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Pneumonia (MCC) **If long bones become damages the spleen can take over,
6 weeks - 18 years RSV (infants only) resulting in splenomegaly**
Mycoplasma
Chlamydia pneumonia Diphtheria
Strep. Pneumonia - It's toxin ADP ribosylated EF-2
18 years - 40 years Mycoplasma - Stops cell synthesis
Chlamydia pneumonia - Gram positive
Strep. Pneumonia - Acquired exotoxin from a virus via transduction
40 years - 65 years Strep. Pneumonia - Causes heart block
H. influenza - Never scrape the membrane b/c it is highly vasular so it will
Anaerobes bleed and also release toxin
Viruses
Mycoplasma Cystic Fibrosis
Elderly Strep. Pneumonia - Sweat test: >60 - definitive positive
Viruses <20 - normal
Anaerobes 30-60 - Heterozygous
H. influenza
Gram negative rods
Inclusion Bodies Chelaytors
Howell-Jolly.
Sickle Cell Methylene Blue - Methemaglobinemia
Heinz.
G-6-PD Sodium Thiosulfate - Cyanide
Zebra.
Niemann Pick CaEDTA - Lead (to test)
Donovan..
Leishmaniasis Penicillamine - Lead (in plasma)
Mallory.
Alcoholism Dimeraprol - Lead (in bone marrow)
Negri..
Rabies
Councilman..
Yellow Fever **Tx for cyanide poisoning
Call-Exner..
Ovarian tumors - Amyl nitrate
Lewy..
Parkinsons - Sodium thiosulfate
Pick.
Pick's Disease - Methylene Blue
Barr Bodies
Female - Transfusion
Aschoff.
Rheumatic Fever
Cowdry Type A..
Herpes Renal Tubular Acidosis (acidosis & hypokalemia)
Auer Rods..
AML Type I High urine pH
Globoid
Krabbe's Disease Acidosis
Russell.
Multiple myeloma Frequent UTI
Schiller-Duvall
Yolk Sac tumor Stones
Basal Bodies.
Smooth Muscle Babies die <1 year
Type II Low urine pH (2)
Allergic Response Hypokalemia
Primary - CONTACT NO carbonic anhydrase
- Neutrophils work in the first 3 days Type III Combo of Type I and II
- Then B-cells produce IgM Normal urine pH
Shows up at 3 days Hypokalemia
Peaks at 14 days Type IV Diabetics
Gone in 2 months Hyperkalemia
- IgG NO aldosterone (Infarcted
Show up at 2 weeks JG apparatus)
Peaks in 2 months
Gone in 1 year Hemolytic Properties of Streptococcus
Secondary - MEMORY - partial hemolysis Green zone
- IgG shows up at day 3 with 5x the concentration - complete hemolysis Clear zone
Highest affinity for antigen - No hemolysis Red zone
Peaks in 5 years
Stays for 10 years Transduction
Bacteria becomes deadly when a virus injects its DNA
Amyloidosis
AL Portion homologous with Ig Light Primary amyloidosis, Transformation
Chain multiple myeloma In a hospital or nursing home the bacteria has
AA Unique N-terminal sequence Chronic Active disease, become deadly by this mechanism
Hodgkin's disease
Pre-albumin/ Single amino acid substitution Hereditary neuropathy, Conjugation
transthyretin nephropathy and Only occurs if bacteria has PILI
cardiopathy
AB B2 microglobin Cerebral artery amyloid, Coumadin vs. Heparin
Alzheimers, Downs Extrinsic Intrinsic
AE Endocrine Aging Tissue Blood
AP Universally associated with all amyloids PT PTT
Factors 2, 7, 9, 10 Factor 3
p.o. i.v.
8-10 hrs delay immediate
C/I in preg. OK in preg
Inhibit Vit K dependant DOC for DVT
factor
Hepatitis B
Incubation: 4-26 weeks (8 wk average)
Acute Disease: 4-12 weeks
Convalescence: 4-20 weeks
Recovery: Years
Immunoglobulins
- Monomer in the blood
IgA - Dimer in secretions
- Protects the mucoscal surfaces and body secretions
IgD - Only known for function is as a surface marker on mature B-cells
- Mediator of Type I hypersensitivity (anaphylaxis)
- Parasite defense
IgE - Responsible for allergies
- Fc portion binds to mast cells and basophils
- Does not fix complement
- Second to be produced during the primary immune response
- Only one to be produced during the secondary immune response
- In memory (secondary) response
Shows up at 3 days with 5x the concentration of primary response
Peaks around 5 years
IgG Some remain in circulation for 10 years
- Has 4 subclasses (antigenic differences in heavy chains and with disulfide bonds)
IgG1 - crosses the placenta due to Fc portion
IgG2 - most common deficiency, susceptible to encapsulated organisms
IgG3 - most memory antibodies
IgG4 - Only one that does not fix complement
- Present only in the primary immune response
IgM - Most effective in agglutination and complement fixation
- Defense against bacteria and viruses
Hyperlipidemias
Type Deficiency Component Misc Information
I Lipoprotein Lipase - defect of the liver type only Chylomicrons
II Receptor or receptor enzyme - IIA, IIB, or B100 LDL Most common in general pop.
III APO E receptor IDL
IV Lipoprotein Lipase - defect of the adipose type only VLDL
V Enzyme and receptor defect - APO CII Chylomicrons & VLDL Associated w/ diabetes melitis
Interleukins and Other Inflammatory Mediators
- Secreted by macrophages
IL-1 - Causes fever and other non-specific symptoms of illness
- Recruits Thelper cells
- Secreted by T cells
- Most potent
IL-2
- Most powerful Chemotactic factor (recruits everyone)
- Must be inactivated prior to transplantation
- Secreted by T cells
IL-3 - Causes B cell proliferation
- Labelled by Thymidine
- Secreted by T cells
IL-4 - Causes B cell differentiation
- Responsible for class switching to IgG and IgE
- Secreted by T cells
IL-5
- Responsible for class switching to IgA
IL-8 - Neutrophil Chemotactic factor
- Suppresses cell mediated response
IL-10
- Tells macrophages and T-cells to stay away if there is a bacterial infection
- Promotes cell mediated response
- If infection in non-bacterial it is released to recruit macrophages and T cells
IL-12 - Activates NK cells to secrete IF-
- Inhibits IL-4 induced IgE secretions
- Changes TH cells into TH1 cells
- Secreted by Leukocytes
- Inhibits viral replication and tumor growth
IF- - Increases NK activity
- Increases MHC (class I and II) expression
- Interferes with protein synthesis
- Secreted by fibroblast
- Inhibits viral replication and tumor growth
IF- - Increases NK activity
- Increases MHC (class I and II) expression
- Interferes with protein synthesis
- Secreted by T-cells and NK cells
- Increases NK activity
- Increases MHC (class I and II) activity
IF-
- Increases macrophage activity
- Co-stimulates B-cell growth and differentiation
- Decreases IgE secretion
- aka Cachectin
- Secreted by monocytes and macrophages
- Induces IL-1
TNF- - Increases adhesion molecules and MHC class I on endothelial cells
- Is a pyogen
- Induces secretion IF-
- Cytotoxic/cytostatic
- aka Lymphotoxin
TNF- - Secreted by T-cells
- Cytotoxic
- Secreted by solid tumors (carcinoma<sarcoma) and monocytes
TGF-
- Induces angiogenesis, keratinocyte proliferation, bone resporption, and tumor growth
- Secreted by platelets, placenta, kidney, bone, T-cells and B-cells
- Induces fibroblast proliferation, collagen synthesis and fibronectin synthesis
TGF-
- Inhibits NK, Lymphokine Activated Killer Cells, Cytotoxic T Lymphocytes, T cell and B cell proliferation
- Enhances wound healing and angiogenesis
**IL = Interleukin** **IF = Interferon** **TNF = Tumor Necrosis Factor** **TGF = Transforming Growth Factor**
EKG Breakdown
Portion of EKG Portion of Heart Phase of Action Potential
P-wave Atrium 0
P-R interval AV Node 2
Q-wave Septum 2
R-upstroke Anterior wall 2
S-downside Posterior wall 2
S-T interval Ventricle 2
T-wave Ventricle 3
U-wave Ventricle 4
Adhesion Molecules
- Homing of lymph nodes to site of inflammation
ICAM-1, ICAL-2, ICAM-3
- Found on T-cells, endothelial cells, dendritic cells
IgCAM - Mediate T-cell interactions BINDING PROTEINS
LFA-3
- Found on lymphocytes, APC
LFA-2 (CD2) - Found on T-cells, NK cells
- Migration thru extracellular matrix
VLA-1 (1)
- Widely distributed
- Tight binding to endothelium
LFA-1 (2)
- Found on lymphocytes
- Tight binding to epithelium
Integrins STOPS THE LEUKOCYTES
- Phagocytosis
CR3 (2)
- Mac-1
- CD11/CD18
- Phagocytosis
CR4 (2)
- Opsonin receptor
- Leukocyte migration and homing
E-selectins
- Found on activated endothelium
BIND CARBOHYDRATES
- Initial binding to endothelium
Selectins L-selectins MEDIATES "ROLLING"
- Found on leukocytes
(slows leukocytes)
- Leukocyte migration to inflammatory sites
P-selectins
- Found on activated endothelium and platelets
Hypersensitivities
(ACID)
Type I - Anaphylaxis
IgE binds to mast cells - degranulates mast cells
IgA activates IP3 cascade - degrades mast cells
Type II - Cytotoxic (humoral) - Goodpasture, Autoimmune hemolytic anemia
Type III - Immune Complex mediated - Rheumatoid arthritis, SLE
Type IV - Delayed (cell mediated) - TB skin test, contact dermatitis, transplant rejection
Mechanisms of Actions
Drug Mechanism
5FU Inhibits thymidylate
Methotrexate Inhibits dihydrofolate reductase
Hydroxyurea Inhibits ribonucleotide reductase
Vincristine/Vinblastin Inhibit microtubule formation
Paclitaxel Inhibits microtubules from migrating
Levamisole Stimulates Natural Killer (NK) cells
1. Kills T-cell and Eosinophils
2. Inhibits macrophage migration
Steroids 3. Inhibits phospholipase A
4. Inhibits mast cell degranulation
5. Stabilizes endothelium
Statins Inhibit HMG CoA reductase
Niacin Decreases VLDL production in the liver
1st generation - Block potassium channels in the islet cells preventing insulin release
Sulfonylureas
2nd generation - Promote insulin release and inhibit gluconeogenesis in the liver
Miglitol/Ascarbose Inhibit glucose absorption from the GI
Metformin Stops gluconeogenesis in the liver
Troglitazone Increases the sensitivity of insulin receptors
Anti-psychotics Block dopamine receptors
Aspirin Irreversible inhibitor of cyclo-oxygenase
K+ Sparing Diruetics Competitive aldosterone receptor antagonist
+
Topical Anesthetics Block Na channels
Quinalones Block topoisomerase (supercoils)
Aminoglycosides Blocks Initiation Factor (IF) 2 on the 30S subunit
Tetracyclines Blocks tRNA binding on the 30S subunit
Rifampin Blocks beta subunit of RNA polymerase
Sulfa Drugs Blocks Para-Amino Benzoic Acid (PABA)
Cephalosporins Inhibit the cell wall
Penicillins Block transpeptidase
Chloramphenicol Blocks peptidyl transferase on the 50s subunit
Clindamycin/Lincomycin Blocks translocase on the 50s subunit
Macrolides Blocks translocase on the 50s subunit
Mitronidazole Increases production of free radicals
Vancomycin Blocks cell wall (phopholipid)
Benzodiazepine Increase the frequency of the GABA receptors via C1 channels
Barbituates Increase the duration of the GABA channels via C1 channels
TCAs Block reuptake of catacholamines, AV conduction and alpha receptors
SSRIs Block reuptake of Serotonin
MAOIs Inhibit MAO
Lithium MOA is unknown but is suspected to be related to it mimicking of Na+
Valproic Acid Blocks Na+ and sometimes Ca2+
Carbamizapine Blocks Na+ and Ca2+
Epinephrine Blocks Beta (2>1) receptors and the Alpha receptors
1st generation - blocks H1 and H2 receptors (H1>H2)
Antihistimines 2nd generation - blocks H2 only
1
Includes Chlamydia, Mycoplasma, ureaplasma, and legionella
2
Simple only (no "Big Mama")
3
H. Flu (not B) and E.coli
* Pseudomembranous colitis, MRSA, and enterococcis
** Protozoa
*** TB