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Plasma cell dyscrasias Multiple Myeloma (MM) The peak incidence is 60 — 70 years old Uncontrolled increased plasma cells production leads toabnormal production of paraproteins Paraproteins are most commonly lg G Clinical features: Hypercalcemia: due to osteoclastic activation Renal impairment: due to renal deposition of immunoglobulins and Bence-Johns protein Anemia: plasma cells replace the normal HCS Bone disease: the most common presentationo Due to an osteoclastic activating factoro Cause lytic lesion on skeletal survey Two of the following 3 are diagnostic: Bone marrow aspiration > 10% plasma cells Paraproteins in plasma and/ or urine (protein electrophoresis) Lytic lesions on skeletal survey Table 17: Diagnostic criteria for multiple myeloma In MM, plasma cells produce dysfunctional antibodies leaving the patient susceptible to infections Renal failure and infection are the most common cause of death in MM bence-Johns proteinuria is detected by immunoelectrophoresis, not routine urinalysis hyperuricemia and normal alkaline phosphatase are expected in MM A high level of light chains in the plasma may lead to hyperviscosity syndrome page 1288 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatme If asymptomatic, no Treatment supportive therapy: high fluid intake, analgesia, allopurinol, protein plasmapheresis for Hyperviscosity Specific treatment: Thalidomide + melphalan + prednisolone: for older patients o Chemotherapy followed by HSCT: improves the quality of life but does not cure MM Bisphosphonates: decrease bone pain and prevent bone fracture Monoclonal qammopathy of unknown significance (MGUS) lg G or lg A spikes in serum protein electrophoresis A small number of plasma cells are present in bone marrow biopsy 1% transform to Multiple Myeloma (The more the number of immunoglobulins in the spike, the more the risk of transformation to Multiple Myeloma) No need for treatment Waldenström macroglobulinemia Overproduction of lg M from malignant B-cells leading to Hyperviscosity No bone lesions Associated with cold agglutinin hemolytic anemia and features of hyperviscosity Treatment: Plasmapheresis to remove the lg M and decrease Hyperviscosity Rituximab, prednisolone, and cyclophosphamide reduce lg M production from abnormal B cells. Page 1289 | INTERNAL1-17AFEEF-MERGED-1.pdf |
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Rheumatology CHAPTER 8 AM JAD K. ALAFEEF Phone number: +962798843824 E-mail: Afeeef. 2005@gmail. com Page 1291 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Introduction to Rheumatology Analysis of arthritis Arthritis can be analyzed as the following Acute vs. chronic Inflammatory vs. non-inflammatory Monoarticular, oligoarticular, or polyarticular Inflammatory arthritis: Hotness, redness, tenderness, pain, and swelling Morning stiffness > 60 minutes Associated with fatigue, fever, and malaise (consfitutionalsymptoms) High synovial fluid leukocyte count (> 2000 u/l)Neutrophils in acute inflammation and monocytes inchronic inflammation. Labs: High ESR, CRP, and anemia of chronic disease Non-inflammatory arthritis: Not hot, tender, or red (bony enlargement and jointeffusion may present in OA) Moming stiffness < 30 minutes No constitutional symptoms Synovial fluid leukocyte count (200 2000 u/l)Monocytes are predominant Normal CRP and ESR Classification according to number of joints involved: Monoarthritis: arthritis involving one joint Oligoarthritis: arthritis involving 2 4 joints Polyarthritis: arthritis involving 5 joints Table 18: Classifications of arthritis Normal Non-inflammatory Inflammatory Septic Leucocytes < 200 200-2000 un > 2000 un > 50000 PMN cells% < 25 < 25 > 50 > 75 Table J 19: Joint aspiration rule in different types of arthritis Page 1292 | INTERNAL1-17AFEEF-MERGED-1.pdf |
C-reactive protein (CRP): It is an acute-phase reactant synthesized by the liver in response to inflammation; it adheres to the bacteria, activates the complement system, and promotes phagocytosis. CRP rapidly responds to inflammation, rises, and falls more quickly than ESR. Level > 0. 8 mg/dl indicates inflammatory condition Level < 0. 8 mg/dl is indeterminate Test ANA Anti-CCP Anti-Sm Anti-ds DNA Anti-UI-RNP ASMA Anti-La/SSB Anti-Ro/SSA Anti-scl-70 Anti-Histone c-ANCA p-ANCA Anti-Jo-1J 20: The acute phase reactant; CRP Autoantibody tests Associated diseases Directed against the nuclear antigen SLE, SSc, Sjögren's syndrome, MCTD Titer does not correlate with the disease activity Rheumatoid factor (RA), directed against the FC portion of lg G Not specific, present in different rheumatologic diseases Anti-cycfic citrullinated peptide Rheumatoid arthritis (most specific) Most specific for SLE (does not correlate to disease activity) SLE; correlate to disease activity, especially in kidney disease MCTD Autoimmune hepatitis Neonatal SLE, Sjögren's syndrome, SSc, RA Subacute cutaneous SLE, Sjögren's, neonatal heart block, SSC, RA Diffuse cutaneous systemic sclerosis Drug-induced SLE Granulomatosis with polyangiitis Not specific Polymyositis Table J 2 J: autoantibodies and associated disorders Page 1293 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Types of hypersensitivity Type Type I Type Il Type Ill Type IV Type VDescription and examples Anaphylaxis, immediate type An antigen reacts with lg E bound to mast cells Anaphylaxis, Atopy, Asthma Cytotoxic type lg G or lg M binds to an antigen on the cell surface AIHA, ITP, Rheumatic fever Immune complex disease Free antigen and antibody SLE, Post-streptococcal GN, EAA Delayed type T-cell-mediated Graft versus host disease (GVHD), chronic EAA, MS, CBS New type Antibodies that recognize and bind to the cell surface receptors, this either stimulating or blocking them Grave's disease, Myasthenia gravis Table 122: Types of hypersensitivity HLA associated diseases HLA type HLA-B27Associated diseases Ankylosing spondylitis Reactive arthritis Enteropathic arthritis HLA-DR4 and DRBI HLA-DR3 Sjögren's syndrome SLE Table 123: different HI-A types and the associated disorders Page 1294 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Raynaud's disease It is a condition characterized by decreased blood flow to the fingers It is more common in female The exact cause is unknown, but several factors are suggested Factors leading to Raynaud's disease: The sensitivity of the small arteries and arterioles to cold (mostly hands) Increased sympathetic tone Psychological instability Presence of cold agglutinins in the blood which causes agglutination of RBCs on exposure to the low temperature Diagnosis: The attack consists of three consecutive phases o Pallor (due to digital arteriolar spams) o Cyanosis (due to dilatation of the capillaries, which are filled with deoxygenated blood) o Redness (present after the flow of oxygenated blood as the attack passes off) The attacks are precipitated by coldness or emotional excitements and relieved by warmth The disease is bilateral and symmetrical Radial and Ulnar pulses are preserved No major gangrene (only minute patches of ulceration or gangrene may present)Grades of Raynaud's disease: Grade l: presents only with Raynaud's phenomena Grade Il: presents with mild trophic changes in the tip of fingers and nails Grade Ill: the presence of gangrene on the tip of fingers Treatment: Conservative measures are tried early (avoid cold, weargloves, Vasodilators as calcium channel blockers)In severe cases, cervicodorsal sympathectomy Page 1295 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Raynaud's Phenomenon: color changes similar to those of Raynaud's disease mayaccompany a large group of organic diseases such as: Thoracic outlet syndrome Certain occupations (Typist, pianist, use of vibrating tools)Collagen disease (Rheumatoid arthritis, SLE, or scleroderma) Vascular disorders (Atherosclerosis, Buerger's diseases)Drugs (Ergot-containing drugs) Treatment: treat the cause Table 124: Raynaud's Phenomenon Erythema nodosum It is an inflammation of subcutaneous fat cells, resulting in tender nodules usually seen in the body's shins and extensor surfaces. Patients with erythema nodosum may have a false-positive result for venereal disease (as in SLE) Clinical features: Flu-like symptoms are the first symptoms Typically, tender, erythematous, nodular lesions Joint pain and inflammation may present for a few weeks Usually, it heals without scarring within 2 weeks and may leave a residual bruised appearance Ulcerative forms: seen in Crohn's disease Causes: (NODOSUM) No cause (idiopathic) Others: Pregnancy, Infection: (Streptococci, TB, Brucellosis) Drugs: (penicillin, sulfonamides, NSAl Ds, Sulfa drugs) Oral contraceptives Steroids Ulcerative co(ltis/ Crohn's disease and other Systemic diseases (sarcoidosis, Behcet's) Malignancy/lymphoma Treatment: Treatment of the underlying cause Cold compressors Bed rest and NSAl Ds Page 1296 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Stevens-Johnson syndrome (SJS) rrvcocutaneocs disease that is often caused by a dug-induced immunologic reaction Mvcosd involvement present in > of SJS tt genero Ry affects adults it is Assodated with first time to Drugs des. peria1En, steroids. NSAl Ds. cephalosporines, C%icd features: Mucosal erosions with erythematous macules Nikobky sign: separation of the superficial skin layer with sight Rubbing and epidermal detachment Erosions and hemorrhagic lesions in the mucous membranes (eyes. rnouthe and genitalia) Diagnosis: Mainly cfinical diagnosis with the history of the cause Biopsy is the most accurate test Complications: (same as Burn complications) Bectrolyte disturbance Secondary infection Treatmerfr. Stop the offending agent Cover the skin and manage fluid and electrolytes Steroids. Cyclosporine, and IVIG, may have a rule in treatment Stevens-Johnson syndrome (SJS) TBSA% involved Mucosal involvement > 90% Of cases Nikolsky sign Present Toxic Epidermis Necrotysis (TEN) > 90% of cases Present Table 125: Stevens-Johnson vs. Toxic Epidermö Necrotyss Page 1297 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Rheumatoid arthritis (RA) RA is a chronic symmetrical polyarthritis of unknown causealso characterized by extra-articular features. Female: male ratio is 3: 1 Risk factors: Genetic factors account for the majority of diseasesusceptibility within the population, and it is associated with HLA-DRBI Environmental factors may play a role: o Smoking: conveys up to a fivefold increase in RA risko Occupational exposure to sifica, asbestos Autoantibodies: Anti-CCP (most specific 95% and 70% sensitivity) RF (70% sensitive), (can be positive in the normal population Autoantibodies are neither necessary nor sufficient for thediagnosis of RA Diagnostic criteria: Feature One large joint Two to ten large joints One — three small joints Four— ten small joints More than ten small joints Negative RF and Anti-CCP (below UNL) Low positive RF and Anti-CCP (< 3 times UNL) High positive RF and Anti-CCP (> 3-time UNL) Normal ESR and CRP Abnormal ESR and CRP Duration of symptoms < 6 weeks Duration of symptoms 6 weeks Points 2 3 5 2 3 A score of 6/10 is needed for the diagnosis Table J 26: The diagnostic criteria for RA Page 1298 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Typical features: RA con present as acute onset with marked systemic features or as chronic relapsing-remitting General symptoms (fever, fatigue, malaise) Arthritis: o Deforming, bilateral, and symmetrical o Inflammatory (Swollen, painful, hot joints in hands and feet) o Gradually gets worse with larger joints becoming involved o Distal interphalangeal joints are rarely affected Moming stiffness > 60 minutes Rheumatoid nodules (most often over bony prominences) Late features (joint deformities): o Swan neck deformity o Boutonniére deformities o Z deformity of the thumb Figure 43: Hand Joints deformities in Rheumatoid Arthritis (J) Normal (2) Swan-neck (3) Boutonniere (4) Mallet deformity Synovitis of the upper cervical spine leading to atlantoaxial subluxation Baker's cyst: extension of inflamed synovium into poplitealspace Rupture of flexor or extensor tendons may occur as a complication Page 1299 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Extra-articular manifestations: Systemic: (Fever, fatigue, weight loss) Musculoskeletal system: (Muscle wasting, Tenosynovitis, Bursitis, Osteoporosis) Skin: o Rheumatoid nodules: usually on extensor surfaceso Pyoderma gangreonosum: painful lesion on lowerlimbs o Rheumatoid vasculitis: purpura, petechiae, splinterhemomhage, livedo reticularis, and digital infarctionmay occur Ocular: o Keratoconjunctivitis sicca (the most common eye manifestation in RA, SLE, and Sjogren's syndrome) o Episcleritis, Scleritis, Uveitis, Keratitis (in more severe Pulmonary: o Pleuritis (the most common pulmonary manifestation) o Exudative pleural effusion o Rheumatoid nodules (peripheral, < 1 cm in diameter) o Pulmonary fibrosis (usually lower lobe fibrosis) Cardiac: o RA is an independent risk factor for CAD and heart failure o Pericarditis (common but often asymptomatic) o Myocarditis, Endocarditis, and rheumatoid nodules in the heart may occur Hematological: (Anemia, Eosinophilia, Thrombocytosis) Lymphatic: (Splenomegaly, Felty's syndrome) Vasculitis: (Mononeuritis multiplex, Visceral Vasculitis) Neurological: (Cervical cord compression, Peripheral neuropathy, Mononeuritis multiplex) Renal: mesangioproliferative Glomerulonephritis, Amyloidosis) page13Ø | INTERNAL1-17AFEEF-MERGED-1.pdf |
The most common cause of death in RA is CAD Feltys syndrome: RA + splenomegaly + neutropenia + leg ulcers Absolute neutrophil count < 2. 0*109/L Fever, anemia, thrombocytopenia, and vasculitis may present It predisposes to recurrent bacterial infection May require the use of granulocyte colony-stimulating factors Caplan's syndrome: RA + pneumoconiosis + lung nodules Poor prognostic factors for RA: Functional limitations Extraarticular disease Positive RF and Anti-CCP Radiographic bony erosions Treatment: Physiotherapy and appropriate exercise (protect joints from damage) Stop smoking (smoking is a risk factor for RA, it decreases the response to DMARDs it exacerbates the Rheumatic lung disease) Analgesia (NSAl Ds): o NSAl Ds are the first-line treatment o Not used as monotherapy o Do not change the destructive course of RA Glucocorticoids: o Can be used orally or intra-articular o Used until the slower acting DMARDs achieve the full effect o The lowest dose and the shortest period are indicated due to side effects Disease-modifying Anti-Rheumatic drugs (DMARDs)o non-biologic DMARDs: Methotrexate is the most widely used one Leflunomide: the first choice if methotrexate side effects or intolerance present Others (sulfasalazine, hydroxychloroquine)o Biologic DMARDs: TNF-alpha inhibitors (e. g., etanercept) Tocilizumab Surgery Rituximab (anti-CD20 monoclonal antibody) Page 1301 | INTERNAL1-17AFEEF-MERGED-1.pdf |
DMARD's Methotrexate TNF-inhibitors Hydroxychloroquine Sulfasalaine Rituximab Prednisone Side effects Liver toxicity Bone marrow suppression, Pulmonary toxicity Reactivation of TB, Infection Retinal toxicity Bone marrow toxicity, Hemolysis in G6PD deficiency, Rash Infection Bipolar disorder Table J 27: DMARDs and their side effects Systemic lupus erythematosus (SLE) SLE is an autoimmune disorder with several autoantibodes Associated with HLA B8, DR2, DR3 The females are more affected than males (F: M ratio is 9:1) Several Autoantibodies associated with this condition Clinical features: General symptoms (fever, fatigue, malaise) Arthritis with early morning stiffness and tenosynovitis Serositis Raynaud's phenomenon Skin manifestations: o Malar butterfly rash o Discoid lupus rash o Photosensitive rash o Painless oral ulcers o Lupus panniculitis (painful induration with overtying erythema) Renal: (Typically proliferative glomerulonephritis-nephritic) Cardio: o Pericarditis (most common cardiologic manifestations in SLE) o Libman-sacks Endocarditis (sterile vegetation) Respiratory: (Pleuritis, Pleural effusion, Pulmonary fibrosis, Alveolitis) Neurologic: (Carpel tunnel syndrome, Chorea, Lymphocytic meningitis) page 1302 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Hematological: (Neutropenia, Lymphoperia, Thrombocytopenia, Anemia) GI: orol ulcer, mesenteric vascufitis (risk of bowel infarction) The Most common presentation is: arthralgia with arthritis and Raynaud's phenomena Anibodies ANA Anti-sm Anti-Ds DNA Anti-histone anti-UI RNP Anti-Ro (SSA) Anti-La (SSB) APS antibodies Characteristics Most sensitive (99%) 20% sensitive, not specific Most specific (>99%), sensitivity 30% Specificity (99%), sensitivity 70%, indicates activity Specific for drug-induced SLE (80 90%) Associated with MCTD Associated with neonatal SLE Usually associated wifh anti-Ro They rnay present in SLE patients Table 128: antibodies associated with SLE Signs of active SLE: High ESR and Anti-ds DNA Low CRP, C, and C4 CRP is not elevated in SLE unless there is serositis or synovitis present. Treafmenf. For mild disease (skin and joint involvement): Analgesia (NSAl Ds) Hydroxychloroquine Prednisolone (short course) For severe disease (heart, renal, or cerebral involvement): I. V methylprednisolone combined with I. Vcyclophosphamide Maintenance therapy: Azafhioprine, Mefhotrexate Page 1303 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Drug-induced SLE: The symptoms are limited to arthritis, fever, and serosifis Anti-Histon antibody is the most appropriate test, but donot order it in a patient with renal involvement of SLE. The most common drugs that can cause drug-induced lupus: Procainamide (the most common offender) Hydralazine (the second most common offender) Other agents: Isoniaid, Tumor necrosis factor (TNF) alphainhibitors, Minocycline, and Quinidine) Discoid lupus erythematosus (DLE): DLE is a benign, autoimmune disorder generally seen in younger females. It can transmit into SLE in < 5% of cases. It is characterized by erythematous, raised rash, sometimes scaly, and photosensitive, which is more common on the face, neck, ears, and scalp. The main treatment is achieved by avoiding sun exposure, topical steroid cream, and hydroxychloroquine (second line) Page 1304 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Antiphospholipid syndrome (APS) Antiphospholipid antibodies (including lupus anticoagulant and Anticardiolipin antibodies) interact with the coagulation cascade Elevated PTT, normal PT. and increased risk of thromboembolism (venous or arterial) and abortions Classical features: Venous thrombosis (DVT, PE, Livedo reticularis, etc. ) Arterial thrombosis (Ml, stroke, gangrenes, etc. ) Neurological involvement (epilepsy, migraine, chorea) Osteoarticular involvement (arthralgia, arthritis) Obstetric conditions (eclampsia, abortion, premature birth) Hematologic involvement (thrombocytopenia, AIHA) Diagnosis: Mixing study (patient plasma mixed with normal plasma; if PTT is still elevated, APS is likely. Nevertheless, if PTT is corrected, clotting factor deficiency is likely) Best: (Russell viper venom test): testing for Antiphospholipid antibodies ANA usually negative Note: Anticardiofipin antibodies are also present in syphilis, so they will give a false-positive result for APS Treatment: For primary thromboprophylaxis: o Low dose aspirin Arterial or initial venous thrombosis: o Lifelong warfarin with an INR target of 2—3 For recurrent venous thrombosis while on warfarin: o Add aspirin and increase the INR target to 3—4 Steroids and immune suppressive drugs can be used Page 1305 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Systemic sclerosis (SS) It is a generalized disorder of connective tissue of unknowncause Systemic sclerosis is also known as scleroderma fibrosis of skin, blood vessels, and viscera More common in female 4:1 Clinical features: Skin changes: o Non-pitting edema o Shiny skin with atrophy and ulceration of finger-tip o Limbs, face, and trunk may be affected Visceral involvement: o GERD (esophageal involvement) o Malabsorption (small bowel involvement) o Lower lobe lung fibrosis o Cardiomyopathy o Real failure and malignant HTN Musculoskeletal involvement: o Raynaud's phenomena o Arthralgia and arthritis o Muscle weakness Classifications: Diffuse cutaneous scleroderma 20%: o Rapid development of symmetrical skin thickening of proximal and distal extremities, face, and trunk o The patient has a greater risk of kidney and visceral involvement earlier. Limited cutaneous scleroderma (CREST syndrome) 80%: o Symmetric skin thickening is limited to the face and distal extremities. o Less frequent involvement of internal organs o After a long time, the patient may have pulmonary HTN and biliary cirrhosis o It was called CREST syndrome: (Calcinosis, Raynaud's phenomena, Esophageal dysmotility, Sclerodactyly, Telangiectasia) Locafized scleroderma: o Limited to skin, subcutaneous tissue, and muscles o Morphea: single or multiple plaques of skin induration o Linear type: sclerotic lesion appears as streaks or band Page 1306 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diagnosis: ANA 90% positive ESR is usually normal RF Positive in 30% Anti-centromere antibody (ACA) associated with limited type Anti-topoisomerase (Anti-Scl-70) — associated with the diffuse type (most specific) Treatment No definite cure for this condition Treatment of complications Steroids may relieve symptoms Nifedipine: for Raynaud's phenomena ACE inhibitors: for HTN crisis in renal involvement even if creatinine is elevated. PPI: for GERD and esophageal dysmotility Treatment of pulmonary HTN Cyclophosphamide: for pulmonary fibrosis (improves dyspnea and PFTs) Sjögren's syndrome An autoimmune disorder of unknown cause Antibodies against lacrimal and salivary glands 90% affect women Pathogenesis: Impairment of exocrine glands The most dangerous complication of Sjögren's syndrome is lymphoma Symptoms: Dry mouth, Dysphagia, Parotid enlargement 30%Dry eyes (keratoconjunctivitis sicca)Less common: (vasculitis, Renal tubular acidosis, chronic interstitial nephritis, Pancreatitis)Diagnosis: Autoantibodies (RF, ANA, Anti-Ro, Anti-La)Schirmer's test: filter paper to measure tear formation Lip or parotid gland biopsy (the most accurate test)Treatment: Artificial Tears Artificial saliva Pilocarpine may stimulate saliva production Pancreatic enzyme replacement Page 1307 | INTERNAL1-17AFEEF-MERGED-1.pdf |
SJögen's syn&ome is associated with: SLE Primary bifiary cirrhosis Potymyositis Hashimoto thyroiditis Mixed connective tissue disease (MCTD) It is a condition of overlapping clinical features Presence of at least two of the following (SLE, Scleroderrna, fibromyositis, and rheumatoid arthritis) Diagnosis: Anti-UI-RNP (anti-UI-Riboneucleoprotein) (highly sensitive) Treatment: According to predominant symptoms Spondyloarthropathies They are also called seronegative arthrifis (negative RA) The gene most strongly associated with seronegative spondyloarthropathies is HLA B27 Usually involves men under the age of 40 years Tis got-JP includes: Ankylosing spondyfifis Reactive arthritis (Reiter's syndrome) Psoriatic arthritis Enteropathic arthritis (associated with IBD) General manresfations: Inflammation of the axial skeleton, tendons, and enthesis They generally involve the spine and large joints Usually asymmetrical ofigoarthritis Lower fimbs are affected more than upper limbs Negative rheumatoid factor (RF) Steroids are not a good treatment for seronegafive Spondyioarthropathies Reactive arthritis and psoriatic arthritis may be more severe in patients with HIV infection Page | INTERNAL1-17AFEEF-MERGED-1.pdf |
Ankylosing spondylitis chronic inflammation affects the sacroiliac joint and spine It affects the Sl joint and progress cranially without skipping Associated with progressive stiffening and fusion of aial skeleton Male to female ratio is 3: I Associated with HLA B27 (70%) Figure 44: Anatomy of the sacroiliac joint (J) Jumbosacral joint, (2) sacroiliac joint, (3) Symphysis pubis Symptoms: Low Back pain is worse at rest (early morning and inactivity) Decreased chest expansion Restriction of lumbar spine movement in all directions Reduced lateral flexion Reduced forward flexion — Schöber's test-a line is drawn 10 cm above and 5 cm below the dimples of Venus. The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible Eflraarticular manifestations: Skin: psoriasis may coexist Ocular: Anterior Uveitis (usually unilateral and recurrent) Gl: asymptomatic intestinal ulcerations GU: Urethritis (rare) Cardiovascular: Aortic insufficiency, Aortitis, CAD, AV block Respiratory: restrictive lung disease (typically upper lobe) Heel pain (due to plantar fasciitis)Enthesis (Achilles tendonitis) Page 1309 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diagnosis: ESR — high, RF-absent Lumber X-Ray: o Maybe normal early in the disease o Sacroifiitis: subchondral erosions and sclerosis. o Square vertebrae with tramline appearance o Bamboo spine: a late finding with a fusion of vertebrae Lumbar MRI (most accurate) Treatment: NSAl Ds Regular exercise Anti-TNF drugs (etanercept, adalimumab, or infiximab) Reactive arthritis (Reiter's syndrome) Reactive arthritis is caused when a joint reacts to an infection elsewhere in the body. May develop days or weeks after Gl or GU infection with Salmonella, Shigella, Campylobacter, Chlamydia, or Ureaplasma urealyticum Male to female ratio is 20:1 Associated with HLD B27 (70%) Symptoms: Conjunctivitis 50% Urethritis Arthritis (Knee and ankle is the commonest sites) Keratoderma blennorrhagica 10% (psoriasiform rash on sole and feet) Circinate balanitis (psoriasiform rash on the penis) Systemic features: Fever, weight loss, Carditis, Aortic regurgitation Diagnosis: Only clinical diagnosis Treatment: NSAl Ds Tetracycline for 3 months (if urethritis present) Sulfasalazine, if no response to NSAID and tetracycline page 1310 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Psoriatic arthritis patients with psoriasis or a family history of psoriasis sometimes there will be no history of psoriasis or a small spot of psoriasis present on the scalp, gluteal cleft, or umbilicus symptoms: Arthritis Usually, in distal interphalangeal joints May precede rash by 10 years Extra-articular symptoms: o Psoriasis of the skin (not always present, or maybe small and un-noticeable during examination) o Nail pitting o Sausage digits o Eyes: Iritis Diagnosis: RA negative ESR: mild elevation X-ray of DIP joints involved shows pencil in a cup deformity Treatment: NSAl Ds Methotrexate (if severe disease not responsive to NSAIDs) Anti-TNF drugs (etanercept, adalimumab, or infliximab) Page 1311 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Osteoarthritis (OA) Chronic slowly progressive erosive damage of the joint surfaces, leading to loss of articular cartilage and pain minimal or absence of inflammation OA is the most common form of arthritis OA is the most common cause of disability in patients over age 65 years The most common affected joints are (the first MCP joint, interphalangeal joints, knee joint, and hip joint) In hands, distal interphalangeal joints (DIP) are more affected than proximal (PIP) Risk factors: Advanced age Female sex Obesity Joint injury and joint overuse Family history Patterns: Nodal OA: o DIP joints (Heberden's nodes) o PIP joints (Bouchards nodes) Non-Noda! OA: Less prominent in DIP joints Erosive OA: o Destructive Subchondral erosion of PIP and DIP joints o Radiographic erosions are seen OA of the knee: Associated with obesity and more common in women OA may follow infectious arthritis, avascular necrosis, or inflammatory arthritis (such as gout, RA, or Pseudogout) Pathogenesis: Cartilage loss Synovial membrane infiltrated with mononuclear cells Osteophytes formation Subchondral bone thickening and cyst formation Page 1312 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Clinical features: Joint pain: Worse in the evening, relieved by rest o Progressive with time o Associated with morning stiffness (less than 1/2 hour) Disability: Muscle wasting o Limited range of motion Joint swelling (effusion), crepitus, and deformity The chronic effusion may lead to the formation of a Baker cyst Diagnosis: X-Ray (narrow joint space, osteophytes formation, cyst formation, and dense subchondral bone) CBC, ANA, RF, and ESR are normal Treatment: Weight loss, moderate exercise, walking stick Analgesia: o Paracetamol is the first line (S 3 g/day) o NSAl Ds second line (unless contraindicated) o NSAl Ds and paracetamol combination may be used o Tramadol: used if paracetamol and NSAl Ds are ineffective or contraindicated Intraarticular steroid injection: o Methylprednisolone or Triamcinolone o Will be effective within days to weeks o Can increase the risk of joint infection, subcutaneous atrophy, and local skin pigmentation o The use is limited to 3 monthly Intraarticular Hyaluronic acid injection: o Analgesic effect for knee OA Joint replacement surgery (Total arthroplasty) Page 1313 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Neuropathic joint (Charcot joint) It is progressive destructive arthritis associated with loss ofpain sensation, proprioception, or both. Associated disorders: Diabetes mellitus (the most common) Amyloidosis Tabes dorsalis (neurosyphilis affecting the spinal cord andthe peripheral nerves) Meningomyelocele Syringomyelia (a cyst or cavity in the spinal cord) Pathogenesis: The joint is subjected to repeated traumas due to the loss ofprotective mechanisms This will lead to progressive cartilage and bone damage The pathologic changes are similar to those found in severe osteoarthritis Clinical features: Usually starts at a single joint and then becomes apparent atother joints Boney overgrowth and progressive enlargement of the affected joints Joint instability, subluxation, and crepitus Diagnosis: Clinical features of the disease and the associated disorders Typical radiologic findings: o Changes of OA with joint space narrowing (initial) o Arthrocentesis: Xanthochromic or bloody non-inflammatory findings Treatment: Cast for 2 — 3 months Treat the associated disorders (e. g., DM) Surgical management (for selected cases) Page 1314 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Infective arthritis Any kind of joint infection, also known as septic arthritis Most common site: knee and wrist joint In I. V drug users: spine and sacroiliac joint is more common Cause: The most common organism is Staphylococcus aureus (40%) Others: (streptococci, E. coli, Pseudomonas) The most common cause of septic arthritis in a recently placed artificial joint is Staphylococcus epidermidis. The risk of infection is directly proportional to the degree of joint damage. Osteoarthritis has a slightly increased risk of septic arthritis due to slight damage Rheumatoid arthritis has the highest risk of septic arthritis due to severe joint damage Source of infection: Hematologic spread (septic skin, endocarditis, UTI) Direct entry to joint (after trauma — penetrating wound) Clinical features: Sudden onset Joint pain aggravated by movement Hotness, redness, and tenderness of affected joint Fever, fatigue, malaise Diagnosis: CBC: leukocytosis Blood culture positive in 50% Joint aspiration with cytology and culture (best) Treatment: Analgesia, Antibiotics, and joint drainage may be needed If prosthetic joint arthritis, remove the joint, treat with antibiotics, and replace the joint after 6— 8 weeks. Antibiotics treatment in septic arthritis: o Flucloxacillin for 4 to 6 weekso If penicillin-allergic patients: use cfindamycin o If gonococcal arthritis: use cefotaxime or ceftriaxone o If the infection is not responding to antibiotics: perform repeated percutaneous aspiration Page 1315 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Intravenous antibiotics are used for I-week until the swelfing subsides, and blood CUItures become negative. This is followed by a I-month course of oral antibiotics. Gonococcal arthritis: It is one of the common causes of septic arthritis in a previously sexually active patient Blood cultures are 40% positive; culture may be positive from genitalia, throat, and rectum The difference in presentation from septic arthritis; Gonococcal arthritis will have polyarticular involvement, tenosynovitis, and petechial rash. Treatment is achieved by ceftriaxone lg IV for 2 days, then ciprofloxacin 500mg PO BID for 7 days Page 1316 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Crystal-induced arthropathies Gout (podagra) Gout is a disease of uric acid metabolism which leads to the accumulation of sodium Urate crystals in (joints, soft tissues, and urinary tract stones) Causes: Overproduction of uric acid: Idiopathic o Increased cell turnover (cancer, chemotherapy) o Enzyme deficiency (Lesch-Nyhan syndrome, glucagon storage disease) Under-secretion of uric acid: o Renal insufficiency o Ketoacidosis or lactic acidosis o Drugs: (thiazide, aspirin) Clinical features: Joint involvement (most common site: 1 st Metatarso-phalangeal joint) Hotness, redness, and tenderness associated with severe pain Tophi: characteristic skin lesion in gout Urate stones and renal colic Precipitants of Gout include: Diuretics (e. g., thiazide) Alcohol Diet rich in meat and seafood Recent surgery or trauma Diagnosis: Synovial fluid aspiration: o Negative birefringent needle shape Urate crystals o High leukocyte count (predominantly neutrophils) Serum uric acid: o Elevated in 95% of caseso The normal uric acid level does not exclude Gout Joint X-Ray: Shows punched-out erosions Page 1317 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatment: Lifestyle modifications: o Adequate hydration o Linit alcohol intake (especially in the acute o Weight loss (for obese patients) o Proper diet (decrease high purine (ietswch and seafood) o High vitarin C intake can reduce the serum uicoöd Between attacks: o Allopurinol (the first line) o Febuxostat (the second line) Additional measures: o Losartan is the drug of choice for HTN in the pteserceof gout o Always stop thiazide diuretic In acute presentation: o NSAl Ds (better than colchicine) — the first fine o Colchicine (if NSAl Ds or steroids cannot be used) o Corticosteroids (if no NSAl Ds are ineffective or contraindicated) o If the patient is taking allopurinol, do not stop it. The indications for uric acid lowering agents: 2 or more attacks in the past year The presence of tophi Renal disease Uric acid renal stones Patients on diuretics Instructions about Allopurinol according to recent guidelines: In the case of acute gouty arthritis, if the patient is already on allopurinol, do not stop it. However, if the patient is not on allopurinol, start it 2 weeks after the acute attack. Colchicine cover should be considered when starting allopurinol ma be continued for 6 months page 1318 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Pseudogout Also known as calcium pyruvate deposition disease Unknown cause but may be associated with hemochromatosis, hyperparathyroidism, hypothyroidism, and true gout. Clinical features: Acute synovitis (hotness, redness, tenderness, pain, swelling) Chronic arthritis (pain + morning stiffness + functional impairment) The knee joint is the most common site DIP and PIP are not affected Diagnosis: Serum calcium and uric acid is normal Synovial fluid aspiration: Positive birefringent cuboidal calcium pyrophosphate crystals Bloodstained or turbid aspirated fluid Joint X-Ray shows Chondrocalcinosis Treatment: NSAIDs (best initial treatment) Intraarticular steroid (if NSAl Ds resistant) Joint aspiration to relieve swelling and pain Colchicine for prophylaxis Figure 45: Joint X-Ray shows Chondrocalcinosis Page 1319 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Vasculitis It is an inflammation of the vessel wall All types of vasculitides can cause: (fever, fatigue, weight loss, arthralgia, and myalgia) Classification: Large vessel: o Giant cell arteritis (Temporal arteritis) o Takayasu's arteritis Medium vessels: o Polyarteritis nodosa (PAN) o Kawasaki's arteritis Small vessels: o Microscopic polyangütis Granulomatosis with polyangütis (Wegener's) o Churg-Strauss syndrome o Henoch Schönlein purpura o Essential cryoglobulinemia Polyarteritis nodosa (PAN) Polyarteritis nodosa (PAN) Vasculitis affecting small and mediumsized arteries More in males than females Chronic hepatitis B and C are associated with PAN The most common cause of death is Myocardial infarction. Clinical features: Fever, malaise, arthralgia, weight loss, hypertension Hematuria, renal failure (need biopsy for diagnosis) Neurological: o The peroneal nerve is the most commonly involved leading to a drop foot o Mononeuritis multiplex o Sensorimotor polyneuropathy Gl: Postprandial angina, Gl bleeding Skin: o Lower extremity ulcers (most common skin symptoms) o Livedo reticularis, purpura, nodules. No lung involvement in PAN Test all patients with PAN for hepatitis B and C Page 1320 | INTERNAL1-17AFEEF-MERGED-1.pdf |
e in of patients Hepa the affected organ shows fibrinoid necrosis of the v" wd (the most occ.-rate) rrdtiple aneuysrr3, bleeding Anfrdd in Hepatifis B related type stead with catt'iopcine or cyclophosphanide Polymyalgia Rheumatica (PMR) occt-r in those over 50 years of age Stror@y with giant cell arteritis $icd featl. res Systemic features: fever, malaise, weight loss Sudden orset of severe pain and stiffness in shoulder, neck, and pe Mc grdle muscles SR: markedly elevated Noerrocytic anemia CPK is not elevated (no muscle destruction) Temporal artery' biopsy: Giant ce!} arterifis Tredme#. Sterdd (rapid response, even at a low dose) Giant cell arteritis (temporal arteritis) TNs disease seems to be on a spectrum of PMR. *icd features: Severe headache and scalp tenderness Jow daudicafion may be present: progressive jaw pain on rnasticafion May present with sudden painless vision loss (maybepermanent or temporary)Symptoms in other arteries: (decreased arm pulse, aorticregurgitation) Page 1321 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diagnosis: ESR very high CRP: high Temporal artery biopsy (most accurate test): it will be falsenegative after 36 hours of steroid therapy Treatment: High dose steroid (do not wait for biopsy) Normal ESR is less than (Age in years/2) (+ 5 for females) Causes of markedly elevated ESR (> 100 mm/hour) Subacute bacterial endocarditis Tuberculosis Giant cell arteritis, PMR SLE, RA Leukemia and Lymphoma Multiple Myeloma Causes of markedly low ESR (O mm/hour) Afibrinogenemia Agammaglobulinemia Extreme polycythemia (HCT > 65%) Increased plasma viscosity Table 129: causes of markedly elevated or markedly low ESR Behcet's syndrome Vasculitis of unknown cause that involves venules, associated with HLA 35 Clinical features: Oral Ulcers, Genital ulcers, inflammatory arthritis Skin: Erythema nodosum, acne Eye: Anterior uveitis, retinal Vasculitis, iritis Neurological: aseptic meningitis Superior vena cava obstruction may occur (venous involvement) Diagnosis: Positive pathergy test is suggestive (puncture site following needle prick becomes inflamed with small pustule forming) Treatment: Oral ulcer: topical steroid Erythema nodosum: colchicine Systemic symptoms: steroid or immunosuppressive therapy Page 1322 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Takayasu's arteritis Usually, effect large elastic arteries like the aorta and its branches Usually present with general features of vasculitis followed by asymmetrical limb pulse Diagnosis: ESR: high, Leukocytosis, Aortography, MRA Treatment: Steroid Surgical (bypassing stenosis or aneurismal site) Dermatomyositis An inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions Associated with cancers in 20% of cases (ovarian, lung, Gl, or lymphoma) No facial or ocular muscle involvement Clinical features: Symmetrical proximal muscle weakness Photosensitivity (Malar involvement) Photo distributed poikiloderma: o Shawl sign: erythema of the back and shoulders o V sign: neck and back or the neck and upper chest o Holser sign: along the lateral thigh Hefiotrope rash: edematous and purplish eyelids Mechanic's hand: palmer fishering and hyperkeratosis Gottron's papules: scaly patches at PIP and MCP joints Diagnosis: High CPK Antibodies: ANA positive (60%), Anti-Mi-2 (25%)EMG Muscle biopsy (best)Treatment: Prednisolone, IVIG, Mycophenolate Polymyositis: A variant of Dermatomyositis where skin manifestations are NOT prominent Anti-Jo-l antibodies are more common in Polymyositisthan in dermatom ositis Page 1323 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Fibromyalgia The cause of fibromyalgia is unknown The female to male ratio is 9:1 It may be associated with RA, SLE, or Sjögren's syndrome Fibromyalgia has an unexplained decrease in opioid receptors, so it has a poor response to opioid analgesia Clinical features: Chronic pain: generalized pain or pain at multiple sites (neck, shoulders, back, hip, etc. ) Stiffness, numbness, fatigue, and sleep disorders It is often associated with somatic conditions such as headaches, TMJ, or pelvic pain. Treatment: Aerobic exercise (the best for functional improvement) Cognitive therapy Medications: o Anticonvulsant (Pregabalin) o Dual serotonin-norepinephrine reuptake inhibitor (Duloxetine, Milnacipran) o SSRI and TCA may be used page 1324 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Neurology CHAPTER 9 AM JAD K. ALAFEEF Phone number: +962798843824 E-mail: Afeeef. 2005@gmail. com Page 1325 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Introduction to neurology The central nervous system (CNS) is formed of two main parts: Intracranial part (cerebrum, brain stem, cerebellum)Spinal part (spinal cord, cauda equina) Cerebrum: Formed of two hemispheres connected via corpuscallosum and the upper part of the brain stem It is divided into 4 lobes (frontal, parietal, temporal, andoccipital lobes) Formed of outer gray matter and inner white matter At the base of each cerebral hemisphere, there areseveral groups of nuclei at different levels within thewhite matter; they form the basal ganglia (thalamus,subthalamus, and hypothalamus) Brain stem: Formed of midbrain, pons, and medulla Connected to the cerebrum and cerebellum bypeduncles The motor nuclei of the cranial nerves in the brain stemare arranged as the following: o Cranial nerves Ill, IV: midbrain o Cranial nerves V, VI, Vll: pons o Cranial nerve IX, X, X', Xll: medulla o Cranial nerves It Il, VI": sensory nerves perceived in special areas in the cerebral cortex Cerebellum: Occupies the most posterior cranial fossa Concerned with coordination, voluntary motor activity, and equilibrium Spinal cord: Lies in the spinal canal The lowermost 3 segments spinal cord in S3. 4. 5 are called conus medullaris The above 4 segments, L5,4 and S12. are called Epiconus Formed of outer white matter and inner gray matter The Gray matter has an H shape (2 anterior and 2 posterior horns) Cauda equina: A collection of lumbosacral roots Filfing the spinal canal below the level of Ll Page 1326 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Cranial nerves The cranial nerves are a set of 12 paired nerves that arise directly from the brain They are as following: Nerve CNI CN Ill CNIV CNVI CN Vil CN Vill General information Name: Olfactory nerve (Sensory) Function: smelling, if impaired, no smell and taste Name: Optic nerve (Sensory) Function: The nerve of vision If impaired, visual field defect will esent Name: Oculomotor nerve (Motor) Function: The nerve of eye movement 3rd nerve palsy will result in outward downward deviation of the eye associated with ptosis Name: Trochlear nerve (motor) Function: Innervates single muscle (superior oblique muscie of the eye) Comes from the posterior side of the midbrain The greatest intracranial length It is the smallest nerve, least number of axons Name: Trigeminal nerve (Mixed) Function: face sensation, biting, and mastication It has 3 divisions (Ophthalmic, Maxillary, and Mandibular) Name: Abducent nerve (Motor) Function: Abduction movement of the eyes If impaired, horizontal diplopia, inward deviation (esotropia) Name: Facial nerve (Mixed motor and sensory) Function: Controls the muscles of facial expression and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue If impaired, Bell's palsy will develop (weakness offacial muscles) Name: Vestibulocochlear nerve Function: Transmits sound and equilibrium(balance) information from the inner ear to thebrain Page 1327 | INTERNAL1-17AFEEF-MERGED-1.pdf |
CN CNX CN Xl CNName: Glossopharyngeal nerve (mixed) Function: Provides motor, parasympathetic andsens information to our mouth and throat. Name: Vagus nerve (autonomic) Function: Parasympathetic control of the heart,lungs, and digestive tract. The longest nerve of the autonomic nervous stem in the human bod Name: Accessory nerve (Motor) Function: Supplies the sternocleidomastoid andtrapezius muscles. Name: Hypoglossal nerve (motor) Function: Innervates all the extrinsic and intrinsicmuscles of the tongue Table 130: the cranial nerves 7th nerve palsy (Bell's palsy) Most are idiopathic, but Lyme disease, viral infection,sarcoidosis, and tumors may be a cause Clinical features: Paralysis of the entire side of the face (upper and lower parts) Difficulty closing eyes, absent wrinkles on the same side of the forehead Hyperacusis: loud sound (7 th nerve supplies stapedius muscle which acts like shock disturber) Taste disturbances (7th nerve supply sensation of taste) Diagnosis: No need for special testing (only clinical diagnosis) but EMG and NCS are the most accurate Treatment: 60% recover fully without treatment The best initial therapy is prednisolone Artificial tears to protect the affected eye Physiotherapy Page 1328 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Aphasia ch centers are located on the left side of the brain (90%); they spee include:Wernicke's area (sensory): left temporal area is responsible for understanding; this area forms the speech before sending it to Broca's area Broca's area (motor): left frontal lobe is responsible for the expression Arcuate fasciculus: the connection between Wernicke's and Broca's area Note: The speech center is located on the left side of the brain in right-handed persons and on the right side of the brain in left-handed persons. Types of aphasia: Wernicke's (receptive) aphasia: Lesions result in sentences that make no sense and word substitution, but speech remains fluent Broca's (expressive) aphasia: Speech is non-fluent and labored Conduction aphasia: Speech is fluent, but repetition is poor. Aware of the errors they are making Global aphasia: Large lesion affecting all 3 of the above areas resulting in severe expressive and receptive aphasia Horner's syndrome Classically, presented with Ptosis, Miosis, anhidrosis, and Enophthalmos Cased by interruption of sympathetic nerve supply to theeye Maybe due to an apical (Pancoast) tumor of the lung Page 1329 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Neurological terms to know Upper motor neuron lesion: is an injury to motor tract abovethe anterior horn (or above the nucleus for cranial nerves)A lower motor neuron lesion: is an injury to motor tract belowthe anterior horn (or below the nucleus for cranial nerves)Muscle tone: a spontaneous local tendon stretch reflexo Hypotonia (also known as flaccidity): decreasedmuscle tone (LMNL) o Hypertonia (also known as spasticity): increasedmuscle tone (UMNL) Tendon jerk (deep reflex): induced local axon stretch reflexby tapping the tendon. o Hyporeflexia: weak or decreased deep tendon reflex(LMNL) o Hyperreflexia: exaggerated deep tendon reflex (UMNL) Clonus: rhythmic contractions induced by a sudden sustained stretch of muscle-tendon Babinski reflex: upward deviation of toes when scratching the dole of foot called positive Babinski, it is a feature of UMNL UMNL Hypertonia without wasting Hyperreflexia Clonus may present Planter reflex (Babinski)LMNL Hypotonia with muscle wasting Hyporeflexia No clonus Planter flexion or no response Table 131: UMNL vs. LMNL Deep tendon reflex Nerve root Ankle jerk Sl,2 Knee jerk Biceps and supinator jerk C5,6 Triceps jerk Finger jerk Table 132: types of deep tendon reflexes and their nerve roots Page 1330 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Dyesatma the f speech cfrfficutty is intactof speech articulation, though the famofion o Herrip$egio: paratysis of one side of the body pao*gia: paratysis of both lower Embs, paratysis of all 4 Ernbs Atom. incoadination of voluntary mof« movement in the absence of motor weakness CT-geo: invdun Wy static, irregular, dysrhyfhmic, sudden jaw movement of any parf of the body, including face, trunk, Errbs Thunderclap headache A thunderclap headache is a severe headache that reaches its maximurn intensity within T minute Cnofid atery Vede&ol Features Thunderclap headache, neck rigidity, phofophobia, vomiting, suspected berry aneurysm. Fronta± thunderclap headache, with visual symptorrz {amaurosis fugax, dpbpia, Homers syndrome) thunderclap headache, nausea, vorrifing. and brain sfem findings (vertigo, afcho, dip!opia, tinnitus, dysarthria) Czebd venous Sudden onset headache in a frrorrboés hypercoagu*able patient J33: D. fferent:c; of Thunderclap headache Red Bags for headache: fist worst headache A&upf orset headache Progession change in the paffem of headache symptorrs more than 1 hour Age < 5 or > 50 years New-onset in a pafienf v;th ma Egnancy or coagulopafhy Change in fhe level of consciousness Headache increased by exertion, sexual activity, or rrnneuver Tab'e i 34 The red f Sogs syrnptorrsl of headache Page 1331 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Subarachnoid hemorrhage (SAH) The most common cause of thunderclap headache 85% are caused by ruptured saccular 'berry' aneurysm More common in women than men 40-year-old Berry aneurysm is more frequent with: Polycystic kidney disease Tobacco smoking High alcohol consumption Hyperfipidemia Clinical features: Sudden severe 'thunderclap" headache, usually occipital May present as a new headache during exertion Vomiting is a frequent symptom Irritability, with photophobia Neck rigidity Loss of consciousness Diagnosis: CT scan (maybe negative) CSF examination 'LP': o High opening pressure o High protein o High RBCs count > 10,000 *106 /L o Xanthochromia: yellow discoloration of CSF due to the presence of bilirubin (2 4 hours after onset of headache) Cerebral angiography (Best) Treatment: Control vital signs Nimodipine 30 — 60mg iv (to prevent vasospasm in the acute phase) Endovascular insertion of coils or surgical clipping of the aneurysm (to reduce recurrence) Page 1332 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Cerebral venous thrombosis cavernous sinus thrombosis: presents after dental or sinus bacterial infection Sudden headache, proptosis, periorbital edema, and ophthalmoplegia Treated with early antibiotics and surgical drainage other forms of cerebral venous thrombosis: Thunderclap headache in a patient who is hypercoagulable Signs of increased intracranial pressure The pain increases with Valsalva Focal findings like 6th cranial nerve palsy. Treated with LMWH and warfarin even in those with hemomhagic parenchymal lesions Headache Syndromes Headache is one of the most common neurological symptoms Type of headache Migraines headache Cluster headache Giant cell arteritis Pseudomotor cerebri (benign intracranial HTN) Tension-type headache Characteristics Throbbing in character, Aura, photophobia, and visual disturbances related to menses, associated with nausea and vomiting, may be associated with chocolate, wine, and cheese. Frequent, short-duration, high-intensity headache, associated with a red, tearing eye with rhinorrhea Jaw claudication, visual symptoms associated with visual loss, tenderness at the temporal area with very high ESR Associated with obesity, venous sinus thrombosis, oral contraceptives, and vitamin A toxicity, mimic brain tumor with nausea and vomiting and visual disturbances Papilledema with diplopia from 6th CN palsy. It is the most common type It is a diagnosis of exclusion Table 135: Differential diagnosis of Headache syndromes Page 1333 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Migraines headache More common in females than males In women may be associated with menstruation Migraine can be precipitated by emotional stress, noises,alcohol, caffeine, and oral contraceptive pills Clinical features: Recurrent, severe headache which is usually: (POUND) Pulsatile One day duration Unilateral Nausea and vomiting Disability Patients with more than 3 of the POUND criteria can bediagnosed with migraine without additional testing Migraine with aura is a strong contributor to stroke when combined with DM, HTN, and obesity Acephalic migraine: the presence of migraine aura without headache Basilar migraine: with brainstem aura (vertigo, ataxia, diplopia, tinnitus, dysarthria) Hemiplegic migraine: migraine associated with a degree of motor weakness Status migrainous: migraine attack > 72 hours duration Treatment: Simple analgesia (aspirin, paracetamol)Antiemetic (symptomatic treatment)Triptans (e. g., sumatriptan) 5-HT agonistso Side effect: increased risk of ischemic eventso Contraindicated in both basilar and hemiplegic migraine Prophylaxis: o Beta-Blockers (e. g., Propranolol, Metoprolol, Timolol) o Valproic acido Topiramate Page 1334 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Cluster headache More common in males than females One of the most painful types of headaches Oicd features: sodden unlaterol severe pain around the eye that may awake the patient from sleep tf may be associated with conjunctiva! injection and tecring tt may be associated with miosis and ptosis Tlöng of headache: Occur in cycfical pattems or clusters. o Once or twice a day, each episode lasting 15 rrinutes to 2 hours Clusters last 4-12 weeks At the time of pain: 0 100% 02: the patient will respond within 15 rrinutes in 80% of cases o Subcutaneous Triptans Prophylaxis: Verapamil Tension-type headache The most common type of headache C&icd features: Wd to moderate bilateral squeezing, dull, like pressure in nature and non-throbbing Radafe forward from the occipital region Predpitated by a stressful event Rest. Pain killers (paracetamol, NSAl Ds..-) Antidepressants Trigeminal neuralgia Unknown cause, but maybe due to compression at the fifth cranial nerve root Unilateral lancinating facial pain in the 2nd and 3rd division of trigeminal nerve territories, which may remit and relapse over a year The pain may be precipitated by touching the face, mastication. or even pronouncing certain words. Page 1335 | INTERNAL1-17AFEEF-MERGED-1.pdf |
(tsl Preg±c Én, Gabmenfin. lc*eeofe Sv$cd (bf resot): ('f tte potent cmt of the higen%d nerve Benign intracranial HTN (BIH) Abo as Pseudonotot cerebi. or icfopathic There on increase htrocrcrid without strvcnrol o' offecfed pa%ents cre femde Assæ-iated with obe Sty, venous inos ttyombosis. OCP we,and A toöcity teoöoche woße in the morring, and with Vabdva rynnevve« c*ways present on examinafion) CSF messt Je 2 mrn H. O MRI: smal ventricles W e. t bss Cab«ic anhy&ase inhbitots: Acetazo'arride (first 5ne), (odd the benefit of weight loss) urrbor punctures Ll..rrbopeötooed shunt ('f faded medcal treatment) Post-herpetic neuralgia Stü-*s assodated with pan syndrome after resoh Jtion in (bout 15% of the cases Ence st-ingles can affect the head. t Ns must be dscussed in the headoche but it can occur at any dermatome in the body. Acycioü and farrcjcbü seem to reduce the incidence of pct-herpetic necral*l Tredrr Efi: (Tricyc Ec antidepcessants. Pregabdn, C(Ybcrnazepine. Phenytoin) Page 13" | INTERNAL1-17AFEEF-MERGED-1.pdf |
Acute stroke Acute stroke is a rapid appearance of a neurological deficit of brain function due to the death of brain tissue The strongest risk factor is HTN Other Risk factors are the same as IHD (DM, obesity, dysfipidemia, male sex, etc. ) Causes: tscherric 85% Thrombosis (most common) o Embofism: lodge in small perforating vessels 'lacunar infarction" Bleedlng 15% The source of embolism in CVA: Heart (e. g., AF) DVT (paradoxical embolus through PFO) Carotid stenosis Presentation: Middle cerebral artery stroke: o Weakness and sensory loss on the opposite side o Loss of visual field on the opposite side of the stroke (homonymous hemianopsia) o Aphasia: speech center present on the left side in 90% of cases Anterior cerebral artery stroke: o Cognitive defect o Urine incontinence o Weakness in Leg more than arm Posterior cerebral artery stroke: o Ipsilateral sensory loss of face o Contralateral sensory loss of limbs o Limb ata)öa Page 1337 | INTERNAL1-17AFEEF-MERGED-1.pdf |
If blockage of the blood vessel is reversed while neurons are stillviable (< 24 hours), this condition Is called TIA, but If the blockage Is prolonged (> 24 hours), infarction and permanent damage withresulting permanent symptoms can occur Diagnosis: Clinically, neurological deficit, with signs of upper motor neuron lesion Neurolmaging (CT, MRI): CT can exclude non-stroke lesions; infarction takes up to 48 hours to show in the CT scan Evaluation for the cause: ECG, Hotter monitor, Echocardiogram, carotid doppler Treatment: Ischemic stroke less than 3-4. 5 hours since onset: Thrombolysis (can increase the risk of hemorrhagic transformation) Ischemic stroke more than 3-4,5 hours since onset: Aspirin If recurrent TIA's: Carotid endarterectomy and angioplasty Ischemic stroke in a patient already on aspirin: add dipyridamole or switch to Clopidogrel Hemorrhagic stroke: control vital signs only (surgical drainage will not help outside posterior fossa) Hospital admission for TIA is recommended for all patients with an ABCD2 score of 23. ABCD2 scoring system for TIA Age 60 years point Blood pressure 140/90 1 point Clinical features: Focal weakness with TIA 2 points Speech impairment without weakness 1 point Duration: 60 minutes 2 point 10-59 minutes I point DM present I point Table 136: ABCD2 score for TIA patients Page 1338 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Epilepsy seinre is a drical syn&oræ caused by an obn«rrß e%ecfr€cd dtschorge in the is o tendency fo have a suzre; a "ng E seiz. re is not epßepsy, But an f« investigaf&b The recurrence rate after the frsf seiwre is Types d seizures Focal Anres: (no loss of consciwsness) sens«y: e g.. déiå vu Srnple mot«: e. g., Jacksonian rr Uch Complex: e. g., Automatism Gerøafzed seinre, (associated wifh loss of consciousness) Tonicdonic (grand Absence (petit rnal) Tonic, Clonic, Myodonic, and Afonic types. Focal to generartzed seiwre: (starts as focal then becorrz gengaüzed) Seconday causes of seizures: Metabofic (Hypoglycemia, hypemafrerria, hyponafrerr%, hypocaicerria, hyporragneserria, Urerria) CNS infection encepha%, abscess) Brain turn«s, trauma, hyporia, CVA, hern«rhage Toxic substances (aicohoi, cocaine) CEricd features: Can varies fo the function of the affected area of fhe brain Ocdpital onset: cause visual symptorns (fights, blobs of cow) Temporal area onset: cause Déjö vu, strip involvement: tingfing sensation, burning sensation Motor strip involvement: jerking Page 1339 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Diagnosis: Rule out secondary causes first Cerebral imaging (CT, MRI) Lab tests to rule out secondary causes (CBC, FBS, KFT, LFT, electrolytes, CXR) EEG (if secondary cause excluded) Treatment: Education of family and patient During convulsion: Place the patient in the left lateral position o Do not insert anything in the mouth (tongue bite unpreventable) o Medications Lorazepam, Diazepam o If prolonged, treat as status epilepticus For epilepsy control, Start treatment under the following conditions: After 2 unprovoked attacks o Single attack with focal finding in imaging or EEG o Single attack after severe head trauma AED Sodium valproate Lamotrigine Carbamazepine Levetiracetam Ethosuximide Lamotrigine, levetiracetam, topiramate, valproate, zonisamide Uses First-line in generalized epilepsy First-line in focal seizure A cost-effective option for focal seizure Effective against tonic-clonic seizure Not effective in absent and myoclonic seizure Wells tolerated Few side-effects Safe in pregnancy First-line in absent seizure It may be used in generalized and focal seizures Table 137: Antiepileptic drugs (AEDs) and their indications page 1340 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Status Epilepticus status epilepticus is a seizure not resolving spontaneously or recurrent seizure without recovery of consciousness for > 5 minutes It can be due to a sub-therapeutic level of anti-epileptic drugs in a patient known to have epilepsy or may be precipitated by secondary causes like metabolic infection, tumor, etc. Treatment: ABC management (airway, breathing, circulation, blood glucose check) Correct underlying cause if present Send lab tests (KFT, LFT, electrolytes) Approach to treat status epilepticus: 1st line: Lorazepam/ Diazepam 2nd fine: Phenytoin/ Fosphenytoin 3rd line: Phenobarbital 4th line: ICU transfer, intubation, ventilation with general anesthesia Essential tremor Essential tremor occurs in both rest and intenfion More common in hands, but the head may be affected-It may affect some skiiis like handwriting Caffeine makes it wotse, and alcohol makes it better The treatment of choice is propranolol Page 1341 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Dementia Dementia: is a decline in memory or other thinking skills severe enough to reduce a person's abifity to perform everyday activities Alzheimer's disease (AD) The most common cause of dementia Slowly progressive loss of memory in older patients > 65 years old Clinical features: Gradual memory impairment to new information Both short and long-term memories may be affected Depression and aphasia are common Diagnosis: Diagnosis of exclusion All patients with memory disturbances should be tested for (812 level, Brain CT scan, and Thyroid function test) Treatment: Donepeil, Rivastigmine, Galantamine Normal-pressure hydrocephalus Also known as Hakim's syndrome Symptoms can be remembered as WWW 'Wet, Weird, Wobbly" o Wet: urinary incontinence o Weird: dementia o Wobbly: wide-based gait/ ataxia Caused by an abnormal accumulation of CSF in the ventricles of the brain Diagnosis: CT and MRI to rule out mass lesions in the brain LP — shows normal pressure Treatment: Ventriculoperitoneal shunt Page 1342 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Other diseases of dementia picks disease (frontotemporal dementia) Abnormal behavior and personality changes precede other symptoms Memory loss No movement disorders Frontal and temporal lobe atrophy in brain imaging Treatment is the same as Alzheimer's disease Creutzfeldt-Jakob disease (CJD) Rapidly progressive dementia and presence of myoclonus The patient is younger than Alzheimer's disease The most accurate test is a brain biopsy EEG and CSF analysis used in the diagnosis Lewy body dementia Presence of parkinsonism plus dementia Presence of vividly detailed hallucinations Huntinqton's disease/chorea Age affected: 30 — 50 years Family history is common CAG trinucleotide repeats on chromosome 4 Presence of dementia + chorea + psychiatric disturbance and personality changes Diagnosis: by genetic testing Treatment: tetrabenazine (for chorea) and antipsychotics Page 1343 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Parkinson's disease (PD) Loss of cells in the substantia nigra resulting in decreased dopamine secretion A clinical syndrome of Bradykinesia + rigidity + tremor + lossof postural reflexes Causes: Idiopathic Repeated head trauma Drugs (e. g., Haloperidol, Lithium, TCA, Metocloprarride) Degenerative diseases (e. g., Alzheimer's disease) Encephalitis Wilson's disease, Huntington's disease Genetic condition Symptoms: Resting tremor improved on catching any subject Bradykinesia (slow movement) Shuffling gait Depression, anxiety Cognitive impairment Rigidity (increased muscle tone) Hypomimia (limited facial expression) Micrographia (small handwriting) Diagnosis: Clinical diagnosis CT Brain to rule out secondary causes If < 50 years, test for Wilson's and Huntington's disease Treatment: Anticholinergics (benztropine) and amantadlne for mild cases Dopamine agonist (best initial therapy for severe parkinsonism) Levodopa/Carbidopa (most effective) COMT inhibitor (tolcapone, entacapone) (used as add on to levodopa/carbidopa, it blocks the metabolism of doparrine) MAO-B inhibitors (selegiline, rasagiline) (single or as add on, it blocks the metabolism of dopamine) Deep brain stimulation (electrical stimulation) Lowy body dementia: parkinsonism + dementia page 1344 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Alcoholic encephalopathies Wernicke's encephalopathy Seen in alcoholism due to Thiamine (Vitamin Bl) deficiency symptoms precipitated by glucose infusion in a patient with alcohofism (Bl is responsible for glucose metabofism) symptoms: Confusion Ataxia Ophthalmoplegia Memory impairment Treatment Thiamine injection Avoid glucose infusion before thiamine Wernicke-Korsakoff disease History of chronic heavy alcohol use Caused by longstanding heavy drinking with an inadequate diet Clinical features: If Wernickers encephalopathy is not treated, it could progress to an irreversibie deficit (Korsakoff syndrome). Severe short-term memory deficit Confabulation Prevention is by proper treatment of Wernicke's encephalopathy No treatment if Wernicke's Korsakoff develop Page 1345 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Neurological autoimmune disorders Multiple sclerosis (MS) It defined as an autoimmune demyelinating disease of the CNS Cell-mediated autoimmune attack of myelin-producing Oligodendrocyte of the CNS More common in white women living in cold climates Common presentations: Visual symptoms (e. g., Optic neuritis, optic atrophy, intemuclear Ophthalmoplegia*) Sensory symptoms (numbness, trigeminal neuralgia, Lhermitte's sign*) Motor symptoms (weakness Most commonly in legs) Cerebral symptoms (ataxia, tremor) Urinary and sexual symptoms (incontinence, impotence) Lhermitte's sign: an electrical sensation at the spine on fimbs on head flexion Intemuclear ophthalmoplegia (INO): inability to adduct one eye with nystagmus in the other eye. Corpus callosum lesion on MRI is pathognomonic for MS because it is high vascular, so strokes are unlikel Clinical courses (types): Relapsing-remitting course (80%) — Most common type Primary progressive course (10%) Secondary progressive disease Fulminant disease (leads to an early death) Diagnosis: MRI (periventricular demyelination) CSF — increased lg G Treatment: Acute relapse: I. V Methylprednisolone for 3 — 5 days Disease-modifying drugs (e. g., Beta-interferon, Fingolimod) Page 134 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Myasthenia gravis (MG) An Autoantibodles to Acetylcholine receptors in the neuromuscular junction Usually, at 15-50 years, women are affected more than men 15% of patients have thymoma, and the majority of others have thymus hyperplasia peniallamine can trigger the antibody-mediated myasthenic syndrome Clinical features: Fatigue and weakness: Ocular: double vision Facial: difficulty chewing o Limb muscles: weakness Symptoms worsen at the end of the day Respiratory muscle involvement (aspiration, pneumonia, respiratory failure) Diagnosis: Tensilon test: I. V anti-cholinesterase (Edrophonium) causes improvement within 30 seconds up to 3 minutes EMG Autoantibodies: (anti-acetylcholine receptor antibodies > 80% of cases) Chest CT scan (to rule out thymoma, thymus hyperplasia) Treatment: Long-acting anticholinesterase, e. g., pyridostigmine Immunosuppression: prednisolone initially Thymectomy Management of myasthenic crisis: (Plasmapheresis, IVIG) page 1347 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Lambert-Eaton myasthenic syndrome Autoimmune response against voltage-gated calcium channel in the peripheral nervous system affecting thesomatic and autonomic nervous system It is a type Il hypersensitivity reaction Associated with small cell lung cancer (as a paraneoplasticsyndrome) or may present independently Clinical features: Limb-girdle weakness (lower limbs first) Hyporeflexia (improved after sustained muscle contraction)Autonomic symptoms: (dry mouth, impotence) Diagnosis: EMG Treatment: Treatment of underlying cancer Immunosuppression (prednisolone and/or azathioprine) 3,4-diamino pyridine (increases the presynaptic Ca concentration) IVIG and plasma exchange Guillain-Barre Syndrome (CBS) Immune-mediated demyelination of the peripheral nervous system Often triggered by an infection (classically Campylobacter jejuni) Most common variation: Acute inflammatory demyelinating polyneuropathy (AIDP) Rare variation: Miller Fisher syndrome (Ophthalmoplegia, ataxia, and areflexia) Clinical features: Paresthesia with pain precedes weakness in ascending pattern The most common cause of death is respiratory failure Diagnosis: Clinical feature of ascending paralysis preceded by infection High CSF protein with normal cell count in CSF Nerve conduction study: delayed conduction page 1348 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatment: Monitoring of Respiratory function (patient may need intubation) IVIG Plasma exchange Steroids have no benefits in CBS treatment. Amyotrophic lateral sclerosis (ALS) It is a progressive degenerative disease that affects both upper and lower motor neurons An autosomal dominant mutation in the copper-zinc superoxide dismutase on chromosome 21 Clinical features: Progressive generalized weakness Dysphagia and nasal speech Neck weakness and head drop Frontotemporal dementia is a common late manifestation Signs of UMNL: hypejreflexia, spasticity, Babinski sign Signs of LMNL: muscle atrophy and fasciculations. Eye muscles, bowel, and bladder functions are preserved in ALS Diagnosis: EMG and NCS: both widespread UMN and LMN injuries that do not fall in a nerve root distribution CSF analysis will be normal Cervical spine MRI to rule out nerve compression Treatment: Riluzole: improves survival by 6 months Noninvasive positive pressure ventilation whenever FEVI < 50% of predicted Percutaneous endoscopic gastrostomy (PEG) tube placement for nutritional support Page 1349 | INTERNAL1-17AFEEF-MERGED-1.pdf |
CNS infections Meningitis It is the inflammation of meninges that presents with headache, fever, and meningism Causes: Patient group Most common organism The most common cause in general Viral meningitis Age 0-1 months Group B streptococci Age I month— 6 years Neisseria meningitidis Streptococcus pneumonia Age 6 years to 60 years Neisseria meningitidis Streptococcus pneumonia Above the age of 60 years Streptococcus pneumonia Neisseria meningitidis Immunosuppressed patients Listeria monocytogenes Post-traumatic meningitis Streptococcus pneumonia Table 138: The most common causes of meningitis Hydrocephalus is most commonly occurring as a complication after H. influenza meningitis Neisseria meningitidis (meningococcal meningitis): Look for a young patient with asplenia who present with sudden high fever and signs of meningitis plus characteristic rash (reddish or purplish rash) It is a rare but serious infection. It needs isolation, and prophylaxis for close contacts (rifampicin, ciprofloxacin, or ceftriaxone) No need to give prophylaxis to nurses who take care of a meningococcal patient, only persons with kissing or another type of saliva-type contact need a prophyla)ds e. who share CUPS, kissin Page 1350 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Clinical features: Headache and fever Neck stiffness Meningococcal meningitis cause rash, usually fatal Signs of meningitis: Kernig's sign: Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees Brudzinski's sign: hip and knee flexion if the neck is flexed Diagnosis: Antibiotics should be started immediately, do not wait for Culture results CSF analysis, CSF Culture (drain LP and then directly start antibiotics) CBC, CRP, blood culture Appearance Glucose Protein WBC Treatment:Bacterial Cloudy Low (< 40 mg/dl) High 10-5000/mm3 Polymorphs Viral Clear Normal (> 45 mg/dl) Normal/high 15-1000/mm3 Lymphocytes Slightly cloudy Low High 10-1000/mm3 lymphocytes Table 139: CSF interpretation for meningitis patients Switch antibiotics according to culture results but do not wait for culture without giving empiric therapy. Age group 0-3 months of age 3 months-50 years Above 50 years Pneumococcat or Hi B Meningococcal meningitis For viral Meningitis Empirical therapy to start I. V cefotaxime and Amoxicillin I. V cefotaxime I. V cefotaxime and Amoxicillin I. V cefotaxime I. V cefotaxime or Benzylpenicillin Acyclovir Table 140: Empirical antibiotic treatment in meningitis Page 1351 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Encephalitis Encephalitis is an acute inflammation of the brain due toeither a viral infection or an autoimmune process The most common cause is a herpes infection Clinical features: The patient presents with headache and fever of acuteonset associated with confusion Photophobia and stiff neck may present Diagnosis: Brain CT scan PCR of CSF (most accurate) Treatment: Antiviral agent (acyclovir) Organophosphate poisoning Organophosphate is a substance that is used widely ininsecticides; most of the war gases are organophosphates as well The time from exposure to the onset of symptoms is 30— 120 minutes The mode of action: Inhibits the enzyme acetylcholinesterase, leading to increased acetylcholine activity at nicotinic and muscarinic receptors in the CNS and skeletal muscles The mode of intoxication: Ingestion: for suicide or accidentally Inhalation (when spraying crops) Dermal absorption Page 1352 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Gl effects Nausea, vomiting Diarrhea Abdominal pain Hypersafivation Eyes Myosis Blurry vision Respiratory Dyspnea, cough Bronchial secretion Wheezing Pulmonary edema Respiratory arrest CNS Anxiety Restlessness Tremor Convulsions Confusion Coma Heart Bradycardia Hypotension Heart block Nicotinic effect Muscle twitching Weakness Fasciculations Respiratory Muscle paralysis Ocular, limbs paralysis Table 14 J: Systemic effects of Organophosphate poisoning Diagnosis: Clinical history and physical examination Acetylcholinesterase activity is less than 50% of the normal Treafmenf: Oxygen Gastric lavage (but never induce vomiting — risk of aspiration) Wash the patient's skin and remove all clothes (to avoid dermal absorption) Atropine 2 mg iv q 15 min until symptoms controlled, then 0. 02 — 0. 08 mg/kg/hour infusion. Use diltiazem to protect the heart if the heart rate exceeds 130 bpm Prafidoxjme I —2 g infusion over 20 minutes (the antidote) Mechanical ventilation, if indicated Page 1353 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Common ENT conditions Meniere disease It is an episodic attack of tinnitus, hearing loss, and vertigolasting for minutes to hours Due to endolymphatic overaccumulation (Endolymphatichydrops) Treatment: Bed rest Antiemetics Antivertiginous drugs (betahistine, meclizine, diphenhydramine) and anticholinergics (e. g., scopolamine)Surgery: Selective vestibular neurectomy or labyrinthectomy Benign Paroxysmal Positional Vertigo (BPPV) It is a spinning sensation upon changes in the position of thehead. Each episode lasts less than I minute Clinical features: Nausea and vomiting Vertigo—Spinning diäness o Paroxysmal (Sudden with a short duration) o Positional: (Induced by a change in head position) Rotatory nystagmus Visual disturbance (difficulty reading or seeing during an attack due to nystagmus) Diagnosis: Clinical diagnosis (Dix—Hallpike test or the roll test, or both) o Dix—Hallpike test: To assess the posterior semicircular canal. Lower your patient quickly to a supine position, with the neck extended Nystagmus will start if the test is positive Page 1354 | INTERNAL1-17AFEEF-MERGED-1.pdf |
o Roll test: To assess the horizontal semicircular canal Done while the patient is supine with their head at 300 of cervical flexion. The examiner quickly rotates the head 900 tothe left side Vertigo and nystagmus will present if the roll test is positive Treatment: Repositioning maneuvers o Epley maneuver o Semont maneuver o Roll maneuver o Brandt-Daroff exercises Medications: Rarely needed o Antihistamines (meclizine) o Anticholinergics (butylbromide 'scopolamine') o Betahistine Page 1355 | INTERNAL1-17AFEEF-MERGED-1.pdf |
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Infectious diseases CHAPTER 10 AM JAD K. ALAFEEF Phone number: +962798843824 E-mail: Afeeef. 2005@gmail. com Page 1357 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Principles of microbiology Bacteria are classified as aerobic and anaerobic types They are further classified according to their staining andshape Examples of anaerobic bacteria: Clostridia (C. difficile, C. tetani, C. botulinum) Spirochetes (Treponema, Pallidum) Bacteroides Gram positive cocci: In chains: streptcocci In clusters: staphylococci In pairs: Enterococci Gram positive bacilli: Large with spores: bacillus, clostridia Small pleomorphic: Corynebacterium, Propionibacterium Filamentous, beaded: Aocardia Actinomyces. Other: Listeria, Lactobacillus Gram-negative cocci: Diplocicci: Neisseria gonorrhea, N. meningitides, Moraxella catarrhalis Other: Acinetobacter Gram negative bacilli: Enterobacteriaceae: E. coli, Klebsiella, Enterobacter,Others: Haemophilus, Proteus, Salmonella, Shigella, Yersinia,Pseudomonas. Acid-fast bacteria: (Ziehl-neelson stain) Mycobacteria Nocardia (weakly acid-fast) Page 1358 | INTERNAL1-17AFEEF-MERGED-1.pdf |
pyrexia of unknown origin (PUO) p U0 is defined as a fever of 380C degree or above for 3 weeks, buf no explanation is found despite investigations by a physician. Causes: Infection (bacterial, viral, fungal, parasitic) Martgnancy (leukemia, lymphoma, MM, solid tumors) Connective tissue disease (SLE, Vascufitis, RA... ) Others (IBD, pancreatitis, hemolytic anemia, sarcoidosis, FMF) Full history and physical examination Lab fests: 0 CBC, Blood Culture, Urine Culture, CSF, CSF Culture o Serology (Autoantibodes, complement, Immunoglobulins) o Echocardiogram, Abdominal U/S o CT/MRI of the chest, abdomen, pelvis, and brain o Biopsy Lymph node, liver, Bone marrow, temporal artery Treatment:-If the cause is obvious after investigations, treat the cause If the cause is still undetectable, use broad-spectrum antibiotics and supportive treatment. Page 1359 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Bacterial infections Brucellosis Brucella is a bacterial zoonosis transmitted directly or indirectly from animals to humans. It may be transmitted by ingestion of raw milk from infectedanimals It is also known as undulant fever or Malta fever It is caused by the Brucella organism (G-negative coccobacilli) The incubation period varies from I week to several months Species and sources: Brucella type B. melitensis B. abortus B. suis B. canis B. ceti The main sources Sheep, goats, and camels Cattle or buffalo Swine Dogs Notes Most common Most aggressive It tends to be-chronic It causes abscess Causes Acute Gl symptoms Marine mammals (seals New species B. pinnipedialis and dolphins) Table 142: Species of brucella and their most common sources Clinical Features: Fever of undulant pattern, night sweat, malaise Hepatosplenomegaty Sacro Tlitis: spinal tenderness may be seen Diagnosis: Isolation of brucellae from blood, CSF, bone marrow, joint fluid, or a tissue aspirate or biopsy sample is definitive in diagnosing brucellosis. Brucella antibody titer AST, ALT, bilirubin bay be elevated Peripheral leukocytes may be normal or low Mild anemia, thrombocytopenia, and DIC may manifest ESR and CRP are usually normal but may be elevated Page 1360 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Treatmestreptomycin lg for 21 days + doxycycline 100 bid for 6 weeks An alternative regimen is doxycycline 100 mg bid + Rifampicin 600 — 900 mg/d for 6-8 weeks. Complications: Infective endocarditis (the most common cause of death) Osteomyelitis (usually vertebral) Others: Meningoencephalitis, orchitis, neuropathy. Toxic shock syndrome (TSS) This condition results from staph aureus or group A streptococcal infection associated with exotoxins released TSS is caused by bacterial exotoxins that act as superantigens. In streptococcal toxic shock syndrome, the streptococcal strains produce pyrogenic exotoxins A, B, or C In staphylococcal TSS, the staphylococcal strains may produce TSSTI or staphylococcal enterotoxins B and C Clinical features: Vomiting, diarrhea. Fever >38. 9 oc (102. 0 OF) and hypotension (SBP mm Hg) Rash that later peels several days after the onset. Diagnosis: Look for menstrual history and the tampon use Look for any abscess, nasal packing, or any gauze packed in the wound Treatment: Identify and remove the source of infection Intravenous fluid Broad-spectrum antibiotics IVIG may be helpful Staphylococci are a normal commensal in human skin and anterior nares A generation of bacteria resistant to methicillin is called Methicillin-Resistant Staph. at. Jreus (MRSA); the drug of choice is vancomycin For Vancomycin-Resistant staph at-Jreus (VRSA), the drugof choice is Da tom cin Page 1361 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Sepsis Sepsis is a systemic inflammatory response to microbial invasion Causes: Gram-negative bacilli (Most common cause) Others: Gram-positive cocci, Viruses, Fungi, Parasites Clinical features: Fever, chills, hypothermia, hypotension, ofiguria, hyperventilation, Skin rash Mental status changes Focal signs that localize the site of infection Features of complications: o ARDS o Renal failure o DIC o Hyperglycemia (common in DM patients) o Hypoglycemia (common in non-DM patients) Diagnosis: CBC, KFT, LFT, Electrolytes Chest X-Ray, ABCs Blood Culture, Urine analysis, and Culture, CSF analysis, and Culture Abdominal U/S Treatment: Empirical broad-spectrum antibiotics then switch according to culture results Treatment the cause Supportive treatment (Fluid, Inotropes, electrolyte maintenance, Blood sugar control, etc. ) Treatment of complications Page 1362 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Lyme disease caused by bacteria Borrelia burgdorferi Transmitted to humans via infected tick bite of (Ixodes) clinical features: There are three stages: stage 1 (early localized disease): a skin reaction around the site of the tick bite "Erythema migrans", associated with fever, headache, and regional lymphadenopafhy. Stage 2 (early disseminated disease): hematologic and lymphatic dissemination, fever, malaise, arthralgia, and metastatic areas of erythema migrans, Other complications (meningitis, cranial nerve palsy, Peripheral neuropathy, carditis, heart block) Stage 3 (late disease): arthritis (large joints), polyneuritis, and encephalopathy Figure 46: Erythema migrans in Lyme disease Diagnosis: Cfinical diagnosis is important with a history of travel to specific areas Anti-Borrelia antibodies (more sensitive in late-stage) Treatment: Doxycycline or Amoxicillin for 1 4 days 15% will develop Jarisch—Herxheimer reaction: a reaction to the endotoxin-fike products due to bacterial death by antibiotics, symptoms resemble bacterial sepsis. P age 1363 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Tetanus Clostridium tetani is a gram-positive spore-forming anaerobic bacteria It is excreted by animal feces to contaminate soil, dust, water, and wounds, including the umbilical stump. Vaccination site... etc. After contamination, the spores germinate and proliferatelocally and produce 2 toxins (tetanospasmin and tetanolysin) which travel along the nerve trunks and bloodstream to CNS and redistribute to the spinal cord, brain, and motor system The Incubation period is 1-14 days, and maybe longer Clinical features: Mild Tetanus: pain and stiffness at the site of injury for a few weeks (mortality < 1%) Generalized tetanus: spasm occurs in descending form with intact consciousness o Trismus: difficult mouth opening (masseter muscle spasm) o Risus sardonicus: (facial spasm and grimacing face) o Laryngeal spasm: (stridor, suffocation) o Opisthotonus: (arched back) o Tonic seizure Cephalic tetanus: o Follow head injury or otitis media o Short incubation period with high mortality o Cranial nerve palsy Tetanus neonatorum: o Infantile form, generalized tetanus 0 3-12 weeks after birth o Umbilicus stump may appear dirty and contaminated o Paralysis o Spasms and stiffness precipitated by touch The most common cause of death is respiratory failure page 1364 | INTERNAL1-17AFEEF-MERGED-1.pdf |
nt and prevention: DTa P immunization at 2,4,6,18 months, and then at 4 years of age At the time of injury: o Surgical management of wound (better to be left open) o Tetanus immunoglobulin or tetanus antitoxin (toxoid) for contaminated wounds of Completed vaccination wound(3 or more doses) <5yr 5-10yr > 10yr None None I-dose TV Clean Non-clean None I-dose TV I-dose TV Incomplete vaccination 3 doses) Complete TV vaccination Complete TV vaccination Tetanus immunoglobulin Table 143: WHO recommendations for tetanus vaccine (TV) and tetanus immunoglobulin administration Typhoid fever (Enteric fever) Organism: salmonella typhi and paratyphi (A, B, C), gram-negative bacilli Humans are only reservoirs Route: oral-fecal transmission Bacteria proliferate in Peyer's patches in the small intestine, then cause primary bacteremia and redistribute to the reticuloendothelial system. Clinical features: Prodromal '1st week': o Headache, anorexia, fever, coated tongue, sore throat, relative bradycardia, abdominal pain, and constipation. 2nd Wee k: o Higher fever o Tachycardia (due to Myocarditis) o Diffuse abdominal pain with splenomegaly and maybe hepatomegaly Rose spots (erythematous Maculopapular rash on lower chest and abdomen) last 7-12 days Page 1365 | INTERNAL1-17AFEEF-MERGED-1.pdf |
week stage of complications: o Intestinal 4th week: Gradual ltnprovament and decline of fever Diagnosis: CBC: anon)la and leucopenia (cluo to loxlc depression on bono Positive' blood culture (40 60 In the week) In tho 2nd week: o Positlvo stool culture o Positlvo WIcla I tost (not specltlc) In the 3M week: Utlno culture PCR Bone marmow cells culture (If affoclecl) Treatment: Bod. rost, light diot Syn)ptornatlc ttoatmont Antibiotics: coftrlaxono or Clprofloxacln with Azlthromycln 5 7 days Evoty I oc riso In temperature Is expected to Increase tho heart rato by 15 20 boats por tnlnuto, fagot's sign (rolativo bradycardia) Is (. 1 condition In which tho patients havo ct lowor hoatt ralo than might bo oxpoc. tod for a 91von body Iornporaturo Tho causos of Fogot's sign are: o Salmonella typhl ßrucolla Logionolla pnoumophila o Mycoplasma pnoutnoniao o Corynobactorium dlphlhorlao o Plasmodium spoclos o Drug fovor o CNS losions o Malignant lymphoma p 1366 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Viral infections Herpes simplex virus (HSV) organism: Herpesvirus type 1 and type 2 Clinical features: Can be a primary or recurrent infection primary: ulcerative stomatitis, Keratitis, Finger infection, Vulvovaginitis, Balanitis, encephalitis Recurrent infection: commonest at Lips (herpes labialis) or genital lesions Treatment: No need for treatment in mild infection-If severe: Acyclovir oral, IV, eye drops Herpes labialis can be activated in case of pneumococcal infection Shingles Organism: Varicella-zoster virus Primary infection: chickenpox (will be discussed in pediatrics) o Fever, pruritus, rash of different stages, history of contact o Treatment: symptomatic only Secondary infection: shingles o This virus may become latent after primary infection, then later in adulthood, will reactivate and present with (Shingles) o Present with severe burning pain at a specific dermatome site with a vesicular rash that does not cross the Medline of the body o Shingles is not contagious o It may be followed by neuropathic pain after resolution (Gabapentin or Pregabalin is the drug of choice for neuropathic pain)o Treatment: Analgesia and antiviral (acyclovir, valacyclovir, Famciclovir) Page 1367 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Infectious mononucleosis (Glandular fever) Organism: EBV (DNA virus) The virus spreads via infected droplets but is rarely blood-borne (It is also known as Kissing disease) Incubation period: 30-50 days Clinical features: Sore throat, Fever, Fatigue, Vomiting Lymphadenopathy (most commonly cervical) Splenomegaly (rapidly occurring, tender, risk of splenic rupture) Hepatitis Myocarditis may occur If ampicillin or amoxicillin is given, a diffuse rash will develop. EBV is an oncogenic virus incriminated in: Nasopharyngeal carcinoma Burkitt's lymphoma Diagnosis: Blood smear (lymphocytosis with atypical lymphocytes) Heterophil antibody (Monospot test) Detection of EBV lg M (specific) 80-100% of patients have elevated liver enzymes Treatment: Supportive only Avoid antibiotics Avoid contact sport for 2-3 weeks; risk of splenic rupture Steroids in selected cases (AIHA, low platelets, meningitis... ) Page 1368 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Rabies It is a viral infection that can cause brain infection Rabies is a DNA rhabdovirus Most commonly transmitted by a dog bite then, the virus travels up at nerve axons to CNS The incubation period is 1-2 months Clinical features: Headache, fever Hydrophobia Hypersafivation Negri bodies (found in the cytoplasm of infected axons) Treatment: Clean wound with soap and water Do NOT stitch the wound (it increases the risk of transmission of the virus to the CNS) Anti-rabies serum: o If the dog is dead, brain biopsy and give anti-rabies serum if positive for the virus o If the dog is live, put in quarantine; give anti-rabies serum if the dog dies within 10 days for any reason o If the dog is not reachable. give the anti-rabies serum Anti-rabies serum is given in 6 doses at: (O, 3, 7. 14, 30 and 90 days) Infiltrate human rabies immunoglobulin around the site of the bite Page 1369 | INTERNAL1-17AFEEF-MERGED-1.pdf |
COVID-19 Coronavirus disease 19 is a disease caused by the beta Coronavirus (SARS-Co V-2 virus) It is a single-strand RNA virus The source of the virus in the first place was transmitted from Bats to humans; then, the virus can be transmitted from human to human Human-to-human transmission is by droplets Incubation period up to 2 — 14 days Poor prognostic factors: Increasing age (> 40 — 50-year-old) Pre-existing comorbidities Males are more affected than females Clinical features: (Mainly respiratory or Gl infection) Some patients do not have symptoms (asymptomatic) Fever (the most common symptom) Cough (with or without sputum) (the 2nd most common) Shortness of breath Upper respiratory symptoms (sore through, runny nose) Gastrointestinal symptoms (Nausea, vomiting, diarrhea) Non-specific symptoms like fatigue, myalgia, malaise, headache, confusion Complications: Adult respiratory distress syndrome Respiratory failure Viremia and septic shock DIC Multiple organ failure Renal failure Diagnosis: CBC (neutropenia, lymphopenia, thrombocytopenia) High AST and ALT level High LDH CXR: bilateral pulmonary infiltration Chest CT scan: bilateral ground-glass opacities, pulmonary infiltrates, multilobar consolidation (the most sensitive) Real-time Polymerase chain reaction (RT-PCR) — detects the viral RNA (the most accurate test) Prevention: Routine vaccination according to the protocol All cases of COVID-19 need complete Isolation Page 1370 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Avoid travel to a disease outbreak area Avoid crowded areas Careful handwashing with soap and water Wearing a surgical mask is not recommended for nonhealthcare workers Treatment: Oxygen therapy: o Sp02 needs to be 90-96%. If Sp02 < 94%, nasal cannula with titration of 02 flow If still < 90 on nasal cannula at a flow rate of 15L/min, switch to face mask A non-rebreathing mask is used if the patient is still hypoxic despite the use of a face mask at a flow rate of 15L/min Consider C-PAP or Bi PAP for COPD patients Mild cases: Paracetamol for fever > 38 c o Encouraging patients to drink fluids Moderate cases: o Paracetamol Prophylactic dose LMWH o Oral vitamin D (2000 IU daily) Severe cases: o Dexamethasone 6mg daily IV for 10 days o LMWH o Favipiravir: 1600 mg twice for the first day Then 600 mg Twice daily for 14— 10 day o Tocilizumab if the following points are present: Evidence of hyperinflammatory state Pulmonary infiltrates on chest imaging Signs of hyperinflammafory status: (at least 3 of the following) Fever > 38 c CRP > 100 mg/L IL6 > 60 pg/ml High Serum ferritin > 5X UNL High LDH Page 1371 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Sexually transmitted diseases Syphilis Mainly sexually transmitted disease Transmitted by: sex, blood transfusion, vertical (transplacental) Organism: the spirochete Treponema Pallidum, incubation period: between 9-90 days Clinical features: There are 3 stages of the disease Primary stage: o Chancre-painless genital ulcer with indurated edges o Local painless lymphadenopathy Secondary stage: (6-10 weeks) o Systemic symptoms: fevers, lymphadenopathy o Rash o Alopecia areata Tertiary stage: o Neurosyphilis: Vasculitis, stroke Memory and personality changes Tabes dorsalis (spinal cord degeneration) o Aortitis: Ascending aortic aneurysms Aortic dissection Aortic regurgitation o Gummas (skin & bone granulomatous lesions) Diagnosis: serology test for syphilis Treatment: For primary and secondary syphilis, a single penicillin injection or oral doxycycline For tertiary syphilis, I. V penicillin Jarisch-Herxheimer reaction: The occurrence of fever and worsening of symptoms after treatment of syphilis. It is managed by aspirin and antipyretics only Page 1372 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Gonorrhea sexually transmitted disease, by vaginal, anal, or oral sex Organism: Neisseria gonorrhea (gram-negative diplococci) Incubation period: 2-10 days Clinical features: It may be asymptomatic ( in men, 80% in women) In men: Mostly symptomatic o Urethritis with urethral discharge o Epididymo-orchitis may present In women: Mostly asymptomatic o Urethral involvement o Bartholin's gland/duct involvement o Endocervical canal involvement o Rectal involvement o Acute pelvic inflammatory disease Diagnosis: Mainly clinical Direct smear (Gram-negative diplococci) Treatment: Ceftriaxone 500mg 1M single dose Chlamydia infection A bacterial infection that is transmitted similarly to gonorrhea Cfinically also similar to gonorrhea In men: urethral symptoms are mild, and < 50% of cases In women: o The most common sites are the cervix and urethra o It may cause vaginal discharge and dysuria o It may cause intermenstrual or postcoital bleeding Treatment: Azithromycin lg PO single dose (first-line) Doxycycfine 100mg bd for 7 days Note: When gonorrhea or Chlamydia is not responsive totreatment, consider that both bacteria may be present at the same time Page 1373 | INTERNAL1-17AFEEF-MERGED-1.pdf |
HIV infection HIV is an RNA retrovirus that affects CD4 (T helper cells) Depletion of CD4 count takes a long period, so it has a longincubation period (from one year to ten years) The main cause of death is decreased CD4 count and opportunistic infections Route of transmission: Sexual contact Exposure to blood or blood products (I. V drug users, occupational) Organ transplantation. Vertical transmission (transplacental, during birth, or breastfed) Kissing is not proven to transmit HIV Clinical features: Primary infection: (2-4 weeks) o Occur in 70% of HIV infections 0 50% asymptomatic 0High viral load o Fever, pharyngitis, lymphadenopathy, myalgia, arthralgia, headache, diarrhea (same symptoms of mononucleosis) o Maculopapular rash (usually at the trunk), oral and genital ulcer o Symptomatic recovery takes 1-10 weeks AIDS phase: o It is the development of opportunistic infections, tumors, and other clinical features. CD4 count The most common diseases (cells/mm3) < 50 50-100 100-200 200 — 500CMV retinitis, Mycobacterium avium/intercellulare Aspergillosis, Candidiasis, Meningitis, CNS lymphoma Cerebral toxoplasmosis, PCP, HIV dementia Oral thrush, Shingles, Kaposi sarcoma Table 144: Diseases affecting HIV patients Page 1374 | INTERNAL1-17AFEEF-MERGED-1.pdf |
nosis: In primary infection: PCR (antibody may be negative) Then HIV antibody test Treatmentprevention (avoid contaminated water, avoid animal-bome infection, control malaria) vector in an endemic area, cotrimoxazole prophylaxis, pneumococcal, influenza, and HBV vaccines) HAART (human antiretroviral therapy) Reduce viral load o Improve CD4 > 200 cells/mm3 o Prolongs life expectancy o Reduce transmission Common parasites Malaria A parasitic infection transmitted by Mosquito (Anopheles) affects blood and liver cells Patients with sickle cell anemia are protected against malaria The mosquito has the plasmodium in their saliva and injects it into the human bloodstream-+ Sporozoites reach the fiver and engage in Asexual reproduction (this is called extra-erythrocytic phase) —i erythrocytic phase: parasite enters the RBCs —+ asexual replication and hemolytic anemia Diagnosis: History of travel to an endemic area General features: fever, headache, splenomegaly Fever is cyclic Signs and symptoms of hemolytic anemia with coombs negative Labs: Blood film (Thick-film: more sensitive, Thin-film: determinespecies) Thrombocythemia is characteristic Page 1375 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Normochromic normocytic anemia Normal white cell count Reticulocytosis Caused by Plasmodium species: Plasmodium species Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae Plasmodium knowlesi Characteristics Complications include: Cerebral malaria Acute renal failure: Blackwater fever ARDS Hypoglycemia DIC The most common cause of non. falciparum malaria Found in Central America and India Can have hypnozoite stage Cyclical fever every 48 hours More common in Africa Can have hypnozoite stage Cyclical fever every 48 hours Associated with nephrotic syndrome Cyclical fever every 72 hours Found in south-East Asia Table 145: Species of Plasmodium and their characteristics Treatment Chloroquine-sensitive areas: ACT or chloroquine Chloroquine-resistant areas: ACT Primaquine: after treatment of ovale or vivax malaria (to destroy liver hypnozoite and prevent relapse) ACT: Artemisinin-based combination therapy ACTS Should be avoided in pregnant women Plasmodium falciparum is chloroquine-sensitive Page 1376 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Chagas disease Also known as American trypanosomiasis Found in Mexico, south and central America Transmitted by Reduviid insect vector Triatominae (Kissing bug) The infected triatomine feeds on the human blood, and it defecates at the same time to make room for the new meal Triatominae in the stool are rubbed into the bite site by the host Other modes of transmission (Through the placenta, Organ donation, Blood transfusion, Ingestion of contaminated food) Clinical presentation: Acute phase: OUsually asymptomatic o Local swelling at the site of inoculation (Romana's sign: usually around one eye when the conjunctiva is the portal of entry) o Fever, lymphadenopathy, cardiomegaly, and hepatosplenomega!y Chronic indeterminate phase: o Asymptomatic increasing levels of antibody o Most infected persons (60-70%) remain in this phase and do not go on to manifest a determinate phase Chronic determinate: o Chronic dilated cardiomyopathy o Esophagomegaly o Megacolon 10 —25 years after acute infection (30-40%) Investigations: Thin and thick blood smears stained with Giemsa stain Serology test PCR Treatment: Acute and Indeterminate phase: Nifurtimox or Benznidazole Chronic determinate:o Symptomatic treatmento Surgery: Heart transplant, Esophagectomy,Colectomy Page 1377 | INTERNAL1-17AFEEF-MERGED-1.pdf |
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Clinical pharmacology CHAPTER 11 AM JAD K. ALAFEEF Phone number: +962798843824 E-mail: Afeeef. 2005@gmail. com Page 1379 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Drugs and their antidotes Anfidofes: substances contract a f«rn The,' may be manufactured by irjecting tt E tonn into on Uirnd in srnd doses and extracting the resuting anfibodf Ar Ædofe Adenosine Theophyffne Atrogine Physosfigrrine Benzodaze Änes Flurrczernl Beta-Bbckers Calcium channel blockers Calcium Dgo%n Digibind Hep«in Protarnine sulfate ton Deferoxarrine Lead Edftafe cf J-sodurn b&fhand Ethanol Morphine N a oxo Paracefarnd N-Ace Mcysfeine Warfain Vitamin K Table 146; Cornrnon drugs and the? antidotes Antibiotics Bacteriostatlc antibiofics: Antibiotics that the growth of bacte(sa Bactericidal antibiotics: Antibiotics that kill the bacteria Befa-lacfam antibiotics: a class of broad-spectrum antibiotics consists of a beta-Iacfam ring in their molecular sfrucfure (e. g., penicilfin, cephalosporins, Carbapenerns, Azfreonam). Page 1380 | INTERNAL1-17AFEEF-MERGED-1.pdf |
classification according to the site of action on bacterial cells: Action site Inhibits cell wall formation Inhibits protein synthesis (by acting on the ribosome) Inhibits DNA synthesis Damages DNA Inhibits folic acid formation Inhibits RNA synthesis Penicillin Cephalosporins Glycopeptides Carbapenems Aminoglycosides Chloramphenicol Clindamycin Macrolides Streptogramin Tetracycfines Quinolones Metronidazole Sulfonamides Trimethoprim Rifampicin Table 147: antibiotics classification and their site of action Bactericidal antibiotics l. Penicillin 2. Cephalosporins 3. Quinolones 4. Aminoglycosides 5. Isoniazid 6. Metronidazole 7. Nitrofurantoin 8. Rifam icin Bacteriostatic antibiotics 1. Chloramphenicol 2. Macrolides 3. Sulfonamides 4. Tetracyclines 5. Trimethoprim Table 148: antibiotic classification and their type of action Page 1381 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Penicillins It is of the most widely effective and least toxic antibiotic The mechanism of action: inhibits bacterial cell wall synthesis Examples are: Amoxicillin, Ampicillin, Dicloxacillin, Nafcillin,penicillin G, penicillin V Penicillin is the initial therapy for otitis media, dental infections, endocarditis prophylaxis, Lyme disease, UTI duringpregnancy Bacteria covered by amoxicillin: (HELPS) H. influenza E. coli Listeria Proteus Salmonella Penicillinase-resistanf penicillin: Penicillinase enzyme is secreted by some bacteria leading to the destruction of Beta-lactam antibiotics resulting in insensitivity to this drug. Their use is restricted to treating infections caused by penicillinase-producing staphylococci, including methicillin-sensitive S. aure US (MSSA). Penicilfinase-resistant drugs include methicilfin, nafcillin, oxacillin, dicloxacillin, cloxacilfin, amoxicillin with clavulanic acid, and ticarcillin with clavulanic acid. Penicilfinase-resistant antibiotics have no activity against grarn-negative bacteria. Beta-lactam antibiotics are the most common antibiotics to cause anaphylaxis Page 1382 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Cephalosporins Beta-lactam antibiotics that cover a wide range of bacteria Cross-sensitivity between cephalosporins and penicillin is 8%: o If penicillin causes skin rash, switch to cephalosporins o If penicillin causes anaphylaxis, switch to non-beta-lactam antibiotics Second Third Fourth Fifth erst cephalexin Cefaclor Ceftriaxone Cefepime ceftaroline Cefazolin Cefuroxime Cefotaxime Cefpirome Cefoxitin Ceftazidime Table 149: cephalosporine generations First Second Third Fourth Fifth G. positive G negative Anaerobes Pseudomonas No No Ceftaidime Yes No MRSA No No No No Yes Table ISO: the bacterial coverage in cephalosporines Indcations: first-generation: Osteomyelitise arthritis, endocarditis, cellulitis Second generation: o Cefuroxime: is a drug of choice for respiratory infections such as otitis, bronchitis, and sinusitis) o Cefoxitin: is a drug of choice in PID (with doxycycline) Third generation: o Pneumococcal pneumonia o Meningitis o Community-acquired pneumonia (with macrolides) o Gonorrhea o Lyme disease involving the heart or brain o Cefotaxime used in the treatment of SBP Fourth generation: o Ventilator-associated pneumonia o Pseudomonal infections Page 1383 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Carbapenems E. g., Imipenem, Meropenem, Ertapenem, Doripenem Covers gram-negative bacilli The difference between all carbapenems and Ertapenem is that all cover pseudomonas while Ertapenem Does not. Fluoroquinolones E. g., Ciprofloxacin, Levofloxacin, Moxifloxacin The best therapy for community-acquired pneumonia Covers gram-negative bacilli, including pseudomonas Ciprofloxacin is used for the treatment of cystitis and pyelonephritis Precautions: o Contraindicated in children (<18 years) and pregnant women (cause bone growth abnormalities) o Can cause tendonitis and Achilles tendon rupture Aminoglycosides E. g., Gentamycin, Tobramycin, Amikacin They are synergistic with beta-lactam antibiotics for enterococci and staphylococci They are nephrotoxic and ototoxic Trimethoprim/sulfamethoxazole (TMP/SMX) Used to treat cystitis, PCP, minor MRSA infections Side effects: hemolysis in G6PD deficiency patients, bone marrow suppression, rash Page 1384 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Doxycycline Used for treatment of Chlamydia, Lyme disease, Cellulitis, Syphilis, Mycoplasma Adverse effects: Tooth discoloration of children, type Il RTA, esophagitis, photosensitivity Some antibiotics that are active against Pseudomonas: Carbapenems (except Ertapenem) (the first line) Tigecycline Cefepime (4th generation cephalosporin) Aminoglycosides (gentamycin, Amikacin) Fluoroquinolones (Except Moxifloxacin) Table 151: Antipseudomonal agents MRSA: methicillin-resistant Staph. aureus: Minor infection with MRSA treated with: TMP/SMX, doxycycline, clindamycin, or Linezotid Major infection treated with Vancomycin Red-man syndrome: a side effect of vancomycin will occur if vancomycin is given as a rapid infusion. Vancomycin must be given over 90 minutes to avoid this syndrome. Page 1385 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Drugs used in DM Oral hypoglycemic agents Biguanides (Metformin): First-line in the treatment of T2DM Work by blocking gluconeogenesis and increasing insufin sensitivity Do not cause hypoglycemia Contraindicated if > 80 years old or CFR less than 30 ml/min (Risk of lactic acidosis) Best for treatment of DM in obese patients (Metformin helps reduce weight) The most common side effect is Gastrointestinal Upset (diarrhea, vomiting, nausea) and rarely Lactic acidosis Sulfonylureas: It can be used as add-on therapy in Metformin fails to achieve the AIC target Stimulate the release of insulin from the pancreas Can cause weight gain; best for non-obese Diabetics Can cause hypoglycemia Sulphonylurea should not be used in renal impairment as there is a risk of hypoglycemia Examples: o Gliclazide, Glipizide, Chlorpropamide Gübenclamide (More risk of hypoglycemia, avoid in elderly) Alpha-glucosidase inhibitor: Decrease intestinal absorption of glucose Side effects (flatulence, abdominal pain, diarrhea) Examples: o Acarbose o Migrltol Thiazolidinediones (glitazones): Enhance action "but not amount" of endogenous insufin Hypoglycemia not happens aarnples: o Rosigfitazone (increased risk of Ml. so withdrawn in 2010) o Piogfitazone (exacerbate heart failure, avoid in HF patients) Page 1386 | INTERNAL1-17AFEEF-MERGED-1.pdf |
Dipepfidyl peptidase-4 (DPP-4) inhibitors: Well tolerated with no increased incidence of hypoglycemia Do not cause weight gain Examples: (Vildagliptin, Sitagliptin) Glucagon-like peptide (GLP) mimetics:-Increase insulin secretion and inhibit glucagon secretion Can be used with Metformin and Sulfonylurea as a third agent Cause weight loss, used if BMI 2 35 kg/m2 Examples: o Exenatide injection BID o Liraglutide injection once daily Insulin Used in TIDM and patients with T2DM who are not controlled or oral agents Can be rapid-acting, short-acting, intermediate-acting, or long-acting Premixed insulin composed of rapid or short-acting combined with intermediated acting insulin The type of insulin that can be given IV is called regular insulin Insulin type Ultra-rapid Rapid-acting Short-acting Intermediate acting Long-acting Examples Faster Aspart Lisprot Aspart, Glulisine Regular insulin Onset Peak 6-12 m 1-3h 5-20 m0. 5-3 30 m 2-4 hh 2-4 h 6-10h Detemir, Glargine 2 h None Duration 3-5 h 3-8 h 5-8 h 18-28 h 20-24 h Table 152: The different types of insulin Page 1387 | INTERNAL1-17AFEEF-MERGED-1.pdf |