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281 Cards in this Set
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- Back
Blood
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a liquid tissue containing seven types of cells that are suspended in a watery substance called plasma
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Types of white blood cells (leukocytes)
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basophils, eosinophils, neutrophils, lymphocytes, monocytes (become macrophages)
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Functions of Blood (3)
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1. Transport oxygen and carbon dioxide
2. Transport of ions, glucose, wastes, and hormones 3. Acts as a defense for the body against foreign materials. |
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Where are blood cells produced?
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Bone Marrow
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What single type of cell does blood form from?
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Multipotent Stem Cell
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Erythropoietin (EPO)
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produced by kidneys and increases production of red blood cells (tells bone marrow to produce more RBCs)
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Thrombopoietin (TPO)
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increases production of platelets
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Interleukin-7
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major cytokine that stimulates stem cells to increase lymphocytes
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Anemia
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shortage of RBCs, shortage of amount of hemoglobin in them, most commonly caused by inadequate intake of iron
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Definition of Anemic and tx
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hemoglobin < 10.....treat with PROCRIT
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#1 WBC
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T Lymphocytes
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Where do T Cells migrate from the bone marrow to mature?
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Thymus
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Components of Blood Plasma and Percentages
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Water 92%
Proteins 6% Salt 0.8% Lipids 0.6% Glucose 0.2% |
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Site of occlusion in vein occlusion
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lamina cribrosa
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How can you tell a vein occlusion is non-ischemic?
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LACK of hemes, CWSs, APD, and being able to see underlying choroid, px has good VA
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What is the main concern in ischemic CRVO?
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neovascular glaucoma
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What is a big cause of CRVO?
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glaucoma (bc lamina cribrosa is compressed in glaucoma)
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Hypoperfusion Retinopathy/Ocular Ischemic Syndrome
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usually unilateral, males > females 2:1, *dot/blot hemes and microanuerysms found only in mid-periphery (=Hypoperfusion Retinopathy); when above are associated with neo of disc, retina, iris, or angle = Ocular Ischemic Syndrome
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Pathogenesis of OIS
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atheromatous ulceration and stenosis at bifurcation of common carotid artery
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Symptoms of OIS (know)
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1) ocular and periorbital pain in 40% of cases
2) prolonged recovery of vision following exposure to bright light (Light Induced Amaurosis) 3) Amaurosis Fugax (TMB) in 5% of cases 4) TIAs |
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Ocular Signs in OIS
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1) dilated but not tortuous veins
2) retinal hemes in mid-peripheral retina (80%) 3) CWSs (5%) 4) Neo of disc (35%) 5) Neo of retina (8%) 6) rubeosis iridis (65%) 7) uveitis- mild anterior (20%) |
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What should you think if you see uveitis in older px?
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Carotid artery disease
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Work up for OIS
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Carotid artery evaluation & echocardiogram
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Tx for OIS
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carotid surgery if needed, aspirin, PRP for neo, stop smoking
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1st and 2nd leading causes of death in OIS
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1) Ischemic heart disease
2) Stroke |
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Hypercoaguable State
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px is constantly making clots bc factor 5 is always turned on (someone below age 50 should not have vein occlusion; if they do, should think hypercoaguable state)
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Primary State conditions that can cause ocular problems (know)
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1. Protein C deficiency
2. Protein S deficiency 3. Antithrombin III 4. Factor V Leiden ** (1 out of 10 ppl) 5. Hyperhomocysteinemia 6. Prothrombin 20210 mutation 7. Antiphospholipid syndrome- miscarriages |
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What proteins turn off the coagulation pathway?
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Protein C and S
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Protein C or S deficiency/Antithrombin III deficiency
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these proteins normally turn factor 5 off; deficiency would leave factor 5 on constantly resulting in venous thromboembolism
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What is the most common hereditary blood coagulation disorder in US?
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Factor V Leiden
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Factor V Leiden
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a defect in factor 5 so that it can never be turned off; resistant to Protein C, found in 10% of caucasions, rare in AA and asians
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Hyperhomocyteinemia
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causes high levels of the amino acid homocysteine; leads to artery and vein occlusion, stroke, upward lens subluxation, heart attack in older males, **treat with B6, B12, and folic acid
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Prothrombin 20210 gene mutation
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**second most common hereditary blood coagulation disorder; elevated levels of plasma prothrombin; increased risk of venous thrombosis; 4% of Caucasians
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Antiphospholipid syndrome
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antibodies to phospholipids activate coagulation cascade; **can lead to BOTH artery and vein occlusions; cause of most miscarriages
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Tx of Hypercoaguable State
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Coumadin, Heparin, Aspirin therapy**
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What ocular finding is characteristic of carotid artery disease?
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midpeipheral hemes
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What do you have to rule out if you see someone younger than 50 with a vein occlusion?
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hypercoaguable state
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Hyperviscosity Syndromes
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if px makes too many RBCs, WBCs, or platelets, buildup occurs and their byproducts make the blood very thck
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3 types of Hyperviscosity Syndromes
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1. Waldenstrom Macroglobulinemia (IgM)
2. Multiple Myeloma (tumor of B cells) 3. Leukemia |
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What is the hallmark ocular sign of hyperviscosity?
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Sausage Link Vessels
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What is a bilateral vein occlusion indicative of?
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Hyperviscosity
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Tx of Leukemia
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Chemo and radiation therapy (ocular manifestations resolve after tx)
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Types of Leukemia
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1. Chronic Lymphocytic Leukemia
2. Chronic Myeloid Leukemia 3. Acute Lymphocytic Leukemia 4. Acute Myeloid Leukemia **most common |
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Multiple Myeloma
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malignant plasma cell tumor- end stage B lymphocyte; tumors cells produce massive quantities of IgG or IgA
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Waldenstrom macroglobulinemia
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neoplastic B cells produce IgM at too high of a rate
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Anemia
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decrease in RBC count, hemoglobin, orhematocrit
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Causes of Anemia
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1. decreased RBC production
2. hemotopoietic cell damage from infection, drugs, or radiation 3. deficiency of factors like iron necessary for heme synthesis 4. increased RBC loss from external blood loss or red cell destruction |
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Sickle Cell Retinopathy KNOW
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1. Seafan neo
2. Black sunbursts- RPE hyperplasia 3. Salmon Patch Hemorrhages |
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***7 types of blood cells
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1. RBCs (Erythrocytes)
2. Platelets (Thrombocytes) 3. White Blood Cells (Leukocytes) a. Basophils b. Eosinophils c. Neutrophils d. Lymphocytes e. Monocytes- become macrophagesd |
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Difference between hypercoaguable and hyperviscosity
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1. Hypercoaguable=blood clots; mid-peripheral hemes
2. Hyperviscosity=too many cells and cell by-products; bilateral vein occlusions |
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Tx of Hypercoaguable syndromes vs Hyperviscosity syndromes
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1. Hypercoaguable- Coumadin, Heparin, Aspirin
2. Hyperviscosity- chemo or radiation therapy, bone marrow transplantation |
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Most common and second most common coaguable states
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1. Factor V Leiden
2. Prothrombin 20210 gene mutation |
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Normal INR (International Normalized Ration) for a px on Coumadin
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2.0-3.0
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What disease do 50% of Giant Cell pxs have?
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Polymyalgia Rheumatic (PMR)- stiffness in neck, shoulder, and hip
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Ocular Manifestions of Giant Cell
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#1. ION
2. acute painless vision loss 3. pale swelling of optic nerve head with flame shaped hemes 4. CRAO 5. CN 3, 4, 6*** 6. CWSs 7. OIS 8. Cilioretinal Artery Occlusion 9. Must refer to ER for sed rate and C-reactive protein |
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Etiology of AAION (vs NAION)
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occlusion of short posterior ciliary arteries with giant white blood cells
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Systemic Presentation of AAION
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Headache, scalp tenderness, jaw claudication, night sweats, weight loss, fever, PMR, depression
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Systemic Testing for AAION
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Immediate C-reactive protein, CBC w/ platelets, Westegren Sed. Rate, carotid artery evaluation, echocardiogram, fluorescein angiography
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Tx for AAION
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IV steroids, temporal artery biopsy, followed by oral steroid
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Blood aqueous barrier
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tight junctions between non-pigmented epithelial cells of ciliary body and blood vessels of iris
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Most common WBC?
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T cell (apprrox 70%)
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What produces antibodies
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B cells
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What matures in bone marrow?
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B cells
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What matures in thymus?
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T cells
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What must you rule out if you see hemorrhages in mid-periphery?
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carotid artery disease
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2 main causes of carotid artery disease?
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1. cholesterol buildup due to high cholesterol
2. GCA |
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Is tehre pain with carotid artery dx?
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yes; known as ocular angina from OIS
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Most common hypercoaguable syndrome?
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Factor V
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Tests for GCA?
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C-reactive protein and ESR
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Are RBCs nucleated?
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NO
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Which blood type is the universal recipient?
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Group AB- cant give blood to anyone unless AB too
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Which blood type is the universal donor?
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Group O- has neither A or B antigens
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Hemoglobin
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Oxygen carrying molecule (marrow stimulated to make hemoglobin by EPO; kidneys produce EPO in response to hypoxia)
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Microcytic Anemias (MCV<80)
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small red blood cells from:
1. iron deficiency** 2. thalassemias 3. sideroblastic anemias 4. lead poisoning |
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Normocytic Anemias (MCV 80-100)
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1. anemia of chronic disease**
2. aplastic anemia 3. sickle cell disease 4. bone marrow infiltration 5. blood loss/hemolysis |
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Macrocytic Anemias (MCV>100)
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1. liver disease
2. myelodysplasia 3. elderly 4. hypothyroidism 5. alcohol 6. drug induced 7. hemolysis 8. megaloblastic anemias (vitamin B12 and folate deficiencies**) |
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Most common cause of anemia?
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iron deficiency (most common) and anemia of chronic disease
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Initial Tests to oder in anemia
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CBC, reticulocyte count, peripheral smear, iron, folate, and B12 levels
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Sideroblastic Anemia
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teardrop shaped cells
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Megaloblastic Anemia
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oval macrocytes, hypersegmented neutrophils, vitamin B121 or folate deficiency
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Neutrophils (myeloid family)
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mobile phagocytes, kill organisms covered with antibodies, fight bacterial infections, clean up dead/damaged tissue
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Basophils (myeloid family)
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granules contain histamine and heparin, role in immedate hypersensitivity rxns
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Eosinophils (myeloid family)
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increased numbers in parasitic infections
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Monocytes (myeloid family)
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clean up debris, phagocytic
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T-cells (lymphoid family)
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70%; initiate and regulate immune response; fight viral infections
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B-cells (lymphoid family)
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synthesize and secrete antibodies
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Platelets
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1st responder to stop bleeding
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Hemophilia- The Prototypical Coagulation Factor Deficiency
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X-linked recessive, low factor VIII or IX levels, deep soft tissue bleeds in joints and muscles, NO PETECHIAE**, tx w/ transfusion of deficient factors
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2 drugs that deactivate key clotting factors
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Heparin and Warfarin
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Acquired Hypercoaguable States- Virchow's Triad
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1. alteration in blood flow (venous stasis)
2. injury to vascular endothelium- major trauma 3. alteration in constitution of blood (hypercoaguability) from cancer, smoking, birth control pill, etc |
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Symptoms of Acute Leukemia
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1. decrease WBC: fever, infection
2. decrease RBC: fatigue, pallor 3. decrease PLT: bleeding 4. enlarged liver, spleen lymph nodes *adults: 80% myelogenous (AML), 20% lymphoblastic (ALL) |
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Autologous (Bone Marrow Transplantation)
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stem cells harvested from patient himself
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Allogeneic (Bone Marrow Transplantation)
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stem cells harvested from a matched donor
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What kind of cells are present in Hodgkins (younger pxs) and non-hodgkins (older pxs)?
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Reed-Sternberg cells
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Transfusion Reactions
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1. Acute Hemolytic Transfusion Rxn (major ABO incompatibility; high mortality)
2. Delayed Hemolytic Transfusion Reaction (slow progression destruction of RBCs) 3. Febril Reaction (donor white cells release inflammatory substances during storage) 4. Allergic rxn |
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Is preseptal cellulitis an orbital disease?
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NO; it is inflammation of periocular structures (lids and skin) ANTERIOR to the orbital septum
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Hordeolum dx and tx
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dx: focal, painless, hard lump; blockage of glands of Zeiss or Moll
tx: hot compresses and topical and/or oral antibiotic like doxycycline or Keflex |
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Chalazion dx and tx
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dx: meibomian gland blockage
tx: hot compresses; can be lanced or removed bc not infectious; if multiple get biopsied |
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Dacryocystitis dx and tx
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dx: painful, swollen and infected lacrimal sac and/or drainage system
tx: oral antibiotics with a topical antibiotic such as a fluoroquinolone or even Polytrim; also give tylenol and codeine *never lance bc do not want to spread infection |
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Clinical Presentation of Preseptal Cellulitis
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1.mild orbital edema usually involving UPPER eyelid only
2. unilateral 3. warmth of eyelid 4. eyelid erythema, tho bulbar conjunctiva is white and quiet 5. **no proptosis, no EOM restrictions, and no pain on eye movement 6. globe is uninvolved 7. VAs and pupils are normal |
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Slit lamp evaluation of Preseptal Cellulitis
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1. AC rxn
2. corneal/conj changes 3. s-shaped inflammation of upper lid |
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Tx of Preseptal Cellulitis
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1. Tetanus toxoid: if traumatic
2. oral antibiotics: Keflex, Ceclor, Augmentin, Bactrim (if px is allergic to PCN), Erythromycin (if px is allergic to PCN and sulfa) 3. warm compresses 4. topical and oral decongestants 5. topical antibiotic: esp Polytrim or Polysporin |
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Is orbital cellulitis an orbital disease??
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YES; an infection/inflammation within retrobulbar tissues within orbit; life threatening; px must be put on IV antibiotics; watch for exudative retinal detachment*
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Etiology of Orbital Cellulitis
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1. extension of preseptal cellulitis
2. **direct extension of sinus infection (#1 cause of orbital and preseptal) 3. following dacryoadenitis, dacrocystitis, acute hordeolum, chalazion 4. following orbital trauma, ocular foreign bodies 5. post-surgical 6. following a systemic illness like bacteremia or septicemia |
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Patient Symptoms/Signs of Orbital Cellulitis
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1. Red, injected eye (*globe is now involved)
2. decreased VA or blindness: ON involved 3. Proptosis (key to dx!)- may cause double vision 4. malaise, fever, and headache- acute illness 5. *external ophthalmoplegia- inability to move eye **3 Ps: Proptosis, external ophthalmoPlegia, Pain 6. possible APD (if ON is involved) 7. disc edema 8. fever 9. increased IOP |
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Tx of Orbital Cellulitis
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IV antiobiotic to cross BBB
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Forced Ductions (paresis vs mechanical involvement)
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1. a paresis will move with forced ductions
2. mechanical involvement: eye will NOT move |
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Orbital Cellulitis with Cavernous Sinus Involvement
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spread of infection of orbital cellulitis to cavernous sinus, leading to cavernous sinus thrombosis; fatal outcome
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Clinical Presentation of Orbital Cellulitis with Cavernous Sinus Involvement
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1. fever
2. progressive proptosis 3. BILATERAL** 4. EOM dysfunction 5. Rising IOP 6. Papilledema 7. Pain *Remember 3 Ps: Pain, external ophthalmoPLEGIA, Proptosis 8. Purple lid skin 9. Severe congestion; bruit 10. fundus shows hemes, tortuosity, ON pallor 11. headache, nausea, vomiting, varying levels of consciousness 12. CN III, IV, and VI palsies |
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Orbital Cellulitis with Mucomycosis
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life-threatening orbital FUNGAL infection; seen in diabetics, transplant pxs, and **severely immuno-compromised pxs
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Dx and tx of Orbital Cellulitis with Mecomycosis
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Dx: proptosis and EOM involvement, **black eschar: ischemic infarction and septic necrosis**; rapid deterioration
Tx: 1. Ketoconazole 2. Enucleation surgery 3. Amphotericin B to clean out hollow globe 4. Immediate hospitalization 5. Mortality rate: 30% |
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Idiopathic Orbital Inflammation
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1. non-neoplastic, noninfectious space-occupying periocular lesion
2. may affect orbit focally, diffusely, or in a tissue-specific manner 3. 5% of all orbital lesions 4. may be acute, recurrent, or chronic 5. UNILATERAL* 6. males = females 7. peak incidence most frequently middle age |
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Signs/Symptoms of Idiopathic Orbital Inflammation
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1. malaise and distress*
2. unilateral* 3. conjunctival chemosis and injection 4. uveitis 5. check vital signs* 6. sinuses are normal in CT scan* (in orbital cellulitis they are full of infectious material bc sinus infection is usually the cause) 7. no bony involvement of orbit* |
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Treatment of Idiopathic Orbital Inflammation *impt
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trial of steroid therapy: 60 to 100 mg po once per day for 2 weeks to 1 month, with tapering dose over several months (also anti-ulcer meds, low dose radiation therapy, immunosuppressive agents, orbital biopsy)
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Anterior Uveitis
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inflammatory cells in the anterior chamber (ddx: HLA-B27, Bechet's, Sarcoidosis, Fuch's Heterochromic Iridocyclitis, JRA, Syphilis, Herpetic, Masquerade syndrome)
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Intermediate Uveitis
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inflammatory cells in vitreous
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Posterior Uveitis
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inflammtion of retina or choroid with or without vitritis
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Panuveitis
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all of above; entire eye involved
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Limited Uveitis
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duration of attack is <3 months
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Recurrent Uveitis
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>3 months between episodes
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Chronic Uveitis
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episodes <3 months apart, not including tx time
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What test should be ordered with anterior uveitis?
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HLA-B27
1. over 50% are HLA-b27 positive 2. 71% if unilateral and recurrent 3. 58% have seronegative spondyloarthropathy |
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What systemic disease has a high association with anterior uveitis?
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Ankylosing spondylitis (45%)
-> 30-40% of pxs with AS will have at least 1 epidose of uveitis |
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Duration of tx for uveitis***
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4-9 weeks per attack (mean duration 6 weeks)
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Avg number of uveitis attacks***
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Median = 3 (range 1-26)
Recurrent uveitis attacks can be associated with CME |
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Reiter's Syndrome (reactive arthritis)***
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85-95% +HLA-B27
Triggers***: 1. Diarrhea or dysentery esp due to food poisoning 2. arthritis (usually within 30 days of infection) |
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Tx for Uveitis***
|
1. Topical corticosteroids for all **always use PRED FORTE
2. oral corticosteroids 3. periocular corticosteroids |
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How to taper steroids
|
only taper when there is a 2-step decrease in number of cells (= 1 grade level decrease)
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Topical corticosteroids
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for anterior disease
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Periocular steroid injections
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for unilateral, intermittent disease; CME
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Oral corticosteroids
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for bilateral, chronic, vision-threatening disease
|
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Immunosuppressive drug therapy
|
steroid-sparing effect in chronic disease after steroids have been stopped
|
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Differences between Episcleritis and Scleritis
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Episcleritis
irritation superficial inflammation ocular complications uncommon systemic disease uncommon tx topical Scleritis painful deep inflammation ocular complications common systemic disease common tx systemically |
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What can you get in Wegener's Granulomatosis?
|
necrotizing scleritis
1. inflammation of small and medium sized blood vessels 2. scleral thinning 3. peripheral ulcerative keratitis |
|
Diagnostic Tests for Scleritis**
|
1. always ddx syphilis & chest x-ray, RPR, FTA antibodies
2. ANCA C & P for Wegener's 3. Urinalysis 4. Chest x-ray 5. Lyme antibody 6. RF, ANA (rarely) |
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4 Connective Tissue Diseases
|
1. SLE
2. Scleroderma 3. Sjogren's 4. MCTD |
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Systemic Lupus Erythematosus (SLE)
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1. 9 xs more common in women than men
2. 20-30 yrs 3. more common in AA, Hispanics, and Asians 4. autoimmune disease |
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Clinical Manifestations of SLE (DOPAMINe RASH)
|
Discoid rash
Oral ulcers Photosensitivty Arthritis Malar rash: butterfly rash Immunological: decreased WBC count Neurological Renal disorders ANA + Serositis + Hematological: anemia, thrombocytopenia **definite SLE: 4 or more criteria |
|
Auto-antibodies tests for Lupus
|
1. Anti-dsDNA
2. Anti-Smith: specific for Lupus** 3. APLA 4. ANA |
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What is the most sensitive test for SLE?
|
ANA (97%) but has poor specificity
|
|
Tx of SLE
|
treat symptoms only:
1. NSAIDS for joints 2. High-dose glucocorticoids if severe and major organ involvement DMARDS: disease-modifying agents 1. antimalarial druge 2. methotrexate: anti-neoplastic agent for disease control |
|
Scleroderma
|
presence of thickened, sclerotic skin lesions; includes abnormalities of vasculature and involvement of multiple organ systems, **can often affect KIDNEY
Also: 1. peak ago of onset 30-40s 2. more common in females and AA 3. ***90% of pxs also have Raynaud's phenomenon |
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Clinical Manifestations of Scleroderma (CREST)
|
Calcinosis: calcium deposits in skin, nodules
Raynaud's Phenomenon Esophageal dysmotility: trouble swallowing and acid reflux Sclerodactyly: fibrosis of skin on fingers, long tapering thin fingers Telangiectasia: small red blood vessels all over body *scleroderma renal crisis: malignant HTN with renal failure is a medical emergency |
|
Tx of Scleroderma
|
difficult to treat; no cure
1. D-penicillamine for skin disease 2. calcium channel blocker for Raynaud's phenomenon 3. ACE inhibitor for renal crisi 4. corticosteroids for pulmonary fibrosis |
|
Sjogren's Syndrome
|
chronic inflammatory disorder caused by a lymphocytic infiltrate that destroys the lacrimal and salivary glands
|
|
Clinical Manifestations and Dx of Sjogren's
|
1. keratoconjuctivitis sicca, or KCS = dry eyes
2. Xerostomia (dry mouth) 3. 70% with +ANA, SS-S in 60-70% 4. + Schirmer test |
|
Tx of Sjogren's
|
wetting agents, corticosteroids if severe symptoms, anti-malarial agents
|
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Mixed Connective Tissue Disease (MCTD)
|
overlap syndome that has features of several connective tissue diseaes such as SLE, scleroderma
*characteristic antibody: Anti-RNP |
|
Seronegative Spondyloarthropathies (SpA)
|
Features:
1.**more common in males than females (unusual for an autoimmune disease) 2. inflammatory back pain worse upon waking 3. peripheral arthritis (joints) 4. enthesitis (inflammation where tendons and ligaments attach to bone) 5. dactylitis (sweating and pain in fingers) 6. UVEITIS 7. sacroiliitis 8. spondylitis (vertebrae) |
|
Ankylosing Spondylitis
|
1. male: female ratio of 4:1
2. 97% of AS px have HLA-B27 3. Get diarrhea after being infected with bug 4. predilection for sacro-iliac joints and spine (bamboo spine); px cant bend over and touch toes 5. elevated ESR 6. **Uveitis: acute, unilateral, recurrent |
|
Tx of Ankylosing Spondylitis
|
1. exercise
2. posture training 3. NSAIDS 4. Sulfasalazine, Methotrexate 5. Anti-TNF agent: Etanercept*** |
|
Reiter's Syndome: Post-Infectous Arthritis or "Reactive Syndrome" Classic Triad
|
1. Urethritis
2. Conjunctivitis 3. Arthritis |
|
Reiter's Syndrome
|
1. most cases occur within 1 to 4 weeks of dysenteric infection
2. 65-85% are HLA-B27+ 3. Arthritis: 100% (predominantly of lower extremeties) 4. Enthesitis 70% 5. Dactylitis 20% 6. Spinal disease 20-30% 7. **Ocular: Uveitis (acute, unilateral and recurrent) and Conjunctivitis 8. **Urethritis (part of classic triad) |
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Tx of Reiter's
|
No good tx:
1. NSAIDS 2. Antibiotics for venereal infection 3. Sulfasalazine, Chloroquine, or Methotrexate |
|
Psoriatic Arthritis
|
1. male:female ratio is 1:1
2. Often HLA-B27+ 3. Arthritis: usually upper extremities 4. "sausage digits" dactylitis 5. extensive skin manifestations (scaly) 6. Tx: NSAIDS, Methotrexate, Cyclosporine, Etanercept, Infliximab, T-cell inhibitors: Efalizumab, Alefacept |
|
Inflammatory Bowel Disease-Associated Spondyloarthropathy
|
1. can occur w/ Crohn's or Ulverative Colitis
2. oligoarthritis predominanly in lower extremities 3. sacroiliitis and spondylitis 4. uveitis** 5. HLA-B27 associated with #3 (but NOT peripheral arthritis |
|
Bechet's Disease
|
1. small medium or large blood vessels
2. associated with HLA-B51 3. TRIAD***1) oral and genital ulcers, 2) uveitis, 3) arthritis 4. Skin: folliculitis, e. nodosum-like lesions 70% 5. tx topical steroids |
|
Dx of Polyarteritis Nodosa
|
1. medium-sized vessel vasculities (ie vessels to heart)
2. joint inflmmation 3. cutaneous ulcers 4. mesenteric ischemia 5. dx: mesenteric or renal angiography showing microaneurysms, or biopsy** |
|
Wegener's Granulomatosis
|
1. granulomatous vasculitis of small arteries, arterioles, and capillaries
2. Triad of organ involvement: upper respiratory tract, lungs, kidney 3. *necrotizing scleritis 4. dx + ANCA (antibody against own neutrophils) 5. tissue dx**: biopsy (sinuses or lung) = GOLD STD 6. tx: steroid & cyclophosphamide |
|
Osteoporosis
|
1.common in elderly men with Vit D deficiency or post-menopausal women
2. **most common skeletal disorder in the world 3. bone mass value 1 to 2.5 SD below DEXA score = osteopenia 4. bone mass value 2.5 or more SD below DEXA score = osteoporosis 5. Type 1: Post-menopausal 6. Type 2: Senile (age-related) 7. dx with DEXA Scans (Dual Energy X-ray Absorptiometry): calculates bone mineral density |
|
Prevention and Tx of Osteoporosis
|
Prevention:
1. calcium intake 2. Vitamin D intake 3. healthy weight 4. avoidance of ETOH, tobacco, and caffeine Tx of Disease: 1. Calcitonin 2. Biphosphonates 3. estrogen 4. Fluoride |
|
Most common joint disease?
|
Osteoarthritis
|
|
Osteoarthritis
|
-degenerative wear and tear
-NOT inflammation -90% of pxs over ago 40 -causes: *obesity, wear & tear, previous inflammation, aging, genetic |
|
Symptoms of Osteoarthritis
|
-joint degeneration but no systemic manifestation
-minimal morning stiffness -pain -crepitus -warmth (will NEVER be hot) |
|
Degenerative Changes in Osteoarthritis
|
early: narrowing of joint space
advanced: enzymatic degradation and thinning of cartilage end stage: bones start touching/rubbing against one another |
|
Three characteristic of Osteoarthritis (KNOW)
|
1) narrowing of joint space
2) osteophytes 3) bony cysts |
|
Gout
|
-crystal deposition disease
-hyperuricemia (high uric acid levels cause crystals to form in joints) |
|
Causes of Hyperuricemia (2)
|
1) under-excretion of uric acid
2) overproduction of uric acid |
|
Acute Gout Attack
|
Podagra- big red inflammation of big toe
Polyarticular- involve multiple joints Tx: resolves on its own |
|
Which drug helps inhibit uric acid formation?
|
Allopurinol
|
|
When should allopurinol not be given?
|
during an acute gout attack bc it will make it worse
|
|
Which drug increases secretion of uric acid?
|
Probenecid
|
|
Pseudogout
|
Calcium Pyrophosphate Dihydrate Deposition (CPPD): NOT uric acid
|
|
Difference in crystals Gout vs Pseudogout
|
Gout crystals are needle-shaped and yellow
Pseudogout crystals are round and blue |
|
Etiology of Infectious arthritis: Septic Arthritis **
|
Neisseria gonorrhea & Staphylococcus sp.
->rapidly destructive; can lost joints |
|
Septic Arthritis: Dx
|
Arthrocentesis: important to culture bc if there is an infection, steroids are contraindicated!
|
|
What is an IgM marker for rheumatoid arthritis?
|
RF
|
|
How much is life expectancy decreased in RA?
|
3-18 yrs bc of disease and tx
|
|
Pathological hallmark of RA?
|
pannus (inflammation of tissues lining joints and is a systemic dx); inflammatory, proliferative synovial membrane (vs osteoarthritis which is not inflammatory and is limited to joints)
|
|
What is the leading cause of death in RA?
|
Coronary Artery Disease: due to inflammation of blood vessels
|
|
Tx of RA
|
NSAIDS
Steroids DMARDS (Methotrexate, Hydroxychloroquine) Antibodies Aggressive early tx |
|
Relapsing Polychondritis
|
episodic inflammation and destruction of cartilaginous structures and connective tissue (cartilage in EARS, nose, respiratory tract)
|
|
What is the gold standard for dx of Inflammatory Myopathies?
|
Muscle biopsy
|
|
Inflammatory Myopathies
|
cannot comb hair, cannot climb stairs
-polymyositis and dermatomyositis: inflammation of muscles with skin changes -proximal muscle weakness(big muscles) and elevated CPK (muscle enzyme) |
|
Tx of Inflammatory Myopathies **
|
Corticosteroids
Other immunosuppressants IVIG: immunoglobulin Physical therapy |
|
Most commonly involved sites in Paget's Disease of Bone
|
**Skull
Sacrum Spine Femur Tibia Pelvis |
|
Paget's Disease
|
abnormal bone remodeling: new weaker bone is formed, resulting in skeletal deformities and pain
|
|
What are the main symptoms of Paget's?
|
*bone pain and deformity
leg bowing |
|
Tx for Paget's
|
analgesics
bisphosphonates to prevent bone resorption (Boniva) surgery NSAIDS |
|
"Everywhere hurts"
|
Fibromyalgia
|
|
Most common cause of musculoskeletal pain in US in women 20-55 yrs
|
Fibromyalgia
|
|
DDx of Fibromyalgia
|
Depression, Chronic Fatigue Syndrome
|
|
What is the most common presenting symptom everywhere (in MD office/ER)?
|
acute back pain
|
|
What is the most common cause of acute back pain?
|
70% are lumbar strains and sprains
|
|
How do you treat acute back pain?
|
40% pxs are better in 1 week
90% pxs are better in 2 months tell px to take NSAIDS and wait it out |
|
What 4 things are most likely associated with carpal tunnel syndrome?
|
1) pregnancy, and women using oral contraceptives
2) Hypothyroidism 3) Diabetes 4) Dialysis pxs |
|
Symptoms of Carpal Tunnel Syndrome
|
numbness and tingling in median nerve distribution; this nerve innervates thumb, pointer, and middle finger, and half of ring finger
|
|
Lateral epicondylitis
|
"tennis elbow"; involves extensor muscles of forearm and lateral epicondyle
|
|
Medial epicondylitis
|
"golfer elbow"; involves flexor muscles of forearm and medial epicondyle
|
|
Which muscle is most common torn in Rotator Cuff Tear?
|
supraspinatus tendon
|
|
What is the purpose of the rotator cuff?
|
to rotate and lift arm; stabilizes shoulder joint; a single tendon
|
|
Largest tendon in body?
|
Achilles Tendon
|
|
Most commonly ruptured tendon?
|
Achilles Tendon
|
|
Familial polypoosis coli
|
Colon cancer 100%
|
|
What is the most prevalent cancer in men?
|
prostate
|
|
What is the most prevalent cancer in women?
|
breast
|
|
What is the most common cause of death from cancer in men and women?
|
lung
|
|
Carcinomas arise from which type of cells?
|
epithelial cells
|
|
Sarcomas arise from what type of cells?
|
cells that make up bone or connective tissue
|
|
Leukemias and lymphomas arise from cells from where?
|
marrow/immune system
|
|
Which type of cancer does not have a reliable screening dx?
|
Lung cancer
|
|
Screening applies to which types of cancer?
|
cervix, breast, colon, prostate
|
|
TNM System
|
tells whether cancer is curable or not
Tumor: size, amt of local invasion? Label T1-T4 Node involvement: any/which ones? Label N0-N3 Metastasis: Yes/no? Label M0 for no, and M1 for yes |
|
Does chemotherapy or radiation therapy damage nuclear DNA?
|
radiation therapy
|
|
What are the risk factors of breast cancer?
|
1. Increased age
2. 1st degree relatives afflicted (3x risk) 3. Genetics 4. Early menarche/late menopause 5. late first pregnancy or nulliparity 6. alcohol comsumption |
|
Breast Cancer Tx
|
1. Surgery
2. Chemotherapy: all tumors >1cm 3. Hormonal Therapy: Tamoxifen: anti-estrogen drug 4. Biologic agents: Herceptin 5. Aromatase inhibitors: Arimidex, Femara *used only in post-menopausal women w/ HR positive tumors |
|
American Cancer Society recommends colonoscopy when?
|
-beginning at age 50, every 10 yrs
-1st degree relative w/ cancer age >60: colonoscopy beginning at age 40, every 10 yrs -1st degree relative w/ cancer age <60: colonoscopy beginning at age 40, every 5 yrs |
|
Hereditary Non-Polyposis Colon Cancer (HNPCC)
|
when 3 1st degree relatives in 2 generations are diagnosed with colon cancer before age 50; almost everyone in family has some colon cancer
|
|
Tx for Colon cancer?
|
Hemicolectomy (removal of polyp) followed by chemotherapy
**Avastin is approved for metastatic colon CA and has minimal SE |
|
How do you grade a tumor in prostate cancer?
|
Gleason score- a high gleason score is worse
|
|
Hormone Therapy for Prostate Cancer
|
LHRH (Luteinizing Hormone Releasing Hormone): agonist combined with testosterone receptor antagonist
|
|
When is chemotherapy used in prostate cancer?
|
only in refractory cases and widespread disease
|
|
What type of lung cancer is most aggressive?
|
small cell lung ca
|
|
What is the #1 risk factor for lung ca?
|
smoking
(also smoking + asbestos exposure) |
|
Is adenocarcinoma more common in males or females?
|
females
|
|
Which type of lung ca is commonly found in smokers?
|
squamous cell carcinoma
|
|
aka oat cell carcinoma
|
small cell lung ca
|
|
Locations of adenocarcinomas, squamous cell carcinoma, and large cell carcinoma
|
adenocarcinoma: peripheral
squamous cell carcinoma: central lesions large cell carcinoma: central |
|
Where does lung ca often spread to?
|
bone and brain
|
|
Prognosis for lung ca?
|
poor; overall 5 yr survival is 10%
|
|
Is there a screening for lung ca?
|
NO
|
|
Gardasil
|
Vaccine to protect against cervical cancer; approved for 9-26 yr olds; effective against HPV 6, 11, 16, 18 (16 and 18 cause 75% of cervical CA)
|
|
Prognosis for Cervical Cancer
|
-94.6% survival at 5 yrs in early stages
-22% survival at 5 yrs in late stages |
|
Risk Factors for testicular cancer
|
-undescended testis (*increased risk even with surgical correction)
-family hx -infertility -HIV infection |
|
Survival Rate of testicular cancer?
|
one of most curable cancers; 5 yr survival exceed 90%
|
|
What should you never do on a testicular cancer px?
|
trans-scotal biopsy
|
|
What is done during orchidectomy in testicular cancer pxs?
|
retro-peritoneal lymph node dissection
|
|
ABCDs of skin lesions
|
Asymmetry
Borders: irregular Color: not uniform Diameter: larger |
|
Major determinant of prognosis of skin cancer?
|
depth of tumor invasion
|
|
What are risk factors for cancer of the esophagus?
|
cigarettes and alcohol
|
|
Barrett's esophagus
|
change in epithelium over time with GERD: predisposes px to esophageal ca
|
|
Dx of esophageal ca?
|
CT of chest/abdomen: *look for enlarge lymph nodes
|
|
Prevalence of ovarian cancer?
|
affects post-menopausal women
|
|
What is associated with decreased risk of ovarian cancer?
|
early first pregnancy, multiparity, oral contraceptive use, breast feeding
|
|
Risk factors for Liver Cancer
|
*Cirrhosis (fibrosis of liver)
*Alcohol *Hepatitis B and C |
|
Should you dilate pregnant pxs?
|
every trimester with tropicamide only
|
|
What is the best glaucoma med for a pregnant px?
|
Propine (alphagan p is 2nd best)
|
|
What is a good rule of thumb for pregnant pxs?
|
No drops of any kind should be given! (do NCT, not goldmann, do no use proparacaine)
|
|
Is there an increase or decrease in BP in pregnant women?
|
decreased blood pressure
|
|
Dermatologic Changes in pregnant px
|
1. Chloasma: blotchy brown hypermelanosis that occurs around eyelids and fades post-partum; due to increased levels of MSH
2. Pre-existing nevi, freckles, and scars increase in size and pigmentation 3. Spider angiomas due to increased estrogen levels (abnormal change) |
|
Visual function in pregnant px
|
-refractive errors remains constant**
-decrease in amplitude of accommodation in 2nd half of pregnancy (may need readers) |
|
IOP in pregnant px
|
decreases
|
|
Pre-eclampsia
|
hypertensive disorder unique to pregnancy; after 20th week of gestation; overall edema of body
|
|
Eclampsia
|
same as pre-eclampsia PLUS seizures and/or coma
|
|
Symptoms of Eclampsia
|
*visual disturbances
*blurred vision *30-100% have ocular symptoms |
|
Hallmark retinal sign of Eclampsia
|
***focal retinal arteriolar vasospasm and narrowing
-also hemorrhage, exudates, CWSs, and eventually disc edema |
|
Should you dilate pxs with PIH (pregnancy-induced hypertension)?
|
YES
|
|
Central Serous Chorioretinopathy (CSC)
|
spontaneous, localized serous retinal detachment (usually in area of macula)
|
|
Symptoms of CSC
|
**Metamorphopsia
-reduced VA -micropsia -dyschromatopsia -refractive shift towards hyperopia |
|
Clinical Manifestation of CSC
|
increased incidenve of gray or white subretinal exudates within the detachment (unique to pregnancy); presumed to occur due to fibrin in subretinal space
|
|
Purtscher-like Retinopathy
|
specifically related to child birth; occlusive vascular disorder; lack of blood flow to eye bc of retinal arteriolar occlusions during pregnancy
|
|
Funduscopic Findings in Purtscher-like Retinopathy
|
multiple, superficial, white retinal patches, resembling large CWSs, often associated with superficial peripapillary hemorrhages (right at disc); resolves spontaneously
|
|
Etiology of Disseminated Intravascular Coagulation
|
disturbance in homeostasis of body's clotting cascade
|
|
Disseminated Intravascular Coagulation occurs in:
|
-complicated abortions
-placental abruption; separation of placenta from uterus b4 baby is born -pre-eclampsia |
|
Clinical Manifestation of Disseminated Intravascular Coagulation
|
-widespread thrombus formation
-choroid most commonly involved -serous retinal detachment due to occlusion of choriocapillaris -fibrin deposition cause by clot formation in microvasculature |
|
Funduscopic Findings of Disseminated Intravascular Coagulation
|
-choroidal hemorrhage
-cystoid macular edema -serous retinal detachment |
|
Amniotic Fluid Embolism
|
-occurs during labor, delivery, or in immediate post partum pd
-mortality rate in 80% range*** -embolic material within amniotic fluid deposits in microvasculature of heart, lung, brain, and eye |
|
Symptoms of Pseudotumor Cerebri (PTC)
|
-increased intracranial pressure
-disc edema -Paton's lines around ONH due to disc edema -CN VI palsy -visual disturbances -headache, nausea, and vomiting |
|
Visual Field of PTC patient
|
enlarged blind spot
|
|
Management of PIH
|
***immediate delivery of baby due to increased mortality risk of mother
|
|
Management of PTC
|
-weight loss
-Diamox, Naptazene -**termination of pregnancy considered last resort (unlike PIH) |
|
2 idiopathic miscellaneous disorders during/after pregnancy
|
1) ptosis
2) Idiopathic Facial Palsy (3x more likely during pregnancy) |
|
Definition of CSME
|
1) exudates within 500 microns of foveola, if associated w/ adjacent retinal thickening
2) thickening of retina within 500 microns of foveola 3) zones of retinal thickening one disc area or larger, any part of which is within one disc diameter or foveola |
|
Are pxs with gestational diabetes at risk for diabetic retinopathy?
|
NO- do not need to be dilated unless they have symptoms
|
|
What is a pathogenic mechanism for diabetic retinopathy?
|
increased retinal blood flow
|
|
Risk factors for progression of DR**
|
1. increased cardiac output
2. increased plasma volume 3. decreased peripheral vascular resistance |
|
Category A Drugs during pregnancy
|
Controlled Studies show NO RISK
|
|
Category B Drugs during pregnancy
|
No Evidence of Risk in Humans; adverse findings in animals
|
|
Category C Drugs during pregnancy
|
Risk cannot be ruled out; human and animal studies are lacking
|
|
Category D Drugs during pregnancy
|
Positive Evidence of Risk; studies in humans have demonstrated fetal risk
|
|
Category X Drugs during pregnancy
|
Contraindicated in Pregnancy; studies have demonstrated positive evidence of fetal abnormalities or risk that clearly outweighs any possible benefit to px
|