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ENI NOTES  Nerves i n the Dermis & Ki > - Sensory Responds...

ENI NOTES  Nerves i n the Dermis & Ki > - Sensory Responds motor Blood : : Adrenergic supply : to touch + , pressure cholinergic , temperature nociception print fibres as rwirgrande in deep D r sin Anae-growing - Melanocytes : pigment- Deep Dermal Plexusibtwn Der mist Subcutis-supply lower follicle - photoprotections immune function - - mid-Dermal plexus : Level of sebaceous glands supply errector - pil: muscles Cells: Antigen Resting Langerhauscells Superficial sollicle Telogen -o hair plexus: just betow Epidermis - Dermal Upper - - Presenting under UV light Exogen-- Expulsion Reduce Glands - : cells follicle glands hair : Polygonal near a to Sebaceous - our Sweat glands : whafoiebeowsebausganseared er # pitredAssociated are as 2) Cortex per sensitivities # Sheath Atopic Dermatitis ONE Anaphylaxis 5) Heule Layer > - + cytokine t leukocyte activity Egte binds most cell Sensitisation. => exposure Phase 1 : , PFgE - n a encountered prote Phase 2 : Same Allergen as above Correodesmosome Most cells - already primed + Coated w/IgE lipids (watertightSeal LKeratohyaline granules Granules (Histamine) , - Releas - pruritus , Brochorestriction toedema mins) Immediate (5 - petwoMysterIgG => WatertightSeal * lipids of the Epidermis => Present Circulate Bode in - Activates classic complement pathway - Destroys cells (phagocytosis) #Three Equine Recurrent Airway Obstruction/ Canine Blue eye -o - immune complex hypersensitivity Formation of complexes - immune - Activation ComplementSystem of - chemotactic neutrophils Neutrophils Caut digest complexesStuck in Blood vessel walls - Releas toxic Granules into +issue > Severe +issue damage = - lots of but lots of IgG IgG - or less Antigens ForTuberosa prolonged onset - Sensitisation phase Antigen Specific Tlymphocytes generated · -> Re Exposure Reactivation of Sensitised cells travel of presentation - > to site = Exotic & Avian Integument * Rats + ferret -> No Sweet glands /only or feet CR overheating - - Ferret of sebaceous glands. ~ Reptiles - - NO SWEAT GLANDS - ( fe m o r a l Dry glands + cloacal pores - Rabbits Few - Furry Feet - - Der mis large for thermoregulation SurgerminatorproduceDana ears Epidermis layers : - Scent glands contains lipid - Dewlap (mature Female) intermediate layer - - cutes Givea pigs - - thick foot padswo hairless behind ears prome to scalding Reptile Revatin : Alpha Flexible To hinges : o btwn scales often a matted sticky sebaceous gland above anus - Betas hard & unique to reptiles Chinchillas Dense Coat - - Need dust baths Fur Slip (handing) Dermis : Contains pigment cells vessels quelona - · large bald ears , nerves + -contain boul plates costoderms in some animals) amester astretchy -ventral Scent skin glands Amphibians ~> Stratum Spongiosuma Stratum Compacture pigment cells: Chromatophores Fats ↳ lie between dermis a epidermis - zymbals glanda base of ear ↳ melamin - black brown grey (tail Slip , -hairless tail , lots of manuary +issue ↳eartedyelloworange a - Edysis : no shedding. ① cells of Stratum intermediate layer replicate to form new 3 layer epidermis ② Lymph & enzymes diffuse btwn old a new epidermis to form cleavage Zone is then shed ⑤ old Skin ④ new Skin hardens Birdemalian - but thinner glandless - feather folleas EpidermalRyersBasa Intermediate outer tornified , a Subcutaneous - yellow fant Bug Holometabolous - adults obigate blood Sucke e , Felis - Diseases : Davis- myxomatosisseeenslave Galva... feline infectious anaemica Rickettsia D Caninum. FliesMolometabolous - Simuliidae Culicidae Ceratopogonidae (Colicoides) Psychodidae muscidae Tabanidae Hippoboscidae Glossinidae Oestridae Sarcophagidae Calliphoridae < Ich  classes of Cell-Surface Receptor protein 3 target G protein - - iOnchannel-linked Receptors Enzyme-linked Receptors - Second messenger signalling - intra cellular Clamp , Calcium ions) intracellular protein molecular switches phosphorylation inactive states kinases & GTPases toggle bon active cells adjust sensitivity to S a ignal to receptor Remove - change sensitivity or ThyroidTy(tri-iodothyronine ↳ Stimulated thyroxine) - as well as Calcitonin by TRHATSH) Regulates Basal metabolic Rate > - for ①Follicular Calls Synthesize Thyroglobulin -Active a y by cells ②Thyroglobulin Split to form +3tTy (TH majority) = Remainder of To made to rT3 ↓ Action of TziTy ↳ inactive = Regulatory to of Tz Ty Functions + Developmento growth - Carbohydrate Metabolism - - Fat metabolism Hypothyroid e/s Acitiology carb metabolism weight gain but no Hxot polyphagia => BMR + Slows Stuckin telogen maintenance of growth = => Skin + coat changes no Gcocorticod on faciculate in the Adrenal gland Cortisol - stress hormone inhibits insulin/storage). promotes Usage of glucose ↳ Gluconeogenesis glycogenolysis proteolysislipolysis , , o for Gluconeogen Muscle entabolism => 3 a fat => lipolysis toprovid Bone => Breakdown for organs Equine Pars Pituitary Intermedia Dysfunction Aetiology of Clinical Signs Pars Distalis : Pars Intermedia Hypothalamus Hypertrichosis- ↑MSH > melanotrophs => POMCL craved Dopamine Laminitis - Somatotrophes GH : [MSH CLIP Bendorphin - persistent hyper insulinemia C P Corticotrophs : POMC , ACTH , BLPH I S e ACTH = BmSH PUPD- > bADH ? Lacto , trophs : prolactin Gonadotrophet Aut Pit weight loss > Catabolic effect on skeletal muscle - sedative effect (ParsInter) Lethargy - > Bendorphin has ACTH Immune Suppression - CMSH In PPID = > Adenoma in Pars Intermedia ↳ MSH... infertility > - Compression of pars distalis ↳ excessive Target production of POMC ↳ Due to lack of control Pinsis inhibitory Biochem : hyperglycaemia/hyper insulinemaneutrophilia/Hypertriglyceridemia from Dopamine from hypothalamus => Allows Adenara to form T estRestinia Imaging > - CTCMRI Catecholamines Blood Comes from medulla suthesis : All Epinephrine in - Tyrosine Nor epinephrine Comes from: d medulla post ganglionic Sympathetic neurons dihydroxy Phenylalanine Tyrosity hydroxyase - : Kinetics ostored in Secretory vesicles ↓ ·Releasedexocytosis via Dopamine · metabolized by liver - kidneys d Norepinephrine/Epinephrine - Receptors - A A2. - B B2 , Catecholamines on Receptors : pha : riction · Pupil dilation contractility Intestinal relaxation -Pilomotor Contraction Bladder sphincter contraction Beta station Bronchodilation Alphatanaesthesia - -Glycogenolysis Lipolysis -  What i s a Hormone? Fendfa/oolitte ↳ messengerthat fix = homeostasi s homeostasi s feedback-enhance the change ↳ positive General pathway of processes Regulated Blood CategoriesEndocrine System transported to Target Cell via By unlesneyforAutenestitial on i s. Hormones 2 ↳ processes. Hormone 3 Binds to receptor - Digestive Utilization of nutrients & -storage development Water Hormones US. Lipid Hormones proteins in Blood -growth a + fluid Balance Require Transport Electrolyte Mereptasuthugh member - - a Reproduction - TheHypothalassies of ANS Endocrine System External environme a - Monitorsb ody's internal A rygland ofManyhomeActio RegulatesSecretion - PituitaryGlad mone Secretion need in Posteriorprintensitof neuroendocrine cells · Secretes Axons Hormonestransported through nerve terminals Anemi releases from S - To posterior pituitary vessel special Blood etabolis obsorption to post absorption is Regulated by mones mesarean digestionlargeorgani laube absorben -During does not fully utilize the nutrients when the body stored glycogenpolymer of as intestine the excess is absorbed from the , des Clipids) ucose and Triglycer trighterides , to protein - liver converts surplus Carbohydrates of + Acid from micrbial proteins In Ruminants most Amino Supply is the fore Stomach synthesized in Glucocorticoid Actions : Fat mobilisation from Stores : > - HAC Plipids (Cholesterd ? ) Parameters : ALP -ALT Cholesterol Bile acid. ↳ stimulate production. , Glucose Catabolises Muscle - * * AA Circ = ↓ parameters : vRea : PGFR Reduced Transit time = - -PBlood glucose low USG- inhibits ADHDirresis Antagonises insulin > = Gluconeogenesis in Liver -> liver enzymes? PGFR i n Ent Block ADM action ↓ a levels in Bone -o PCa circ Release neutrophils from marginated pool neutrophilia Stress -> Leukogram Down Regulates immune Response (Tcel-Ball) ↓ Mineral corticoids- Na +H20 Retention  Growth Hormone + IGF = Support Growth /long term) a Short term = starvation response is mator GHIH clipolysis - insulin resistance) ↳ GH Mediated by IGF-1 ever Tissues GH stimulated by : + ↓ Blood Glucose Growth Hormone &Growth ↓ blood free fatty acids ↑ nuclear by promoting protein synthesis : transcription I translation ↓ protein ↑ amino acid transport ↓ tranna stress excitement + exercise , , ↓ catabolism of proteins ↳ Protein IGF-1 - Synthesis , lipolysis promotes , Stimulatedbya hyperglycemia cantagonise insolve - Promotes Bone growth grow bone (by ? Chondrocytes + Osteogenic cells) = a tissue of OR Bthickness Bone 2 Functions : ↑ partilage deposition pinsclimGrowthStimulatestosGF- = Anti insulin = starvation => works as Glucagon  Exocrine : The Pancreas Glucose transporters = GLUTI INS RBLs independenta - = = , Excine Pancreas GLUTC Liver = - Islet Glucose sensors GLUTy=Requireinsulin ge to let a Somatostatic Insulin Glucagont - , G by Cells in slets of langerhans hypegm Stresavailibility. insulin on GlUT inhibits glycogenols Somatostativ = a Glucose Stimulates PromotesConversion glycogenesis of glucose to Seet Secreted by Hypothalamus No Glut 4 in stomach intestine - inhibitsgucone a - brain except , pancreas , , Suppresses - sacts on insulin-Glucagon Secretion GHFH Fusin soluble (caut be e - Preprohormone - given po meditate prohormone (proinsulin)viaCalcium - Secreted by B cells in pancrease Liver - hepatic portal usin - Regulated byinsuling/Amino acids. GIhormones (incretins) such gastic inhibitory Peptide as (GIP) like + glucagon peptide(GlP 1). And ANS/PSNSPSNSA) ↳ released by cells si Lovagus (Adrenalive Insulin Release : (P Glucose i n Blood GLUT2 : Islet glucose sensor @ Calcium s i m e GLUTL transporter allows Glucose to enter Bell Diabetes Mellitus Phosphorylation of glucose by glucokinase thaps glucose a a b Dogs Glucose ④ inhibits insulin : Immune mediated (Tcell) destruction ofcells OR # insiliv receptors ATP sensitive potassium channels PancreatitDei o intracellular dependent insula sensitivity potassium i s => depolarization = ⑥ voltage gated calcium channels activated Binding ⑦ influx of Calcium Cats Condition of insulin triggers exocytosis of insulin (HAC to receptor activates acromegaly phaeochromocyto Obesity/diet induced : , pathway , Tyrosine kinase not insulin destruction of is let GLUTH = insulin responsiveGlucose transporters dependent amyloid (cytotoxic insulin latreadingit - says can let Glucose into cell Glucagon Synthesised as preproglucagon Metabolised by liver a kidney Primarily acts on Liver Acelsprimarilyrespond Also Secreted o Bloodwo alongside insulin e nesis in response to PAAs Gormones e sells in Duodenum+ Stomach stedbypenopeptidesastomachdistensional sthypertentechie made s Secretin : by drodenum Stimulated by Ht in Small intestine Effects : Stimulates release of Bicard rich pancreatic obiliary fluid CheystokininMadebyDvoden Effects & Stimulates secretion of pancreatic AAs enzymes in small intestine contraction Gastric inhibiting peptide+ glucagon like emptying of gall t t bladder. Stimulated by gastric peptide made by proximal small intestine : Fat Glucose tamino acid ina secretiona * insulin sensitivity of motility potentiates release of insulin in to Blood glucose - Secretion leaves a civi zygomatic modified parotid o - in ducts (Na +a out , Hoztkin) ↳ intercalated ducts-Secrete HCO +absorb 21- ↳Stricted ducts - Secrete kt absorb Na o a HCOz & Secretory ducts Convey ↳ - Saliva to the Mouth · Mandibular Composition Sublingual · - aas all Paivatypes digestion Carbohydrates Amylase - = of parotid: Runsacrossmastermuspensiup a - Bicarb to buffer Stomach/Rumen Bicarb for > most set as keeping mouth pH 7 5 -serous in. Phosphate puffer > buccal opposite upper 1st molar zygomatic provides Ca for teeth (maintain enamel : mucosa Opens Hydroxyapatite in upper > - - Sublingual : Monostomatic part : opense sublingual naruncle a Mandibulargland mrus > Urea/ammonia - Rodents serous Mandibular : caruncle base of ling Sublingual gland a Opens sublingual : mucus - mixedSerost -Serous in Rodents In dogs : -ele -gam incisors : x0l-x03 - 83/3 Canine : XO4 premolarixos-xo8 Molar : X09-TpBot213 Oval mucosa = lips Deciduous all Species Formulae across Deutine have Bu t out : Formed by Odonto blasts molars primary laid down as tooth grows ↳cat Secondary laid down after eruption make smaller pulp - 5-4 3 Horse : 304 , Tertiary : Reaction , to damage 3 , 0 - 1 3 4 , -. 3 ↳ XOI Erupts &Zo Syr Alveolar bone formed by osteoblasts 2 in wear 5 Xo2 - 23 ·bmonter nee -. x03-304 5 Dementum made by eementoblasts. Enamel made by ameloblasts ⑳speed Feene a occlusal Sure * in cats + dogs · All adult teeth Cementum periodontal ligament to Bone Should be in - 6 months by  i n formi t Dental Nerve blocks · mandible middeteal - maxillary max Canine : Infraorbital maxillary ·maxmokumaxia Max pr: Infreorb + maxillary aente inferior Alveolar mandibular e : middle mental inferior Alveolar mandibular Pm : Inferior Alveolar Mandib Molar Interior : illary cauda Alveolar Ixx nfra orbital O - - X &X D I = - -- & - X Cardal Tmiddle mental mandibular ofHeG s bacterslet Will s produce peptides that Epithelial layer - the lumen Many folds, Connective. Submucosa-thicker layer of connective +issue ↳ Blood vessels ↳lympvessel ks of nerrous i n wall of intestines : Submucosal Plexus muscularis - primarily Smooth Muscle cells ↳ Responsible for mixing a transport movements of digestive tract Serosa-Peritoneum (inside lines abdominal wall /parietal layper - visceral layer lives organs #porta 3. Portal tract = One hepatic Artery , One Bile ducts one portal vein portal canal-space * · · > Bile four cell Endothelial cells Gall Bladder o types Blood flow in * Gall Liver : Heo, in epithelial opposite directions cells modify kupfer ce lls Defend against Vascular carried pathogens + remove debris hepatic Stellate Cells (Ito) +issue Sibrosis Retinol metabolism Function : Storage Concentration & release , > - of BileFunctionFadigestion the patiEretodrugstduodenum bile bile by removing Na + e) a containing portal tract Central vein receives blood from Sinusoid & Returns it to circulation & duodenum pile duct joins wh pancreatic ducts + empties via hepatic vein , into lomen & ampulla of water spinter prevents backflow of clume allows to builda Enzymes involved in metabolism ↳ opens in response to CCR Glycolysis aspartate aminotransferase (AST) : Gluconeogenesis Alanine aminotransferase (ALT) : Synthesises plasma proteins detergent emulsify fats : Bile = to Serum Albumin exclusively by hepatocytes Ammonia needs be converted to crea - - to VLDL Bilirubin > move insoluble fet Synthesises (yellow) around - HDL - Fibrinogen - prothrombin -transferrin Synthesises Cholestero - steroid hormones Cholesterol - - Bile acids > cholesterol derivatives - choicacidminids cougard ↳ BileSalt aphospholipids Endogenous Detoxification Exoea - - Haem breakdown - macrophage eats damaged RBs > excretion via Bile Phase 1 : involves Cytochrome P450 heamoglobin recycled - Phase 2 : Glucuronidation gebetamin attachments ess Ligaments Caveat + CoronaryLigament: Diaphragm-liver C falciform ligament ventral side & Triangular ligaments ro l · UREA Cycles Aminoid metabolism urea/Nitrogen metabolism = Ammotoxic need toconvert urea to Intracellular proteins S Diet ~o Y Amino Acids Deamination wr dretoacids * NHyt -> Excretion (Fish/Amphibians) liver Glucose Blood Gluconeogenesis COO Kr~rea ebsthe o "Biosynthesis of Amino did a Ureas > Kidney Respiration Frea Urine westland ad Metabolism - Biochemistry FedageteabsorbedTransportedachylomicronsthrough lymph lole lipids : · Absorptionmine Pinot hydrolyze triglycerides Fatty acid t o SI Fastingnindve,Glucagonpolysis breakdownTAGS Pancreatic lipases A a 3 chylomosa s. enterocytes packagedinto G smaller Molecules absorbed by fromTAG Breakdown substrate for Gluconeogenesis - Glycero used as a fasting into Ketone bodies to be used alternate energy Continued Conversion of Excess Acetyl COA by Brain & Muscles - sportation as = : lipoproteins/chylomicrons transport via Lymphatic System => Adipose muscle - Remnants of * Chylomicrons taken up via liver Starvation : Plipolysis ↑Ketogenesis , 24 hist SoTriglycerides musclespring utilizationot ketonebodiesbyreducesneedforglucosespares catabolizedA is needed muscle protein being stored in Adipose +issue for when is energy As ketone bodies provide Alternate for braint other organs of protein breakdown b to muscle - source mass energy , rate preserve bism : Lipolysis : response to hormones (glucagon * Adrenaline) = triglycerides in Adipose +x hydrolyzed into Freefatty acids - Glycerol no catalyzed by HSL Beta Oxidation : Free fatty acids transported to mitochon. Dreaks down fas into acetyl COA units to enter Krebs cycle mesRetolysistesting exerciseAcetyl-CoA Converted to before bodies in Liver-transported to issues to be converted back to