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CPII Exam 2 - Coggle Diagram

- - - - maj contrib to maint colloidal oncotic P - 75%
      - transporter
        
        Ca, Mg, unconju bili, drugs, horms...
  - - - avian and reptiles
    - - bind and trnspt thyroxine and retinol
  - - - acute phase prot (APP)
      - Ig
      - C'
      - clotting factors
      - trnspt prot, lipoprot, fibrinogen
  - - - APP and trnspt prot
    - - APP (incl fibrinogen), trnspt prot, some Ig (IgM and IgA)
    - - all Ig
  - - - converted to fibrin during hemostasis to form a clot
  - - - refractometry
        
        msmt of total solids
        
        incl prot, gluc, electrolytes, lipids, urea...
        
        temp dep - run at RT
        
        interference: lipemia, choles, urea, gluc, synth colloid soln
        
        typ measured on plasma but can use serum
      - biuret
        
        spectrophotometry
        
        will be lower than TP/TS by refractometer
      - alb dye binding
        
        most common chem analyzer method for measuring alb
        
        bound by dye and measured
        
        interference: bind alb if low = false inc alb; hemolysis
    - - CALC
        
        [glob] = [serum TP] - [alb]
      - TP msmt on chem analyzer
      - fractionated glob by SPE
        
        sep based on size and charge
        
        differen cause of hyperprot -- mono vs polyclonal gammopathies
        
        can also be run on urine
      - immnoelectrophoresis/immunofxn
        
        ID subclasses of IG
        
        useful to recog monoclonal gammopathy
    - - LA
      - heat precip
        
        2 tubes > 1 heated and 1 not = heat removes fibrinogen
        
        cannot docu hypofibrinogenemia
      - Clauss modif (QFA)
        
        determ by addn of high [thrombin] to citrated plasma and msmt of time for form fibrin
        
        longer time to clot = lower fibrinogen
        
        docu dec fibrinogen
  - - - neonates
        
        alb and glob are low
        
        high water content
        
        immuno inexperiece
      - elderly
        
        progressive inc in Ig
        
        sm dec in alb
    - - dec alb a varia glob
  - - - dec produc
      - inc loss
      - rela shift of water
    - - inc produc
      - rela shift of water
    - - nonselective = both alb and glob affec
        
        nonselective hypoprot
        
        inc loss
        
        hemorr
        
        external blood loss
        
        GI/PLE
        
        SI mucosal dz, lymphatic dz, intes blood loss from parasitism
        
        exudative skin dz
        
        thermal and chem burns/gen skin dz
        
        3rd space loss/seques
        
        body cavity fl
        
        can appear as selective if inflamm present
        
        dilutional
        
        age/preg
        
        fl overload
        
        edematous disorders (CHF, cirrhosis)
        
        nonselective hyperprot
        
        dehyd/hemoconc
      - selective = only alb or glob affec
        
        selective HYPOalb
        
        dec produc/intake
        
        liver dysfunc
        
        inflamm: neg APP
        
        dec typ mild (<30%) if sole reason
        
        GI parasitism
        
        parasites steal aa from host
        
        starvation/cachexia
        
        SEVERE neg prot bal
        
        RARE
        
        Addison's dz - mech unk
        
        intes malabsorp/maldiges
        
        Ex: EPI
        
        defic absorp of aa
        
        inc loss
        
        prot losing nephropathy (PLN)
        
        glom dz
        
        alb molec are sm and neg charged = pass thru
        
        glob gen too lg to pass thru
        
        proteinuria w hypoalb
        
        can lead to nephrotic synd
        
        1 more item...
        
        selective HYPOglob
        
        FPT
        
        neonates have min [Ig]
        
        failure of neonates to ingest or absorb colostral Ab
        
        results in lower [IgG]
        
        inherited or acq immunodefic is RARE
        
        selective HYPERalb
        
        DEHYD - literally the only one
        
        selective HYPERglob
        
        inc produc
        
        inflamm
        
        APP
        
        inc in pos APPs and dec in neg APPs
        
        chronic inflamm = polyclonal gammopathy
        
        typ polyclonal = mixture of clones recruited
        
        rare monoclonal
        
        1 more item...
        
        also dec alb
        
        acute inflamm = monoclonal gammopathy
        
        perform SPE
        
        neoplasia
        
        monoclonal gammopathy (gmp)
        
        narrow based peak (steeper than alb)
        
        bi-clonal gmp (2 narrow peaks)
        
        single neoplastic clone produce 2 Ig that migr sep
        
        result from inc produc of single (maybe 2) Ig
        
        often glob higher w neoplasia than inflamm
        
        MM
        
        plasma c neoplasm of bm
        
        Bence Jones proteinuria
        
        SPE peaks in beta or gamma region
        
        B c lymphoma and lymphocytic leuk - may be polyclonal
        
        magnitude often impt
        
        liver dz
        
        post colostrum
    - - hyperfib
        
        inflamm
        
        dehyd
        
        others - preg, neoplasia
      - hypofib
        
        inc consump
        
        DIC or local
        
        inc fibrinogenolysis
        
        dec synth
        
        hepatic insuffic
        
        congen or inherited afibrinogenemia (RARE)
- - - - islet of Langerhans contain endocrine pancreas c
        
        alpha
        
        secre glucoagon
        
        inc gluc
        
        beta
        
        most numerous
        
        insulin secre
        
        drives gluc into c
        
        delta
        
        somatostatin
        
        inhib GH, TSH, insulin...
        
        pancreatic polypeptide
        
        GI motil, metab, food intake
    - - dietary - intes absorp
        
        anorexia NOT common cause of hypoglycemia bc of gluconeogenesis
        
        consider body condition and how prolonged/extreme
        
        sm/young ani may be more prone
      - gluconeogenesis - occurs in liver and some in kidney
        
        glycogenolysis
    - - inc blood gluc
        
        growth horm (GH)
        
        thyroid horm
        
        cortisol
        
        catecholamines
        
        glucagon
      - dec blood gluc
        
        insulin
        
        acts primarily on liver, musc, fat
    - - direct
        
        serum or whole blood analysis
        
        sep early - w/in 30 min bc RBC and WBC consume gluc
        
        portable gluc monitors
        
        many types
        
        sp varia
        
        adeq precision but questionable accuracy
        
        sig
        
        may underestim gluc lvls
        
        be consis w method
      - indirect
        
        blood gluc highly varia and change rapidly
        
        better to have long term indicator of gluc lvls
        
        hyperglyc = non-enz irreversible glycation of prot = can measure
        
        Ex
        
        fructosamine
        
        glycated prot/ab (gluc bound in blood)
        
        indicator of 2-3 gluc control
        
        can be used in cats to disting btwn stress induced and DM hyperglycemia
        
        quick, easily automated, economical
        
        can be affec by serum prot conc and rates of prot turnover
        
        hypoprot and hyperthyroidism may dec results
        
        impt to use lab specific RI
        
        avoid smpl hemolysis
        
        glycated hgb (a1c)
        
        rxn in RBCs btwn gluc and hgb over life of RBC
        
        reflects avg gluc over 2-3 mo (dog) and 6 wks (cat)
        
        not widely avail or used in vet med
    - - low production
        
        liver failure
        
        sepsis
        
        young ani/toy breed
        
        low tis stores and prot
        
        low gluconeogen
        
        hypoadrenocorticism (Addison's dz)
        
        no cortisol for gluconeogen (and inc insulin medi tis uptake)
      - inc use/uptake
        
        in vitro artifact
        
        mk leukocytosis, bact in smpl, or cell utiliz
        
        xylitol toxicity
        
        stim insulin release, hepatic necrosis
        
        paraneoplastic
        
        insulinoma
        
        hypoadrenocorticism (Addison's)
        
        inc insulin medi uptake in musc
        
        sepsis
        
        inc utiliz by M0 irch tis or poss bact
        
        uncommon
        
        extreme exertion, mk bact in blood (hemotropic mycoplasma in LA)
        
        insulin overdose
        
        bov ketosis and preg toxemia
      - dec intake
        
        starvation is UNCOMMON
        
        typ assoc w poor body condition except in neonates and toy breeds
    - - post-prandial (monogastric)
        
        2-4 hrs post meal inges
      - stress
        
        may be epi or endog coricosteroid related
      - corticosteroid
        
        exog (cause insulin resis)
      - DM
        
        insulin defic or insulin resis
      - hyperadrenocorticism (Cushing's)
        
        metab synd in horses EMS = obesity, laminitis, insulin resis, DM very rare in horses
      - uncommon
        
        hyperthyroidism
        
        pancreatitis - B c destruc or stress in acute setting
        
        drugs - xylazine in horses, somogyi effec w insulin
        
        milk fever in cattle - hypoCa and hypoP
        
        prox duod obstruc in calves - can be severe
      - lvls in stressed cats can be v high and = glucosuria
        
        300-400 mg/dL in blood (renal threshold ~280 mg/dL)
        
        stressed dogs = <150-200
        
        stressed horse = <200-250
        
        stressed cow = <300-500
      - sick cats tend to have higher lvls of stress induced hyperglycemia than healthy cats
      - can differen stress from DM by fructosamine
      - DM
        
        cats
        
        hyperglycemia >500 mg/dL
        
        glucosuria
        
        azotemia - pre +/- renal
        
        varia electrolytes and mnrls
        
        ALT, ALP, choles can be inc
        
        may see Heinz bodies, anemia of chronic dz
        
        dogs
        
        sim to cats but gluc does not get over 150-200 w stress
        
        lower renal threshold for gluc ~180 mg/dL
  - - - if in neg E bal
        
        dec gluc = dec insulin and inc glucagon = inc HSL lipolysis = fa E from fat
        
        fa delivered to liver converted to acetyl-CoA + dec oxaloacetate lvls (used up from gluconeogenesis)
        
        acetyl-CoA cannot enter TCA cycle w/o oxaloacetate = inc ketogenesis
    - - ketonuria - paper strips
      - milk strips in cattle detect BHB
      - chem analyzers
      - some glucometers
    - - metab stress - preg, post lact in LA
      - starvation/ketosis in LA
      - diabetic ketoacidosis in SA
    - - blood msmt of ketones more sensi then urine
      - mild inc in serum ketones may be noted nonspecifically (hepatic lipidosis, CKD, hyperthyroidism in some cats)
      - sign inc assoc w DKA
      - inc serum ketones not linearly corr to severity of hyperglycemia in DM
  - - - liver secre VLDLs into circu
      - VLDLs hydrolyzed by LPL to usable choles rich LDL in musc and adipose (choles rish LDL to be used as E by other tis)
      - liver can also synth HDLs - these are good bc they can remove excess choles from tis and circu
    - - processed for blood trsnpt as lipoprot
        
        lipoprot classif by density - HDL, LDL, VLDL, chylomicrons (CM)
        
        not routinely fractionated in ani
        
        CM trnspt GI lipid to musc and fat
      - secre into intes lymphatics which enter blood
      - lipoprot lipase (LPL) hydrolyze CM primarily at musc and fat to usable components for E and storage
    - - activated by insulin
    - - alt, stores can enter ketogenesis cycle
    - - insulin
        
        anabolic - promotes lipid storage in periph tis and activates LPL
      - glucagon
        
        catabolic - stim brkdn of lipid in tis via HSL
      - glucocorticoids
        
        catabolic - stim brkdn of lipids via HSL and antagonize insulin
      - thyroid horm
        
        promote tis uptake to LDLs
    - - choles = all lipoprot, but typ HDL, LDL, few VLDL
      - trigs = all lipoprot but mostly CM and VLDL
      - NEFA (non esterified fatty acids) sometimes measured in LA for neg E bal
      - hyperlipidemia = nonspecific inc circu lipids - incl 1 or both hypercholes/hypertrig
      - hyperlipemia/lipemia = inc trigs in CM and some VLDL = lactescence (lipemia) of plasma
      - hyper/hypotrig
      - hyper/hypocholes
    - - mostly PSS/liver dysfunc
      - hypoadrenocorticism
        
        may be only finding in atyp Addison's
        
        concurrent hypoalb, hypogly, no steroid leukogram, lymphocytosis, poss eosinophilia, hypoNa, hyperK, 30-50% of dogs hve high ALT and ALP
      - rarely neoplasia
      - PLE (lymphangectasia, IBD, infectious, neoplasia)
        
        leakage in gut
        
        gluc typ norm, often assoc w panhypoprot +/- low blood mnrl (Ca, Mg, P)
    - - post prandial
      - idiopathic/primary familial metab dz
        
        Schnauzers and Shetland sheepdogs
        
        Schnauzers can get primary hypertrig that lacks elev in choles
      - secondary disturbances MEMORIZE
        
        hypothyroidism
        
        T4 needed to activate LPL
        
        DM
        
        insulin unable to activate LPL
        
        obstruc cholestasis
        
        lack of lipid clearance
        
        hepatic lipidosis
        
        lipid sourced from adipocytes for E outpaces abil of liver to metab it and lipid accum in liver
        
        hyperadrenocorticism (Cushing's)
        
        insulin antag
        
        pancreatitis
        
        dec LPL activity, cholestasis (dec clearance and inc hepatic synth)
        
        nephrotic synd
        
        dec LPL acitivity? dec alb compensation?
        
        dietary/obesity
        
        severe inflamm - dec LPL activity - NOT common
  - - - dec cal intake / inc E demand
      - ffa/nefa recruited to liver = liver overwhelmed = re-release lipoprot to circu
      - liver can accum fat = fat "toxicity"of liver
      - inc liver enz, maybe dec liver func
      - can also cause renal tubular lipidosis and renal failure
      - mini horses and ponies often for hyperlipemia
      - hyperlipidemia
        
        milder, norm liver func
      - hyperlipemia
        
        more severe, gross lipemia, inc enz and dec liver func
    - - dogs and cats
      - defic of insulin (type I) or insulin action (type II)
      - pathophys
        
        hyperglycemia: lack of insulin can cause vasc fl shifting if severe. Liver perceives low gluc and worsens hyperglycemia from glycogenolysis and gluconeogenesis
        
        osmotic diuresis: glucosuria oblig water mvmt and electrolytes to be lost
        
        fatty liver: fa released for E and are incorp into liver as state of cellu starvation perceived
        
        ketocidosis: dec fa conversion to trigs and inc fa conversion to ketones. does not occur in all cases but causes much more clin illness
      - physio effec of insulin
        
        gluc transloc into c
        
        dec P and K due to transloc into c
    - - dogs and cats
      - results from exocrine pancreatic damage
      - chronic pancreatic inflamm/fibrosis can affec endocrine pancreas
      - inflamm can cause release/activ of pro-enz in pancreas and peritoneal cavity = autodiges
      - can get SIRS response
      - poss labs
        
        CBC
        
        leukocytosis, often neutrophilia
        
        +/- steroid/stress leukogram
        
        dehyd/polycythemia or anemia of chronic dz
        
        DIC can occur
        
        hyperglyc (stress and poss islet c damage)
        
        pre-renal azotemia
        
        hypoCa - fat saponification, horm alt and dec alb lvls
        
        inc liver enz - local effects or spillover
        
        varia changes to blood prot
        
        inc holes/trig COMMON - cholestasis and alt lipoprot theorized
        
        amylase/pancreatic lipase - have lim
      - feline pancreatitis
        
        clin signs not specific and lab diag a problem
    - - hyper
        
        hyperglycemia
        
        inc ALP in >90% dogs, maybe inc ALT and GGT
        
        +/- thrombocytosis
        
        +/- inc choles and lipemia
        
        steroid leukogram
        
        +/- hypoCa
        
        clin signs: panting, PU/PD, polyphagia, musc wasting, distended abd, thin hair coat
        
        glucosuria uncommon
        
        Cushing’s dz
      - hypo
        
        Addison's dz
        
        "the great pretender"
        
        often vague clin signs - diarr, vom, lethargy, anorexia, +/- PU/PD
        
        ptx have immun-medi destruc of adrenal cortex
        
        leads to lack of mineralocorticoids (aldosterone) and glucocorticoids (stress horm)
        
        no mineralocorticoids = hyperK and hypoNa
        
        no glucocorticoids =
        
        = lymphocytosis or lack of lymphopenia, eosinophilia, mild non-regen anemia
        
        = hypocholes, hypoalb, hypoglyc
        
        "typical addison's" = lack of mineralocorticoids AND glucocorticoids
        
        "atypical addison's" = lack of glucocorticoids
    - - hyperthyroidism
        
        cats
        
        present w inc wt loss despite inc appetite
        
        ALP can be elv from bone turnover
        
        ALT and poss AST can be elev
        
        azotemia - prerenal +/- concurrent renal
        
        lymphocytosis/eosinophilia uncommon
        
        hyperglycemia is inconsis
        
        anemia of chronic dz
        
        sm #s of Heinz bodies may be seen
        
        can dec fructosamine!
        
        not common in dog, horse, cow