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Patho Complete Exam 2 Notes

by: Haley

Patho Complete Exam 2 Notes NURS 239 001

GPA 3.5

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About this Document

All of the notes for exam 2.
Pathophysiology I
Nursing, pathophysiology, immunology
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This 16 page Bundle was uploaded by Haley on Wednesday February 17, 2016. The Bundle belongs to NURS 239 001 at University of New Mexico taught by Drexler in Fall 2015. Since its upload, it has received 34 views. For similar materials see Pathophysiology I in Nursing and Health Sciences at University of New Mexico.

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Date Created: 02/17/16
Adaptive Immunity  ● 3rd line of defense in immunity where the B cells remember the pathogen so  that the body can fight off a future infection.   ○ The T cells fight the infection.  ● Two Types of Cells:    T Cells (Lymphocytes)  B Cells (Lymphocytes)   Cytotoxic: killers  Differentiate into plasma cells  Helper: tell killers to “come over  Produce 5 types of antibodies  here!” (site of infection)  Suppressor: inhibits kills “that’s  Recognition and memory  enough!”    ● Lymphatic organs: make immune response    Central Organs  Peripheral organs  Bone Marrow  Spleen  Thymus  Lymph nodes and lymph tissue    ● Lymph nodes:  ○ Near arteries  ○ Take pathogen to node  ○ Travel to cardiovascular system to dispose of  ● Immunocompetent: cells growing up  ● Lymphoid stem cell is made in bone marrow  ○ B cells are made in bone marrow  ■ Go towards humoral immunity  ● Create: Memory B Cell  ○ Remembers pathogen  ● Create: Plasma Cell→   ○ Produces antibodies  ○ Gammaglobulin  ○ T cells are made in thymus  ■ Go towards cellular immunity  ● Create: T Helper cell  ○ Activate cytotoxics to kill  ● Create: Cytotoxic T cell  ○ CD8: cluster of differentiation: identify type of  receptor on pathogen and destroy  ● Create: Suppressor T cell  ○ Stops process     Innate Immunity​  immunity that you are born with  ● Innate immunity wants to prevent microbe:  ○ Colonization   ○ Spread  ○ Entry    Adaptive Immunity  ● Two types:    Cell mediated  Humoral   CD8: killers!  Secrete antibodies from plasma  CD4: helpers! CD4 produces→   Memory cells  TH1: activate macrophages and  Antibodies: IgA, IgD, IgE, IgG, IgM  cytokines→ phagocytosis occurs by  IgG: activates complement, passive  macrophages and cytokines  immunity in newborns, antibody  They are globular and thick  TH2: activate B cells→ B cells  IgA 15%, IgG 75%, IgM 10%, IgD 0.2%,  differentiate→ B cells release antibodies  IgE 0.04%    ● Antibody Function: Neutralize antigen, clump up (agglutinate), spread out  (precipitation)  ○ Lock and key system with receptors  ○ Neutralize toxins from Gram Negative bacteria  ● Major Histocompatibility System (MHC): produced by human leukocyte antigen  (HLA)  ○ MHC 1: recognize CD8s  ○ MHC 2: recognize CD4s, TH1s and TH2s  ● Antigens  ○ Pathogens  ➢ Virus  ➢ Bacteria  ➢ Fungi   ➢ Parasite  ○ Noninfectious  ➢ Pollen  ➢ Food  ➢ Bees  ○ Clinical  ➢ Transplant  ➢ Transfusion  ● Responses    Primary  Secondary  First time interacting with the antigen  Reactivation of adaptive immune  response because of recognition!  Lower titer for IgG and IgM  High titer for IgG and low for IgM  Slow and many symptoms  Fast and often no symptoms    ● How can host defense fail?  ○ Virus mutates: takes longer to make new antibodies for new virus type  ○ Viral latency: hides in cells and activates later (28 days later)   ○ Immunodeficiency: not enough immunity  ● Alloimmunity: body cannot tell the difference between self and nonself   ○ Damages organs or systems  ○ Graft rejection    ● Autoimmune disease: Lupus, RA, thyroid    AIDS    HIV: virus  →   AIDS: syndrome  Flu symptoms    Other opportunistic infections: candida,  kaposi endothelial tumors, pneumonia  Virus continues to replicate     Patients eventually dies    ● Altered host defense from secondary immunodeficiency   ○ CD4s and helper Ts are infected with HIV  ● Loss of cell mediated and humoral immunity   ○ Loss of CD4 TH1s   ■ Cannot activate macrophages and cytokines  ● Some manifestations:  ○ Anorexia  ○ Diarrhea  ○ Fatigue  ○ Weakness  ○ Opportunistic infections!  ○ Memory loss  ○ Night sweats  ○ Swollen lymph nodes  ● Diagnostic:   ○ H&P   ○ Risk factors?   ➢ Homosexual, needles, blood  ○ Signs and symptoms: flu‐like  ➢ Seroconversion: period of time from exposure to HIV to develope  antibodies  ● Lab  ○ Viral load  ○ Detection of antibodies for HIV  ○ CD4 helper lymphocyte cell counts  ● Treatment  ○ HARRT: suppress viral replication→ delay disease progression  ○ Early treatment is better!  ○ Use drug combo to reduce drug resistance of HIV  ● Seroconversion: how long it takes for an antibody to develop and be detected  in the bloodstream  Hypersensitivity     (I)Hypersensitivity  Immediate exaggerated response to antibody  Reaction (HSR)  Allergy  (II) Antibody  Tissue Specific  Mediated HSR  Blood transfusion, drug reactions, Rh factor  (III) Immune  Vasodilation and increased permeability  complex mediated   Lupus, Rheumatoid Arthritis (RA)  (IV) Cytotoxic T  Antigen creates memory in the dermis, 2nd response is  lymphocyte  stronger  mediated HSR  Contact dermatitis (think of cat allergy)    Anaphylaxis   ● Exaggerated response (type I)  ○ Triggered by allergy  ● Antigen→ IgE→ histamine→ vasodilation→ bronchial smooth muscle  contraction (narrowing of airway)→ increased vascular permeability   ○ Individual has been sensitized to antigen before   ○ IgE is released  ○ Mast cells and basophils degranulate   ○ Local and systemic responses occur  ➢ Dilation of smooth muscle  ➢ Narrowing airway  ➢ Increased vascular perm  ○ Vasoactive amines and other mediators are released  ○ Mast cells release histamines when encountering allergen  ● Phase 1   ○ Difficulty breathing  ○ Flushing  ○ Itching  ○ Angioedema (swelling of dermis)    ● Phase 2   ○ Difficulty breathing  ○ Severe hypotension  ○ Severe edema  ● Diagnostic  ○ H&P  ○ Allergy testing (painful!)  ● Treatment  ○ Symptomatic:  ➢ Drugs to open airway (Bronkaid, albuterol)  ➢ Drugs to constrict vascular smooth muscle (Oxytocin,  vasopressin)   ➢ Limit inflammation (Ibuprofen, aspirin)   ○ Preventative  ➢ Desensitization  Rh Isoimmunization  ● Type II cytotoxic antibody‐mediated reaction  ○ Mom: Rh‐ (anti‐D antibodies)  ○ 2nd baby: Rh+ (D antigen)  ➢ They share blood  ➢ Mom’s antibodies attack baby’s red blood cells by hemolysis  ● Manifestations  ○ Anemia  ○ Too much bilirubin in blood (bilirubin is a breakdown product of heme;  due to hemolysis of blood cells)   ➢ Bilirubin in tissues= yellow→ jaundice  ➢ Liver is unable to conjugate bilirubin and cannot get rid of it  ○ Kernicterus: brain damage from excessive jaundice  ○ Hearing loss  ○ Cerebral palsy: movement, speech, muscle tone and posture disorder;  abnormal development   ● Diagnostic  ○ H&P  ○ Identify D antigen and anti‐D antibodies  ○ Amniocentesis to measure bilirubin  ○ Sample fetal blood  ● Treatment  ○ Reduce risk  ○ Transfuse baby with rhogam through placenta  ○ Blood transfusion of new blood for fetus    SLE (Lupus)   ● Type III   ● Autoimmune  ● Uses innate and adaptive immune systems  ● Caused by antigen  ○ Epstein‐barr virus  ● B cells: produce antibodies  ● T cells: promote inflammation  ● Systemic: complex deposits in certain organs    Local  Systemic  Kidney→ glomerulus: stopped up so  Speech difficulty  you cannot pee  Capillary bed  Pulmonary    Autoimmune    ● Manifestations  ○ Butterfly rash   ○ Seizures  ○ Serositis  ○ Heart  ○ Hematologic effects  ○ Glomerulonephritis  ○ Lymphadenopathy   ○ Arthritis  ● Diagnostic  ○ H&P  ○ Lab: C3 and C4 (complements)   ● Pharm  ○ Anti‐inflammatories  ○ Disease modifying anti‐rheumatoid   ○ Anti‐malarial for cell membrane  ○ Immunosuppressants  ● Type IV   ○ T lymphocytes→ T cells activate→ memory cells  ○ Contact dermatitis  ➢ TB test  ○ Sensitization→ T cells activate→ (elicitation) memory cells develop  sensitivities  ○ Direct cell‐mediated toxicity  ➢ CD8 cytotoxic cells attack cells with recognized antigens (antigen  could be harmful or non harmful)   ➢ So cell mediated toxicity causes MORE damage  ● Hepatitis B  ○ Body attacks liver  ○ Antigen specific T lymphocytes  ➢ Skin reaction is small and itching  ➢ APC and TH1 mediate   ➢ Reaction with self proteins bind to MHC   ● This is seen as foreign  ➢ The antigen is sensitized into system  ➢ The pathogen is reintroduced (elicited) into system  ● T cell memory in dermis creates local reaction  ○ TB circle    Rheumatoid Arthritis   Osteoarthritis  Autoimmune  Singular  Systemic  Wear and tear of joints  Moving of joints  Bone degradation     Gout​: uric acid crystals trapped in joints  ● Pain and swelling from crystals     Fibromyalgia: ​widespread muscle pain and tenderness  ● No cure  ● Genetically linked    Infection  ● Tissue destruction from invasion of microbes  ○ Communicable: spread from person to person   ➢ Blood  ➢ Fluid  ➢ Skin  ○ Noncommunicable: spread not by person  ➢ Vectors  ➢ Fomite  ➢ Inanimate object  ● ALL communicable diseases are infectious but not all infections are  communicable!  ● Capacity to cause disease:  ○ Communicability   ○ Immunogenicity  ○ Infectivity  ○ Mechanism of action  ○ Pathogenicity   ○ Portal of Entry  ○ Toxigenicity  ○ Virulence  ● Acute Infection  ○ Exposure: ​first contact  ○ Incubation: exposure→ symptoms  ○ Prodrome: ​ onset of signs and symptoms (eeyore‐like)  ○ Clinical Illnesssigns and symptoms specific to disease  ○ Convalescence: t​ired but leads to full recovery    Local Infection  Systemic Infection  heat  fever  redness  weakness  swelling  headache  heat  malaise  edema  anorexia  incapacitation: limited movement  nausea  lymphadenitis: inflammation of lymph    nodes  purulent exudate:WBCs      ● Toes vs. whole body for local vs. systemic  ● Complications of Infection  ○ Septicemia: ​ when an unknown pathogen enters into bloodstream  ○ Bacteriemia:​  confirmed bacteria in bloodstream   ➢ Treat with antibiotics  ○ Massive vasodilation​ → septic shock  ➢ High heart rate, low blood pressure= vasodilation  ○ Chronic infection:​  lasts weeks to years  ➢ Prefix mono: means activates monocytes  ➢ Examples:  ● Fibromyalgia  ● MRSA: recurrent infections  ○ Can still spread even if host is symptomless    ● Treatment of Infection  ○ Antimicrobial drugs  ■ Antifungals: break cell wall  ■ Antivirals: slow replication  ■ Anti‐bacterials: inhibit protein synthesis, break cell walls  ○ Symptom Reduction  ■ Aspirin  ■ Fluids to squeeze out infection  ● Chain of Infection  ○ Infectious agent→ reservoir→ portal of exit→ portal of entry→ host  ■ Prevent with handwashing!  ● Bacteria  ○ Shape of bac?  ○ Is it positive or negative?   ■ Gram negative releases toxins in the body  ○ Endotoxins or exotoxins?  ● Viruses  ○ Use body cells to make more virions  ■ Attaches to plasma membrane  ■ Releases enzymes to weaken membrane  ■ Penetrate cell  ■ Uncoating  ■ Replicates  ■ Matures and escapes by budding  ● Fungal Disease  ○ Reproduce through:  ■ Budding  ■ Division  ○ Multiply inside or outside cell  ○ Superficial, deep or opportunistic  ○ Entry:  ■ Inhalation  ■ Wounds  ○ Mold: aerobic  ○ Yeast: anaerobic  ● Parasites  ○ Symbiotic relationship  ■ Negative  ○ Unicellular to large worms  ○ Usually transmitted through vectors  ○ Direct tissue damage  ■ By host immune system  ■ By parasite    ● Protection  ○ Antimicrobials  ○ Vaccines  ■ Different coats for pathogens→ vaccines have to constantly  change to match coat or might not be effective because of coat  change  ■ Scientists find largest strain of pathogen and use the vaccine for  that large strain  ■ Herd immunity: 85% of population achieves immunity→  prevention  ● Immune Deficiencies  ○ Primary: congenital  ○ Secondary: acquired with another condition, more common    ● Recurrent infections: check risk factors!  ● Multiple infections could be occurring at the same time   ● Replacement therapy: gamma globulins, blood products, stem cells, steroids    Influenza  ● Airway epithelial cells are infected by virus  ● Transmission: respiratory droplets  ● Result: infected epithelial cell necrosis  ● Manifestations  ○ Cough  ○ Sore throat  ○ Nasal congestion/drainage  ○ Chills  ○ Fever  ○ Body aches  ○ Malaise  ● Diagnostic  ○ H&P  ○ Rapid viral assays  ○ Prevention  ○ Symptomatic care  ■ Fluids, rest, over the counter  ○ Antiviral drugs  Viral Hepatitis   ● Liver inflammation from infection of hepatitis virus(es)  ○ Acute  ○ Chronic  ● Transmission: ​ fecal‐oral, body fluids of the infected  ● Result: hepatic necrosis (liver dies)  ● Types A‐E   ○ Refer to Table 5.3  ○ A&E: fecal oral  ○ B,C,D: infected blood and fluids  ○ B&D: mother to fetus  ● Manifestations  ○ Prodrome: fatigue, anorexia, low fever  ○ Icterus: jaundice, enlarged liver, clay stools, irregular urine  ○ Recovery: long, when enlarged liver decreases  ● Diagnostic and Treatment  ○ H&P  ○ Detection of viral antibodies  ○ Prevention  ○ Symptomatic care  ■ Safe sex  ■ Careful with needles  ■ Careful with seafood  ○ Antivirals   UTI   ● Ascending infection from wiping and cleaning  ● Women are more likely  ● E. Coli is most common   ○ Think of butt proximity  ● Result: necrosis of urinary tract epithelium   ○ Damage to nephron  ● Manifestations:  ○ Burning pee  ○ Bladder spasms  ○ Cloudy pee: purulent with WBCs in it  ○ Lower back pain  ○ Bloody urine  ● Diagnostic and Treatment  ○ H&P  ○ Urinalysis and urine culture  ■ Look at specific gravity  ○ Antimicrobials  ○ Symptomatic care  ■ Anti‐inflammatory  ■ Cranberries  Tinea  ● Group of fungal infections  ● Transmission: direct contact  ● Dermophyte thickens (keratinizes) cells  ● Types:  ○ Corporis: ringworm  ■ Epidermis  ■ Ring pattern  ○ Versicolor: affects melanocytes  ■ Discoloration  ■ Hypopigmentation  ○ Capitis: hair loss and breakage  ■ Keratin build‐up on hairs  ○ Pedis: athlete’s foot  ■ Build up between and around toes  ○ Cruris: erythema, itching  ■ Redness  ■ Blob shape  ○ Unguium: nail thickening, discoloration  ■ Bar rot  ● Wet and ret: powder  ● Dry and flakey: cream  ● Diagnostic:   ○ H&P  ○ Microscopic exam  ○ Look for fungus with wood light  ○ Prevention: stay away from gross wet places!  ○ Antifungals  ○ Fungal cultures  Meningitis: Bacterial  ● Inflammation in brain and spinal cord  ● Transmission: respiratory droplets  ● Result: Bacteria proliferate in CNS and exudate damages and obstructs CNS  structures leading to reduced oxygen in the brain  ● Manifestations:  ○ Severe and rapid onset  ○ Severe headache  ○ *Photophobia: light fear  ○ *Nuchal rigidity: stiff neck  ○ Loss of consciousness  ○ Vomiting  ○ Seizures  ● *Meningitis vs. Migraine   ○ Meningitis only symptoms  ● Diagnosis  ○ H&P   ■ Kernig sign: raise knee test  ● Pulls on meninges  ■ Brudzinski sign: move head forward  ● Pulls on posterior meninges  ○ Blood and CSF analysis and cultures  ○ Spinal Tap  ● Know Table 5.4!  Bacterial Meningitis   Viral  Fungal  Rapid onset: <24 hours  1‐7 days  >7 days  Severe  Mild‐moderate  Mild  Neutrophils  Lymphocytes  Lymphocytes  Antibiotics  Symptomatic   Antifungals    ● Treatment:  ○ Prevention  ○ Antimicrobials for ​EVERYONE IN THE HOUSE  ○ Symptom care 


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