Mechanisms of Disease Exam 1

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Pathology of Osteoarthritis 1. gross level 2. microscopic level 3. biochemically: 1. - first, cartilage irregularities and splitting
- next, ulceration and loss of cartilage
- next, bone on bone contact then eburnation (polished bone)
2. - fibrillation of cartilage
3. - decreased glycosaminoglycan content of cartilage, including less chondroitin sulfate, less keratin sulfate and less hyaluronic acid
- increased MMP activity, which plays role in degradation of extracellular matrix of cartilage
Pathogenesis: OA is primarIly a disease of ________ of joints.: hyaline cartilage
Pathogenesis: the initiating event in OA is ______ which results in _______.: mechanical stress, which results in change in chondrocyte metabolism - proteolytic enzyme production (MMPS)- disruption of cartilage matrix
In OA, mechanical stress means...: any compressional stress which too forcefully jams the 2 articulating surfaces of hyaline cartilage together.
As OA progresses, crystals of _______ are shed into the joint fluid and are commonly found in severe OA.: calcium phosphate
Clinical features of OA: -pain and stiffness of joint, worse with use, better with rest, or vv.
-morning stiffness <30 min
-gelling
-osteophytes impinging on dorsal roots &/or spinal cord - radicular sx in limbs:pain, numb, weak
In OA, pain may be due to:: -inflammation of the periosteum (periostitis) at sites of bone remodeling
-subchondrial microfractures
-irritation of synovial nerve endings by osteophytes
-synovial inflammation from chemical junk
On physicacal exam, OA presents:: -warmth and soft tissue swelling of joint is minimal
-tenderness and bony enlargement of joint
-Crepitus from cartilage irregularities
-possible locking due to a loose piece of cartilage
-varus deformity of knee in 50% due to worse loss of cartilage
In OA, classic enlargement occurs at which joints?: PIP joints (Bouchard's nodes) and DIP joints (Heberden's nodes)
Radiologic features of OA:: -asymmetric joint space narrowing due to cartilage loss
-subchondral bone sclerosis
-subchondral bone cysts
-osteophytes
Labs of Osteoarthritis:: -Dx of OA is almost always by H&P and can be confirmed by XR
-WBC count in synovial fluid should be <200 cells per cubic mm
Treatment of OA:: -APAP, NSAIDS
-capsaicin cream (Zoxtrix)
-oral chondroitin sulfate or glucosamine
-intra-articular steroid injections
-intra-articular injection of hyaluronic acid derivatives
-arthroplasty (joint replacement)
The most feared possibility when a patient presents with a joint which is red, hot, swollen, painful joints is:: Septic arthritis
Which form of arthritis is monoarticular?: Septic arthritis
Septic arthritis is caused by...: bacterial joint infection
Hydrolytic enzymes from neutrophils destroy joint fast by irreversible cartilage reabsorption possibly resulting in sepsis and death.: Septic arthritis
Bacterial access to joint occurs by...: -hematogenous spread (endocarditis, IV drug use)
-contiguous osteomyelitis
-joint penetrating injury
-prosthetic joint
-joint injection
SA in children is often linked to _____ because of _____.: osteomyelitis because of open epiphyses
SA in teens & adults is often linked to _______.: Neisseria gonorrheae infection
Labs of SA:: -of all causes of SA, blood culture is + in 50%
-synovial fluid constituents indicate decreased glucose, increased protein & lactate, WBC count >10,000/ul
Treatment of SA:: -treat early with antibiotic
-Rocephin (ceftriaxone) or Nafcillin IV plus gentamicin IV
Name 3 diseases that present with red, hot, swollen joints.: 1. Septic arthritis
2. Gouty arthritis
3. Reiter's disease
Clinical features of Lyme Disease: -rash in 50% of people
-if untreated, fatigue, fever, headache &/or arthralgias
If Lyme Disease goes untreated, a minority develop the following complications:: -arthritis (knee)
-neorologic: headaches, meningeal signs (nuchal rigidity), cranial nerve dysfunction (facial nerve-bilateral Bell's Palsy)
-Cardiac(AV block)
ELISA detects replacement of IgM with IgG and is confirmed by Western Blot.: Lyme Disease
Treatment of Lyme Disease: -Prevention: tick repellants
-Antibiotics: rash/arthritis - po Vibramycin (doxycycline) or Amox (amoxicillin); carditis/meningitis - IV Rocephin (ceftriaxone)
Arthritis which occurs after genitourinary, gastrointestinal and possibly respiratory infection.: Reiter's Syndrome aka Reactive Arthritis
Originally referred to as the clinical triad of arthritis, conjunctivitis, and nonconococcal urethritis.: Reiter's Syndrome aka Reactive Arthritis
Considered one of the seronegative spondyloarthropathies (SNSA): Reiter's Syndrome aka Reactive Arthritis
SNSA: seronegative spondyloarthropathies
The SNSAs are:: -Reactive Arthritis
-Lyme Arthritis
-Psoriatic Arthritis
-Gouty Arthritis
-Osteoarthritis
-Septic Arthritis
Seronegative denotes absence of _________.: rheumatoid factor
Nongonococcal urethritis with C.trachomatus is frequently the trigger for _________.: Reiter's Syndrome
Clinical features of Reiter's Syndrome: -typically begins 2-4 weeks post gastroenteritis or venereal infx.
-nongonococcal urethritis
-conjunctivitis usually accompanies or follows
urethritis
-articular manifestations typically appear last
-extraarticular manifestations
-dactylitis or sausage digits -asymmetric oligoarthritis of lower extremities -enthesopathy: articular manifestations of Reiter's Syndrome aka Reactive arthritis
entheses: attachment sites of tendons to ligaments
-Circinate balanitis -Keratodermal blennorrhagica: Extra-articular manifestations of Reiter's Syndrome aka Reactive arthritis
Circinate balanitis: shallow ulcer of glans or shaft of penis
Kertodermal blennorrhagica: papulosquamous rash most often on palms or soles.
Immunohistochemical studies of synovium reveal antigenic material from infecting organisms but no viable organisms.: Reiter's Syndrome aka Reactive arthritis
-increased sed rate & C-reactive protein -synovial fluid: turbid,WBC count >5000/ul,low viscosity: Labs for Reiter's Syndrome aka Reactive arthritis
Consider Reactive arthritis when:: -asymmetric oligoarthritis esp. in young person
-extra-articular manifestations
-h/o prior infections supports Dx
Treatment of Reactive arthritis: -NSAIDs & exercise until arthritis remits
-rarely, systemic or intra-articular steroids
-DMARDs if no response to NSAIDs
DMARDs: Disease Modifying Anti-Rheumatic Drugs
-increased epidermal cell turnover leading to acanthosis (thickening) -pink-to-salmon plaques covered with silver scales -nail changes (oil slick discoloration,pitting,thickening,oncholysis) -Auspitz sign -Koebner phenomenon: The skin condition Psoriasis
Auspitz Sign: multiple small bleeding points on skin when scrape gently or lift scales due to dilated tortuous capillaries under plaque
Koebner Phenomenon: psoriatic lesion develops at the site of minor skin trauma, surgical suture lines, etc.
T/F: Psoriatic Arthritis is a seronegative spondyloarthropathy.: True.
T/F: Psoriatic Arthritis appears in psoriasis patients who have extensive skin leasions.: True.
___________ arthritis may really be another form of Reactive Arthritis, ie. reactive to Staph and Strep antigens in ____________.: Psoriatic Arthritis...psoriatic skin lesions.
-oligoarthritis most comm. spread through small joints (PIP,DIP, MCP), sausage digits -Arthritis mutilans -Extra-articular involvement (psoriatic skin lesions, nail changes, sausage digits, enthesopathy): Psoriatic Arthritis
-pencil in cup deformity at phalanges -acro-osteolysis=resorption of distal bone tuft of distal phalanx -joint space loss: Radiologic features of Psoriatic arthritis
Treatment of Psoriasis (Skin Disease): -topical steroids (kenalog cream)
-topical coal tar preps (Psorigel)
-Vit. D derivatives (Dovonex)
-Vit. A derivatives(Soriatane)
-PUVA=pulsed UVA light
-Rheumatrex (methotrexate)
-Enbrel (etanercept)
Treatment of Psoriatic Arthritis: -NSAIDs
-intra-articular steroid injections
-Enbrel
-DMARDs (Rheumatrex, Azulfidine)
A metabolic disease; hyperuricemia in the blood, which has musculoskeletal consequences: Gouty Arthritis
Uric acid comes from the breakdown of _______, _______ & ________.: purines, adenosine & guanosine
Patients with Gout: -mostly men, peak in 40s
-hyperuricemia
-at higher plasma concentrations of urate, monosodium urate crystals precipitate out of solution into cooler peripheral joints (ankles, toes) and tissues (ears & fingers)
Clinical Presentation of Gout: -abrupt: usually one joint(MTP,ankle,knee). Pt often well at bedtime, awakes w/podagra. exquisitely painful.
-attack resolves in days to weeks despite crystals still in joint
Factors which precipitate acute attack of Gout: -start of uric acid therapy (allpurinol)
-start of diuretic therapy
-surgery/trauma, severe illness, stroke, acute myocardial infarction
-alcohol binges
Clinical Presentation of Gout 1. Intercritical Phase 2. Subsequent Attacks 3. If untreated: 1. all quiet, but most have recurrence w/in 2 years of 1st attack
2. often worse: high fever & chills suggesting septic joint;more likely to involve upper extremity joints &/or multiple joints
3. shorter intercritical phases & progressive joint destruction;urate crystals in soft tissue
gouty tophi: urate crystals in soft tissue
(ear pinnae,olecranon bursa,fingers & toes, achilles tendon)
Diagnosis of Gout: -Pt presents with abrupt onset mono or oligoarthritis of lower extremity
-Hyperuricemia >6-7mg/dl
-aspiration of fluid shows needle-shaped, negatively bifringent, monosodium urate crystals
Treatment for Acute Attack of Gouty Arthritis: -NSAIDS:Indocin(indomethacin),Advil(Ibuprofen),Anaprox(naproxen)
-Cochicine-90% get relief and this supports dx of gout
-Steroids-if can't use above
_______ is contraindicated for treatment of Gout because in small doses it may worsen hyperuricemia.: Aspirin
Prophylaxis and Uric Acid Lowering TX of Gout: -lose weight and lose the boose
-avoid dehydration and diuretics
-get serum urate below 5mg/dl
In a condition called ______, calcium pyrophosphate crystals are at fault. These crystals are ____________ bifringent.: Pseudogout, positively
Diagnosis of Pseudogout: -patient presents with abrupt onset mono or oligoarthitis
-serum urate level NOT elevated
-aspiration of joint fluid shows: calcium pyrophosphate crystals and NO bacteria
Treatment of Pseudogout: -urate lowering drugs are irrelevant
-NSAIDS
-Cochicine(may or may not be beneficial for acute attack but given prophylactically it decreases the # & duration of attacks
-intra-articular steroids will terminate attacks in resistant cases
A chronic inflammatory systemic disease dominated by joint destruction: Rheumatoid Arthritis
________ arthritis is considered a symmetric polyarthritis: Rheumatoid
symmetric polyarthritis: arthritis that affects homologous joints on both sides of the body
Joints commonly affected in RA are:: -MCP and PIP joints
-carpal bones and wrist
-Knees and MTP joints
-synovial microvasculature -hyperplasia of Type A & B synoviocytes -early T cell emigration & infiltration into synovial tissue -proliferation of blood vessels and of synovial fibroblasts (hypertrophic synovium) -hypertrophied: Earliest changes of Rheumatoid arthritis
Pathogenesis: Joint damage in ______ arthritis is of immune origin, ie. an autoimmune disease, in genetically disposed individuals.: Rheumatoid
The autoimmune response of this disease is due partly to Type 3 Hypersensitivity , ie. immune complex-mediated tissue injury. 80% of pts have RFs, which result in the attraction of WBC causing inflammation.: Rheumatoid arthritis.
RFs: Rheumatoid factors - autoantibodies to the Fc portion of IgG in the serum and synovial fluid.
Essential for Diagnosis of RA: documentation of inflammatory synovitis
-by synovial fluid leukocytosis (WBC >2000)
-typical erosions on XR
-RF found in 80% of patients -increased ESR and C-reactive protein (CRP) -anemia of chronic disease: Labs of RA
Synovial hypertrophy and pannus formation may cause peripheral nerve entrapment in selected joints.: Rheumatoid Arthritis
morning stiffness greater than 2 hours: Rheumatoid Arthritis
morning stiffness less than 30 minutes: Osteoarthritis
-frozen shoulder (adhesive capsulitis) -ulnar nerve entrapment-paresthesias of 4th/5th digi -Baker's Cyst(post.herniation of joint capsule) -Tarsal Tunnel Syndrome-entrapment of post.tibial nerve-parethesias of sole -MTP Subluxations<: Rheumatoid Arthritis
Deformed hands: -MCP and PIP joints involved -nodules in finger tendons (locking) -tendon rupture-Swan Neck & Boutonniere Deformity -Opera Glass hands-ulnar deviation at MCP joints, radial deviation at wrists: Rheumatoid Arthritis
Extraarticular Manifestations of Rheumatoid Arthritis: -Skin: nodules in skin,bursae,tendons &/or over pressure points
-Ocular: Keratoconjunctivitis sicca
-Respiratory: interstitial fibrosis, pluerisy/pleural effusion
-Heart: pericardial effusion, restrictive pericarditis w/sns of RHF
-GI: gastritis & peptic ulcer dz from NSAID tx
-Blood: anemia of chronic dz
-NSAIDS (Advil,Arthrotec, Daypro,Alleve) -Corticosteroids(glucocorticoids) -DMARDS: Treatment for RA
The prototype of autoimmune diseases, characterized by production of antibodies to components of cells in the nucleus.: Systemic Lupus Erythematosus (SLE)
Dominated by: -severe fatigue -arthralgias/arthritis -some permutation of its many systemic effects, many of which are vasculitic: SLE
Used to be called connective tissue diseases or collagen vascular disease because of the prominence of effects in connective tissue and in blood vessels themselves: SLE and other autoimmune diseases
central disturbance is rampant production of auto-antibodies to a variety of self antigens in/on the cell surface, cytoplasm or nucleus: SLE
In SLE, auto-antibody production is due to immune cell abnormalities of the _____: B cells, T cells and monocytes
In SLE, abnormalities to immune cells cause:: -B cell hyperactivity leading to hyperglobulinemia
-Increased # of Ab producing cells
-Heightened responses to both foreign and self Ags
Immuno complex (IC) deposition results in inflammation and vasculitis of various organs and tissues: SLE
Anti-nuclear antibodies bind to self-antigenic components of _____, _____, _____, _____: DNA, RNA, nuclear proteins, protein-nucleic acid complexes
Labs: -generic ANAs -anti-dsDNA Abs -anti-Smith Abs -C reactive protein is low even when sed rate is high: SLE
_____ Abs in a lupus patient may fluctuate over time but _____ Abs remain more constant.: anti-dsDNA, anti-Smith
Skin manifestations: -malar, butterfly rash -general erythema, often photosensitive -discoid lesions=red papules or plaques with thick scale and hypopigmented center -alopecia -mucus membrane lesions -Raynaud's Phenomenon: Skin Manifestations of SLE
Musculoskeletal manifestations: -arthralgias & arthritis -arthritis similar to RA but not erosive -myalgias -fibromyalgia: Musculoskeletal Manifestations of SLE
Manifestations of Renal Dysfunction: -glomerulonephritis, nephrotic syndrome, renal failure: Renal Manifestations of SLE
Neuropsychiatric Manifestations: -CNS problems, cranial and peripheral neuropathies, psychiatric problems: intractable headaches, seizures,chorea,CVA,cranial neuropathies,peripheral neuropathies,organic brain syndrome: Neuropsychiatric Manifestations of SLE
Serositis: -Pleurisy -Pericarditis: serositis of SLE
GI Manifestations: -abdominal pain, nausea/vomiting, anorexia due to diffuse peritonitis, pancreatitis, IBD, mesenteric vasculitis: GI Manifestations of SLE
Pulmonary Manifestations: -pneumonitis -pulmonary hemmorhage due to pulmonary vasculitis -pulmonary hypertension: Pulmonary Manifestations of SLE
Cardiac Manifestations: -pericarditis -myocarditis -- CHF -endocarditis -coronary vasculitis -atherosclerosis leading to AMI: Cardiac Manifestations of SLE
Vascular Manifestions -acute necrotizing vasculitis: Vascular Manifestions of SLE
Reticuloendothelial System -splenomegaly -lymphadenopathy, at single or multiple sites, nodes soft & tender: Reticuloendothelial Manifestions of SLE
Hematologic Manifestations -increased sed rate -cytopenias: Hematologic Manifestations of SLE
Treatment for SLE: -avoid sun
-NSAIDs & steroids
-DMARDs
Clinical course of SLE: -usually relapsing-remitting
-some have downhill course to death in months
-10 year survival = 70%
Dominated by fibrotic and degenerative skin changes.: Scleroderma
Includes the changes of scleroderma plus systemic fibrosis and systemic vascular injury.: Systemic Sclerosis
Scleroderma is aka ____. Systemic Sclerosis is aka ____.: Limited Scleroderma
Diffuse Scleroderma
CREST comprises most of the manifestations of ________ and it stands for_______.: -Limited Scleroderma
-Calcinosis, Raynaud's Phenomenon, Esophageal Dysmotility, Sclerodactyly, Telangectasias
Calcinonis: subcutaneous tissues develop calcifications that are either palpable, visible as radio-opacities on Xray or both. Fingertips most often.
Raynaud's Phenomenon: Painful, triphasic color change in acral areas, ie. fingers, toes, nose, ears. In response to cold exposure or stress, the acral arterioles constrict (ischemia-white). Next the area becomes cyanotic (blue) probably because the arterioles redilate slightly and perfusion is so minimal that blood releases oxygen. Next, arterioles dilate greatly (reactive hyperemia -very red)
Esophageal Dysmotility: atrophy and fibrosis of the esophagus causes:
-dysphagia
-LESD which causes GERD, Barrett's esophagus (metaplasia of epithelial cells of lower esophagus leading to precancerous lesion) from chronic GERD
Sclerodactyly: -first manifestation to occur in crest is diffuse edema of fingers and hands later replaced by skin thickening and tightness
-eventually, claw-like hand w/tapered fingers w/tight, shiny skin
-skin change later affects face, pulling into a tight mask with bared teeth
Telangectasias: -most commonly result from alcohol abuse
-permanently dilated blood vessels of the nose and cheeks
-in Scleroderma, it is more widespread and occurs w/o alcohol
anti-centromere antibodies: Limited Scleroderma
SCL-70 antibodies: Diffuse Scleroderma aka Systemic Scleroderma
Fibrotic and vascular changes that originally affected only the hands, esophagus and face intensify in those areas and cause problems in other systems: Diffuse Scleroderma aka Systemic Scleroderma
Skin Manifestations of Systemic (Diffuse) Scleroderma: -skin changes spread to arms, legs, trunk
-scattered hyperpigmentation of skin creates S&P appearance
-involved skin loses sweat glands and hair follicles
-hand skin becomes so tight that finger motility is impaired
-mouth becomes so tight that eating & oral hygiene become difficult
-ischemia of the fingers causes skin ulcers, necrosis and then loss at the tips
GI Manifestations of Systemic (Diffuse) Scleroderma: -anywhere from mouth to rectum
-fibrosis of small bowel leading to hypomotility, cramping, bloating
-colon develops wide-mouth saccular diverticuli
Cardiac Manifestations of Systemic (Diffuse) Scleroderma: -pericardial effusion may impair ventricular filling
-coronary vasospasm leads to left ventricular dysfunction
-systemic hypertension leading to left ventricular hypertrophy and failure
-pulmonary fibrosis leading to pulmonary hypertension and right ventricular hypertrophy and failure
Pulmonary Manifestations of Systemic (Diffuse) Scleroderma: -pulmonary fibrosis (restrictive lung disease & right ventricular failure)
-fibrosis causes decreased alveolar oxygen uptake
Kidney Manifestations of Systemic (Diffuse) Scleroderma: -marked sclerosis of arteries -->decreased GFR--> progressive azotemia and increased renin secretion--> malignant hypertension
Musculoskeletal Manifestations of Systemic (Diffuse) Scleroderma: -joint pain and stiffness due to skin tightness and tendon involvement
-friction rubs/crepitus of large joint (knee) due to fibrosis of synovium
-flexion contractures of fingers, wrist and elbow from fibrosis of synovium and periarticular structures
Clinical Course of Systemic (Diffuse) Scleroderma: -unpredictable, generally slowly progressive
-CREST syndrome may remain nonprogressive for long periods
-prognosis is poor if cardiac, pulmonary or renal involvement
Treatment for Systemic (Diffuse) Scleroderma: -no cure and nothing alters course of disease for long. Therefore, treatment is symptomatic.(Treat individual manifestations)Also, steroids provide no benefit in this time of inflammation.
Treatment for: -Raynaud's -GERD -Hypertension: -calcium channel blockers, angiotensin II receptor blockers
-antacids, anti-histamines (H2 blockers), proton pump inhibitors
-ACE-inhibitors
Immune-mediated inflammatory disorder of exocrine glands dominated by salivary and lacrimal gland dysfunction (dryness).: Sjogren's Syndrome
Primary Sjogren's Syndrome: when mucous membrane dryness and its related effects occur in isolation, it is called ______.
Secondary Sjogren's Syndrome: When other autoimmune diseases, notable RA, SLE and Systemic Sclerosis, may themselves cause similar exocrine gland degeneration and dysfuntion, it is known as ________.
Clinical Features of Sjogren's Syndrome: Dysfunction of:
1. Lacrimal Gland - dry, irritated eyes with foreign body sensation; corneal abrasions
2. Salivary Gland - dry mouth, oral sores and dental caries;lingual and labial fissures, dysphagia and GERD, parotid and/or submandibular gland swelling and tenderness
3. other mucous membrane - dry vaginal membranes (dyspareunia);recurrent or persistent sinusitis, dry tracheobronchial membrances leading to URI (pneumonia);pancreatic dysfn leading to nutrient malabsorption
anti-SS-A Ab aka anti-Ro Ab anti-SS-B Ab aka anti-La Ab: Sjogren's Syndrome
Pathology: Emigration of CD4 T-lymphocytes come in direct contact with ductal epithelial cells, causing cell mediated gland destruction: Sjogren's Syndrome
Diagnosis of Sjogren's Syndrome: -suspect SS if patient presents with chronically dry eys and mouth, esp. with mild joint pain
-ROSE BENGAL TEST=staining of cornea for abrasion
-Whole Saliva Sialometry=patient sucks on sugarless candy for 3 min. and spits watching for decreased secretions.
-SCHIRMER's Test=measure of the quant. of tears secreted in 5 min. in response to irritation by a strip of Schirmer's filter paper under each lower eyelid.
-young moisten 15mm, 1/3 of elderly moisten 10mm, SS will moisten <5mm
Labs: -salivary gland biopsy -70% have elevated ESR: Labs for Sjogren's Syndrome
Treatment for Sjogren's Syndrome: -avoid meds w/anticholinergic effects since much exocrine gland function is cholinergic
-treat Keratoconjunctivitis sicca, Xerostomia, dyspareunia, nephritis, pneumonitis, neueropathy, etc.
Treatment for Keratoconjunctivitis sicca: -hypotears (artificial tears)
-HydroEye caps = blend of omega-6 fatty acids and mucin
Treatment for Xerostomia: -stimulate saliva (sugarless gum, chewing paraffin or sucking on fruit pit, oral pilocarpine)
-Evoxac(cevimeline)=cholinergic agonist-salivation
-Fluoride treatment against caries in absence of saliva
Inflammatory disease of muscle.: Polymyositis
Inflammatory disease of muscle with a variety of dermatologic manifestations.: Dermatomyositis
four main categories of clinical features of PM & DM: 1. Proximal muscle weakness
2. Elevated serum levels of skeletal muscle enzymes
3. Electromyographic evidence of myopathy
4. Biopsy evidence of muscle inflammation
5. Skin rash - permits the Dx of Dermatomyositis
slow onset over 3 to 6 months without an identifiable precipitating event: Polymyositis/Dermatomyositis
3 main components of Acute Inflammation: 1. Local Hyperemia:from local arteriolar vasodilation-inc'd flow volume but dec'd flow velocity-neutros & RBC to site
2. Vascular Permeability:leakage of water,plasma proteins and neutrophils into tissue-swelling & pain
3.Leukocyte Emigration:accumulation, leakage & subsequent movement of neutrophils into the tissue by dec'd laminar flow
Histamine, Bradykinin, Leukotrienes, IL-1, TNF: chemical mediators of inflammation aggravate leakiness
after moving into the tissues, the neutros move toward the site of injury along gradients of _____.: chemotactic factors (chemical junk)
Vasoactive amines: chiefly histamine, found in mast cells adjacent to capillaries and venules, and in circulating basophils and platelets.
Histamine causes _____, _____ and therefore ______.: arteriolar dilation, venular leakage, edema.
Eicosanoids: the prostaglandins and leukotrienes
Prostaglandins and Leukotrienes lead to:: fever, pain, edema, vasodilation, bronchospasm
Which pathway do NSAIDs block?: cyclooxygenase pathway
Which pathway do steroids block?: phospholipid-induced production of arachidonic acid
a) Leukotriene receptor antagonists b)5-lipoxygenase inhibitor: a) Accolate (zafirlukast)
Singulair (montelukast)
b) Zyflo (zileuton) - off market
Acute phase reactions associated with injury or infection and induced by IL-1,IL-6, and TNF: -fever,lethargy,dec'd appetite,inc'd neutrophil count,ACTH release leading to corticosteroid release,hepatic synthesis of various proteins (acute phase reactants)
acute phase reactants: -fibrinogen
-C-reactive protein
-complement
In inflammation, the increased levels of _____ in the blood cause the sed rate to increase significantly.: fibrinogen
What role does Nitric Oxide play in the inflammation process?: vasodilation
Lysosomal enzymes: -elastase
-alpha1-antitrypisin: counteracts elastase
Outcomes of Acute Inflammation (4): 1. Complete resolution
2. Scarring
3. Abscess formation: occurs when injury is due to pyogenic bacteria
4. Progression to chronic inflammation
Chronic inflammation is seen in what 4 settings?: 1. persistent infection
2. prolonged exposure to toxic agents
3. autoimmune disease
4. sarcoidosis
Chronic inflammatory cells: macrophages, lymphocytes, plasma cells
Granulomatous Inflammation: distinctive form of chronic inflammation, characterized by aggregation of activated macros that develop a squamous "epitheloid" appearance. It may also become surrounded with fibroblasts and connective tissue
The role of the lympatics:: to remove inflammatory fluid and debris from the interstitial space
To prevent the normal net leakage of plasma proteins into the brain, and to prevent exposure to drugs, toxins or hormones that may enter the body, brain capillaries have:: blood brain barrier - tighter endothelial cell junctions
_______ allows penetration of the BBB by antibiotics, which is typically very selective.: Vascular permeability caused by inflammation
Morphologic Patters in Acute and Chronic Inflammation (4): 1. Serous Inflammation
2. Fibrinous Inflammation
3. Suppurative Inflammation
4. Ulceration - necrosis and erosion

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