Immunology & Microbiology Study Notes: Key Concepts & Mechanisms | Lecture notes Immunology

IMMUNOLOGY

1. Kupffer cell- liver MF

2. Abs- 2 Heavy chains, 2 light chains

oFc portion = same/constant for all Abs in same class. c’ proteins bind here on IgG and IgM***

oIgG- 75%, valence = 2

oIgM- 14%, 1st responder, forms pentamer via J chain, valence = 10, found in active dz

oIgA- 8%, mucosal lymph nodes, 1° Ab in tears, can form dimer, valence = 4

oIgE- 1-2%, Valence = 2, not free in blood, involved w/ allergies/parasites

3. MHC 1

oChromosome 6 encodes MHC/HLA. Present on almost all host cells + APCs (MFs, B cells, Dendritic cells, PMNs,

Langerhan cells). Absent in RBCs and some neurons. Self-recognition, recognized by CD8 TC. Referred to as HLA in

autoimmune Dz

4. MHC 2

oFound on Thymic epithelial cells *BOARDs* and APCs. APCs bind Ags to MHC 2 to present to CD4 of TH1 and TH2

5. Diapedesis - WBCs squeezing through endothelial cells

6. INNATE MMUNITY

oSKIN, Stomach acid, mucousal membranes w/ Lysozymes. Monocytes (in blood) arrive after granulocytes (PMNs) and become

Mfs (upon entering tissue)

oIFNs α, IFN β- produced by virally infected cells to warn neighboring cells to stop protein replication (halts virus replication)

oIFN γ- produced by Lymphocytes, Natural Killer cells to STOP CANCER / TUMOR growth *BOARDs*

oIFN α Tx- Hep C, Hairy-cell leukemia, Kaposi Sarcoma

oIFN β Tx- Relapsing MS **TEST**

oIFN γ Tx- Chronic granulomatous Dz (TB, Sarcoidosis)***

oNatural Killer (NK) cells- Non-specific Lymphocytes, 1st line of defense against TUMORs *BOARDs*, No Ag recognizing

site / APC used, Viral/Tumor protection

oOpsonization- Abs bind to Ags and flag for phagocytosis

oc’ Functions- activated by Ab-Ag complex (1)Direct lysis (2)Chemotaxis of PMNs/MFs (3)Opsonization (4)Degranulate

Mast Cells (↑Histamine) to ↑Diapedesis

i. c’-1 located / produced in cornea and concentrated in periphery near conj vessels w/ IgG

ii. c’ Classic Pathway

1. IgG / IgM form Ab-Ag complex  c’-1 binds Fc portion of IgG / IgM  c’-1 cleaves c’-4  c’-4 cleaves c’-2

 MAC (Membrane Attack Complex ) is formed on membrane of Ag and lysis occurs

iii. c’ Alternative Pathway- activation of c’ by IgA/Bacterial ENDOTOXINS initiate process

7. ADAPTIVE IMMUNITY

oB-cell activation- 2 methods (1) Ag binds directly to Surface IgM or IgD on B cell. (2) TH2’s CD4 binds B Cell’s MHC 2

and TH2 secretes IL-4 to stimulate B cell

oTC (CD 8)- binds infected cells/tumor cells via MHC 1. Responsible for Transplant rejection

oAPCs = B cells, MFs, PMNs, Monocytes (in blood)

oTH1 – cellular immunity, only communicates w/ APC’s (excluding B cells) MHC 2 receptor via TH1’s CD4

i. IL-2 - TH1 growth factor  RESTASIS inhibits IL-2 Production **TEST**

ii. IL-3 - Multi-colony stimulating factor (widespread growth of Myeloid (PMNs, MFs, etc) in BM)

iii. IFN-γ - ↑MF activity, ↓TH2 activity

iv. CD40 Ligand

oTH2 – humoral immunity, stay in lymph node to activate B cells

i. IL-4 - TH2 growth factor, ↑B cell activity, ↓ TH1 activity

ii. CD40 Ligand

oMF + DCs

i. IL-12 - Tells T0 cells to ↑ TH1 differentiation

ii. IL-4 - Tells T0 cells ↑TH2 differentiation

oTC (CD 8)

i. Fas ligand- triggers apoptosis

ii. Cytotoxins (Perforins- make holes, Granzymes- causes DNA damage)

iii. IFN-γ - ↑MF activity, ↓TH2 activity

oTreg/suppressor, NKT, Breg

i. IL-10 - suppresses IR after pathogen cleared, ↑TH1 apoptosis

ii. TGF-β

oMF at infection site

i. IL-1 - energize MFs, ↑inflammation, FEVER, ↑platelet

ii. IL-6 - Fever, Chemotaxis, Lectin-mediated c’ pathway

iii. IL-8 - Chemoattractant (major)

oPMNs

i. Lactoferrin – binds Fe

oLT- chemotactic agent for MFs and PMNs, ↑mucous production from Goblet cells, ↑VP

8. 1° Exposure- 5-10 days to response w/ measurable Abs, IgM made first

9. 2° Exposure- Fast response, <2 hrs to produce Abs, IgG made first **TEST**

10. TISSUE TRANSPLANT REJECTION- TC cells attack tissue via Type 4 Hypersensitivity

oHYPERACUTE REJECTION- within mins, Ab-mediated because recipient had preformed Abs against donor tissue

oACUTE REJECTION- Weeks after, T cell-mediated due to foreign MHC rejection

oCHRONIC REJECTION- Mos-yrs after, Ab-mediated and IRREVERSIBLE

11. IMMUNOLOGICAL TEST

oESR- 1 hr non-specific inflammatory test

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IMMUNOLOGY

Kupffer cell- liver MF
Abs- 2 Heavy chains, 2 light chains o Fc portion = same/constant for all Abs in same class. c’ proteins bind here on IgG and IgM *** o IgG - 75% , valence = 2 o IgM - 14% , 1st^ responder, forms pentamer via J chain , valence = 10 , found in active dz o IgA - 8% , mucosal lymph nodes, 1° Ab in tears, can form dimer , valence = 4 o IgE- 1-2%, Valence = 2, not free in blood, involved w/ allergies/parasites
MHC 1 o Chromosome 6 encodes MHC/HLA. Present on almost all host cells + APCs ( MFs , B cells , Dendritic cells, PMNs , Langerhan cells ). Absent in RBCs and some neurons. Self-recognition, recognized by CD8 TC. Referred to as HLA in autoimmune Dz
MHC 2 o Found on Thymic epithelial cells BOARDs and APCs. APCs bind Ags to MHC 2 to present to CD4 of TH1 and TH
Diapedesis - WBCs squeezing through endothelial cells
INNATE MMUNITY o SKIN, Stomach acid, mucousal membranes w/ Lysozymes. Monocytes (in blood) arrive after granulocytes (PMNs) and become Mfs (upon entering tissue) o IFNs α , IFN β - produced by virally infected cells to warn neighboring cells to stop protein replication (halts virus replication) o IFN γ - produced by Lymphocytes , Natural Killer cells to STOP CANCER / TUMOR growth BOARDs o IFN α Tx - Hep C , Hairy-cell leukemia, Kaposi Sarcoma o IFN β Tx - Relapsing MS TEST o IFN γ Tx - Chronic granulomatous Dz ( TB , Sarcoidosis )*** o Natural Killer (NK) cells - Non-specific Lymphocytes, 1 st^ line of defense against TUMORs BOARDs, No Ag recognizing site / APC used, Viral/Tumor protection o Opsonization - Abs bind to Ags and flag for phagocytosis o c’ Functions - activated by Ab-Ag complex (1)Direct lysis (2) Chemotaxis of PMNs/MFs (3) Opsonization (4) Degranulate Mast Cells ( ↑Histamine ) to ↑Diapedesis i. c’-1 located / produced in cornea and concentrated in periphery near conj vessels w/ IgG ii. c’ Classic Pathway
IgG / IgM form Ab-Ag complex  c’-1 binds Fc portion of IgG / IgM  c’-1 cleaves c’-4  c’-4 cleaves c’-  MAC (Membrane Attack Complex) is formed on membrane of Ag and lysis occurs iii. c’ Alternative Pathway - activation of c’ by IgA/Bacterial ENDOTOXINS initiate process
ADAPTIVE IMMUNITY o B-cell activation - 2 methods (1) Ag binds directly to Surface IgM or IgD on B cell. (2) TH2’s CD4 binds B Cell’s MHC 2 and TH2 secretes IL-4 to stimulate B cell o TC (CD 8) - binds infected cells/ tumor cells via MHC 1. Responsible for Transplant rejection o APCs = B cells , MFs , PMNs , Monocytes (in blood) o TH1 – cellular immunity , only communicates w/ APC’s ( excluding B cells ) MHC 2 receptor via TH1’s CD i. IL-2 - TH1 growth factor  RESTASIS inhibits IL-2 Production TEST ii. IL-3 - Multi-colony stimulating factor (widespread growth of Myeloid (PMNs, MFs, etc) in BM) iii. IFN-γ - ↑ MF activity, ↓ TH2 activity iv. CD40 Ligand o TH2 – humoral immunity , stay in lymph node to activate B cells i. IL-4 - TH2 growth factor, ↑ B cell activity, ↓ TH1 activity ii. CD40 Ligand o MF + DCs i. IL-12 - Tells T 0 cells to ↑ TH1 differentiation ii. IL-4 - Tells T 0 cells ↑ TH2 differentiation o TC (CD 8) i. Fas ligand - triggers apoptosis ii. Cytotoxins ( Perforins - make holes, Granzymes - causes DNA damage) iii. IFN-γ - ↑ MF activity, ↓ TH2 activity o Treg/suppressor , NKT , Breg i. IL-10 - suppresses IR after pathogen cleared, ↑ TH1 apoptosis ii. TGF-β o MF at infection site i. IL-1 - energize MFs , ↑inflammation, FEVER, ↑platelet ii. IL-6 - Fever, Chemotaxis, Lectin-mediated c’ pathway iii. IL-8 - Chemoattractant (major) o PMNs i. Lactoferrin – binds Fe o LT - chemotactic agent for MFs and PMNs, ↑mucous production from Goblet cells , ↑VP
1° Exposure - 5-10 days to response w/ measurable Abs , IgM made first
2° Exposure - Fast response, <2 hrs to produce Abs, IgG made first TEST
TISSUE TRANSPLANT REJECTION- TC cells attack tissue via Type 4 Hypersensitivity o HYPERACUTE REJECTION - within mins , Ab-mediated because recipient had preformed Abs against donor tissue o ACUTE REJECTION - Weeks after, T cell-mediated due to foreign MHC rejection o CHRONIC REJECTION - Mos-yrs after, Ab-mediated and IRREVERSIBLE
IMMUNOLOGICAL TEST o ESR- 1 hr non-specific inflammatory test

i. Non-specific indicator of inflammation somewhere in the body ii. Levels normally rise w/ age TEST Rule of Thumb :

Males : ESR limit = Age/
Females : ESR limit = (Age + 10)/ o CRP- non-specific inflammatory test. CRP is produced by LIVER during acute inflammation i. Normal is <0.5 (In cases of GCA, is often >2.45) ii. Age does NOT influence CRP TEST iii. Anemia does NOT influence CRP o HLA-B27 - UCRAP, JIA (boys > girls) o HLA-B29 - Birdshot o HLA-B51 - Behcet’s Dz BOARDs o HLA-B54 - Glaucomatocycltic crisis MICROBIOLOGY BACTERIA
Prokaryotes (Bacteria and Archaebacteria)- no true nucleus, complex cell wall w/ Peptidoglycan, 70S ribosome, no mitosis/meiosis, no phagocytosis
Gram+  Simple thick Peptidoglycan Cell Wall outside cell membrane
Gram- o Outer membrane- Lipopolysaccharide ( Lipid A Endotoxin , Core polysaccharide , O-Ag side chain - detected by IR but can change to hide) + Porins , o Periplasmic space- location of β-lactamases o Sandwiched in Middle between Outer and Inner membrane – Complex, thin Peptidoglycan Cell Wall o Inner membrane - Cell membrane
LAG phase - active growing w/o dividing
LOG phase - growing AND divide at exponential pace , Abx most effective in this stage TEST
STATIONARY phase - nutrient becomes depleted, cell number = constant
DEATH phase - population decline
Obligate Aerobes - require O 2 as final e-^ acceptor in ETC
Facultative anaerobes - better growth in O 2 presence, but not required
Anaerobic organisms - Fermentation or anaerobic respiration for energy. Death upon exposure to Air
SPOREs - Gram+ RODs form endospores w/ limited nutrition ( Bacillus anthracis , Clostridium botulinum )
Binary fission (asexual) 3 phases- Initiation ( Elongation ), C period ( Chromosome replication and Protein synthesis ), Division (2 daughter cells produced)
PLASMID - small, circular EXTRA -chormosomal DNA molecule that can replicate independent of Bacterial chromosome  Provides drug resistance , or toxin genes
Transformation - DNA segment taken up by bacteria is incorporated into bacterial chromosome
Transduction - DNA segment taken up by bacteriophages ( VIRUS ) and is incorporated into bacterial chromosome
Conjugation - DNA segment xferred by donor cell to recipient cell via sex pilus coded by an “ F plasmid ”
Transposition - “ jumping genes ” coding for movement , resistance , pathogenicity within a bacterial chromosome that changes place or moves to different DNA molecules
GRAM (+) COCCI o S aureus - cocci, Catalase + (turns H 2 O 2 to H 2 O), Coagulase + (forms fibrin layer to wall off WBCs in an abscess ), may produce β-lactamase/PCNase to break down β-lactam rings in PCNs and Cephalosporins. Causes 50% of all ocular infections ***, can cause acute bacterial endocarditis (heart valve attack), can cause hypersensitivity chronic blepharitis w/ SEIs near limbus, TOXIC SHOCK SYNDROME - Enterotoxins act as Super-Ags by binding directly to TH cells to induce IR, from food poison, dirty tampons o S epidermidis - diplococci, Catalase + , more prevalent than S aureus, less pathogenic , #1 cause of Acute Post-Op Endophthalmitis o Strep pneumoniae - #1 cause of Bacterial Pneumonia BOARDs. facultative anaerobe , Catalase (-) ***, Pediatric bacterial conjunctivitis and Corneal ulcer , pneumonia , meningitis , Otitis media o Strep pyogenes - grows in chains , Catalase (-) ***, AKA Group A Strep , pharyngitis, strep throat, scarlet fever , rheumatic fever , impetigo , Toxic shock , rarely causes ocular conjunctivitis, dacryocystitis , central ulcers
GRAM (+) RODs – not common source of ocular infections o Bacillus anthracis - LARGE, BOX-CAR shaped, spore forming, anthrax in humans, found in wools, furs, hides o Clostridium - obligate anaerobe rods that produce spores , C perfringens (gas gangrene) TEST, C botulinum (botox), C tetani (tetanus) o Corynebacterium diptheria - club-shaped , aerobic , cause Diphteria , can penetrate intact epithelium
GRAM (-) RODs o P aeruginosa - motile , Oxidase (+) , 1-3 Flagella , grape juice odor , blue-green pigment , CL ulcers, burn victims, +/- HYPOPYON in corneal ulcers. Tx: FQs o H influenza - URI , Otitis media , sinusitis, Pneumonia , meningitis , commonly affects children , Vaccine against H influenza Type B , cultured on Chocolate Agar (Thayer-Martin)
GRAM (-) COCCI o Neisseria gonorrhea - diplococci , STD or via birth canal, vision threatening corneal ulcer that may cause Corneal Perforation , Neonates Tx’s w/ Silver nitrate or Erythomycin , cultured on Chocolate Agar (Thayer-Martin) o Neisseria meningitidis - Coffee bean-shaped , Tetrad grouping , meningitis , culture on Blood Agar o Moraxella - Coffee bean-shaped , causes PseudoGonococcal conjunctivitis and ANGULAR BLEPHARITIS , contaminated eye-makeup o Bordatella pertussis - Whooping cough TEST
GRAM (-) ENTERIC Bacteria

Toxoplasmosis- infected cat litter or undercooked meat, obligate intracellular parasite, not xferred from human-human, TORCH, starts in retina (Vitreous involved more often) and spreads to choroid. Biggest risk of causing vertical xfer infection in 3rd^ Trimester

BIOCHEMISTRY

Cytosol - Glycolysis occurs here (1st^ step of Carbs broken down to ATP)
Nucleus - Area of DNA replication , mRNA Transcription , tRNA Transcription a. Nucleolus - Inside the Nucleus. Site of rRNA Transcription
RER - Surrounds perinuclear space, makes Extracellular proteins
SER - continuous w/ RER. No Ribosomes here. Makes Lipids (Steroids in Adrenal Cortex), stores Glycogen , and detoxifies lipid soluble drugs , Stores and releases Ca for M contractions
Golgi Apparatus - UPS, modifies proteins
Mitochondria - Location of Kreb’s Cycle and Oxidative Phophorylation.
Gap Junctions - Cell-2-Cell communication, found in heart (rapid synchronized response) and areas where blood is not in close proximity (Intraocular lens fibers (HIGHEST CONC. THAN ANYWHERE IN THE BODY), Stromal Keratocytes, between Rod BP cells and ON BP cells, Horizontal cells
Paracrine signaling - signal to local neighboring cells (NTs in Synapse)
Signal Transduction - Ligand (hormone, photon) binds Transmembrane Receptor (Rhodopsin) Activates GTP into a G protein (Transducin GT)  Activates Adenylate Cyclase which produces 2°messengers (mainly cAMP molecules (β1 and β2 ↑cGMP, α 2 ↓cGMP)  cAMP activates Protein Kinase A (phosphorylates/activates multiple proteins allowing Signal Amplification )
Chemical Bonds Strongest to Weakest - Covalent > Non-Covalent [ Electrostatic (between (+) and (-) molecules), Hydrogen (between 2 electronegative atoms that are covalently bound to electropositive H), Van der Waals interactions (transient)
Proteins a. Essential AA i. 9 total, cannot be made by body and obtained through diet. (1) Histidine (decarboxylation cause Histamine), (2) Isoleucine, (3) Leucine, (4) Lysine, (5) Methionine (Asparagus),(6) Phenylalanine , (7) Threonine, (8) Tryptophan, (9) Valine 1. SC Anemia - Valine substituded for Glutamic Acid ….causes Hb to have ↓O2 2 carrying capacity, ↓solubility, ↑aggregation within RBCs 2. Phenylalanine (essential) is a precursor to Tyrosine (conditionally-essential). PUK Dz- can’t turn Phenyl into Tyrosine a. Deficiency in Phenylalanine = ↓Tyrosine (becomes essential in diet) = ↓Catecholamines, Albinism, ↓AAs 3. Tryptophan is a precursor for Serotonin b. Non-essential AAs i. 11 total. Aspartate (can turn to ketone in body) ii. Glycine - Heme precursor, NA precursor iii. Aspartate - NA precursor iv. Glutamine - NA precursor c. Conditionally essential (may turn Essential during times of Stress) i. Glutamine, Arginine, Cysteine, Tyrosine 1. Tyrosine - AA precursor converted by TYROSINASE into Melanin within Melanosomes of Melanocytes ( Albinism has deficiency in this), Epinephrine + NE precursor. Deficiency can cause ↓Sympathetic activity d. Ketogenic AA break down into Acetyl CoA e. Glucogenic AA break down into Pyruvate f. Protein- >100 AA’s linked together i. 3° structure- stabilized by Covalent Di-Sulfide bonds TEST ii. 4° structure- Multimers formed together via Non-covalent + Covalent Di-Sulfide bonds (Hemoglobin) g. Enzymes- Catalysts that ↓activation energy to initiate a rxn. IgM – surface of immature B cells. IgD- suface of mature B cells i. Acetyl Co A (4 primary roles) 1. 1) At the end of Glycolysis, Pyruvate is converted into acetyl CoA, which is xferred to Kreb’s / TCA cycle to make ATP, NADH, FADH2- REQUIRES presence of O 2 2. 2) Converted into cholesterol , which can be incorporated into cell membranes or can be converted into steroid hormones 3. 3) Converted into ketone bodies , which are used as an alternative energy source during periods of fasting 4. 4) Acetyl CoA forms the core of fatty acids 5. Acetyl CoA cannot be used to produce glucose! 6. Glycolysis - Pyruvate (Carb) broken down into Acetyl Co A 7. β-Oxidation - Lipids (FA core) broken down into Acetyl Co A 8. Transaminase Reduction - Proteins broken down into Acetyl Co A ii. Xanthine Oxidase - responsible for formation of URIC Acid iii. Glycogen Phosphorylase- Breaks down Glycogen into Glucose in the liver as a response to Glucagon from α-cells in the Pancreas h. Collagen- #1 abundant protein in body (30%) i. Collagen core always contains Glycine-x-y repeats *** Most common AAs in x-y positions are Proline and Lysine ii. Type 5 collagen - most important in maintaining corneal transparency via ↓Light Scattering. Located in Stroma and maintains spacing of Type 1 collagen iii. Collagen made by Hydroxylase enzyme using the cofactor VITAMIN C (deficiency causes Scurvy )

iv. Fun Fact: SLE and RA are autoimmune conditions w/ body attacking collagen v. Osteogenesis imperfecta- Type 1 collagen defect vi. Ehlers-Danlos syndrome- Type 1 ( MAINLY ) and Type 3 collagen defect vii. Osteoporosis- ↓Collagen in skin and bones i. Elastin - similar to Collagen, but more elastic due to absence of HydroxyLysine j. Proteins in Tear Film i. Buffer Ophthalmic drugs and maintain a stable pH due to containing many functional groups w/ different pK values Enzyme Kinetics

Km - [S] Conc. when rxn rate is 50% of Vmax …. measures enzyme of affinity for substrate. ↓Km = ↑Affinity, ↑Km = ↓Affinity a. Competitive Inhibition i. Inhibitor competes w/ [S] in binding active-site of Enzyme. Vmax stays same but ↑Km (↓ affinity) ii. Lineweaver-Burke plot - x-intercept shift to right b. Non-Competitive Inhibition i. Inhibitory ligand at allosteric site stops enzyme function, but [S] can STILL bind Enzyme (Enzyme affinity for [S] doesn’t change). ↓Vmax , but Km stays the same ii. Lineweaver-Burke plot - y-intercept shifts upward c. Positive Allosteric ligand binds Enzyme= ↑Enzyme affinity for substrate= ↓Km. x-intercept shift to Left d. Negative Allosteric ligand binds Enzyme= ↓Enzyme affinity for substrate= ↑Km. x-intercept shift to Right e. Cooperativity- [S1] binds to active site and ↑affinity off active site for [S2] f. Positive Feedback - end-product binds to enzyme at allosteric site and ↑enzyme activity. Childbirth (OXYTOCIN ↑Contraction ) and Platelet clotting cascade g. Zymogen - inactive enzyme / proenzyme is activated by proteins into active form h. NUTRITIONAL DISORDERS
ANOREXIA NERVOSA - W>M. Distorted self-body image. Fear of being fat. <85% ideal body weight. Miss >3 consecutive menstrual cycles
BULIMIA NERVOSA - Binge eating >2x/wk for >3 months. Vomit, over-exercise, use laxatives
Vitamin A- development, maintenance of epithelial tissue, ↓infection risk a. Vit A Deficiency- Squamous metaplasia, Xerophthalmia (Bitot’s spots), Pneumonia, Nyctalopia, skin dryness , ↑Infection risk b. Vit A Toxicity- Yellowed skin (mistaken for jaundice), hepatomegaly, splenomegaly, bone pain
TR ai N P rivate B rad F irst C lass (TRN B PFC)
Vitamin B 1 (Thiamine)- Carbohydrate + AA Metabolism a. Thiamine deficiency - ↓Energy metabolism, BeriBeri (jaundice, polyneuropathy, edema, cardiac failure), Toxic Optic Neuropathy b. ALCOHOLISM - Sx’s: Gallstones, alcohol hepatitis “Fatty-liver”, Cirrhosis (#1 contributor, Jaundice, hypoalbuminemia, ↓coagulation factor, PORTAL HTN), WERNICKE-KORSAKOFF Syndrome (DRY BeriBeri) - Thiamine deficiency causing Wernicke ( Ophthalmoplegia , Confusion, Ataxia, bleeding in brain, muscle wasting, delirium, heart failure), Korsakoff (Memory loss). Ocular: Toxic optic neuropathy (bilateral temporal Optic N pallor w/o edema) c. Of all the water -soluble vitamins, Thiamine is depleted fastest. Its levels are also low in Diabetics
Vitamin B 2 (Riboflavin) - ↓risk of CAT a. Riboflavin deficiency- photophobia, corneal NEO, DRY EYE, DRY skin changes, cheilosis, seborrheic dermatitis, Interstitial Keratitis
Vitamin B 3 (Niacin)- important cofactor for NAD and NADP and ↓VLDL and LDL levels a. Niacin deficiency- Pellagra (dermatitis, photosensitivity, dementia) b. Niacin Toxicity- Niacin maculopathy at high doses, itching, rash, flush skin
Vitamin B 6 (Pyridoxine) - Coenzyme for Transamination (AA synthesis) - Pyridoxine deficiency- Anemia, convulsions, Homocysteine
Vitamin B 9 (Folic Acid) - Purine and Pyrimidine synthesis (DNA SYNTHESIS) a. Folic acid, Vit B 9 Deficiency- #1 deficiency worldwide , caused by alcoholism , Toxic Optic Neuropathy , Spina Bifida and ↓DNA Replication
Vitamin B 12 (Cyanocobalamin) a. Cyanocobalamin deficiency- ↓NT synthesis, Pernicious anemia, peripheral neuropathy**
Vitamin C- Cofactor to (1) Hydroxylase enzyme in Collagen Synthesis , (2) Dopamine synthesis (3) NE synthesis. Antioxidant, Wound healing, Bone formation, Capillary integrity a. Vit C Deficiency- Scurvy (joint/bone pain, bleeding gums)
Vitamin D - found in liver, egg, saltwater fish, ↑Ca and ↑Phosphate absorption in Small intestine a. Vit D Deficiency- Rickets in children - bone malformation, ↓cartilage. Osteomalacia in adults - Bone softening due to ↓Ca absorption b. Vit D Toxicity- Most toxic vitamin …Hypercalcemia  which is associated w/ SARCOIDOSIS , kidney stones, HAs

Immunology & Microbiology Study Notes: Key Concepts & Mechanisms, Lecture notes of Immunology

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IMMUNOLOGY

BIOCHEMISTRY