front 1 Gram + or - cause | back 1 Thickness of peptidoglycan cell wall |
front 2 Why does gram + or gram - matter? | back 2 Thickness of peptidoglycan wall will determine the type of antibiotics we will use |
front 3 Fungi divisions | back 3 Yeasts |
front 4 Molds shape | back 4 Hyphae - fingerlike |
front 5 Yeasts shape | back 5 Buds |
front 6 Fungi cell walls can produce | back 6 vitamin D |
front 7 Helminth | back 7 Worm parasite |
front 8 4 infectious agent categories | back 8 Bacteria |
front 9 Adaptive immune system consists of | back 9 T & B cells |
front 10 Innate immune system consists of | back 10 Macrophages |
front 11 Nonspecific immune system consists of | back 11 Skin, mucous membrane, stomach acid, lysozomes |
front 12 Gut Microbiota/Microbiome | back 12 Diverse microorganisms in and on the human body. Need to be fed to produce properly. |
front 13 Microbiota produces most of this vitamin in the body: | back 13 Vitamin K |
front 14 Nosocomial infections | back 14 occur when replacement of the normal flora occurs in the hospital setting |
front 15 Innate immune system | back 15 General system we are born with |
front 16 Adaptive system | back 16 Specific, takes exposure |
front 17 Immunization gives exposure for: | back 17 Adaptive immunity |
front 18 Virus can cause damage to tissues in two was | back 18 directly/indicrectly |
front 19 Chigella produces cytotoxin that causes | back 19 intestinal cells to die off. This produces hemorrhagic diarrhea |
front 20 Cell being infected hurts the host | back 20 Immune system removes that cell |
front 21 Direct cell damage from microorganism | back 21 cytoxin |
front 22 Indirect damage from microorganism | back 22 inflammation |
front 23 Acute | back 23 <4 weeks |
front 24 Subaccute | back 24 4-12 weeks |
front 25 Chronic | back 25 12 weeks or longer |
front 26 Recurrent acute | back 26 4 or more episodes per year |
front 27 IL-1 | back 27 cytokine that is proinflammatory, produces fever |
front 28 opportunistic infection | back 28 waits dormant for immune system to be distracted, takes the opportunity |
front 29 Symptoms of a UTI | back 29 Burning, have to pee a lot. |
front 30 Gram positive bacteria | back 30 Have thicker peptidoglycan walls so they hold on to dye more |
front 31 Gram negative bacteria | back 31 Thinner wall |
front 32 Infective endocarditis | back 32 Almost always infects the left side of the heart |
front 33 IV Drug user endocarditis affects: | back 33 The right side |
front 34 PRR stands for | back 34 Pattern Recognition receptors |
front 35 What type of receptors fall under the PRR category? | back 35 Toll-like receptors, nucleotide binding oligomeriation domain like receptors |
front 36 What activates PRRs | back 36 Exogenous organisms interacting with host cells |
front 37 What does PAMP stand for? | back 37 Pathogen-associated molecular patterns |
front 38 What happens when Pathogen associated molecular patterns are activated? | back 38 Activation of a pro-inflammatory cascade that plays a role in pathogen recognition and inactivation. |
front 39 Pathogen associated molecular patterns | back 39 PAMPS |
front 40 Which type of hypersensitivity response causes creation of immune complexes? | back 40 Type III |
front 41 Diarrhea classified as | back 41 Secretory |
front 42 Secretory diarrhea | back 42 Presents as watery, Enterotoxins activate intestinal enzyme activity, loses water and electrolyes |
front 43 Inflammatory diarrhea | back 43 Presents as mucus-y, |
front 44 Hemorrhagic Diarrhea | back 44 E.Coli most common, toxin destroys RNA, prevents cells from reproducing, bloody. |
front 45 Common causes of secretory diarrhea | back 45 v.cholerae |
front 46 Common causes of inflammatory diarrhea | back 46 Mucus-y |
front 47 During inflammation we get these common effects | back 47 Vasodilation |
front 48 Fever is caused by | back 48 IL-1, systemic proinflammatory mediator |
front 49 Warmth in inflammation is caused by | back 49 Vasodilation increasing blood flow |
front 50 Redness is caused by | back 50 Vasodilation increasing blood flow |
front 51 Swelling is caused by | back 51 Vasodilation increasing capillary permeability, allowing antibodies, compliment and white blood cells to cross the endothelium and reach the site of injury. |
front 52 How does the pH change during inflammation? | back 52 The pH is lowered |
front 53 Why is the pH lowered in inflammation? | back 53 It creates an inhospitable environment for invading microbes. |
front 54 Why do we get vasodilation in inflammation? | back 54 Vasodilation helps increase blood flow to the area which helps deliver the proteins needed for clotting, inflammation, healing and remodeling. |
front 55 Neutropenia | back 55 Low Neutrophils, <1000cells/microliter |
front 56 These 3 types of cells are phagocytic | back 56 Macrophages, Neutrophils, Monocytes |
front 57 Low neutrophils increases chance of what | back 57 infection |
front 58 Extreme neutropenia is defined as | back 58 <500cells/liter |
front 59 Chediak-higashi syndrome: | back 59 Autosomal recessive, neutrophils have a profound defect in the formation of intracellular granules. |
front 60 In this syndrome, neutrophils have a lack of intracellular granules | back 60 Chediak-higashi |
front 61 In this syndrome neutrophils intracellular granules cannot fuse with phagosomes and form phagolysosomes. | back 61 Chediak-higashi |
front 62 Myeloperoxidase deficiency | back 62 Most common neutrophil disorder |
front 63 In this syndrome phagocytosis, chemotaxis and degranulation are nrormal, but metabolic pathways are impaired. | back 63 Myeloperoxidase deficiency |
front 64 Most patients with this neutrophil disorder are asymptomatic | back 64 Myeloperoxidase deficiency |
front 65 Chronic granulomatous disease | back 65 genetically heterogeneous group if disorders characterized by the failure of phagocytic cells to produce superoxides. |
front 66 Osler lesions | back 66 ouchy on hands and feet |
front 67 Janeway lesions | back 67 Just on hands and feet, no ouchy |
front 68 What do we believe causes osler lesions and janeway lesions? | back 68 Depositions of immune complexes |
front 69 Pathogenic bacteria like s pneumonia and n meningitidis secrete: | back 69 IgA protease that inactivates host antibody and facilitates mucosal attachment |
front 70 Two theories for passing blood brain barrier | back 70 Trojan horse, tight junction opening from cytokine |
front 71 Bacteria have this that let them survive in the CSF | back 71 Large capsules |
front 72 IL-1, IL-6, Metalloproteinases and tumor necrosis factor are thought to be: | back 72 Inflammatory mediators for meningitis |
front 73 Types of cerebral edema | back 73 Vasogenic |
front 74 Vasogenic cerebral edema is caused by : | back 74 Increase in the blood brain barrier, dilation of the blood vessels |
front 75 Cytotoxic cerebral edema is caused by | back 75 Toxic factors released b bacteria or neutrophils |
front 76 Interstitial cerebral edema is caused by | back 76 Obstruction in the flow of CSF |
front 77 Mast cells produce these two inflammatory mediators | back 77 Histamine and LeukotrinesL |
front 78 Hitamines and Leukotrines mediate | back 78 vasodilation in inflammation |
front 79 Stages of inflammation | back 79 Vascular response Leukocyte recruitment |
front 80 Vascular response in inflammation | back 80 Starts with vasoconstriction, turns into vasodilation |
front 81 Leukocyte recruitment consists of | back 81 Neutrophils being guided to the area through chemotaxis |
front 82 Phagocytosis | back 82 nom nom nom |
front 83 Aside from histamine and leuktrines, these are key players in inflammation | back 83 Prostaglandin |
front 84 Cell membranes, phospholipids, when inflammation takes place, this phospholipid can be converted into arachadonic acid which is split into | back 84 Leukotrines or prostaglandins |
front 85 The enzyme that is required for leukotrine production is | back 85 Lipogenase |
front 86 The enzyme required to convert arachadonic acid into prostaglandins is | back 86 COX |
front 87 COX | back 87 Cyclooxygenase |
front 88 Term for wbc leaking into tissues | back 88 fenestration |
front 89 How is skin different from mucosa? | back 89 skin is distinct from mucosa in that it contains adnexal structures such as the eccrine units that exude sweat and the folliculosebaceous apocrine units that produce hairs and oils |