Final Exam 1 Flashcards
Genetics, Altered Cells, Immunology, Cancer, Fluids/Acid-Base, Neuro, Renal
<p>silent, missence, and nonsense are all what type of genetic mutation</p>
<p>base pair substitution</p>
<p>mutation -> new codon -> same AA</p>
<p>silent mutation</p>
<p>mutation -> new codon -> new AA</p>
<p>missense mutation</p>
<p>mutation -> new codon -> stop codon</p>
<p>nonsense mutation</p>
<p>insertion or deletion of 1 or more base pairs</p>
<p>frameshift mutation</p>
<p>Chromosomes and pairs of somatic cells</p>
<p>46 chromosomes in 23 pairs (diploid)</p>
<p>Chromosomes and pairs of gametes</p>
<p>23 chromosomes as singles (haploid)</p>
<p>cells w/ a multiple of the normal number of chromosomes</p>
<p>euploid cells</p>
<p>cells w/ compete extra sets of chromosomes</p>
<p>polyploidy (usually spontaneous aborted or stillborn)</p>
<p>describe the chromosomes in triploidy and tetraploidy cells</p>
<p>- triploidy = 3 complete sets of chromosomes- tetraploidy = 4 complete sets of chromosomes</p>
<p>a cell that does not contain a multiple of 23 chromosomes (missing or additional individual chromosomes)</p>
<p>aneuploidy</p>
<p>name 2 types of aneuploidy cells and which type is worse</p>
<p>monosomy and trisomy; monosomy is worse due to the lack of genetic material</p>
<p>aneuploidy is a result of what?</p>
<p>nondisjunction - homologous chromosomes or sister chromatids fail to separate during mitosis or meiosis</p>
<p>intellectual disability, distinctive facial features, and increased risk of leukemia</p>
<p>Down Syndrome/Trisomy 21</p>
<p>short stature, neck webbing, spaced nipples, usually sterile, but no intellectual disability</p>
<p>Turner Syndrome/Monosomy X</p>
<p>breast development, small testicles, typically sterile and some intellectual impairment</p>
<p>Klinefelter Syndrome/XXY condition</p>
<p>low birth weight, severe intellectual disability, microcephaly, heart defects, and characteristic high pitched cry</p>
<p>Chromosome 5 - deletion of short arm/Cri-du-chat syndrome</p>
<p>Name 4 types of abnormalities in chromosome structure</p>
<p>- deletion- duplication- inversion- translocation</p>
<p>exchange of material between 2 non-homologous chromosomes</p>
<p>reciprocal translocation</p>
<p>long arms of 2 non-homologous chromosomes combine at the centromere to form a single chromosome and the short arms are usually lost</p>
<p>Robertsonian translocation</p>
<p>On what chromosomes do Robersonian translocations occur?</p>
<p>13, 14, 15, 21, and 22</p>
<p>more common in males; causes intellectual disability (2nd most common under Down syndrome)</p>
<p>gap on long arm of X chromosome/Fragile X Syndrome</p>
<p>Patau syndrome</p>
<p>trisomy 13</p>
<p>Edward's syndrome</p>
<p>trisomy 18</p>
<p>what is the recurrence of autosomal dominant</p>
<p>50%</p>
<p>List 3 examples of autosomal dominant disorders</p>
<p>Huntington's disease, Von Willebrand's disease, and Marfan's syndrome</p>
<p>% of individuals w/ a genotype who also exhibit the expected phenotype</p>
<p>penetrance</p>
<p>individuals w/ disease-causing genotype but not the phenotype</p>
<p>incomplete penetrance</p>
<p>What is a common example of incomplete penetrance</p>
<p>retinoblastoma - about 90% who carry the gene will get the disease (90% penetrance)</p>
<p>What AD disease is known for its delayed age of onset (about 40 y/o)?</p>
<p>Huntington's disease</p>
<p>What is the recurrence of autosomal recessive?</p>
<p>50% carrier, 25% normal; 25% affected</p>
<p>List 3 examples of AR diseases</p>
<p>cystic fibrosis, sickle cell anemia, and albinism</p>
<p>List 3 examples of X-linked inheritance</p>
<p>color blindness, Duchenne muscular dystrophy, and hemophilia A</p>
<p>range of phenotypes that vary between patients and specific genotype</p>
<p>expressivity</p>
<p>Example of expressivity</p>
<p>neurofibromatosis</p>
<p>traits in which variations are caused by combined effect of multiple genes (polygenic)</p>
<p>multifactorial inhertence</p>
<p>certain number of factors/genes must be affected before phenotype is expressed</p>
<p>threshold of liability</p>
<p>What chromosome is cystic fibrosis linked to?</p>
<p>chromosome 7</p>
<p>Decrease or shrinkage of cell size</p>
<p>atrophy</p>
<p>Increase in size of cells</p>
<p>hypertrophy</p>
<p>Increase in the number of cells (from an increased rate of cellular division)</p>
<p>hyperplasia</p>
<p>Abnormal changes in size, shape, or organization of mature cells</p>
<p>dysplasia</p>
<p>Reversible replacement of one mature cell type by another</p>
<p>metaplasia</p>
<p>What 2 types of cellular adaptation occur in non dividing cells?</p>
<p>atrophy and hypertrophy</p>
<p>Physiologic vs Pathologic atrophy</p>
<p>- Physiologic: normal process that usually occurs in early development (ex. thymus in children)- Pathologic: due to decreased pressure, use, blood, nutrition, hormones, or stimulation (ex. disuse atrophy in skeletal muscle)</p>
<p>chronic malnutrition atrophy is often accompanied by what?</p>
<p>autophagy -> autophagic vacuoles contain cellular debris and enzymes</p>
<p>Physiologic vs Pathologic cardiac hypertrophy</p>
<p>Physiologic: temporary and preserves myocardial structure (ex. endurance training, postnatal development, and pregnancy)Pathologic: includes aging, strenuous exercise, sustained workload or stress</p>
<p>Explain compensatory hyperplasia. Where is it significant?</p>
<p>adaptive and allows for some organs to regenerate(epidermal and intestinal epithelia, hepatocytes, BM cells, and fibroblasts)</p>
<p>Explain hormonal hyperplasia</p>
<p>occurs in estrogen-dependent organs in response to hormonal stimulation (uterus and breast)</p>
<p>Explain pathologic hyperplasia</p>
<p>abnormal proliferation of normal cells (usually in response to excessive hormonal stimulation or GF on those cells)</p>
<p>2 most common examples of pathologic hyperplasia</p>
<p>- hyperplasia of the endometrium (over secretion of estrogen)- BPH (due to changes in hormonal balance)</p>
<p>Dysplasia is also known as what?</p>
<p>atypical hyperplasia -> not a true adaptive change</p>
<p>T/F: Dysplasia means the presence of cancer</p>
<p>False; dysplasia does NOT indicate cancer and may not progress to cancer if stimulus is removed early on</p>
<p>If metaplasia is not reversed, what can it advance to?</p>
<p>Dysplasia and possible cancerous transformations</p>
<p>Explain the general mechanisms of cellular injury (regardless of cause)</p>
<p>- depletion of ATP
- mitochondrial damage
- O2 and O2-derived free radical membrane damage
- protein folding defects
- DNA damage
- calcium level changes</p>
<p>Most common cause of hypoxia</p>
<p>ischemia (reduced blood supply)</p>
<p>What causes ischemia</p>
<p>narrowing of arteries (arteriosclerosis) or complete occlusion by clots (thrombosis)</p>
<p>Explain what causes a cell to swell w/ hypoxic injury</p>
<p>decreased mitochondrial O2 -> decreased ATP -> Na/K pump failure -> increased intracellular Na -> increased intracellular H2O -> swelling</p>
<p>Explain what causes a decrease in protein synthesis w/ cellular hypoxic injury</p>
<p>increase intracellular H20 -> dilation of ER -> detachment of ribosomes</p>
<p>Explain what causes nuclear chromatin clumping w/ cellular hypoxic injury</p>
<p>decrease in O2 -> decrease in ATP -> increase anaerobic glycolysis -> decrease glycogen -> increase lactate -> decrease pH -> chromatin clumping &amp; DNA damage</p>
<p>Explain changes to Na, K, and Ca during cellular hypoxic injury</p>
<p>- increased intracellular Na- increased extracellular K- increased intracellular Ca</p>
<p>Where is intracellular Ca released from?</p>
<p>mitochondria and smooth ER</p>
<p>Name 4 mechanisms for ischemia-reperfusion injury</p>
<p>- oxidative stress- increased intracellular Ca- inflammation- complement activation</p>
<p>Name 3 types of reactive oxygen species (ROS)</p>
<p>- hydroxyl radical (OH-)- superoxide radical (O-)- hydrogen peroxide (H2O2)</p>
<p>How does cell structure change after reperfusion injury?</p>
<p>ischemic cell = swollen
| reperfusion injured cell = necrotic</p>
<p>main systems affected by lead (Pb)</p>
<p>nervous system and blood</p>
<p>carbon tetrachloride (CCl4) affects what organ</p>
<p>liver</p>
<p>Explain how CO causes hypoxic injury</p>
<p>has a higher affinity for hemoglobin than O2 -> carboxyhemoglobin</p>
<p>Sxs of CO poisoning</p>
<p>dizziness, weakness, N/V, headache, tinnitus, confusion, and chest pain</p>
<p>Primary systems affected by ethanol</p>
<p>brain and liver</p>
<p>What nutrition deficiencies are associated w/ ethanol?</p>
<p>Mg, B6, thiamine, and phosphorus; folic acid is a problem for chronic drinkers</p>
<p>bleeding into skin or underlying tissues -> takes time to appear</p>
<p>contusion (bruise)</p>
<p>collection of blood in soft tissue that appears quickly</p>
<p>hematoma</p>
<p>wound is longer than it is deep -> usually has significant external bleeding w/ little internal bleeding</p>
<p>incised wound</p>
<p>penetrating sharp-force injury deeper than it is long</p>
<p>stab wound</p>
<p>produced by items w/ sharp points but dull edges (ex. stepping on a nail)</p>
<p>puncture wound</p>
<p>What will affect the appearance of an entrance gunshot wound?</p>
<p>range of the gunshot</p>
<p>What is seen w/ contact range entrance gunshot wound?</p>
<p>- searing of the edges- blowback (gaping or jagged)- muzzle imprints</p>
<p>What is seen w/ intermediate range entrance gunshot wound?</p>
<p>- tattooing/stippling: fragments of gunpowder abrade but don't enter the skin</p>
<p>appearance is the same regardless of range</p>
<p>indeterminate range entrance wound AND exit wound</p>
<p>Necrosis vs Apoptosis</p>
<p>- Necrosis: unprogrammed death; cellular swelling -> lysis; inflammation; many cells affected
- Apoptosis: programmed, organized disassembly; membrane bound shrinkage; no inflammation; one cell or small clusters</p>
<p>nucleus gets smaller -> DNA condenses into shrunken particles</p>
<p>pyknosis</p>
<p>fading away of nuclear envelope and nuclear material</p>
<p>karyolysis</p>
<p>nuclear fragmentation</p>
<p>karyorrhexis</p>
<p>Explain coagulative necrosis and where it occurs</p>
<p>- ischemia -> decrease pH -> protein degeneration -> albumin becomes firm and opaque</p>
<p>- occurs inkidneys, heart, adrenal glands</p>
<p>Explain liquefaction necrosis and where it occurs</p>
<p>- autolysis (hydrolytic enzymes) and heterolysis (bacterial infection) -> tissue becomes soft, liquefies, and segregates -> forms cysts</p>
<p>- occurs inneurons and glial cells of the brain</p>
<p>Types of bacteria involved in liquefaction necrosis?</p>
<p>- Staph- Strep- E. Coli</p>
<p>Explain caseous necrosis</p>
<p>- mycobacterium (TB) is walled off in a granuloma -> cells disintegrate but not completely digested (combo of coagulative and liquefaction) - will resemble cottage cheese (soft and granular)</p>
<p>Explain fat necrosis and where it occurs</p>
<p>- occurs by lipases -> break down triglycerides -> release FAs that combine w/ Ca, Mg, and Na (saponification) -> white and chalky</p>
<p>- occurs in thebreast, pancreas, and other ABD organs</p>
<p>Dry vs wet gangrene</p>
<p>- Dry: poor perfusion (coagulative necrosis)- Wet: poor perfusion + pyogenic infection (liquefactive necrosis)</p>
<p>Explain gas gangrene</p>
<p>caused by species of Clostridium -> produces hydrolytic enzymes and toxins -> destroy connective tissue and membranes -> gas bubble form in muscle cells -> death caused by shock</p>
<p>What occurs during algor mortis?</p>
<p>- body temp decreases 1 degree per hour- by 24 hours -> body temp = environment</p>
<p>What is the main event of livor mortis and how it is physically seen?</p>
<p>- blood pools at the lowest point of the body (due to gravity)- purple discoloration where blood pools (line of demarcation)- can see pupils dilate and become nonreactive to light due to decreased retinal pressure (decrease muscle tension)</p>
<p>What is the timeframe for rigor mortis? What causes rigor mortis?</p>
<p>- starts within 6 hours after death and lasts for approximately 36 hours (then body becomes flaccid)</p>
<p>-acid builds up in muscles -> delete ATP -> myosin doesn't work for relaxation -> rigid muscles (small muscles first)</p>
<p>What is postmortem autolysis (putrefaction)?</p>
<p>breakdown of tissues that occurs between 24-48 hours (all cells start necrosing)</p>
<p>What speeds up/slows down the process of postmortem autolysis?</p>
<p>- warm environment speeds it up- cold slows it down</p>
<p>Lines of defense (3)</p>
<p>- 1st: innate (natura/native) immunity- 2nd: inflammation- 3rd: adaptive (acquired) immunity</p>
<p>What 3 things are part of innate immunity?</p>
<p>- physical barriers- epithelial cell-derived chemicals- normal microbiome</p>
<p>List 4 characteristics of the inflammatory response</p>
<p>- occurs in vascularized tissues- activates rapidly (in seconds) after damage occurs- depends on activity of both cellular and chemical components- nonspecific</p>
<p>At the beginning of the inflammatory reaction, what are 3 vascular responses that occur?</p>
<p>- vasodilation- increased vascular permeability- WBC adherence to the inner walls of vessels and migration through vessels</p>
<p>What causes edema at the site of injury?</p>
<p>increased vascular permeability -> plasma proteins leak from capillary bed -> oncotic pressure -> fluid will follow protein out of capillary -> edema</p>
<p>Who are the 1st and 2nd responders at a site of inflammation?</p>
<p>1st responder: neutrophil2nd responder: macrophage (from monocyte)</p>
<p>List the 3 plasma systems</p>
<p>- complement- clotting- kinin</p>
<p>Symptoms of acute inflammatory response and causes?</p>
<p>- vasodilation (erythema/warmth)- vascular permeability (edema)- cellular infiltration (pus)- thrombosis (clots) -> helps encapsulate bacteria- stimulation of nerve endings by kinin (pain)</p>
<p>cells filled w/ granules and located in loose connective tissue close to blood vessels</p>
<p>mast cells</p>
<p>What 3 types of granules are released by mast cells?</p>
<p>- histamine- chemotactic factor for neutrophils- chemotactic factor for eosinophils</p>
<p>List 3 mediators synthesized by mast cells</p>
<p>- platelet activating factor (PAF)- prostaglandins- leukotrienes</p>
<p>Function of PAF</p>
<p>platelet activation and vasodilation</p>
<p>Function of prostaglandins</p>
<p>increased vascular permeability, neutrophil chemotaxis, and pain</p>
<p>Explain histamine's function after being released from mast cells</p>
<p>vasoactive: temporary rapid constriction of large blood vessels and dilation of post-capillary venues; retraction of endothelial cells lining capillaries (junctions)</p>
<p>Explain the compliment system</p>
<p>- C3 -> C3b + C3a- C3b -> C5 -> C5b + C5a- C5b -> C6-9 -> membrane attack complex- MAC forms pores in pathogen membrane to damage it</p>
<p>What in the compliment system creates opsonin? What is the function of opsonin?</p>
<p>- C3b- coats surface of bacteria and increases their susceptibility to phagocytosis</p>
<p>potent anaphylatoxin in the compliment system -> mass cell release of histamine</p>
<p>C3a</p>
<p>Anaphylatoxin and chemotactic factor in compliment system -> leukocyte (neutrophil) migration</p>
<p>C5a</p>
<p>main protein in a blood clot</p>
<p>fibrin</p>
<p>What activates the extrinsic pathway of the clotting system?</p>
<p>tissue factor (TF) - released by damaged endothelial cells in blood vessels (external trauma)</p>
<p>What activates the internal pathway of the clotting system?</p>
<p>activated when the vessel wall is damaged (trauma inside the blood vessels)</p>
<p>- Factor unique to extrinsic pathway- Factor unique to intrinsic pathway- Factor activated by both pathways</p>
<p>- Extrinsic: VIIa- Intrinsic: XII (Hageman Factor) -> XIIa- Both: Xa</p>
<p>Describe the common pathway of the clotting cascade</p>
<p>Xa -> thrombin -> fibrinogen -> fibrin -> blood clot</p>
<p>functions to activate and assist inflammatory cells; interacts closely w/ coagulation system</p>
<p>Kinin system</p>
<p>What activates the kinin system?</p>
<p>activation of Hageman factor (XII) to XIIa (aka prekallikrein)</p>
<p>Functions of bradykinin</p>
<p>- vasodilation (like histamine)- induce pain (w/ prostaglandins)- smooth muscle contraction- increase vascular permeability- leukocyte chemotaxis</p>
<p>Cytokines that cause vasodilation (3)</p>
<p>- prostaglandins- histamine- NO</p>
<p>Cytokines that cause vascular permeability (4)</p>
<p>- histamine- bradykinin- leukotrienes- PAF</p>
<p>Cytokines that cause pain (2)</p>
<p>- prostaglandins- bradykinin</p>
<p>Cytokines that cause fever (4)</p>
<p>- IL-1- IL-6- TNF-a- prostaglandins</p>
<p>Cytokines that activate leukocytes (2)</p>
<p>- IL-1- TNF-a</p>
<p>activate T-cells without MHC-II or antigen to activate them -> widespread activation of immune system</p>
<p>Superantigens</p>
<p>List acute phase reactants (5)</p>
<p>IL-1, IL-6, IL-8, TNF-a, and C-reactive protein</p>
<p>What does C-reactive protein tell about inflammation</p>
<p>global test for inflammation (doesn't tell cause or location; only that it exists)</p>
<p>increased neutrophils?</p>
<p>acute bacteria/acute inflammation</p>
<p>increased lymphocytes?</p>
<p>viral infection/chronic bacterial infection</p>
<p>increased monocytes?</p>
<p>inflammation</p>
<p>increased basophils?</p>
<p>allergic reaction</p>
<p>increased eosinophils?</p>
<p>parasitic infection</p>
<p>type of innate lymphocyte</p>
<p>natural killer cell (NK cell)</p>
<p>How do cytokines limit inflammation?</p>
<p>- inhibit production- inhibit macrophage proliferation- destroy histamine and leukotrienes</p>
<p>How do cytokines help w/ repair and healing?</p>
<p>- activate macrophages- stimulate fibroblast growth- stimulate endothelial growth</p>
<p>Explain VEGF function and how it relates to cancer and chemo</p>
<p>- VEGF is angiogenic -> vascular growth- found in some cancers to help them develop blood supply- some chemo targets this -> will also delay healing</p>
<p>What does the erythrocyte sedimentation rate test?</p>
<p>how fast RBCs settle at the bottom of the test tube -> faster may mean inflammation</p>
<p>How do cytokines help w/ phagocytosis?</p>
<p>- adherence and diapedesis- chemotaxis- opsonins- activate and increase macrophages</p>
<p>Type I interferons (IFN)</p>
<p>INF-a and INF-b</p>
<p>Type II interferon (IFN)</p>
<p>IFN-y</p>
<p>IL that is pro inflammatory an endogenous pyrogen (causes fever)</p>
<p>IL-1</p>
<p>IL that directly induces hepatocytes to produce proteins needed for inflammation and stimulate differentiation and growth of BM cells</p>
<p>IL-6</p>
<p>List 3 systemic effects of TNF-a</p>
<p>- induces fever (endogenous pyrogen)- increased synthesis of inflammation proteins by liver- muscle wasting (cachexia) and intravascular thrombosis in cases of severe infection/cancer</p>
<p>What IL is anti-inflammatory?</p>
<p>IL-10</p>
<p>What cells secrete TNF-a?</p>
<p>macrophages</p>
<p>macrophages that predominate in early inflammation and become a component of purulent exudate</p>
<p>neutrophils (PMNs)</p>
<p>Life cycle of monocytes</p>
<p>produced in the BM -> travel to site of inflammation about 24 hours after neutrophils -> develop into macrophages</p>
<p>defense against parasites and regulation of vascular mediators</p>
<p>eosinophils</p>
<p>adherence of leukocytes to endothelial cells</p>
<p>margination</p>
<p>emigration of cells through endothelial junctions</p>
<p>diapedesis</p>
<p>protein filled watery exudate that indicates early inflammation</p>
<p>serous</p>
<p>thick, clotted exudate -> indicates more advanced inflammation</p>
<p>fibrinous</p>
<p>pus filled exudate that indicates bacterial infection or inflammation (supperative)</p>
<p>purulent</p>
<p>2 types of exudate that indicate bleeding</p>
<p>serosanguinous and sanguinous</p>
<p>Risks that lead to dysfunctional wound healing</p>
<p>- hemorrhage- fibrous adhesion- hypovolemia- lack of nutrients- poor control of glucose levels- infection</p>
<p>raised scar from original skin level (4mm above skin)</p>
<p>keloid scar</p>
<p>scar that is larger than it should be</p>
<p>hypertrophic</p>
<p>process by which the extensive diversity of antigen receptors on B and T cells is established</p>
<p>clonal diversity</p>
<p>develop from B cells -> produce antibodies</p>
<p>plasma cells</p>
<p>T cells that identify and kill target cells</p>
<p>cytotoxic T cells</p>
<p>come from both B and T cells and activate rapidly during a second infection w/ the same microbe</p>
<p>memory cells</p>
<p>infection/exposure immunity</p>
<p>active natural</p>
<p>vaccine immunity</p>
<p>active artificial</p>
<p>maternal immunity</p>
<p>passive natural</p>
<p>IVIg (immunoglobulins/serum/antibodies)</p>
<p>passive artificial</p>
<p>T/F: passive immunity does not lead to memory</p>
<p>True</p>
<p>3 parts to an antibody</p>
<p>- 2 identical antigen binding fragments (Fab)- Fc portion that is responsible for most biological functions of antibody</p>
<p>How do Abs indirectly affect Ags</p>
<p>activate innate immune system -> complement and phagocytes</p>
<p>best complement activating antibody</p>
<p>IgM</p>
<p>best opsonin antibody</p>
<p>IgG</p>
<p>antibody that is part of mucosal immunity</p>
<p>IgA</p>
<p>antibody that responds to allergic reactions and parasites to activate mast cells</p>
<p>IgE</p>
<p>only antibody that crosses the placenta</p>
<p>IgG</p>
<p>processing of antigen and gene rearrangement for a specific immune response</p>
<p>clonal selection</p>
<p>Which cells are APCs</p>
<p>dendritic cells, macrophages, and B cells</p>
<p>What cells are HLA class II found on</p>
<p>all APCs</p>
<p>What cells are HLA class I found on</p>
<p>all nucleated cells</p>
<p>What is presented by each class of HLA and to what cells are they presented?</p>
<p>- HLA I: present endogenous antigens for cytotoxic T cells (CD8) -> gives thumbs up that the cell is okay- HLA II: present exogenous antigens ingested to T-helper cells (CD4) -> activate adaptive immunity</p>
<p>T/F: APCs have both HLA I and HLA II on their surface</p>
<p>True: all nucleated cells have HLA I</p>
<p>What immunoglobulins do B cells produce before class switching?</p>
<p>IgM and IgD</p>
<p>immunoglobulins released during primary exposure</p>
<p>IgM (major) and IgG (minor)</p>
<p>immunoglobulins released during secondary exposure</p>
<p>IgG (major) and IgM (minor)</p>
<p>Most abundant immunoglobulin in the body</p>
<p>IgG</p>
<p>ability to produce soluble toxins or endotoxins (greater influence pathogen's degree of virulence)</p>
<p>toxigenicity</p>
<p>opportunistic bacteria that is commonly found on skin and nasal passages but is also a major cause of HAI and abx resistance</p>
<p>staphylococcus aureus</p>
<p>T/F: S. aureus uses biofilms to colonize but doesn't produce toxins</p>
<p>False: produces and secretes exotoxins as well as uses biofilms</p>
<p>proteins created and secreted by the bacteria to have a virulence effect -> can damage plasma membranes or inactivate enzymes needed for protein synthesis</p>
<p>exotoxins</p>
<p>Explain how endotoxins can activate inflammatory response and produce fever</p>
<p>When bacterial cell dies -> membrane is disrupted -> releases LPS (lipid A portion) -> lipid A exposed to the immune system -> causes fever, shock, and DIC</p>
<p>what type of bacteria produce endotoxins?</p>
<p>gram-negative bacteria</p>
<p>Explain what causes endotoxic shock</p>
<p>bacteria growing in blood (septicemia) -> release endotoxins -> activate complement and clotting systems -> increased capillary permeability -> large volumes of plasma escape to surrounding tissues -> hypotension -> shock</p>
<p>antigenic drift vs shift</p>
<p>- antigenic drift: minor change in surface antigens due to mutations -> leads to weakened protection against virus- antigenic shift: major change where genome is segmented and undergoes recombination (usually zoonotic)</p>
<p>What 2 proteins classify influenza and what do they do?</p>
<p>- H protein (hemagglutinin): attachment and fusion (entry into cell)- N protein (neuraminidase): facilitates release of viral proteins from host cell</p>
<p>large microorganisms w/ thick, rigid cell walls without peptidoglycan</p>
<p>fungus/mycoses</p>
<p>- most common cause of fungal infections- opportunistic fungus that is normally found in the skin, GI tract, and vagina but can cause localized infection if overgrown -> disseminates if immunocompromised</p>
<p>Candida albicans</p>
<p>eukaryotic, unicellular microorganisms include malaria, amoeba, and flagellates</p>
<p>protozoa</p>
<p>What causes antibiotic resistance?</p>
<p>- genetic mutations- lack of compliance (selective resurgence)- overuse (destruction of normal microbiome)</p>
<p>Lab/serum tests used to evaluate immunodeficiencies</p>
<p>- CBC w/ diff- quantitative determination of immunoglobulins- assay for total complement</p>
<p>List the 6 stages of viral infection of a host cell</p>
<p>- attachment- penetration- uncoating- replication- assembly- release</p>
<p>What do all viruses contain?</p>
<p>genome and capsid</p>
<p>MOA of most antibiotics (4)</p>
<p>- inhibition of function/production of cell wall/membrane- prevent protein synthesis- blockage of DNA replication- interference w/ folic acid metabolism</p>
<p>x-linked disorder where IgM production is greatly depressed; clinical triad iseczema, thombocytopenia, and immune deficiency</p>
<p>Wiskott-Aldrich Syndrome</p>
<p>What cells are destroyed by HIV? What is the purpose of these cells?</p>
<p>CD4 Th cells -> necessary for development of plasma cells and CD8 cytotoxic T cells</p>
<p>How is HIV spread?</p>
<p>blood-borne and sexual contact (more common)</p>
<p>What do retroviruses use to implant their ds DNA into host cells?</p>
<p>- reverse transcriptase: RNA -> DNA- HIV integrase: inserts DNA into host genes</p>
<p>Describe the general steps of HIV life cycle (6)</p>
<p>- virion binds to CD4 and chemokine receptor- fusion of membrane w/ host cell membrane -> genome enters cytoplasm- reverse transcriptase -> integration of virus genes into host genome- transcription of HIV genome into RNA- synthesis of proteins and assembly of virion core- budding and release of mature vision</p>
<p>current regimen for treatment of HIV (combination of drugs)</p>
<p>antiretroviral therapy (ART)</p>
<p>Name 2 lab tests use to determine the progression of HIV</p>
<p>- HIV RNA levels: determines viral load- CD4 T cell count</p>
<p>Normal CD4 T cell count and value that begins to cause opportunistic infections</p>
<p>- Normal: 800-1000- Opportunistic infections: < 200</p>
<p>Describe typical HIV progression without treatment</p>
<p>- exposure: viral load is high (first 6-12 weeks)
- clinical latency: viral load is low (no sxs) but it could still be transmitted (12 weeks - 7 years); CD4 count drops slowly over time
- Constitutional sxs as viral load begins increasing
- Opportunistic diseases occur as CD4 < 200</p>
<p>Clinical symptoms of AIDS</p>
<p>- cachexia (severe weight loss)- Kaposi sarcoma- PCP pneumonia- other atypical or opportunistic infections or cancers</p>
<p>Hypersensitivity I, II, III are mediated by what? How does this differ from hypersensitivity IV?</p>
<p>- mediated by Abs- Type IV is cell mediated</p>
<p>type I hypersensitivity is mediated by what?</p>
<p>IgE mediated against environmental antigens (allergens)</p>
<p>sensitizing exposure and re-exposure in type I hypersensitivity</p>
<p>- sensitizing exposure: allergen binds to APC -> B cell + Th2 cell -> plasma cell -> creates IgE -> binds to IgE Fc receptor on mast cell- re-exposure: allergen enters -> binds to IgE on mast cells -> mast cell degranulation -> histamine release -> edema/smooth muscle contraction/mucous secretion</p>
<p>Symptoms of type I hypersensitivity</p>
<p>- itching/urticaria- angioedema- hypotension- bronchospasm (anaphylaxis)- dysrhythmia</p>
<p>type II hypersensitivity is mediated by what?</p>
<p>specific cell or tissue (tissue-specific antigens)</p>
<p>Ex. of type II hypersensitivity</p>
<p>- Graves disease (hyperthyroidism)- myasthenia gravis- Hemolytic disease of newborn (HDNB)</p>
<p>type III hypersensitivity is mediated by what?</p>
<p>immune complex mediated (not organ specific) -> antigen-antibody complex circulate and later deposited in vessel walls or extravascular tissues</p>
<p>Ex. of type III hypersensitivity</p>
<p>- serum sickness (includes Raynaud phenomena)- arthus reaction- SLE</p>
<p>type IV hypersensitivity is mediated by what?</p>
<p>cell-mediated; either cytotoxic T lymphocytes or lymphokine-producing Th1 and Th17 cells -> direct killing of target cells</p>
<p>Ex. of type IV hypersensitivity</p>
<p>- graft rejection- TB skin test- contact dermatitis (poison ivy, metals, and latex)</p>
<p>autoimmune disease characterized by production of a large variety of antibodies (autoantibodies)</p>
<p>systemic lupus erythematosus (SLE)</p>
<p>Explain how SLE is a type III hypersensitivity</p>
<p>causes deposition of circulating immune complexes containing antibody against host DNA</p>
<p>List some of the clinical manifestations of SLE</p>
<p>- arthritis/arthralgia - vasculitis/rash - renal disease - hematologic changes - CV disease - photosensitivity -presence of ANA (antinuclear antibodies) in blood</p>
<p>3 types of transplant rejection</p>
<p>- hyperacute: due to preexisting ab to the antigens of the graft - acute: cell-mediated immune response (type IV) against unmatched HLA antigens - chronic: takes months-years; weak cell-mediated reaction against minor HLA antigens</p>
<p>6 characteristics of benign tumors</p>
<p>- grow slowly- well-defined capsule- non invasive (don't grow past capsule)- well differentiated (similar to original cells)- low mitotic index- don't metastasize</p>
<p>6 characteristics of malignant tumors</p>
<p>- grow rapidly- not encapsulated- invasive- poorly differentiated (anaplasia)- high mitotic index- can spread distantly (metastasize)</p>
<p>pre-invasive epithelial malignant tumors of glandular or epithelial origin that have not broken through the basement membrane or invaded surrounding stroma</p>
<p>carcinoma in situ (CIS</p>
<p>What type of benign tumor does cause problems?</p>
<p>brain tumors -> limited space to grow so will affect the functions of surrounding tissues</p>
<p>increase in catecholamines indicates what?</p>
<p>adrenal medullary tumor (ex. pheochromocytoma)</p>
<p>increase in ACTH indicates what?</p>
<p>adrenal, pituitary, or hypothalamic tumors</p>
<p>increase in b-HCG indicates what?</p>
<p>germ cell and hepatic cancers</p>
<p>increase in carcinoembryonic antigen (CEA) indicates what?</p>
<p>colon, lung, pancreas, or breast cancer</p>
<p>alpha fetoprotein (AFP) is used to monitor what types of cancers?</p>
<p>hepatic and germ cell (testicular and ovarian)</p>
<p>CA-125 is used to monitor what type of cancer?</p>
<p>ovarian</p>
<p>What problem has been found with prostate specific antigen (PSA)?</p>
<p>many false positives -> approximately 75% of men w/ increased PSA don't have prostate cancer on biopsy</p>
<p>cancer is mainly a disease of what?</p>
<p>aging</p>
<p>4 types of gene mutations related to cancer</p>
<p>- secretion of growth factors- increased GF receptors- signal on cell-surface receptor is mutated in the "on" position- Intracellular signaling protein to promote replication</p>
<p>genes that regulate normal cellular proliferation</p>
<p>proto-oncogenes</p>
<p>mutation gained in proto-oncogene so that it can't slow down</p>
<p>oncogene</p>
<p>the "guardian of the genome" - signal to undergo apoptosis</p>
<p>p53</p>
<p>How do cancers participate in angiogenesis</p>
<p>secrete angiogenic factors such as vascular endothelial growth factor (VEGF)</p>
<p>Explain how cancer cells use telomeres to become immortal</p>
<p>cancer cells can secrete telomerase to restore and maintain telomeres -> allow for continuous division without stop</p>
<p>List the 6 hallmarks of cancer</p>
<p>- Self-sufficiency (in growth signals)- Evading growth suppressors- Tissue invasion and metastasis- Replication immortality- Induce angiogenesis- Resist cell death (apoptosis</p>
<p>genes tested for breast cancer</p>
<p>BRCA1/BRCA2</p>
<p>hereditary nonpolyposis colorectal cancer (no polyps present -> requires regular screenings)</p>
<p>Lynch syndrome</p>
<p>familial adenomatous polyposis is cancer of the colon/rectum caused by mutations in what gene?</p>
<p>APC</p>
<p>gene associated w/ thyroid cancer</p>
<p>RET</p>
<p>gene associated w/ retinoblastoma</p>
<p>RB1</p>
<p>T/F: most cancer is inherited</p>
<p>False: most is NOT inherited</p>
<p>chronic infections w/ H. pylori are associated w/ what?</p>
<p>- PUD- stomach carcinoma (most stomach cancers)- MALT lymphomas</p>
<p>entry of tumor cells into circulation</p>
<p>intravasation</p>
<p>exit of tumor cells from circulation</p>
<p>extravasion</p>
<p>Most common metastasis sites</p>
<p>brain, bone, liver, and lung</p>
<p>TNM staging</p>
<p>- Tumor: # equals size of tumor and local extent- Node: higher # means more nodes involved- Metastasis: # indicates extent of metastasis</p>
<p>increase in \_\_\_\_ comes from mutations of proto-oncogenes -> oncogenes</p>
<p>pro-growth signals</p>
<p>decrease in \_\_\_\_ comes from mutations in tumor-suppressor genes</p>
<p>anti-growth signals</p>
<p>examples of oncogenes</p>
<p>- c-ras- myc- fos- jun</p>
<p>most common genetic defects found in human cancers</p>
<p>mutations of tumor-suppressor genes</p>
<p>What triggers the extrinsic pathway of apoptosis?</p>
<p>Fas - "death receptor"</p>
<p>What is one of the most important activators of the Fas receptor</p>
<p>TNF-a</p>
<p>T/F: pain is one of the first signs of cancer</p>
<p>False; little/no pain is associated w/ early stage of cancer</p>
<p>What is the most frequently reported symptom of cancer and cancer treatment?</p>
<p>fatigue</p>
<p>What is included in cachexia (5)?</p>
<p>- anorexia- early satiety- weight loss- taste alternation- altered metabolism</p>
<p>Causes of anemia in cancer (4)?</p>
<p>- chronic bleeding due to iron deficiency- severe malnutrition- medical therapies (chemo)- malignancy in blood forming organs</p>
<p>Causes of leukopenia and thrombocytopenia in cancer?</p>
<p>- direct tumor invasion to the bone marrow- chemo drugs are toxic to the bone marrow</p>
<p>symptom complexes triggered by cancer but not caused by direct local effects of the tumor; commonly due to biologic substances released from the tumor or by immune responses triggered by the tumor</p>
<p>paraneoplastic syndrome</p>
<p>in what cancers are paraneoplastic syndromes most often seen?</p>
<p>breast, lung, and ovarian cancer</p>
<p>What system is most affected by paraneoplastic syndromes?</p>
<p>nervous system (can cause various neurological disorders that precede other cancer symptoms)</p>
<p>obstruction of blood flow through the SVC</p>
<p>superior vena cava syndrome</p>
<p>What type of cancer is most common w/ SVC syndrome</p>
<p>adenocarcinoma of the right lung</p>
<p>- Most common symptom of SVC syndrome</p>
<p>- Other symptoms of SVC syndrome</p>
<p>- dyspnea (most common)</p>
<p>- other sxs:cough, chest pain, headache, head fullness, and facial swelling</p>
<p>chemo given before localized (surgical or radiation) treatment of cancer -> seeks to shrink tumor so that surgery many spare more normal tissue</p>
<p>neoadjuvant chemotherapy</p>
<p>chemo given after surgery with the goal of eliminating micrometastasis</p>
<p>adjuvant chemotherapy</p>
<p>the first lymph node to which cancer cells are most likely to spread from a primary tumor</p>
<p>sentinel node</p>
<p>4 tissue types affected by cancer treatment</p>
<p>mainly includes labile cells (continuous replication)- GI tract- bone marrow- hair and skin- reproductive tract</p>
<p>important factor in development of cancer -> causes cell mutation</p>
<p>chronic inflammation</p>
<p>Explain how cytokines can lead to cell mutation</p>
<p>cytokines are supposed to help the inflammatory process but when overproduced -> cause damage to tissues</p>
<p>Risk factor for cancers of the lung, lower urinary tract, upper aerodigestive, liver, kidney, pancreas, cervix, uterus, and myeloid leukemia</p>
<p>tobacco</p>
<p>What are some dietary sources of carcinogens?</p>
<p>- cooking fat, meat, or protein- naturally occurring carcinogens associated w/ plant food substances (alkaloids or mold byproducts)</p>
<p>What type of cancer are obese women at increased risk of and why?</p>
<p>breast cancer due to increased estrogen in their tissues</p>
<p>Risk factor for oral cavity, pharynx, larynx, esophagus, liver, colorectal, and breast cancers</p>
<p>alcohol consumption</p>
<p>What risk for cancer is dose related?</p>
<p>ionizing radiation</p>
<p>3 effects of UVA and UVB</p>
<p>- released TNF-a in epidermis- production of ROS- promotes skin inflammation and release of free radicals</p>
<p>3 types of skin cancer</p>
<p>- basal cell carcinoma (BCC)- squamous cell carcinoma (SCC)- melanoma (melanocytes)</p>
<p>incidence of BCC and SCC strongly correlate with what?</p>
<p>lifetime sunlight exposure</p>
<p>EBV is linked to what types of cancers?</p>
<p>nasopharynx and Hodgkin's and non-Hodgkin's lymphoma</p>
<p>6 types of cancers associated w/ HPV</p>
<p>- cervix- penis- vulva- anus- oropharynx (tongue and tonsils)</p>
<p>outdoor pollution is associated with what type of cancer?</p>
<p>lung cancer</p>
<p>3 main factors that lead to altered epigenomic marks</p>
<p>- lifestyle- carcinogen exposures- occupational exposures</p>
<p>What is ECF composed of?</p>
<p>- interstitial fluid (spaces between cells)- intravascular- lymphatics- transcellular (joint, intraocular, and CSF)</p>
<p>Describe whether each electrolyte is found more in ICF or ECF- Na- Cl- Ca- K- Mg</p>
<p>- Na = ECF- Cl = ECF- Ca = ECF- K = ICF- Mg = ICF</p>
<p>Name 4 factors in the absorption of fluid</p>
<p>- ADH- RAAS- ANP- renal function</p>
<p>What primarily regulates water balance?</p>
<p>antidiuretic hormone (ADH); aka vasopressin</p>
<p>What is another method the body uses to raise fluid volume or decrease plasma osmolarity other than ADH?</p>
<p>thirst -> increase fluid intake</p>
<p>Describe the RAAS system</p>
<p>decreased renal perfusion (decreased plasma volume) -> renin secreted -> Ang I -> Ang II -> ADH (water absorption) and Aldosterone (salt reabsorption) -> increased blood volume</p>
<p>What secretes renin and when?</p>
<p>juxtaglomerular cells when BP is low</p>
<p>What releases aldosterone and what stimulates it release?</p>
<p>released from the adrenal cortex; stimulated by Ang II or directly by increased plasma K</p>
<p>What causes production of ANP and BNP? What will ANP/BNP do?</p>
<p>- caused by cardiac distention (ECF volume increased, Na and H2O retention, increased BP)</p>
<p>-decrease RAAS - increase GFR - increase Na and water excretion (natriuresis and diuresis) - vasodilation (decrease BP)</p>
<p>3 lab tests used to measure renal function</p>
<p>- GFR- serum creatinine- serum BUN</p>
<p>What is the minimum normal urine output?</p>
<p>30 mL/hr</p>
<p>Normal blood osmolarity</p>
<p>275-295 mosm/Kg</p>
<p>What is responsible for the ECF water balance</p>
<p>Na</p>
<p>What will isotonic IV solution do? Ex. of isotonic solution</p>
<p>- remain in vessels -> add to blood volume</p>
<p>- 0.9% NaCl solution</p>
<p>What will hypertonic IV solution do? Ex. of hypertonic solution</p>
<p>- contains high Na -> will pull fluid from cells into vessels (useful in cerebral edema)</p>
<p>-3-5% normal saline</p>
<p>What will hypotonic IV solution do?</p>
<p>- contains low Na -> fluid will be pulled into the tissues from the vessels</p>
<p>-0.45% normal saline</p>
<p>Pathophysiology of edema (3)</p>
<p>- increased capillary permeability (proteins moves to interstitial space)- low levels of serum proteins- hydrostatic pressures increased due to venous obstruction, Na or water retention</p>
<p>Non-pitting vs pitting edema</p>
<p>- Non-pitting: swollen cells due to increased ICF volume- Pitting: increased interstitial fluid volume</p>
<p>T/F: A loss or gain of saline affects the volume of both ICF and ECF</p>
<p>False; saline is confined to the extracellular compartment -> does not affect volume of the intracellular compartment</p>
<p>Clinical presentation of isotonic fluid loss</p>
<p>- orthostatic hypotension- tachycardia- weight loss- decreased skin turgor and slow capillary refill- low urine output- hypovolemic shock</p>
<p>Clinical presentation of isotonic fluid excess</p>
<p>- hypertension - weight gain- edema- signs of CHF- may have increased urine output</p>
<p>Cause of hyponatremia</p>
<p>- excessive hypotonic IV- excess water intake (includes psychogenic polydipsia, tap water enemas, and NG irrigation)- vomiting/diarrhea- fresh water drowning- SIADH</p>
<p>What will happen to serum Na and cells with hyponatremia?</p>
<p>low serum Na and cellular swelling</p>
<p>Clinical presentation of hyponatremia and why?</p>
<p>- confusion, lethargy, coma- headache, weight gain- nausea- seizure, weakness, muscle twitching- decrease in Na concentration changes the cell's ability to depolarize and repolarize normally -> alters APs of neurons and muscles- will also see cerebral edema (causes many neurological changes)</p>
<p>Most important way to determine if someone is retaining fluid or losing fluid</p>
<p>Daily weights</p>
<p>Normal Na level</p>
<p>135-145 mEq/L</p>
<p>Causes of hypernatremia</p>
<p>- chronic diarrhea, vomiting and fever (water loss)- no access to water (decreased thirst)- diabetes insipidus- drowning in salt water- tube feedings- diaphoresis and diuresis- primary hyperladosteronism- Cushing syndrome</p>
<p>clinical manifestations of hypernatremia and why?</p>
<p>- confusion, lethargy, coma- seizure- fever- dry mucous membranes- hyperreflexia- pulmonary edema- CNS signs due to brain cells shrinking and Na can't cross BBB; also due to alterations in membrane potential</p>
<p>normal K levels</p>
<p>3.5-5.0 mEq/L</p>
<p>4 factors that enhance cellular uptake of K</p>
<p>- insulin- epinephrine- aldosterone- alkalosis (K is lo)</p>
<p>4 factors that enhance K release</p>
<p>- acidosis (H+ takes over cells)- cell lysis- strenuous excersice- increased ECF osmolarity</p>
<p>causes of hyperkalemia</p>
<p>- excess K intake- diuretics- large blood transfusions- decreased renal excretion- Addison's disease (decreased aldosterone)- crush injuries and burns (cell lysis)</p>
<p>Clinical signs of hyperkalemia</p>
<p>- muscle weakness/paralysis - cardiac dysrhythmias/arrest - hypopolarization (lowering) of RMP (easier to excite) - anxiety, numbness/tingling, N/V/D -tall, peaked, T wave</p>
<p>Causes of hypokalemia</p>
<p>- anorexia or NPO- diuretics- V/D- NG suction- intestinal drainage</p>
<p>Clinical signs of hypokalemia</p>
<p>- hyperpolarization (increasing) of RMP- muscle weakness/paralysis- paralytic ileus- dysrhythmias</p>
<p>Normal total Ca level</p>
<p>9-11 mg/dL</p>
<p>Normal ionized Ca level</p>
<p>4.5-6 mEq/L</p>
<p>Causes of hypercalcemia</p>
<p>- hyperparathyroidism (increased PTH secretion)- immobilization (stimulation breakdown of bones)- leukemia- diuretics</p>
<p>Clinical signs of hypercalcemia</p>
<p>- weakness and CNS depression- decreased NM excitability</p>
<p>Causes of hypocalcemia</p>
<p>- dietary deficiency (vitamin D)- laxative abuse- diarrhea- pancreatitis- malabsorption</p>
<p>Clinical signs of hypocalcemia</p>
<p>- cramps and seizures - increased NM excitability -low T wave</p>
<p>What is trousseau sign</p>
<p>- identifies hypocalcemia- inflate BP cuff on arm and will see flexion at wrist (carpal spasm)</p>
<p>What is Chovstek sign</p>
<p>- identifies hypocalcemia- tap the facial nerve anterior to the ear to elicit ipsilateral facial contraction</p>
<p>Normal Mg level</p>
<p>1.5-2.5 mEq/L</p>
<p>causes of hypermagnesemia</p>
<p>laxatives and antacids</p>
<p>Clinical signs of hypermagnesemia</p>
<p>- decreased reflexes- muscle weakness- drowsiness- respiratory depression- cardiac arrhythmias</p>
<p>causes of hypomagnesemia</p>
<p>alcoholism, poor nutrition, and malabsorption</p>
<p>Clinical signs of hypomagnesemia</p>
<p>- muscle cramps/spasm- tetany- seizures- hyperactive reflexes- cardiac arrhythmias</p>
<p>Normal Pi levels</p>
<p>2.5-4.5 mg/dL</p>
<p>causes of hypophosphatemia</p>
<p>- alcoholism- malabsorption- diarrhea- DKA- diuretics- antacids- dialysis</p>
<p>Clinical signs of hypophosphatemia</p>
<p>- anorexia- malaise- paresthesias- muscle weakness- decreased reflexes- confusion- impaired cardiac function</p>
<p>causes of hyperphosphatemia</p>
<p>- phosphate containing enemas- crushing injury- adrenal insufficiency- hypoparathyroid disease</p>
<p>Clinical signs of hyperphosphatemia</p>
<p>- increased NM excitability- Ca deposits in body tissues- hypocalcemia</p>
<p>Which electrolyte imbalances will cause weakness/poor muscle tone?</p>
<p>- hyperkalemia- hypokalemia- hypercalcemia- hypermagnesemia</p>
<p>Which electrolyte imbalances will cause twitchy/crampy muscles?</p>
<p>- hypocalcemia- hypomagnesemia</p>
<p>Normal blood pH</p>
<p>7.35-7.45</p>
<p>Normal blood PaCO2</p>
<p>35-45 mmHg</p>
<p>Normal blood HCO3 (bicarb)</p>
<p>22-26 mEq/L</p>
<p>causes of metabolic acidosis</p>
<p>- loss of base or addition of acid- DKA- lactic acidosis- EtOH poisoning</p>
<p>What is the compensation of metabolic acidosis?</p>
<p>hyperventilation (respiratory compensation) -> excrete more CO2</p>
<p>Clinical presentation of metabolic acidosis</p>
<p>- N/V/D- confusion/coma- Kussmaul breathing (deep and rapid)</p>
<p>causes of metabolic alkalosis</p>
<p>- addition of base or loss of acid- vomiting (loss of acid)- antacid tablets (gain HCO3)- diuretics (volume contraction)</p>
<p>What is the compensation of metabolic alkalosis?</p>
<p>hypoventilation (respiratory compensation) -> retain more CO2</p>
<p>Clinical presentation of metabolic alkalosis</p>
<p>- increased NM irritability- tetany- seizures- confusion- lethargy- coma</p>
<p>Respiratory acidosis compensation</p>
<p>decreased ventilation -> CO2 goes up -> kidneys increase HCO2 regeneration and acid excretion</p>
<p>causes of respiratory acidosis</p>
<p>CNS depression, airway obstruction, pneumonia, PE, COPD</p>
<p>Clinical presentation of respiratory acidosis</p>
<p>- headache- lethargy- confusion- tremors/seizures- cardiac arrhythmias</p>
<p>Respiratory alkalosis cause and compensation</p>
<p>increased ventilation (hyperventilation) -> CO2 decreases -> kidneys decrease acid excretion</p>
<p>Clinical presentation of respiratory alkalosis</p>
<p>- diaphoresis- NM irritability- carpopedal spasms- tingling around fingers/mouth- seizures/coma</p>
<p>What is the relationship between calcium and phosphate?</p>
<p>extracellular concentrations are inversely related -> both regulated by the same hormones</p>
<p>5 patterns of neurologic function that are critical to evaluate</p>
<p>- level of consciousness- pattern of breathing- pupillary reaction- oculomotor responses- motor responses</p>
<p>Explain the rhythm of Cheyne-Stokes respiration</p>
<p>- increased levels of CO2 -> tachypnea- CO2 levels decrease -> leads to apnea until CO2 accumulates again</p>
<p>4 criteria for brain death</p>
<p>- unresponsive coma (no motor or reflex movements)- no spontaneous respiration (apnea)- no brainstem functions (dilated, fixed pupils; no gag or corneal reflexes)- isoelectric EEG</p>
<p>death of the cerebral hemispheres exclusive of the brain stem and cerebellum (no behavior or environmental responses but brain can maintain homeostasis)</p>
<p>Cerebral death (irreversible coma)</p>
<p>complete unawareness of the self or surrounding environment and complete loss of cognitive function; can be seen in survivors of cerebral death</p>
<p>persistent vegetative state (VS)</p>
<p>sleep-wake cycle are present, eyes open spontaneously, and BP and breathing are maintained without support; brainstem reflexes intact but cerebral function lost</p>
<p>persistent vegetative state (VS)</p>
<p>individuals may follow simple commands, manipulate objects, gesture or give yes/no responses, have intelligible speech, and have movements such as blinking/smiling</p>
<p>minimally conscious state (MCS)</p>
<p>defect of pattern recognition -> failure to recognize the form and nature of objects (can be tactile, visual, or auditory)</p>
<p>Agnosia</p>
<p>agnosia is commonly associated w/ what neurological problem</p>
<p>CVA</p>
<p>Broca vs Wernicke</p>
<p>- Broca's area: helps in producing coherent speech- Wernicke's area: helps in speech processing and understanding language</p>
<p>acquired mental disorder characterized by deficits in attention and coherence of thought and action; secondary to intoxication, metabolic disorders, or nervous system disorders</p>
<p>acute confusional states (ACS); may also be called delirium</p>
<p>progressive deterioration of cerebral functions due to neurofibrillary tangles and plaques -> lead to neuronal death and brain atrophy</p>
<p>Alzheimer's disease (AD)</p>
<p>state of continuous seizures lasting more than 5 minutes or rapidly recurring seizure before the person has regained consciousness</p>
<p>status epilepticus</p>
<p>normal ICP</p>
<p>5-15 mmHg</p>
<p>causes of increased intracranial pressure (IICP)</p>
<p>increased intracranial content- tumor growth- edema- excessive CSF- hemorrhage</p>
<p>ICP may not change in this stage due to compensatory mechanisms</p>
<p>Stage 1 IICP</p>
<p>stage with continued expansion of intracranial contents and pressure may compromise neuronal oxygenation and systemic arterial vasoconstriction may occur to overcome IICP</p>
<p>Stage 2 IICP</p>
<p>Clinical manifestations of stage 2 IICP</p>
<p>subtle and transient - confusion- restlessness- drowsiness- slight pupillary and breathing changes</p>
<p>stage where ICP begins to reach arterial pressure and brain tissues experience hypoxia and hypercapnia -> rapid deterioration</p>
<p>Stage 3 IICP</p>
<p>Clinical manifestations of stage 3 IICP</p>
<p>- decreased levels of arousal- widened pulse pressure (systolic increases)- bradycardia- small, sluggish pupils</p>
<p>stage of IICP where brain tissue herniates from compartment of greater pressure to compartment w/ less pressure -> blood supply compromised -> further hypoxia in herniated tissues</p>
<p>Stage 4 IICP</p>
<p>Clinical manifestations of stage 4 IICP</p>
<p>- progression to deep coma- ipsilateral dilation and fixation of pupils -> bilateral dilation and fixation of pupils- abnormal breathing (Cheyne-stokes, ataxic, or central neurogenic hyperventilation)- pulse pressure begins to decrease (as brain herniates and ICP decreases)- pulse slightly irregular</p>
<p>At what stage of IICP is surgical or medical intervention the best?</p>
<p>Stage 2 IICP</p>
<p>Cause of hydrocephalus</p>
<p>interference of CSF flow- decreased reabsorption- increased production- obstruction within ventricular system</p>
<p>NT necessary to make muscle tone smooth</p>
<p>dopamine</p>
<p>AD hereditary degenerative disorder that causes severe degeneration of basal ganglia and frontal cerebral atrophy -> depletion of basal ganglia GABA (inhibitory NT)</p>
<p>Huntington disease (HD or Chorea)</p>
<p>severe degeneration of basal ganglia involving dopaminergic nigrostriatal pathway -> dopamine deficiency (inhibitory NT) and unopposed cholinergic activity (promotes muscle tone)</p>
<p>Parkinson disease (PD)</p>
<p>Classic manifestations of PD</p>
<p>- resting tremor- rigidity- bradykinesia/akinesia- postural disturbance (stooped)- short shuffling steps- cognitive-affective symptoms</p>
<p>Diagnostic hallmark of PD? What does it lead to later in disease?</p>
<p>- Lewy body formation in neurons (protein misfolding and accumulation of alpha-synuclein)- Lewy body dementia later in disease</p>
<p>temporary loss of all spinal cord functions below the lesion</p>
<p>spinal shock</p>
<p>neurodegenerative disorder that diffusely affects upper and lower motor neurons of the cerebral cortex, brain stem, and spinal cord (corticospinal tracts and anterior roots)</p>
<p>amyotrophic lateral sclerosis (ALS or Lou Gehrig disease)</p>
<p>Clinical manifestation of ALS</p>
<p>progressive muscle weakness leading to respiratory failure and death; pt has normal intellectual and sensory function until death</p>
<p>posture/response characterized by upper extremities flexed (held close to body) and lower extremities that are externally rotated and extended;occurs when the brainstem is not inhibited by the cerebral cortex motor area</p>
<p>decorticate posture/response</p>
<p>posture/response characterized by increased tone in extensor muscles and trunk muscles w/ active tonic neck reflexes (head is neutral and all 4 extremities are rigidly extended);caused by severe injury to the brain/brainstem</p>
<p>decerebrate posture/response</p>
<p>broad-based gait where person walks in small steps and the head and body are flexed -> due to basal ganglion dysfunction and seen in Parkinson disease</p>
<p>basal ganglion gait</p>
<p>exaggerated emotional response; excessive crying (left hemisphere) or laughing (right hemisphere); may not be appropriate to environment</p>
<p>hypermimesis</p>
<p>loss of emotional language (aprosody); inability to understand emotional in speech and facial expression or inability to express emotion</p>
<p>hypomimesis</p>
<p>brain injury at the site of impact</p>
<p>coup injury</p>
<p>injury from the brain rebounding and hitting opposite side of skull after impact</p>
<p>contrecoup injury</p>
<p>fracture at the base of the skull; pts can leak spinal fluid from their ears/nose and have raccoon eyes</p>
<p>basilar skull fracture</p>
<p>4 types of vertebral injuries</p>
<p>- simple fracture- compressed fracture (wedge; vertebral body compressed anteriorly)- comminuted fracture (vertebral body shattered into several fragments)- dislocation</p>
<p>normal activity of the spinal cord ceases at and below the level of injury due to lack of continuous nervous discharges from the brain; transient</p>
<p>spinal shock</p>
<p>causes of spinal shock</p>
<p>presence of hemorrhage or edema at the spinal cord; also due to transection of the cord which would not be transient</p>
<p>clinical manifestation of spinal shock</p>
<p>complete loss of reflex function (skeletal, bladder, bowel, sexual function, thermal control, and autonomic control) below level of lesion</p>
<p>syndrome of sudden, massive reflex sympathetic discharge associated w/ spinal cord injury at T6 or above where descending inhibition is blocked</p>
<p>autonomic hyperreflexia (dysreflexia)</p>
<p>Explain the cause of autonomic dysreflexia</p>
<p>- sensory receptors below level of cord lesion are stimulated- intact autonomic nervous system reflexively responds -> increase BP (sympathetics)- baroreceptors in cerebral vessels, carotid sinus, and aorta sense HTN and stimulate parasympathetics- HR decreases but vessels don't dilate because efferent impulses can't pass through cord</p>
<p>most common causes of autonomic dysreflexia</p>
<p>distended bladder or rectum; also caused by pain receptors in the skin, penis, and uterus</p>
<p>in autonomic dysreflexia, stimulation of the sympathetic nervous system will cause what (4)?</p>
<p>- vasoconstriction- hypertension- skin pallor- pilomotor spasms (goosebumps)</p>
<p>in autonomic dysreflexia, what parasympathetic response will occur above lesion (4)?</p>
<p>- arterial dilation- flushed skin- headache - sweating</p>
<p>fracture of the lamina (usually in the lumbar region; L5) and it causes a separation between adjacent vertebrae</p>
<p>spondylolysis</p>
<p>secondary to spondylolysis; anterior displacement (sliding) of the inferior vertebral segment</p>
<p>spondylolisthesis</p>
<p>condition due to a compressed nerve in the spine that can cause pain, numbness, tingling, or weakness along the course of the nerve/dermatome</p>
<p>radiculopathy</p>
<p>arise from arterial occlusions caused by thrombi formation in arteries supplying the brain or intracranial vessels</p>
<p>thrombotic stroke</p>
<p>involves fragments that break from a thrombus formed outside the brain (usually heart, aorta, or common carotid)</p>
<p>embolic stroke</p>
<p>stroke usually caused by occlusion of a single, deep perforating artery that supplies small penetrating subcortical vessels; will have pure motor or sensory deficits</p>
<p>lacunar stroke</p>
<p>a mass of blood is formed as bleeding continues into the brain -> adjacent brain tissue is displaced and compressed -> causes ischemia, edema, IICP, and necrosis</p>
<p>hemorrhagic stroke</p>
<p>most common type of brain aneurysm that is usually due to congenital abnormalities in the arterial wall; occur in large intracranial vessels and will cause subarachnoid hemorrhage if ruptured</p>
<p>saccular (berry) aneurysms</p>
<p>aneurysm that results from diffuse arteriosclerotic changes and are found most commonly in the basilar arteries or terminal portions of the internal carotid arteries</p>
<p>fusiform (giant) aneurysms</p>
<p>acute febrile illness, usually of viral origin, with nervous system involvement</p>
<p>encephalitis</p>
<p>acquired inflammatory disease causing demyelination of the peripheral nerves w/ relative sparing of axons; acute onset w/ ascending motor paralysis that usually occurs after respiratory or GI infection</p>
<p>Guillain-Barre syndrome</p>
<p>chronic inflammatory disease involving degeneration of CNS myelin, scarring (sclerosis or plaque formation), and loss of axons</p>
<p>multiple sclerosis</p>
<p>chronic autoimmune disease where IgG antibodies are produced against ACh receptors -> block binding of ACh and decrease muscle contraction</p>
<p>myasthenia gravis</p>
<p>symptoms of myasthenia gravis</p>
<p>- weakness and fatigue- ptosis (drooping of eyelid)- diplopia- difficulty chewing</p>
<p>most common types of urinary calculi</p>
<p>- calcium oxalate or calcium phosphate- struvite - uric acid</p>
<p>What causes nephrolithiasis</p>
<p>- supersaturation of one or more salts- precipitation of a salt from liquid to solid state- growth into a stone via crystallization or aggregation</p>
<p>How are kidney stones evaluated?</p>
<p>- imaging studies determine location of stone (KUB/CT/IVP)- UA to analyze contents of stone</p>
<p>Treatment of kidney stone</p>
<p>- high fluid intake- decreased dietary intake of stone-forming substances- stone removal</p>
<p>benign encapsulated tumors located near the cortex of the kidney</p>
<p>renal adenoma</p>
<p>most common renal neoplasm</p>
<p>renal cell carcinoma (RCC)</p>
<p>symptoms are renal cancers</p>
<p>- usually no early symptoms- later sxs include gross, painless hematuria and dull, achy flank pain</p>
<p>most common metastasis sites of RCC</p>
<p>- lung- liver- bone- thyroid- CNS</p>
<p>most common bladder malignancy</p>
<p>transitional cell carcinoma</p>
<p>risk factors for RCC</p>
<p>- smoking- obesity- analgesic use</p>
<p>symptoms of acute cystitis</p>
<p>- urinary frequency- dysuria- urinary urgency- lower ABD pain and/or suprapubic pain</p>
<p>nonbacterial or noninfectious cystitis</p>
<p>interstitial cystitis</p>
<p>symptoms of interstitial cystitis</p>
<p>- bladder fullness- urinary frequency - small urine volume- chronic pelvic pain- dyspareunia</p>
<p>acute infection of the renal pelvis and interstitium; most common cause is vesicoureteral reflux; associated w/ E. coli, proteus, and pseudomonas</p>
<p>acute pyelonephritis</p>
<p>symptoms of pyelonephritis</p>
<p>- fever/chills- flank or groin pain- other symptoms characteristic of a UTI</p>
<p>Common causes of glomerulonephritis</p>
<p>- type II, III, or IV hypersensitivity- drugs or toxins- vascular disorders (vasculitis)- systemic disorders (DM- post-strep infection</p>
<p>most common cause of end-stage renal failure</p>
<p>glomerulonephritis</p>
<p>What lab work will be seen w/ glomerular disease?</p>
<p>- decreased GFR- increased plasma creatinine and urea- reduced creatinine clearance</p>
<p>Explain how glomerular disorders can lead to edema</p>
<p>increased glomerular capillary permeability -> passage of plasma proteins into urine -> hypoalbuminemia -> decreased vessel oncotic pressure and fluid moves into interstitial space -> edema</p>
<p>excretion of 3.5 g or more of protein in the urine per day; due to glomerular injury</p>
<p>nephrotic syndrome</p>
<p>clinical manifestations of nephrotic syndrome</p>
<p>- hypoalbuminemia -> edema- hyperlipidemia and lipiduria (low albumin stimulates lipoprotein synthesis by liver)- vitamin D deficiency (decreased D activation by kidneys)- proteinuria- microscopic hematuria and RBC casts</p>
<p>causes of decreased renal perfusion</p>
<p>- hypotension- hypovolemia (hemorrhage or fluid loss)- sepsis- inadequate cardiac output- renal artery stenosis</p>
<p>most common cause of intra renal kidney injury/failure</p>
<p>acute tubular necrosis (ATN)</p>
<p>urine output less than 400ml/day</p>
<p>oliguria</p>
<p>urine output less than 50 ml/day</p>
<p>anuria</p>
<p>Elevated levels of urea and other nitrogen compounds in the blood.</p>
<p>azotemia</p>
<p>Stage of CRF w/ normal kidney function (GFR >90 ml/min); HTN</p>
<p>stage 1 CRF</p>
<p>Stage of CRF w/ mild kidney damage (GFR 60-89 ml/min); possible elevation of BUN and creatinine and HTN</p>
<p>stage 2 CRF</p>
<p>Stage of CRF w/ moderate kidney damage (GFR 30-59 ml/min); mild w/ HTN</p>
<p>Stage 3 CRF</p>
<p>Stage of CRF w/ severe kidney damage (GFR 15-29 ml/min)</p>
<p>Stage 4 CRF</p>
<p>ESRF w/ GFR < 15 ml/min</p>
<p>Stage 5 CRF</p>
<p>symptoms of stage 4 and stage 5 CRF</p>
<p>- moderate HTN- EPO deficiency anemia- hyperphosphatemia and hyperkalemia- hyperlipidemia- metabolic acidosis- salt/water retention</p>
<p>systemic manifestations seen due to urea accumulation because of renal dysfunction</p>
<p>uremic syndrome/uremia</p>
