biochem_mod5_ms1

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soren101
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59067
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biochem_mod5_ms1
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2011-02-03 01:01:54
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biochem mod5 ms1
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endo/reproductive
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  1. KNOW BMAX (Ro) AND KD AND HOW MEASURED GRAPHICALLY.
    BMAX AND Ro= NUMBER OF AVAILABLE RECEPTORS = X-INTERCEPT

    KD = AFFINITY; THE LOWER THE KD, THE HIGHER THE AFFINITY = -1/SLOPE

  2. Gs COMPONENTS AND EFFECTORS
    INITIATING SIGNAL - B-ADREN AMINES, GLUCAGON, PARATHYROID HORMONE, etc

    DOWNSTREAM SIGNAL - ADENYLATE CYCLASE

    INC cAMP --> STIM PROT KIN A
  3. Gq COMPONENTS AND EFFECTOR SITES
    INITIATING SIGNAL - ACh, A-ADREN AMINE, NEUROTRANSMITTERS

    DOWNSTREAM - PLC-B CLEAVES PIP2 INTO DAG & IP3 --> INTRACELLULAR Ca++

    Ca++ & DAG STIM PKC

    Ca++ STIMS CALMOD-DEPENDENT PROT KIN
  4. Gi COMPONENTS AND EFFECTOR SITES
    INITIATING SIGNAL - ACh, A-ADREN AMINES, MANY NEUROTRANSMITTERS

    DOWNSTREAM SIGNAL - INHIBITS ADENYLATE CYCLASE
  5. 3 WAYS TO TERMINATE G-PROT RECEPTOR SIGNALING
    1) INTRINSIC GTPase OF G-alpha SUBUNIT

    2) DIS-ASSOCIATION OF LIGAND

    3) PHOS OF RECEPTOR BY A RECEPTOR KINASE, CAUSING B-ARRESTIN TO BIND TO RECEPTOR AND PREVENT RECEPTOR FROM ACTIVATING G-PROT EVEN WHEN LIGAND IS BOUND (DESENSITIZATION)
  6. MECHANISMS OF CHOLERA AND PERTUSSIS
    CHOLERA - ADP-RIBOSYLATE Gs IN INTESTINE CAUSING LOSS OF GTPase ACTIVITY. ADEN CYCL ALWAYS ON AND cAMP ELEVATED

    PERTUSSIS - ADP RIBOSYLATES Gi IN AIRWAY TISSUES CAUSING INABILITY TO EXCHANGE GTP/GDP. ADEN CYCL ALWAYS ON AND cAMP ELEVATED
  7. 3 WAYS IN WHICH RECEPTORS WITH INTRINSIC TYROSINE KINASE ACTIVITY CAN SIGNAL
    1) RAS PATHWAY - EGF BINDS TO RECEPTOR AND INC TYROSINE PHOS --> RECRUITS MOLECULES CONTAINING SH2 DOMAINS (Grb-2) --> PROT ACTIVATIONS --> RAS --> MAP KINASE --> DNA SYNTH

    2) PLC-gamma - ACTIVATION BY EGF RECEPTOR INC DAG, IP3, AND PKC. TUMOR PROMOTORS ACTIVATE PKC SIMILARLY TO EGF

    3) PI3-K - CATALYSES ATTACHMENT OF PHOS GROUP TO 3 CARBON OF PIP2 (SAME PIP2 THAT BREAKS TO DAG AND IP3), PIP2 --> PIP3 --> ACTIVATES PROT KIN CASCADE THAT INCLUDES PDK1 AND PKB (Akt)

    GROWTH AND METABOLISM
  8. WHAT IS SPECIAL ABOUT CYTOKINE, GH, AND PROLACTIN RECEPTORS
    NON-INTRINSIC TYROSINE KINASE RECEPTORS

    BUT, RECRUIT TK
  9. HOW DO NATRIURETIC PEPTIDES SIGNAL?
    BINDING TO RECEPTORS WITH GUANYLATE CYCLASE ACTIVITY

    REGULATE Na AND BLOOD PRESSURE

    cGMP --> PROT KIN G
  10. EXAMPLES OF LIGAND GATED ION CHANNELS ON NEUROTRANSMITTER RECEPTORS
    NICOTINIC CHOLINERGIC RECEPTOR ON MOTOR END PLATE
  11. RECEPTOR MEDIATED INTERNALIZATION
    FORM OF DOWN-REGULATION
  12. BIOLOGICAL ACTIONS OF GH AND IGF-1
    METABOLIC STRESS CAUSES RELEASE OF GHRH: FASTING, HYPOGLYCEMIA, EXERCISE, SLEEP, AAs

    IGF-1 REGULATES GROWTH AND METABOLISM, MEDIATES MANY OF THE GROWTH EFFECTS OF GH.

    • GH:
    • LIPOLYSIS
    • PROT SYNTH
    • BONE,MUSCLE,CART, SOFT TISSUEGROWTH
    • GLUCONEOGENESIS
    • INHIB MUSCLE GLUC UPTAKE

    • IGF-1 (SIMILAR TO INSULIN EFFECTS)
    • MUSCLE GLYCOLYSIS
    • PROT SYNTH
    • BONE,MUSCLE, etc
  13. SIGNAL TRANSDUCTION FOR GH AND IGF-1
    • GH
    • RECEPTOR ACTIVATES TYROSINE KINASE JAK --> TPs TRANSCRIPTION FACTORS CALLED SIGNAL TRANSDUCERS & ACTIVATORS OF TRANSCRIPTION (STATs) --> BIND TO DNA PROMOTER/ENHANCERS ENCODING IGF-1. ALSO, INC FFA OX WILL ACTIVATE PYRUV CARB AND INH PYRUV DEHYD AND PFK-1 --> INH PFK-1 INCREASES GLUC-6-P --> INH HEXOKINASE --> INH GLYCOLYSIS & STIM GLUCONEOGEN

    • IGF-1
    • SIMILAR TO INSULIN RECEPTOR --> BIND a-SUBUNIT ACTIVATES TYROSINE KINASE OF b-SUBUNIT --> AUTOPHOS --> TYROSINE PHOS OF IRS & Shc --> BIND AND ACTIVATE PI3 KIN AND Grb-2 RESPECTIVELY --> MET & GROWTH CASCADE --> SKEL MUSCLE GLUC UPTAKE, INH OF GLUCONEOGEN IN KIDNEY.

    LIVER & ADIPOSE HAVE VERY FEW IGF-1 RECEPTORS
  14. GH EXCESS
    GIGANTISM BEFORE PUBERTY & ACROMEGALY AFTER

    • DUE TO:
    • PITUITARY DAMAGE

    MUTATION IN Gs CAUSING INC GH SYNTH & SECRETION --> DESTROY INTRINSIC GTPase ACTIVITY

    GH RESISTANCE: LARON SYND. GH RECEPTOR MUTATION. POSSIBLE GIVE IGF-1
  15. GH DEFICIENCY
    GH GENE DELETION

    PITUITARY DAMAGE

    MUTATIONS IN GH PRODUCTION & SECRETION: GHRH, GHRH RECEPTORS, TRANSCRIPTION FACTORS FOR GH GENE

    IF SHORT STATURE BUT NO GH DEFICIENCY, DON'T GIVE GH
  16. THERAPEUTIC USES OF IGF -1
    1) CATABOLIC ILLNESS/NEGATIVE NITROGEN BALANCE: GIVE BOTH GH AND IGF-1

    2) ALS, MUSC DYST, SARCOPENIA (MUSC LOSS DUE TO AGING

    3) TYPE II DIABETES: DON'T GIVE GH!

    4) OSTEOPENIA, OSTEOPOROSIS, BONE FRACT REPAIR: IGF-1 MIGHT BE CRITICAL FOR PTH ACTION

    5) INCLUDE IGF-1 BINDING PROTS WITH IGF-1 TO INC HALF-LIFE
  17. ABUSE OF GH AND IGF-1
    GH RELEASED IN PULSATILE MANNER SO MEASURMENTS MAY BE INACCURATE: SERUM IGF-1 AND BINDING PROT BETTER INDICATOR

    INTRAMUSCULAR IGF-1 INJECTION HARD TO DETECT

    CANCER RISK IN PROSTATE, BREAST, & COLON
  18. STRUCT OF CHOLESTEROL
    AMPHIPATHIC 27 CARBON STRUCT

    A B C D RINGS

    KEY REGULATOR OF MEMBRANE FLUIDITY: INC CHOL MAKES MEMs LESS FLUID AND INC Tm BY DISRUPTING INTERATIONS OF FATTY ACIDYL CHAINS AND COMPLEXING WITH PHOSPHOLIPIDS

    SYNTHED MAINLY IN LIVER, INTESTINES, AND STEROIDOGENIC TISSUES
  19. ENZYME CATALYZING COMMITED STEP OF CHOLESTEROL SYNTH
    HMG-CoA REDUCTASE
  20. REGULATION OF CHOLESTEROL SYNTHASE
    1) NEGATIVE FEEDBACK BY HMG CoA REDUCTASE -- SYNTH CONTROLLED BY TRANSCRIPTION FACTOR SREB THAT BINDS TO DNA SEQUENCE SRE ON 5' SIDE. INACTIVATED BY ANCHORING TO ER OR NUC MEM. RELEASED BY PROTEOLYTIC CLEAVAGE WHEN CHOL LEVELS ARE LOW

    2) RATE OF HMG CoA REDUCTASE TRANSLATION INHIBITED BY MEVALONATE METABOLITES AND DIETARY CHOL

    3) DEGRADATION OF REDUCTASE: 2 DOMAINS. CYCLIC DOMAIN CATALYSES AND MAMBRANE SENSES DEGRADATION SIGNALS. INC STEROLS CAUSE CHANGE OLIGOMERIZATION STATE LEADING TO PROTEOLYSIS.

    4) PHOS BY AMP-ACTIVATED PK DECREASES ACTIVITY OF REDUCTASE. CHOL SYNTH STOPS WHEN ATP IS LOW.
  21. KEY STEPS OF CHOL SYNTH (PIC)
  22. BILE SALT SYNTH (PIC)


    CHOL + 7a-HYDROXYLASE --> THC --> CHOLYL CoA (ACTIVE INTERMEDIATE) + GLYCINE OR TAURINE --> GLYCOCHOLATE (MAJOR) OR TAUROCHOLATE.

    SERIES OF HYDROXYLATIONS BY P450
  23. CHYLOMICRONS AND THEIR REMNANTS
    CHYLOs HAVE VLD AND ARE RELEASED FROM INTESTINES IN FORM OF LARGE LD CHYLOs

    TAGs RELEASED BY LIPOPROTEIN LIPASES LINING BLOOD VESSLES AND TRANSPORTED BY ALBUMIN

    LIVER TAKES UP CHOL RICH REMNANTS
  24. VLDLs
    EXCESS TAGs AND AND CHOL IN LIVER RELEASED AS VLDLs

    BOTH VLDLs AND CHYLOs DEGRADED TO CHYLO REMNANTS
  25. IDLs
    RESULTING REMNANTS FROM VLDLs ARE IDLs. HALF TAKEN UP BY LIVER AND HALF CONVERTED TO LDLs BY MORE TAG REMOVAL
  26. LDLs
    RICHEST IN CHOL

    MAJOR CARRIER OF CHOL

    TRANSPORT CHOL TO PERIPHERAL TISSUES AND REG DE NOVO SYNTH

    SHELL CONTAINS SINGLE PROT apo B-100 WHICH RECOGNIZES TARGET CELLS

    AMOUNTS OF CHOL AND CHOL ESTERS IN LDLs ARE AROUND 2/3 OF TOTAL PLASMA CHOL
  27. HDLs
    DIFFERENT FUNCTION

    SHUTTLES CHOL THROUGHOUT BODY

    PICKS UP UNESTERIFIED CHOL RELEASED FROM DYING CELLS (HDL3 --> HLD2)

    EXCHANGES PROTS AND CHOL ESTERS WITH VLDLs AND CHYLOMICRONS
  28. FORMATION OF CHOL ESTERS
    RENDERS CHOL MORE HYDROPHOBIC THUS EASIER TO TRANSPORT

    LCAT IN PLASMA FOR HDLs

    ACAT INTRACELLULAR TO MAKE VLDLs. HIGH UNESTERIFIED CHOL DISRUPTS CELL MEM INTEGRITY
  29. LIVER AND CHOL METABOLISM
    MAJORITY OF BODY'S LDL RECEPTORS

    MAJOR SITE OF CONVERSION OF CHOL TO BILE ACIDS

    HIGHEST LEVEL OF HMG CoA REDUCTASE
  30. UPTAKE OF LDLs
    1) APO-PROT B-100 ON LDLs BIND TO PROT CLATHRIN ON CELL PM (LOCATED IN COATED PITS)

    2) RECEPTOR-LDL COMPLEX INTERNALIZED BY ENDOCYTOSIS. RECEPTOR THEN RECYCLED BACK TO MEM IN SEPARATE VESICLE

    3) LDL VESICLE FUSES WITH LYSOSOME WITH VARIETY OF DEGRADING ENZYMES.

    4) UNESTERIFIED CHOL USED FOR MEM BIOSYNTH, STORED USING ACAT, MADE INTO STEROIDS IN CERTAIN CELLS, OR RELEASED
  31. REGULATORY EFFECTS OF INTERNALIZED CHOL
    1) INH HMG CoA REDUCTASE

    2) ACTIVATES ACAT

    3) LOWERS SYNTH OF LDL RECEPTORS (SREBP - SAME AS CHOL SYNTH CUZ BOTH HAVE SRE) -- EXCESS CHOL LEADS TO INC BLOOD CHOL [ ], WHICH ACCUMULATES

    • LDL RECEPTOR HAS:
    • EGF SIMILAR TO TRANSDUCIN b-SUBUNIT
    • O-LINKED GLYCOSYLATION TO EXTEND RECEPTOR INTO LUMEN
  32. POMC
    LARGE PRECURSOR MOLECULE THAT CONTAINS:

    ACTH --> INC cAMP --> PKA

    MSH
  33. ACTH PROMOTES ...
    CHOL RELEASE FROM CHOL ESTERS

    CHOL TRANSPORT INTO MITOCHONDRIA

    CHOL SIDE CHAIN CLEAVAGE --> PREGNENOLONE
  34. CUSHING'S SYNDROME
    GENERAL MUSCLE CATABOLISM

    UNUSUAL REDISTRIBUTION OF FAT

    GLUC INTOLERANCE

    IMMUNE SUPPRESSION

    ELECTROLYTE IMBALANCE, esp INC NA CAUSING HYPERTENSION

    HYPERPIGMENTATION

    • URINE CORT - 1000nmol NORM <250
    • SERUM CORT - 500 / <50 AT MIDNIGHT
    • SERUM ACTH - 100 / <80
    • INABILITY TO SUPPRESS WITH DEXAMETHSONE
  35. ADDISON'S DISEASE
    LIFE THREATENING

    AUTOIMMUNE DESTRUCTION OF ADRENAL CELLS

    IMPAIRED FORMATION OF ADRENALS

    DEFICIENT ACTH RECEPTORS

    IMPAIRED STEROIDOGENESIS: LOW CORT BUT HIGH ACTH (HYPERPIGMENTATION)

    SECONDARY: LOW ACTH

    HYPOGLYCEMIA, HYPOTENSION, DEHYDRATION, HIGH INFLAM RESPONSE

    TREAT WITH CORT
  36. FAMILIAL GLUCOCORT RESISTANCE
    HIGH CORT BUT NO EVIDENCE OF HYPERGLUCOCORT RESPONSE

    MUTANT CORT RECEPTOR WITH <1000 FOLD AFFINITY

    GR IN HYPOTHAL AND PIT ALSO MUTATED, CAUSING INC CRH --> ACTH --> CORT
  37. GLUCOCORTS AND ANDROGEN SYNTH (PIC)


    RED - 17a-HYDROXYLASE

    PURPLE - 17,20-DESMOLASE --> ANDROGENS

    GREEN - 3b-DEHYDROGENASE

    PINK - 21-HYDROXYLASE

    BLUE - 11b-HYDROXYLASE (MITO)
  38. 21-HYDROXYLASE DEFICIENCY (GLUCOCORTS)
    LOW CORT, INC CRH ACTH AND DHEA

    MALES --> PRECOCIOUS PUBERTY

    FEM --> MASCULINE APPEARANCE & MALE EXTERNAL GENITALIA

    LIFE-THREATENING DUE TO NA WASTING AND DEHYDRATION
  39. 17a-HYDROXYLASE DEFICIENCY (GLUCOCORTS)
    LOW CORT, INC CRH ACTH MINERALCORTS (DEOXYCORTICOSTERONE) --> LOW RENIN HYPERTENSION

    VARIABLE ALDOSTERONE LEVELS

    MALES: NO ANDROGENS --> FEM APPEARENCE & EXT GENITALIA

    FEM: NO ESTROGENS --> DEFECTIVE SECONDARY SEX CHARACTERISTICS AND NO MENSTRATION.
  40. 11b-HYDROXYLASE DEFICIENCY (GLUCOCORTS)
    CAN RESULT IN BIPHASIC EFFECTS ON NA RETENTION: LOSS OF ALDOSTERONE --> NA WASTING AND DEHYDRATION EARLY IN LIFE

    BUT WEAK MINERALOCORT DEOXYCORTICOSTERONE CAN CAUSE Na RETENTION LATER IN LIFE
  41. ADH
    aka VASOPRESSIN

    INC BLOOD OSMOLALITY (NaCl [ ] DUE TO RETENTION OR WATER LOSS) BATH HYPOTHAL OSMORECEPTORS

    RELEASED BY POST PIT

    INC cAMP IN RENAL TUBULAR CELLS --> PKA --> AQUAPORIN-2 --> WATER REABSORPTION

    ALSO INC SMOOTH MUSCLE CONTRACTION BY Gq --> INC CYTO Ca --> PKC & CALMOD ACTIVATED

    • DISORDERS:
    • DIABETES MELLITUS INSIPIDUS - TREAT W/ ADH

    HEREDITARY NEPHROGENIC DIABETES INSIPIDUS: RARE - MUTATION IN ADH RECEPTOR

    SYNDROME OF INAPPROPRIATE ADH SECRETION (SIADH): TUMOR PRODUCING ADH
  42. SYNTH OF PREGNENOLONE
    REMOVAL OF 6-CARBON SIDE CHAIN FROM CHOL TO FORM PREG

    CATALYZED BY CYTOCHROME P450 ENZYME CHOL DESMOLASE

    STIMULATED BY ACTH
  43. STEROID RECEPTOR ACTIVATION
    STEROID IN CIRCULATION DISSOCIATES FROM TRANSPORT PROT

    DIFFUSE INTO CYTO OR NUC

    BIND TO INACTIVATED RECEPTOR (INACTIVATED BY HEAT SHOCK PROTS)

    TRANSLOC TO NUC

    BIND TO HRE (HORM RESPONSE ELEMENT)

    SYNTH OF NEW PROTS
  44. ANDROGEN RESISTANCE SYNDROME (ARS)
    DIFICIENT a5-REDUCTASE-2 --> DEC DHT

    AUTOSOME RECESIVE MUT

    PROMOTES DEV OF MALE EXTERNAL GENITALIA AND PROSTATE DURING EMBRYOGEN
  45. 17a-HYDROXYLASE DEFICIENCY
    DEFICIENT SYNTH OF CORT --> INC ACTH --> CONGENITAL ADRENAL HYPERPLASIA

    INC DEOXYCORT --> INC MINERAL CORT --> LOW-RENIN HYPERTENSION

    VARIABLE ALDOSTERONE

    REDUCED ANDROGEN AND ESTROGEN
  46. 21 HYDROXYLASE DEFICIENCY
    MOST COMMON CAUSE OF CONGENITAL ADRENAL HYPERPLASIA

    IMPAIRED CORT SYNTH

    INC ANDROGEN SYNTH --> PRECOSIOUS PUB (MALE) AND MALE GENITALIA (FEMALE)
  47. ESSENTIAL FATTY ACIDS
    CANNOT SYNTH BECAUSE OF LOCATION OF DOUBLE BONDS CLOSER THAN 7 Cs AWAY FROM o END

    2 SEPARATE BIOSYNTH PATHWAYS FOR LENOLEIC AND LENOLENIC ACID

    LINOLEIC ACID, o-6: MAINTAINS HEALTHY SKIN BY PREVENTING WATER LOSS. ACYLGLUCOSYLCERAMIDE (SPHINGOLIPID)

    LENOLENIC ACID, o-3: --> 4,7,10,13,16,19-DOCOSAHEXAENOIC ACID IN RETINA.

    o-3 THOUGHT TO ENHANCE CARDIO HEALTH BY REDUCING FAT PRODUCTION

    DEC FAT SYTH BY INH FATTY ACID SYNTHASE AND HMG-CoA REDUCTASE

    INC FATTY ACID DEGRADATION BY INC LIPOGENIC ENZYMES ACYL-CoA DEHYD AND CARNITINE PALMITOYLTRANSFERASE I.

    NEURONS ACCUMULATE FOR MEM
  48. AUTACOIDS
    LOCALLY ACTING HORMONES

    MOSTLY DUE TO RAPID DEGRADATION

    • 5 CATEGORIES TO KNOW:
    • PROSTAGLANDINS, THROMBOXANES, LEUKOTRIENES, HETEs, AND PAF (NOT DERIVED FROM LENOLEIC)
  49. LENOLEIC ACID --> PROSTAGLANDINS AND THROMBOXANES
    LENOLEIC ACID --> ARACHIDONIC ACID --> CLEAVED BY PHOSLIPASE A2 FROM MEM --> COX ENZYME CONVERTS TO PROSTAGLANDIN PGG2 (COMMITED) --> PEROXIDASE CONVERTS TO PGH2
  50. THROMBOXANE A AND PROSTACYCLIN
    THROM INDUCES PLATELET AGG WHILE PROSTA DOES OPPOSITE
  51. PROSTAGLANDIN E AND F
    E INDUCES RELAXATION OF SMOOTH MUSCLE AND F DOES OPPOSITE

    E ALSO INHIBITS GASTRIC ACID SECRETION, INFLAMMATION, FEVER, & PAIN
  52. WHY STEROIDS USED TO DEC INFLAMMATION
  53. 5-LIPOXYGENASE
    CONVERTS ARACHIDONIC ACID TO 5-HPETE

    BIOSYTH OF HETEs AND LEUKOTRIENES

    LEUKOs MADE MOSTLY IN LEUKOCYTES AND MAST CELLS -- INDUCE ASTHMA
  54. REGULATION OF PROSTAs, THROMBOs, LEUKOs, AND HETEs
    PHOSPHOLIPASE A2 INH BY STEROIDS SUCH AS PREDNISONE AND DEXAMATHASONE. ADRENAL STEROIDS PROBALY DO SAME

    ASPRIN INH COX (PROSTAs AND THROMBOs) BUT NOT LIPOXYGENASE (LEUKOs AND HETEs)

    COX SELF-DESTRUCTS

    ALL INACTIVATED METABOLICALLY -- VERY SHORT HALF-LIVES
  55. 3 ISOZYMES OF COX
    1 - FOUND IN PLATELES, ENDO CELLS, KIDNEY, & LINING OF STOMACH. THROMBO SYNTH, PLATELET AGG, AND GASTRIC ACID SECRETION

    2 - INFLAMMATION (LEUKOCYTES)

    3 - ALT SPLICE OF COX 1, LARGELY IN BRAIN AND MEDIATES PAIN SENSATION
  56. DRUGS FOR COX ISOZYMES
    ASPRIN - INH ALL BUT PREFERS COX 1. ANTI-INFLAMM FROM INH COX 2 & SIDE EFFECTS FROM INH COX 1 (STOM ACID, ULCERS, BLEEDING)

    COX 2 - CELEBREX, ROFECOXIB (VIOXX), MELOXICAM (MOBIC). INH INFLAMM WITHOUT COX 1 SIDE EFFECTS. ALSO INH CANCER DEV BY INDUCING APOP.

    VIOXX PULLED - SO SPECIFIC TO COX 2 THAT INH PROSTACYCLIN PRODUCING CELLS IN HEART/AORTA/LARGE ARTERIES.

    COX 3 - ACETAMINOPHEN (TYLENOL) DIMINISHES PAIN WITHOUT INH INFLAMM
  57. ANANDAMIDE AND 2-ARACHIDONYLGLYCEROL
    o-6 FATTY ACIDS

    ACTS ON CANNABINOID RECEPTOR

    2-ARACH PRESENT IN BRAIN >170 ANANDA & HELPS PROTECT NEURONS DURING BRAIN INJURY BY INH INFLAMM
  58. PAF
    NOT ESSENTIAL FATTY ACID, BUT PHOSPHOLIPID & AUTACOID

    CAUSES PLATELET AGG, EDEMA, HYPOTENSION, ALLERGIC INFLAMM, PSORIASIS, ITCHING, ASTHMA AND SHOCK
  59. DIETARY ASPECTS OF ESSENTIAL FATTY ACIDS
    o-3: IMP FOR NUTRITION. WHEN INCLUDED IN MEMs TEND TO EXCLUDE CHOL

    INH INFLAMM IN CHONDROs --> HELP ARTHRITIS

    HIGH o-6 DIETS PRODUCE MORE PROSTAs, THROMBOs, AND LEUKOs THAN ANCESTORS --> INC BLOOD CLOTS, ASTHMA, ALLERGIES, HEART DISEASE, CANCER AND DIABETES. BUT GREATER RESISTANCE TO INFECTION
  60. PROSTAGLANDINS CAN HAVE OPPOSITE EFFECT IN DIFFERENT TISSUES
    KNOW THIS
  61. ROLE AND MECHANISM OF ACTION OF CALCIUM
    ESSENTIAL PROCESSES: ENZ ACTIVITY, HORMONAL RESPONSES, BLOOD COAGULATION, MUSCLE CONTRACTILITY & IRRITABILITY

    FORMS: FREE, COMPLEXED (CHELATED) BY ORGANIC IONS LIKE CITRATE, AND PROT BOUND (45%) PRIMARILY ALBUMIN

    LOW SERUM Ca STIMS FORMATION OF 1,25 DIHYDROXYD3 INC INTESTINAL ABSORPTION. VIT D NEEDED FOR Ca ABSORPTION

    IF LOW Ca, 1,25(OH)2D3 AND PTH STIM BONE REABSORPTION
  62. HORMONES THAT REG Ca BALANCE
    INTESTINES, BONE, KIDNEY

    INTESTINES: ACTIVE VIT D 1a,25-(OH)2D3 INC BOTH Ca AND PHOSPHORUS

    BONE: PTH INC BOTH, ACTIVE VIT D INC Ca, CALCITONIN (CT) DEC BOTH

    KIDNEY: PTH INC Ca REABS AND DEC PHOS REABS, CT DEC BOTH, ACT VIT D INC Ca
  63. PTH AND Ca
    PTC RELEASED BY CHEIF CELLS IN PT. RECEPTORS SENSITIVE TO SERUM Ca ACTIVATE G-PROT Gs WHEN Ca [ ] FALLS

    ACTS ON INTESTINES, BONE, AND KIDNEY

    ALSO A PROT RELATED HORMONE WITH SIMILAR ACTIONS (PTrH)

    SERUM PHOS INC DEPRESSES SERUM Ca BY REDICING BONE RESORPTION AND DECREASING VIT D
  64. CALCITONIN (CT)
    PEPTIDE HORMONE RELEASED BY C CELLS IN THYROID GLAND

    LOWERS SERUM Ca [ ] BY INH OSTEOCLASTS AND KIDNEY EXCRETION

    HYPOCALCEMIA AND ACCOMPANYING HYPOPHOSPHATEMIA AFTER CT RELEASE

    INC INTRACELLULAR Ca AND IP3 SUGGESTING PLC AND ADENYLYL CYCLASE

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