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23 Cards in this Set
- Front
- Back
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Leukocyte Adhesion Deficiency Type 1
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Presentation: Recurrent skin and periodontal infections, delayed seperation of umbilical stump, granulocytosis
Pathophys: Lack of b-chain of LFA-1 and MAC-1 integrins leads to reduced firm adhesion in acute inflammation |
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Leukocyte Adhesion Deficiency Type 2
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Presentation: Recurrent skin and periodontal infections, delayed seperation of umbilical stump, granulocytosis
Pathphys: Fucose metabolism to lack of sialyl-Lewis X). Reduces rolling and initial attachment of leukocytes to endotehial cells (less severe) |
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Chdeiak Higashi syndrome
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Presentation: Recurrent skin and periodontal infections, esp. with Stap aureus. *Autosomal recessive also associated with albinism, neuropathy, retardation
Pathophys: Characterized by neutrophils and monocytes having large granules; cells have defect in ability for membranes to fuse, thereby having poor formation of phagosomes and lysosomal fusion with phagosomes |
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Chronic Granulomatous Disease
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Presentation: Severe recurrent infections of skin, lung, liver, bones esp. with catalase positive organisms; severely diminsed peroxide
Pathophys: lack of components of NADPH oxidase system either sex-linked (cytosolic component) |
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Neutrophil specific granule deficiency
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Presenation: Autosomal recessive characterized by recurrent infections of skin, ears, sinuses; delayed wound healing, and bleeding tendency
Pathophys: Lack of neutrophil specific granules and abnormal eosinophils and platelets |
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Myeloperoxidase deficiency
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Presentation: Fungal infection common; only appears as problem when patients have other issues (diabetes mellitus, steroid therapy)
Pathophys: autosomal recessive having defective or no production of myeloperoxidase (makes clorox from peroxide in lysosome) |
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Congestive Heart Failure: Left-sided heart failure
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Presentation: Dypsnea, Pulmonary Edema, Left sided S3 sound, Mitral valve regurgitation, Paroxysmal nocturnal dypsnea
Pathogenesis: Decreased ventricular contraction (systolic dysfunction), Noncompliant ventricle (diastolic dysfunction), Increased workload (increased afterload or preload) |
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Congestive Heart Failure: Right-sided Heart Failure
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Presentation: Prominence of jugular veins, right sided S3 heart sound due to volume overload in the ventricle, tricuspid valve regurgitation, painful hepatomegaly, depedent pitting edema and ascites
Pathogenesis: Decreased contraction, noncompliant right ventricle, increased afterload, increased preload |
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Shock
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Presentation: restless, agitated, pale and cold, rapid thready pulse, arterial hypotension, metabolic acidosis, changes in mental status
Cause: Hypovolemic, Cardiogenic, Septic, Neurogenic, Anaphylactic Pathogenesis: Initation of symtpoms, compensation (vasoconstriction, redistribution of flow to vital organs, tachycardia, renal fluid conservation) |
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Morphologies of shock
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Kidneys: Acute tubular necrosis
Heart: subendocardial hemorrhages Lungs: adult respiratory distress syndrome Brain: hypoxic encephalopathy GI tract: focal mucosal hemorrhages and necrosis |
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Clinical Significance of Hemmorhage
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1. Loss of Blood volume
2. Tissue damage 3. Iron deficiency anemia |
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Virchow's triad (pre-disposing factors for thrombus formation)
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1. Endothelial Injury (ex: trauma)
2. Hypercoagulability (increase clotting) 3. Stasis and turbulance (ex: DVT) |
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Stasis dermatitis
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Presentation: Orange discoloration around the ankles
Cause: deep venous insufficiency, rupture of penetrating branches Treatment: compression therapy, topical treatment |
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Superficial Venous thrombi
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Presentation: tenderness, local inflammation
Causes: IV drugs, varicose veins (rarely embolize) |
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Deep venous thrombosis
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Presentation: difficult to diagnosis (SOB)
Cause; most common site is leg (femoral, popliteal), also iliac, periprotstatic, ovarian |
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Factor V Leiden
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-Most common hereditary thrombosis syndrome
-Mutant form of factor V cannot be degraded by protein C and protein S |
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Disseminated intravascular coagulation (DIC)
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-Presentation: Gram neg sepsis, shock, carcinoma, amniotic fluid embolism/obstetric complications
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Factors which affect severity of ischemic injury
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1. Nature of vascular supply
2. RATe of development of occlusion 3. Vulnerability to hypoxia 4. Oxygen content in blood |
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Features used to distinguish benign from malignant
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Differentiation and anaplasia
Rate of growth local invasion metastasis |
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Urticaria
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Pruritic elevation of the skin
Cause: mast cell release of histamine, Type I IgE mediated reaction associated to certain foods, insect bites, drugs |
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Acute Generalized Exantehmatous Pustulosis
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Presentation: non-follicular pustules on edematous, erythematous skin (rash occurs 2 days to 3 wks after drug administration)
Associated drugs: B-Lactam antibiotics, Macrolides, Diltiazam, Antimalarials |
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Drug Rash With Eosiniphilia and Systemic Symptoms
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Presentation: fever, edema and follucular accentuation (vesicle, bullae, pustules), lymphadenophthy -->Big head
Associated Drugs: Sulfonamides, anticovulsants |
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Stevens-Johnson Syndrome (SJS), Toxic Epidermal Necrolysis
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Erythema mutliforme that involveds the skin and mucous membranes
Presentation: non-infectious ulceration of the mouth (SJS), TEN: lesions that are poorly defined, and macular with purpuric centers that coalesce=Nikolsky's sign-->epidermis can be readily rubbed off with the finger Drugs: Sulfonamides, Allopurinol, Cephalosporins, Imidazole |
