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NSG 211 EXAM 1 Review
Pathophysiology (NSG 211)
Marian University
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PATHO/PHARM 2022Preview text
EXAM 1: NSG 211 EXAM REVIEW
1. Definitions:
Idiopathic – Things arise spontaneously, the cause is unknown. This is a person specific reaction and unpredicted. ** NOT AN ALLERGIC REACTION Iatrogenic – Acquired from treatment or examination during pt. care Acute – sudden onset (Less than 6 months) Typically remediates after treatment Chronic – S/Sx that have lasted longer than 6 months Nosocomial – Disease acquired during a hospital visit, stay, or procedure Communicable – Disease being transmitted from one infected person to another (contagious) Notifiable (or Reportable) – some diseases that have to be reported to state board of health (STI’s)
2. Define Epidemiology, Morbidity, Mortality, Prevalence, Incidence and Homeostasis:
Epidemiology – study of communicable diseases and how they develop Mortality – death Morbidity – QOL decrease due to disease (i. congestive heart failure, osteoporosis, etc. all at once is comorbidity). Prevalence – proportion/number of people over a given time who have a condition/disease (time frame/no time frame) Incidence – measure of the probability of occurrence of a given medical condition in a population within a specified period of time (i. incidences of the flu from January to March vs April to June) Homeostasis – stable, equilibrium, the norm – the condition to which your body tries to default
3. Cell Growth Patterns and Definitions:
Hypertrophy – enlargement of an organ or tissue from the increase in size of its cells Hyperplasia – (a.k. hypergenesis) an increase in the amount of organic tissue that results from cell proliferation. It may lead to the gross enlargement of an organ Metaplasia – one mature form to another Dysplasia – a broad term that refers to the abnormal development of cells within tissues or organs Atrophy – decrease in cell size Benign vs. Malignant – Benign is not typically cancerous. Malignant typically cancerous. A benign tumor is a tumor that does not invade its surrounding tissue or spread around the body. A malignant tumor is a tumor that may invade its surrounding tissue or spread around the body.
4. Cell Injury Process (causes and characteristics): Hypoxia, Ischemia, Death/Necrosis
Hypoxia – deprivation of O 2 to tissue/cell, can affect whole body or be local Ischemia – inadequate tissue perfusion/ blood flow, #1 of causing cellular damage
Death – Necrosis: death of a cell(s), not enough ATP energy; nasty; inflammatory Apoptosis: ORGANIZED self destruction and death
Types of Necrosis: Gangrene: an area of necrotic tissue which has been infected by bacteria; if bloody ischemic can die in nasty blood clot (coagulative); cheesy (casius); liquefied
Types of Exudate: (interstitial fluid formed in the inflamed area) Serous: clear yellow fluid, thing (under blisters) Fibrinous: has fibrin, Thrombin enzyme causes fibrinogen to convert to fibrin, blood clotting, in plasma of blood; sticky Purulent: pus Abscess: walled off sack full of PUS Hemorrhagic: bloody
Types of Tissue Healing and Tissue healing abnormalities 1 st Intention Healing: cleaner; well approximated; less granular tissue – less scar formation 2 nd Intention Healing: dirty; not healing well; more granular tissue – more scar formation Keloid: big scar; hypertrophic scar Contracture: less functional form of healing tissue (scar tissue) occurring over flexor surface; decreases mobility; can also have tendons and ligaments
5. Inflammation Process (Innate Immunity: Typical manifestations, Complications):
Major chemical mediators of inflammation: Histamine, Bradykinin, Leukotriene, Tumor Necrosis Factor (TNF) Acute: infection, ulcers, tissue swelling, muscle spasms – of short duration Chronic: persisting for a long time
Manifestations of both Acute and Chronic inflammation
Medications for Inflammation Acetylsalicylic Acid (ASA): ASPIRIN an NSAID Nonsteroidal Anti-Inflammatory Drugs (NSAIDS): Non-steroid anti-inflammatory drugs Aspirin, ibuprofen naproxen (Aleive) Glucocorticoids: Prednisone, Cortisone – cover up inflammation; stop healing for innate immunity; good for short term; decrease permeability & leukocytes & histamines; blocks all aspects of the immune response Can cause immune tissue atrophy; catabolism of tissue, and muscle wasting
6. Immunity Process (Innate vs. Adaptive Immunity)
IgM: bound to B-cell “First Responder” Wagon wheel - does not cross placenta IgA2 : secretions (saliva, tears), colostrum for newborns (first liquid to come out of the breast of a monster- important for infant). IgE: Eosinophil / mast cells degranulation (type I HS) - a lot of histamine associated with this (allergies) IgG and IgM : large activators of complement
Cell-Mediated (T, B): CD4+ T-helper cell (architect of all immunity): NK Natural Killer T-cells: ”natural born killers”, destroy foreign cells (cancer) without activation
Lines of Immunity Defense:
Phagocytosis: engulfing foreign antigens Complement System: opsonization “tattle tale cells” – “HERE’S AN ANTIGEN! ALARM!” Specific Immunity: ● cells of specific immunity (macrophages & lymphocytes)
khanacademy/test-prep/mcat/organ-systems/the-immune-system/a/innate-immunity
7. Types of Immune Response:
Primary: What Ig is highest? IgM Secondary: What Ig is highest? IgG Natural: you get the disease and acquire Ab (chickenpox or varicella) Artificial: you did not have to get the disease (HepB we give a vaccination you don’t have to go through the disease) Natural Active: acquired through active illness Artificial Active: acquired thorough immune activation by vaccination (body responds as though it’s a true infection) Natural Passive: placenta or breast milk, passed on through childbirth Artificial Passive: subject is given antibodies by another organism (antivenin, rabies shot, RhoGham to expecting mothers ○ Rhogam- given to expectant mother is Rh – and the child is Rh+ ○ Type I: Allergic Reactions: IgE mediated (eosinophils and Mast cells).· ○ IgE mediated (eosinophils and mast cells)- histamine response ○ When mast cells degranulate they release histamine- vasodilation, capillary permeability (edema), airways obstruction, hypoxia. ○ Grass pollen- presented as an APC- begin a b cell humoral response and makes IgGs for grass pollen and so the next time you come into contact you have a hyperimmune response. Then you become edematous and you have a “stuffy” nose
Type I: Allergic Reactions: mild, from coughing and a runny nose, to a life-threatening reaction known as anaphylaxis. A person becomes allergic when their body develops antigens against a substance
Type II: Tissue Specific Hypersensitivity: 2 major types: ● #1: ABO Incompatibility (alloimmune reaction to a foreign HLA antigen) ○ Incompatible blood will result in host blood will attack donor blood ■ Destroys red blood cells (hemolysis), ■ Causes a massive IgG and complement inflammatory response and manifests with SOB, chest pain, diaphoresis, jaundice, urticaria, and even death ○ Blood typing: ■ Type A = A antigens you have B antibodies (can receive A and O) ■ Type B = B antigens and A antibodies (can only receive B and O) ■ Type O = Universal donor. No antigens and has both A/B antibodies (can receive O blood) ● Rh = Rh+ or Rh- ● Type AB = A/B antigens but no antibodies ● #2: ADCC: Antibody- dependent cell mediated cytotoxicity – involves NK T Cells ○ An antibody binds to a cell receptor and changes its physiological function ■ **ADCC is organ specific/ tissue specific ○ EXAMPLE: Graves’ Disease (Hyperthyroidism) ■ Pituitary TSH stimulates the thyroid hormone production and increases T3 and T and then the brain detects the higher levels of T3/4 and releases pituitary TSH to balance everything out again ○ Autoantibody at TSH receptor site causes the NK T cells to mistakenly bind and activate function of the TSH receptor and causes an increase in thyroid hormone production which goes to the brain to try and stop it but it’s not being stimulated by the brain but by a T cell – out of homeostasis. ○ Hyperthyroidism – Graves’ disease. And will keep going until the thyroid is gone must have treatment such as radiation or iodine
Type III: Immune Complex Hypersensitivity: ● Ab-Ag Immune Complex reactions (global effects-does not go away) – always involves an Ag-Ab Complex and systemic (not tissue specific) ○ Complement activation causes widespread host cell damage (distinction from Type II: damages is not organ-specific, can attack anywhere) ○ If Ag-Ab complexes not removed properly, remain blood borne and deposit in various tissues throughout the body (not tissue specific) – ex: acute rheumatic fever ○ If antigen protein of Ag-Ab complex is OWN host’s tissue – ex systemic lupus Erythematosis
Type IV: Cell-Mediated or Delayed Hypersensitivity (24-72 hr):
Local signs: Inflammation Pain Tenderness Exudate Tender local nodes
Systemic signs: Fever Fatigue Weakness Headache Nausea
11. Differences in Gram (-)- and Gram (+) bacterial infection to host (consider cell wall characteristics)
Gram (-): does not uptake stain. Typically contains endotoxins in the cell wall. No release of endotoxins (just inside cell) until cell dies Gram (+): uptakes stain, thick PGL (gram stain: cell wall composition-peptidoglycan: complex cell wall composition) layer. Often produce exotoxins as part of life function. Antibiotics can attack at PGL layer. Antibiotics relieve endotoxin symptoms.
12. HIV cause: What cell of immune system is primarily affected? Can HIV be destroyed with medications?
RNA retrovirus that infects T helper cells of host (Th CD4+ cell). HIV cannot be destroyed, but medications can slow down the process (somewhat like remediation).
13. AIDS cause and definition (hint CD4+ / T-h): What cell(s) is(are) affected? Which type(s) of immunity affected?
Acquired-immuno-deficiency Syndrome – a disease in which there is a severe loss of the body's cellular immunity, greatly lowering the resistance to infection and malignancy
Starts with HIV and it infects T helper cells. When someone is HIV+ the body has detected HIV virus and made B lymphocytes antibodies – no disease yet (can go months or years as HIV+)
Advances to AIDS when an unknown trigger (stress or another virus) initiates viral replications through HIV protease – wakes up T cell proliferation and the ones that were activated to HIV they go out and try to find the infected cells but the infected cells are T helper cells (CD4) and they assassinate the T helper cells (the architects of immunity)
14. Cancer
Types of Cell Differentiation and Types of Cell Growth.
Hyperplasia, Metaplasia, DYSplasia, ANAplasia. Malignant or Benign
Risks of Cancer Development Genetic Factors – Viruses – Radiation – Chemicals – Biologic Factors – Age – Diet – Hormones Modifiable vs. NonModifiable risk factors
Modes of Cancer Spread Through the circulatory (blood) system (hematogenous) Through the lymphatic system Through the body wall into the abdominal and chest cavities (transcoelomic)
Stage I, II, III, IV Stage I- confined to organ Stage II- locally invasive to surround tissue Stage III regional node spread Stage IV- metastasis to distant sites – breast cancer but find cancer in left inguinal node
Tumor Grading Scale : TNM A system to describe the amount and spread of cancer in a patient's body, using TNM. T describes the size of the tumor and any spread of cancer into nearby tissue; N describes spread of cancer to nearby lymph nodes; and M describes metastasis (spread of cancer to other parts of the body) T – size of the primary tumor N – extent of regional Node involvement (# of nodes) M – signs of distant invasion/metastatic spread
Laboratory Data Complete Blood Count with White Blood Count Differential (CBC with Diff) Normal total WBC Count 3 – 10 x 10 9 /L
Normal Differential %: Neutrophils 40 – 60% immature are “bands” or “stabs” Lymphocytes 20 – 40% T lymphocytes, B lymphocytes Eosinophils 1 – 4% Allergic, histamine releasers Monocytes 2 – 8% Suggest infection recovery Basophils 0 – 1% Involved in allergic conditions, along with eosinophils
NSG 211 EXAM 1 Review
Course: Pathophysiology (NSG 211)
University: Marian University
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