Term
| What areas of the cell are susceptible to injury? |
|
Definition
Genetic apparatus
Membrane integrity
ATP production in mitochondria |
|
|
Term
| Most rapidly dividing cells in the body? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Isoenzymes released ONLY by the HEART: |
|
Definition
| Creatinine kinase, troponin |
|
|
Term
| Isoenzymes released ONLY by the LIVER: |
|
Definition
|
|
Term
| Isoenzymes released by the HEART and LIVER: |
|
Definition
|
|
Term
| Decreased ATP production in cells leads to... |
|
Definition
| Cellular influx of Na and water - cells swell |
|
|
Term
| How can low blood flow lead to further injury? |
|
Definition
Low blood flow = low ATP production
Also, local ischemia creates anaerobic conditions which allow for the growth of certain anaerobic bacteria (e.g. Gangrene) - can treat condition by reperfusing the area with oxygen |
|
|
Term
| Most common radicals in the body? |
|
Definition
| Superoxide radicals (O2-); negatively charged due to extra electron |
|
|
Term
| Consequences of radical injury |
|
Definition
Lipid peroxidation - loss of membrane integrity
DNA damage - e.g. thymine dimers can halt DNA replication
Enzymatic dysfunction - changes in conformation of protein alter function |
|
|
Term
| How can free radicals be formed in the body? |
|
Definition
Normal enzymatic byproducts
Reperfusion injury (reperfusion = increased O2 flow post injury = more likely to see superoxide)
Radiation damage forms random free radicals
Promotion by free Fe (forms OH and O2- radicals) |
|
|
Term
|
Definition
| Part of the synthesis pathway of ATP; generates superoxide radicals as a byproduct |
|
|
Term
|
Definition
| Convert CCl4 -> CCl3. (radical form of carbon trichloride); excess CCl4 in the body causes liver damage because of radical accumulation |
|
|
Term
| Enzymes/metabolites which protect us from radical damage: |
|
Definition
Superoxide Dismutase
Catalase
Glutathione Peroxidase
Antioxidants (Vit C and E) |
|
|
Term
|
Definition
Takes 2 superoxide + 2 protons -> 2 hydrogen peroxide and oxygen
Needs Zn as a cofactor |
|
|
Term
|
Definition
Present in cells with high [O2] e.g. RBCs
2 H2O2 -> 2 H2O and O2; breaks down hydrogen peroxide into less harmful products (hydrogen peroxide readily generates OH radicals) |
|
|
Term
|
Definition
Needs Se as a cofactor
H2O2 + 2 GSH -> GSSG + 2 H2O (2 GSH are oxidized to form a glutathione dimer, GSSG) |
|
|
Term
| 2 different antioxidants and their properties |
|
Definition
Vitamin C - water soluble; protects cytosol in cell
Vitamin E - lipid soluble; protects cell membrane |
|
|
Term
|
Definition
| Death of a GROUP of cells due to injury |
|
|
Term
|
Definition
Due to LOSS OF BLOOD SUPPLY (ischemia)
See solid cell outline retained, but have denatured proteins within cell (solid mass) |
|
|
Term
| Example of coagulative necrosis |
|
Definition
|
|
Term
|
Definition
| Enzymes within the cells break down contents - leaves a "liquid mass" |
|
|
Term
| Example of Liquifactive Necrosis |
|
Definition
|
|
Term
|
Definition
| Dead cells walled off by WBCs - forms GRANULOMA; technically a form of COAGULATIVE necrosis (solid mass) |
|
|
Term
| Example of Caseous Necrosis |
|
Definition
| Tuberculosis (granulomas in lungs) |
|
|
Term
|
Definition
| Programmed death of individual cells |
|
|
Term
| What process is at the root of apoptosis |
|
Definition
| Decreased cytoskeletal formation (surface blebs) |
|
|
Term
| What causes the blebs seen on cells undergoing apoptosis? |
|
Definition
| Internal caspases - denatures internal cytoskeleton of the cell |
|
|
Term
|
Definition
| Decreased size of cells; caused by - lack of use, malnutrition, age |
|
|
Term
|
Definition
| Increased size of cells; caused by - increased use, overstimulation w/ hormones |
|
|
Term
|
Definition
| Increased # of cells (seen in uterine enlargement during pregnancy) |
|
|
Term
|
Definition
Replacement of one cell type by another; usually causes loss of some function
(Replacement of RTE in lungs to squamous epithelium for protection in smokers) |
|
|
Term
|
Definition
Disordered arrangement, growth, nuclear shape
Due to chronic irritation; often precancerous |
|
|
Term
|
Definition
Undifferentiated cells - all cells look similar (no gene repression)
Hallmark of cancer |
|
|
Term
|
Definition
| Excessive growth of new cells (abnormal); can be benign (contained tumor in fibrous cap) or malignant (can become metastatic) |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Toxic response to innocuous agents (e.g. Type I hypersensitivity - allergic reaction) |
|
|
Term
| Two different causes of chronic inflammation |
|
Definition
The stressor causing the inflammation is still present
The immune response cannot be turned off |
|
|
Term
| Examples of chronic inflammation |
|
Definition
Rheumatoid Arthritis - WBCs kill off muscle and joint cells
Ulcerative Colitis - WBCs ulcerate normal colon |
|
|
Term
| Stages of the immune response |
|
Definition
Vasodilation - increase flow which leads to hyperemia
Increased cap permeability - leads to edema
WBC infiltration - destroy damaged cells & pathogens |
|
|
Term
| Innate vs. Acquired Immune Response |
|
Definition
Innate - non-specific, short term
Acquired - specific, delayed response |
|
|
Term
| WBC's involved in the INNATE immune response |
|
Definition
Eiosinophils
Basophils
Neutrophils
Monocytes/Macrophages |
|
|
Term
| WBC's involved in ACQUIRED immune response |
|
Definition
Monocytes/Macrophages
Lymphocytes/Plasma cells |
|
|
Term
|
Definition
| Attraction of cells to certain areas due to differing concentrations of various chemical substances |
|
|
Term
|
Definition
| Lining up of the neutrophils along the vascular wall; attach to wall via SELECTINS |
|
|
Term
|
Definition
| Migration of neutrophils across capillary endothelium after margination |
|
|
Term
| What do the neutrophils exit the capillaries from? |
|
Definition
|
|
Term
|
Definition
Recognize microbe that is coated in opsonins - opsonins facilitate binding and flag antigen
Engulfment - neutrophil surrounds coated antigen
Degradation in phagosomes - oxidative burst to create superoxide -> conversion to H2O2 -> MPO converts to form a hypochlorite radical (bleach antigen) |
|
|
Term
| Process of Degradation in Phagosomes (chemical rxn) |
|
Definition
1. Oxygen undergoes oxidative burst with NADPH to form superoxide radical
2. Superoxide radical converted by peroxide dismutase into hydrogen peroxide
3. H2O2 converted by myeloperoxidase to form hypochlorite radical |
|
|
Term
| Average neutrophil life-span |
|
Definition
|
|
Term
| Monocytes vs. Macrophages |
|
Definition
Monocytes - in blood
Macrophages - in tissue |
|
|
Term
| Relative occurrence of edema, neutrophil population, and macrophage population changes in the innate immune response |
|
Definition
1st see edema peak @ 12 hours
Then neturophil population peaks @ 24 hours
Then macrophage population peaks @ 48 hours (last because they need to be converted from monocytes) |
|
|
Term
|
Definition
NOT a protein (N compound)
Released by mast cells & basophils
Release stimulated by - IgE/antigen binding to mast cells; complement & interleukin interactions
Effects - bronchoconstriction, vasodilation, increased vascular permeability |
|
|
Term
| Histamine is released by? |
|
Definition
|
|
Term
|
Definition
| Bronchoconstriction, vasodilation, increased cap permeability |
|
|
Term
|
Definition
Collection of PROTEINS made in the liver
Function as CHEMOTAXINS or OPSONINS
Stimulated by antigen-antibody complexes or bacteria
Forms membrane attack complex |
|
|
Term
| Membrane Attack Complex (MAC) |
|
Definition
| Formed by complement - punches pores into bacterial membrane to cause water influx and osmotic lysis |
|
|
Term
| Types of arachidonic acid metabolites |
|
Definition
| Luekotrienes, Prostacyclins, Prostaglandins, Thromboxanes |
|
|
Term
| Enzyme which converts arachidonic acid to leukotrienes |
|
Definition
|
|
Term
| Enzyme which converts arachidonic acid to prostacyclins/glandins, thromboxanes |
|
Definition
|
|
Term
| How is arachidonic acid formed? |
|
Definition
| Formed from dietary Linoleic acid |
|
|
Term
| Where is arachidonic acid normally stored and how is it released? |
|
Definition
Normally stored in the CM; released by phospholipase A2 (this enzyme is activated by complement)
Complement indirectly activates arachidonic acid |
|
|
Term
| How can you alter phospholipase A2 function? |
|
Definition
| Introduce cortisol to the body; reduces phos-ase A2 function, less arachidonic acid conversion |
|
|
Term
|
Definition
| Vasodilation, bronchospasm, increased vascular permeability |
|
|
Term
| Effects of NSAID's on Leukotrienes |
|
Definition
| NO EFFECTS (NSAID's only affect COX, not lipoxygenase) |
|
|
Term
| Where are leukotrienes released from ? |
|
Definition
|
|
Term
| Effects of Prostaglandins (PGE, PGF) |
|
Definition
| Promote vasodilation & edema; mediate fever & pain |
|
|
Term
|
Definition
| Promote platelet aggregation (clotting), vasoconstriction |
|
|
Term
| Effects of Prostacyclins (PGI2) |
|
Definition
| Vasodilation and inhibit clotting (antagonistic to Thromboxanes) |
|
|
Term
| Which is more sensitive to NSAID inhibition, thromboxanes, or prostacyclins? |
|
Definition
| Thromboxanes; that is why as a clotting treatment Pt can take NSAIDS (vasodilation and less clotting predominates as those are the effects of prostacyclins) |
|
|
Term
|
Definition
| Interleukins, TNF, interferon |
|
|
Term
| Function of IL1 (interleukin) |
|
Definition
| Activate T cells; acts on brain as a pyrogenic; increase vascular permeability |
|
|
Term
|
Definition
| Causes proteolytic enzyme release in cells (apoptosis); also pyrogenic |
|
|
Term
|
Definition
| Interferes with viral replication; only works on UNINFECTED CELLS (primes cells before viral infection, then promotes cell death of infected cell) |
|
|
Term
| Systemic signs of inflammation |
|
Definition
Increased ESR (more RBC agglutination, faster ESR)
Elevated C-reactive protein levels (opsonin)
Leukocytosis - acute inflammation = high # of immature neutrophils; chronic inflammation = high # of lymphocytes
Fever |
|
|
Term
| Leukocytosis & Acute vs. Chronic Inflammation |
|
Definition
Acute - high #'s of immature neutrophils
Chronic - high # of lymphocytes |
|
|
Term
| Eosinophilia is commonly seen when... |
|
Definition
| Parasitic infections & allergies |
|
|
Term
| Leukopenia is commonly seen with... |
|
Definition
| Viral infection (low WBC count) |
|
|
Term
| How is granulation tissue formed at the wound site? |
|
Definition
| By increased mitosis of nearby cells (WBC's, fibroblasts, etc.) |
|
|
Term
|
Definition
Stimulate angiogenesis at wound sites
VEGF - vascular endothelial growth factor
FGF - fibroblast growth factor |
|
|
Term
| Complications of scar tissue |
|
Definition
No glands, follicles, nerves
Rigidity can lead to keloid formation
Adhesions between structures
Stenosis |
|
|
Term
| Difference in cause between coagulative necrosis and liquifactive necrosis? |
|
Definition
Coagulative - caused by ischemia to region of cells
Liquifactive - caused by enzymatic breakdown from w/in |
|
|
Term
| What often accompanies metaplasia? |
|
Definition
| Loss of function of the "replaced" tissue (when RTE -> squamous, lose function fo cilia so debris cannot be wiped away) |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Removal of surface cells; death & damage of surface cells |
|
|
Term
|
Definition
| Watery fluid loss; in burn victims |
|
|
Term
|
Definition
| High fibrin content; leaves scar tissue |
|
|
Term
|
Definition
| Yellow due to necrotic cells (pus); necrotic cells contain Hb and S break-down products (yellow colour) |
|
|
Term
| What is the 1st line of defense in the innate immune response? |
|
Definition
| Neutrophil attack (can be phagocytotic); 1st to get to inflammation |
|
|
Term
| Examples of chemotaxins which draw neutrophil to damaged location.... |
|
Definition
| Bacterial peptides, complement, prostaglandins |
|
|
Term
| Where do opsonins that have coated an antigen bind to? |
|
Definition
| They bind to antigen receptors on leukocyte (neutrophil) |
|
|
Term
|
Definition
|
|
Term
| What can stimulate histamine release? |
|
Definition
Tissue Trauma
Released from IgE primed mast cells
Presence of complement, interleukins |
|
|
Term
| What chemical mediator activates phospholipase A2? |
|
Definition
| Complement (collection of proteins made in the liver) |
|
|
Term
| Two alternative functions for COMPLEMENT |
|
Definition
| Can function as CHEMOTAXINS or OPSONINS |
|
|
Term
| Where are thromboxanes formed? |
|
Definition
| In platelets (thrombocytes) |
|
|
Term
| Where are cytokines produced? |
|
Definition
| Active lymphocytes & macrophages |
|
|
Term
| What do fibroblasts need for collagen production? |
|
Definition
|
|
Term
| How can healing be delayed? |
|
Definition
| Large doses of glucocorticoids (break down individual amino acids, antagonistic to healing) and lack of insulin (diabetes; insulin provides substrates needed for healing) |
|
|
Term
| Relation of repair rate in cancer cells vs. normal cells |
|
Definition
| Cancer cells repair SLOWER -> use of fractionated doses of radiation to kill cancer cells (normal cells have time to heal in between doses) |
|
|
Term
| Types of Acquired Immunity |
|
Definition
Active - direct exposure to pathogen
Passive - maternal antibody transfer to fetus; vaccine injection |
|
|
Term
| Main cell type involved in acquired immunity |
|
Definition
|
|
Term
| Different types of lymphocytes |
|
Definition
Effector Cells - short life span, carry out direct attack on antigen
Memory Cells - long life cycle (reproduce), remember antigen |
|
|
Term
|
Definition
| Make Ig's (HUMORAL RESPONSE; indirect) |
|
|
Term
|
Definition
| Directly attack the antigen (CELL MEDIATED RESPONSE) |
|
|
Term
|
Definition
|
|
Term
|
Definition
Plasma cells - secrete Ig's; effector cells
Memory B cells |
|
|
Term
|
Definition
75% of plasma antibodies (most common)
Can cross placenta
Monomeric |
|
|
Term
|
Definition
Present in secretions
Dimeric |
|
|
Term
|
Definition
Present in allergic responses
Monomeric |
|
|
Term
|
Definition
2nd most common Ig
Involved in PRIMARY RESPONSE & BLOOD GROUP REACTIONS
Pentameric |
|
|
Term
|
Definition
| Unknown function - may activate B cells/antibodies |
|
|
Term
|
Definition
| IgM is main respondent to NEW antigen; non-specific response |
|
|
Term
| Secondary Immune Responses |
|
Definition
| Due to re-exposure of antigen; now IgG predominates the secondary response (compare to IgM for primary) |
|
|
Term
| What cells are MHC class I not present on? |
|
Definition
| RBCs (only present on nucleated cells) |
|
|
Term
|
Definition
| Binds peptides from antigens to kill cells; kills cell w/ MHC |
|
|
Term
|
Definition
Opsonins
Agglutinate antigens
Activate other immune cells (T cells)
IgM/IgG complex activates complement
Degranulate mast cells |
|
|
Term
| Where do T lymphocytes mature? |
|
Definition
|
|
Term
|
Definition
CD4 markers; activate B cells and Tc cells via cytokines
Preferentially killed by HIV
Twice as many normally as Tc cells |
|
|
Term
|
Definition
CD8 markers; Attack the antigens present w/ MHC bound
Activated by Th cells |
|
|
Term
|
Definition
|
|
Term
|
Definition
More rapid than Tc cells; kill virally infected and tumor cells
Don't need MHC complex to attack
Secrete interferon |
|
|
Term
| What is secreted by NK cells? |
|
Definition
|
|
Term
| Only see identical MHC's in .... |
|
Definition
|
|
Term
| What kills cells w/ MHC I bound? |
|
Definition
| Tc cells (bind to MHC and lyses cell |
|
|
Term
|
Definition
Present on ANTIGEN PRESENTING CELLS (macrophages, dendritic cells)
APC does not die |
|
|
Term
| Where does MHC II bind on Th cells? |
|
Definition
|
|
Term
|
Definition
| No antigens, only A & B Ig's -> universal donor |
|
|
Term
|
Definition
| A & B antigens, no antibodies -> UNIVERSAL RECIPIENT |
|
|
Term
| Problems w/ Rh positive/negative blood donations? |
|
Definition
| Rh- can be given to anyone (no antigen present); see problems when Rh- mom gives birth to Rh+ baby (if second birth is Rh+, REALLY BAD = secondary immune response) |
|
|
Term
|
Definition
Allergic reactions; need initial exposure, then get type I on subsequent re-exposure
Mediated by IgE |
|
|
Term
|
Definition
Mediated by T cells
Delayed response (need to recruit T cells) |
|
|
Term
| Types of type IV hypersensitivity? |
|
Definition
|
|
Term
| Desensitization treatment |
|
Definition
| Get small amounts of antigen injected (stimulates IgG production); get IgG to compete w/ IgE for binding preference with the antigen (reduce type I response) |
|
|
Term
|
Definition
| Obstruction of tube, diabetes (presence of glucose in urine as a food source) |
|
|
Term
| Cystitis vs. Pyelonephritis |
|
Definition
Cystitis = bladder infection
Pyelonephritis = renal infection |
|
|
Term
|
Definition
| Dysuria (painful), urgency (stimulation of sensory neurons), systemic infection signs (fever, leukocytosis), bacteriuria, hematuria, cell casts (specific to pyelonephritis) |
|
|
Term
| Why are there no cell casts found in cystitis? |
|
Definition
| Because there are no tubes in the bladder for them to form in |
|
|
Term
| Glomerulonephritis is most commonly seen... |
|
Definition
| Post-streptococcal infection (2 weeks post); due to type III hypersensitivity |
|
|
Term
| How does glomerulonephritis occur? |
|
Definition
| Antibody-antigen complexes get lodged in glomerular capillaries -> activates complement = inflammation |
|
|
Term
| SEVERE glomerulonephritis |
|
Definition
See a decrease in GFR; due to accumulation of scar tissue formed in glom capillaries
Also see vascular congestion; increased BUN and creatinine; increase in ANGII and aldos (increased BP) |
|
|
Term
| Serum complement levels in glomerulonephritis? |
|
Definition
| DECREASED LEVELS; all complement is trapped in kidneys at site of inflammation |
|
|
Term
| Symptoms of Glomerulonephritis |
|
Definition
Flank & back pain
Proteinuria, hematuria, cell casts
Facial Edema (water retention; lose plasma proteins in urine so less oncotic pressure)
Metabolic Acidosis
Oliguria |
|
|
Term
|
Definition
Excessive insoluble salt intake
Lack of fluid intake |
|
|
Term
|
Definition
Less soluble in ALKALINE (precipitate)
MORE SOLUBLE in ACIDIC (acidify urine to treat) |
|
|
Term
|
Definition
Less soluble in ACIDIC URINE (precipitate)
More soluble in ALKALINE URINE (eat bicarbonate to treat) |
|
|
Term
| What causes uric acid accumulation? |
|
Definition
| Byproduct of gout, side-effect of chemo |
|
|
Term
| Acute vs Chronic Renal Failure |
|
Definition
Acute - can be iatrogenic, calculi; decline in GFR so that kidneys cannot function
Chronic - due to long term DM/HTN; scar tissue development & decreased GFR |
|
|
Term
| What is present in peritoneal dialysate? |
|
Definition
| Bicarbonate ions, electrolytes, glucose |
|
|
