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Y2B1 Part 2

Year 2 Block 1 Weeks 5-8

Zymogens Inactive precursors that are converted into active enzymes as part of the coagulation cascade
Cofactors Regulatory proteins that enhance functionality of corresponding coenzymes
What makes up a complete enzymatic complex and which enzyme is the exception 1. Enzyme + protein cofactor + procoagulant membrane surface 2. Thrombin
Most enzymes in coagulation are ______ similar to ____ Serine proteases; Trypsin
Procofactors 1. inactive coagulation prots in circulation w/o enzymatic abilities 2. regulatory role in enhancing enzymatic activity 3. Needs to be cleaved by certain enzyme to be fully active
Which coagulation factors are involved in the extrinsic coagulation pathway Tissue Factor (thromboplastin), Factor 7 (Proconvertin), Factor 7a (enzyme)
Name the zymogen of the extrinsic coagulation pathway Proconvertin aka Tissue Factor 7
Name the cofactor of the extrinsic coagulation pathway Thromboplastin aka Tissue Factor
Name the zymogen of the contact coagulation pathway Factor 12 (Hageman), Prekallikrein (Fletcher)
Name the cofactor of the contact coagulation pathway High MW kininogen (Will-Fitz-Flaujeac)
Name the enzyme of the contact coagulation pathway Factor 12a & Kallikrein
Name the zymogen of the intrinsic coagulation pathway Factors 11 (Plasma thromboplastin antecedent), 9 (Christmas)
Name the procofactor of the intrinsic coagulation pathway Factor 8 (antihemophilic factor)
Name the zymogen of the common coagulation pathway Factors 10 (Stuart-Prower), 2 (Prothrombin), 8
Name the procofactor of the common coagulation pathway Factor 5 (Labile)
Name the substrate of the common coagulation pathway Fibrinogen (Factor I)
What is the final product of common coag pathway Fibrin
Serpin Superfamily of inhibitors of serine proteinase found in plasma & tissues; employ a suicide substrate mechanism (they make bait)
Which coagulation inhibitors are part of the Serpin family 1. Antithrombin 2. Heparin cofactor II
Which coagulation inhibitors are Kunitz inhibitors Tissue Factor Pathway Inhibitor aka Extrinsic Pathway inhibitor
Kunitz inhibitor Protein in legume seeds that fxns as protease inhibitor specific for either trypsin or chymotrypsin
Name the zymogen of the coagulation inhibitors Protein C
Name the coagulation inhibitor that is an enzyme as well as an inhibitor Activated Protein C
Name the cofactors (enhance the coenzymes) of the coagulation inhibitors Protein S & Z, Thrombomodulin
Name the enzymes of the coagulation inhibitors Protein Z dependent protease inhibitor & Activated protein C
Name the zymogen involved in Fibrinolysis Plasminogen, Prourokinase
Name the enzymes involved in Fibrinolysis 1. Plasmin 2. Urokinase 3. Single chain tissue-type plasminogen activator 4. Double chain tissue-type plasminogen activator
Name the Fibrinolysis inhibitors 1. A2-antiplasmin 2. Plasminogen activator inhibitor-1 3. Thrombin activatable fibrinolysis inhibitor (aka Carboxypeptidase U, B, R)
Name the Fibrinolysis inhibitors of the Serpin family 1. A2-antiplasmin 2. Plasminogen activator inhibitor-1
Name the non-specific inhibitors of the coagulation cascade 1. C1 inhibitor 2. A2-Macroglobulin 3. Protease nezin 1 4. Protein C inhibitor
How does activated protein C inhibit enzymatic activity & which pathway does it inhibit 1. Cleaves target protein, cutting it into pieces so it cant be used 2. Common pathway (I think)
How does antithrombin inhibit enzymatic activity 1. employing a "suicide substrate" mechanism 2. Stable complex formed when inhibitor binds to enzyme & alters enzyme so it permanently can't be released
List the 4 diff ways that inhibitors can work in the coagulation cascade 1. Damage target prot 2. Active site inhibitors bind to enzyme 3. Bait peptide attracts enzyme, never lets it go 4. Modify substrate
_______ is the ONLY coagulation protein that's permanently attached to the membrane surface Tissue Factor
Contact activation on neg-charged phospholipid cell membranes is important for bradykinin generation & is involved in angiogenesis
_____ is major inhibitor of FXIIa in contact pathway C1-inhibitor
What are FXIIa's primary coagulation substrates within the contact pathway Prekallikrein, HK, FXI
What are the primary inhibitors of enzyme kallikrein within the contact pathway C1-inhibitor & a2-macroglublin
List all of the possible inhibitors of enzyme kallikrein within the contact pathway 1. C1-inhibitor 2. a2-macroglublin 3. protein C inhibitor 4. heparin-AT
List the roles of the common pathway 1. Coagulation (minor) 2. Vasoactive inflamm effects 3. Fibrinolysis 4. Complement activation
Which enzyme(s) of the common pathway play a role in vasoactive inflamm effects 1. Bradykinin 2. Kallikrein
Which enzyme(s) of the common pathway play a role in Fibrinolysis 1. Kallikrein 2. FXIIa
Which enzyme(s) of the common pathway play a role in complement activation 1. FXIIa
Which enzyme(s) of the common pathway play a role in coagulation 1. FXIa
Auto-activation of FXIIa may occur when FXII binds to neg charged surface esp in presence of ____ Zinc
What converts prekallikrein (PK) to kallikrein? FXIIa on neg-charged surface
What are kallikrein's primary substrates within the contact pathway Hageman factor (12) & HK (high MW kininogen)
How is bradykinin released from domain 4 during contact pathway When kallikrein cleaves kininogens
___ absolutely required for binding of HK to membrane surfaces Zinc
von Willebrand's factor 1. Adhesive glycoprotein made by endothelial cells & megakaryocytes 2. Extracellular vWF is found in sub endothelium & circulating in plasma in multimeric form 3. Main fxn is promote adhesion of platelets
Where is a small % of vWF stored? Weibel-Palade bodies
Weibel-Palade bodies 1. storage granules of endothelial cells 2. they store & release von willebrand factor & P-selectin thus playing role in hemostasis & inflamm
vWF fxns 1. Promote platelet adhesion to exposed subendothelium 2. platelet to platelet aggregation along w/ GPIIb/IIIa complex & fibrinogen 3. Form tight complex w/ factor VIII which prolong's VIII's half life (not as imp in dogs) stabilizes this factor
Glycoprotein Iib/IIIa complex 1. integrin complex found on platelets 2. Receptor for fibrinogen & vWF 3. Helps in platelet activation 4. Need Ca to form complex
How Glycoprotein Iib/IIIa complex is formed 1. Platelet activation released ASP & TXA2 which bind to their respective receptors 2. Incr inracellular Ca which allows complex to form
What occurs after Glycoprotein Iib/IIIa complex is formed 1. Once complex is formed it can bind to fibrinogen (factor I) & many platelets can stick together 2. Coag cascade stabilizes clot as thrombin converts soluble fibrinogen into insiluble fibrin strands which crosslink by factor XIII I make stabilized clot
Which animal's platelets does not carry large amts of vWF Dog
Type 1 vWD 1. Most common 2. all multimers present but at reduced amt
Type 2 vWD 1. More effective, large multimers absent 2. German pointers
Type 3 vWD 1. Most severe 2. all multimers absent 3. Assoc with life-threatening hemorrhagic bleeding episodes 4. Scottish terriers, Shetlands, Ches Bay retrievers, Dutch kooikers
How do you typically test for vWF 1. ELISA with concen expressed as vWF:antigen 2. 70-180% vWF;Ag is normal & unlikely to transmit dz 3. 0-49% is abnormal range 4. Don't determine bio activity or multimeric disturb
What is the global test of primary hemostasis Buccal mucosal bleeding time
What factors affect vWF:Ag levels 1. Blood drawn frm cephalic or jugular (higher in jug) 2. Strenuous exercise, EP, pregnancy
Which elements/factors inhibit Thrombosis 1. Antithrombin III bound to heparin-like molec -> inactiv thrombin & factors 10,11a 2. Tissue factor pway inhibitor (inactivates 7a & 10a) 3. prostacyclin, nitric oxide, ADP inhibit platelet aggreg 4. Tissue plasminogen activator
4 phases of wound healing inflammation, debridement, repair, and maturation
In inflamm phase of wound healing, extrinsic coagulation mechanism is activated by _____ thromboplastin released from injured cells
What initiates the transition from the inflamm phase to debridement phase during wound healing WBCs leaking from blood vessels into wounds
In Debridement phase of wound healing which cells are essential and which are not Monocytes essential, neutrophils are not
Role of monocytes in wound healing 1. Make growth factor (-> tissue form & remodeling) 2. Become macrophages in wounds at 24-48 hours
Macrophage roles in wound healing 1. Secr collagenases removing necrotic tissue, bacteria, foreign material 2. Coalesce to form multinulceated giant cells w/ phago fxn 3. Secr chemotactic & growth factors 4. Recruit mesenchymal cells to stimul angiogenesis & modulate matrix prod
Which words are used to describe repair phase of wound healing 1. Starts 3-5 day after injury 2. Macrophages stimulate DNA & fibroblast proliferation (stimul by TGF beta to produce fibronectin) 3. Incr type I collagen 4. Capillary angiogenesis 5. Granulation tissue formed
Granulation tissue in wound healing 1. formed at each wound edge, and it fills defects and protects wounds 2. barrier to infection & surface for epithelial migration 3. Source of myofibroblasts for muscle contraction
Epithelialization in wound healing 1. mobilization, migration (determined by integrins), proliferation, and differentiation of epithelial cells 2. occurs faster in a moist environment
When does epithelialization in wound healing begin 1. begins immediately (24-48 hours) in sutured wounds with good edge to edge apposition 2. in open wounds when an adequate granulation bed has formed (usually 4-5 days)
Chalone 1. water soluble glycoproteins found in epidermis 2. inhibits epithelial mitosis in normal tissue but is diminished in wounds 3. allows epithelial cells along wound margins to divide and migrate across the granulation tissue
Process of scab removal 1. epithelial cells slide fwd until wound surface covered 2. migrating cells move under scabs, make that dissolve scab base
Wound contraction in wound healing 1. Decr wound size 2. Fibroblastic invasion into the wound necessary for contraction to begin 3. Wound contraction stops when: wound edges meet, tension is excessive, or when myofibroblasts are inadequate
Maturation Phase of Wound Healing 1. Starts when collagen properly deposited in wound (17-20 days later) 2. Most rapid gain in strength occurs 7-14 days after injury as collagen rapidly accumulates in the wound 3. Normal tissue strength is never regained
What is open wound "golden period" Wounds less than 6-8 hrs old (w/ minimal trauma & contamination)
Primary Wound Closure 1. Performed only if < 6-8 hrs since injury and the wound is clean 2. Wound cleaned by lavage & debridement, good hemostasis present, & there is no tension or dead space 3. immediate suture closure of viable tissue without tension
Delayed Primary Wound Closure 1. Used for mild contaminated wounds (such as with feces, saliva, purulent exudate_ 2. min traumatized wounds w/ unsure tissue viability, edema, skin tension 3. done 2-5 days after the wound occurs 4. requires lavage & debridement while open
Primary healing Occurs with clean, incised wounds that are held together
Second intention healing 1. wound tissue unsuitable for closure techniques, large skin defects and extensive tissue devitalization, infxn, wounds older than 6-8 hrs 2. healing by granulation tissue, wound contraction, and epithelialization
Secondary Wound Closure 1. Closure after granulation tissue formed due to contaminated wounds 2. > 5 days after injury 4. Granul tissue & epithelized skin edges excised & closure performed
When is secondary wound closure okay to do 1. wound severely contaminated/traumatized 2. epithelialization & contraction won't totally close wound 3. healing by secondary intention is undesirable
Diff betw primary vs secondary hemostasis 1. Primary = small, minimal vascular injury 2. Secondary = when vascular damage is more extensive, it also undergoes secondary hemostasis
Intrinsic pathway becomes activated when Blood comes in contact with negatively charged surface
Extrinsic pathway becomes activated when Blood comes in contact with material from damaged cell membranes
Intrinsic & Extrinsic pathways converge to form Common pathway that culminates in generation of thrombin, and ultimately stable fibrin
Where are all coag factors & cofactors formed? Liver
Which coag factors are vitamin K dependent Factors 2, 7, 9, 10
Sum up Primary Hemostasis in a few sentences 1. initial vascular and platelet response to injury 2. Platelet adhesion, activation, aggregation 3. Formation of primary platelet plug
Platelet Adhesion in Primary Hemostasis 1. platelets normally don’t adhere to themselves or endothelial membranes (bc of neg charge) 2. adhesion mediated by platelet receptors 3. certain cytokines & hypoxia trigger release of vWF frm endothelial cells; vWF binds to the glycoprotein receptors
Platelet Activation in Primary Hemostasis Binding of thrombin -> platelet receptor conformational change -> starts intracellular signaling cascade -> rel Ca & thromboxane A2 -> exocytosis of dense granules
Platelet Aggregation in Primary Hemostasis 1. ADP, serotonin, thromboxane A2 activate more platelets 2. vWF frm activated platelets binds to platelet receptor GpIb/Ia -> activate more platelets & forms molec bridges 3. Gp IIb/IIIa activation allows binding fibrinogen 4. = primary platelet plug
What promotes platelet aggregation in Primary Hemostasis ADP, serotonin, thromboxane A2 activating additional platelets
Summarize secondary hemostasis Intrinsic (contact pathway) or extrinsic (tissue factor pathway) -> prothrombinase complex -> thrombin (key enzyme in hemostasis) -> fibrin (insoluble & stabilizes clot)
Summarize Intrinsic/contact pathway of secondary hemostasis 1. Kallikrein activates Factor 12 -> activates 11 then 9 then 8 2. Activated factors 8 & 9 + ca & neg charged phospholipids -> tenase complex 3. Tenase activates factor 10 4. Factor 12a also actives PK to K ->more 12 can be made
ApTT tests which part of clotting cascade Intrinsic
In secondary hemostasis, what activated factor is made at the end of the extrinsic AND intrinsic pway Factor 10
Summarize extrinsic pathway of secondary hemostasis 1. Tissue factor released frm damaged cells 2. Tissue factor binding to factor 7 leads to its factor 7's activation 3. Complex of factor 7a, Ca, TF -> Cleaving of factor X to Xa
Summarize common pathway of secondary hemostasis 1. Started by factor 10a-> prothrombinase complex made of factors 5, 2 (prothrombin) & Ca 2. This complex makes thrombin which binds fibrinogen coverting it to unstable fibrin monomers 3. monomers crosslink by factor 8a to form insoluble stable prot
How do you remember which tissue factors are involved in the extrinsic pway of secondary hemostasis 3+7 =10 1. 3 looks like the little E 2. Tissue factor (III) makes complex w/ Ca & Factor 7a to allow cleavage of Factor 10 to its activated form
How do you remember which tissue factors are involved in the common pway of secondary hemostasis 10/5=2 ....10-2=8.. 10, 5, 2, 8
What type of rodenticide is most common Anticoag rodenticides
Name the 2 most common 1st gen anticoag rodenticides 1. Warfarin & indanedione 2. Indandione rodenticides include pindone, chlorophacinone, difethialone
Name the 2 most common 2nd gen anticoag rodenticides & which is most commonly used active ingredient bromadialone & brodifacoum (most commonly used active ingredient)
How much active ingredient can be found in warfarin, difethialone (of indandione), and 2nd gens 1. Warfrain- 0.025% 2. Difethialone- .0025% 3. 2nd gen- .005%
Some plants can cause bleeding similar to whats seen in anticoag rodenticides, name them 1. Aesculus 2. Melilotus 3. Anthroxanthum 4. Gallium 5. Dipteryx 6. Trillium 7. moldy lespedeza
Meds like _____ cause same clin syndrome as anticoag rodenticides warfarin & bishydroxycoumarin
In dogs what is the half life is warfarin & brodifacoum Warfarin- 14.5 hrs Brodifcoum- 120 days or 6+- 4 days
Warfarin toxicosis, bromadialone toxicosis, brodifacoum & other 2nd-gen anticoag toxicosis duration of action in dogs 1. Warfarin toxicosis- 14 d 2. bromadialone toxicosis- 21 d 3. brodifacoum & other 2nd-gen anticoag toxicosis- 30 d
Anticoag rodenticide MOA 1. inhibition of K 1-2-3-epoxide reductase enzyme -> block vitamin K-dependent clotting factor synthesis 2. Thus affecting factors 2, 7, 9, 10 so includes intrinsic, extrinsic, common pathways
List the main risk factors assoc with anticoag rodenticide tox 1. Age (very young or old) 2. Nonrums 3. Hypothyroidism 4. High-fat diet 5. Prolonged oral ab therapy 6. preexisting hepatic dz
Clinical signs from anticoag rodenticide tox 1. Nonspecific 2. Signs usually don't appear till 3-7 days after ingestion bc coag system maintains its integrity until clotting factors already present degrade naturally 3. Most common is acute dyspnea frm bleeding into chest cavity
Clin path for anticoag rodenticide tox 1. PT & aPTT incr 2. ACT incr = hemorrhage 3. Platelet values, TCT, FDP normal until bleeding starts 4. PIVKA incr to rodenticide poisonings and other vitamin K-responsive coagulopathies
Diagnostics for anticoag rodenticide tox 1. Post-mortem analysis of liver 2. Test for anticoagulants
What is used to monitor at baseline, 48, 72 hrs to see if decontam successful or if animal did/did not ingest toxic dose; which is ideal & why; and when should this be done? 1. PT or PIVKA 2. PT better bc elevates BEFORE animal becomes clinically ill 3. Test b4 vitamin K treatment
Poisons that cause hemolytic anemia in dogs or all species 1. Allium 2. brown recluse spider 3. Naphthalene 4. propylene glycol 5. Zinc
Poisons that cause coagulopathy in dogs or all species 1. Anticoag rodenticides 2. Brown recluse spider 3. Coumarin glycosides 4. Pit vipers 5. Sulfonamides 6. Aspirin
Shock Abnormal physio state where there's inability to deliver adequate oxygen to meet the metabolic needs of the body
List the 4 types of shock 1. Hypovolemic 2. Cardiogenic 3. Distributive 4. Obstructive
Hypovolemic shock 1. Decr intravascular volume from loss or poor intake 2. Ex- bl loss, vomit, diarrhea, burns
Cardiogenic shock 1. Heart fails to provide enough cardiac output 2. Ex- Heart block, CHF, cardiac arrhythmia
Distributive shock 1. Change in vascular capacitance -> peripheral vasodilation & abnormal redistribution of blood flow 2. Ex- Anaphylaxis, neurogenic, sepsis
Obstructive Shock 1. Obstruction of outflow from heart 2. Ex- Hemothorax, aortic stenosis, heartworm 2
When there is decreased tissue perfusion, what are ways that the body ultimately tries to incr tissue perfusion 1. Incr circulating volume 2. Incr CO 3. incr fluid retention
How does the body incr cardiac output in response to decr tissue perfusion 1. Symp nerv system activated & releases catecholamines 2. Tachycardia, peripheral vasoconstriction happens -> incr CO
How does the body incr fluid retention in response to decr tissue perfusion 1. RAAS & ADH release 2. RAAS -> incr renal & water reabsorption, incr K+ excretion -> incr fluid ret 3. ADH rel -> vasoconstriction -> incr kidney tubule ability to reabsorb water -> incr fluid ret
What role does ADH (antidiuretic hormone) play when there is decr tissue perfusion Leads to vasoconstriction -> incr kidney tubule ability to reabsorb water -> incr fluid retention
How does the body incr circulating volume in response to decreased tissue perfusion Decr hydrostatic pressure -> fluid shifts from interstitial space to intravascular space -> incr circulating volume
Stages of Shock 1. Compensated 2. Decompensatory 3. Terminal
MDR1 1. Gene encoding for P-glycoprotein (ATP-dependent drug transporter) involved in transporting drugs & other toxins out of brain tissue 2. Canine version of MDR1 gene is on chromosome 14
MDR-1 1. Mutant (non-functional) form of canine MDR1 gene first seen in Collies insensitive to ibuprofen
What does it mean when dogs have MDR1 hypersensitivity 1. Adverse neuro rxns to drugs that are substrates of P-glycoprotein (ATP-dependent drug transporter encoded by MDR1 gene) 2. Hypersaliv, ataxia, blind, coma, death etc
List the P-glycoprotein substrate drugs used in Mellow Yellow 1. Doxycycline 2. Dexamethasone 3. Cyclosporin A 4. Ivermectin
Ibuprofen MOA 1. Stops conversion of arachidonic acid into prostaglandins by reversibly blocking COX enzyme axns 2. Decr prod of inflamm mediators such as PGE2, F2alpha 3. Inhib COXI enzymes (decr prod of substances that maintain normal gastric mucosal barriers, etc)
When ibuprofen inhibits COX I enzymes, what does this cause Decr in production of substances needed to maintain normal gastric mucosal barriers, renal blood flow (due to decr prostaglandins), platelet aggregation; GI signs (diarrhea, vomit, ab pain, blood in vomit within 24 hrs of ingestion)
Where are senescent/old RBCs usually phagocytosed by macrophages? Name all the options and the most common one Liver (kupffer cells), Bone marrow, Spleen (most common)
Hemolysis/RBC destruction depends on what 1. Phosphatidylserine expression on cell surface 2. Decr cell deformability (cant change form as well when going thru capill) 3. Binding of IgG and/or complement 4. Oxidative damage
When macrophages degrade erythrocytes, what is the watse product called? Bilirubin
Classic sequela of hemolytic anemia (intravascular, extravascular, both) 1. Hyperbilirubinemia (incr plasma concen of bilirubin) 2. Icterus if severe
Acute Intravascular hemolysis (AIH my acronym) Hemoglobinuria contributing factor in renal tubular necrosis (hemoglobinuric nephrosis) which occurs often with AIH
Where is primary site of extravascular erythrophagocytosis Spleen
Extravascular hemolysis Often results in splenomegaly due to incr RBC destruction by splenic macrophages
List the hallmarks of IMHA 1, Spherocytosis 2. Autoagglutination
Spherocytes 1. Made when spleen macrophages phago part of RBC plasma membrane bound w/ autoantibody 2. Decr deformability of cells so cannot go thru splenic red pulp & sinusoidal walls 3. Retained in spleen assoc w/ macrophag w/ risk of more injury & destruction
Autoagglutination 1. Due to cross-linking of abs bound to RBCs 2. Seen as clusters of RBCs under microscope 3. Macroscopically seen as grainy blood consistency
Howell-jolly body 1. Small nuclear remnant that may be incr w/ incr hemolysis 2. In healthy, low # RBCs w/ H-J rel frm marrow are quickly removed via spleen macrophages 3. If H-Js easily seen w/o reticulocytosis may = splenic dz 4. maybe incidental in cats
How can oxidative damage cause hemolytic anemia 1. Normal antioxidative pways that make reducing agents (ie glutathione, NADH, NADPH) compromised or overwhelmed
Nonregenerative anemias 1. Lack of reticulocytosis on CBC 2. Anemia of inflamm, anemia of chronic dz, iron deficiency
In which animal does reticulocytosis not occur Horse
Hepcidin 1. Acute phase prot made in liver 2. Limits iron availability 3. Hepcidin expression incr with inflame, infxn, Fe overload & decr w/ anemia or hypoxia
In common erythrocyte morphologic abnormalities: Macrocyte 1. Huge 2. Seen with regenerative anemia, FeLV, congenital in some poodles
In common erythrocyte morphologic abnormalities: Microcyte 1. Very small 2. Iron 3. Portosystemic shunts 4. Normal in akita & shibu dogs
In common erythrocyte morphologic abnormalities: Polychromasia 1. Reticulocytosis (regen anemia) 2. Bluish color
In common erythrocyte morphologic abnormalities: Basophilic stippling Lead tox, regen anemia (esp ruminants)
In common erythrocyte morphologic abnormalities: Howell-Jolly Bodies 1. Small, round, bluish/black inclusion usually off-center 2. Regen anemia, Splenic dysfunction
In common erythrocyte morphologic abnormalities: Hypochromasia 1. Incr pallor/pale & deformability 2. Iron deficiency
In common erythrocyte morphologic abnormalities: Heinz bodies 1. Pale round inclusion may bulge; stains blue with methylene blue 2. Seen when theres oxidative damage
In common erythrocyte morphologic abnormalities: Poikilocyte Nonspecific term for shape abnormality
In common erythrocyte morphologic abnormalities: Spherocyte 1. Abnorm small with uniform staining 2. Seen with extravascular hemolysis
In common erythrocyte morphologic abnormalities: Schistocyte 1. Small, irreg RBC fragment often crescent shaped 2. Seen with Microangiopathies (DIC, hemangiosarcoma, glomerulopathy) & Incr RBC deformability (eg Fe def)
In common erythrocyte morphologic abnormalities: Acanthocyte 1. Few irreg projections 2. Seen with abnorm lipid metabolism (ie liver dz), microangiopathies, incr RBC deformability
Which RBC morphologic abnormalities would you see with regenerative anemia 1. Macrocyte 2. Polychromasia (bluish color) 3. Basophilic stippling (esp in ruminants) 4. Howell-jolly body
CBC hallmarks of regenerative anemia 1. Reticulocytosis (except horse) 2. Polychromasia, anisocytosis (RBCs unequal sizes) 3. Maybe Incr MCV & decr MCHC
CBC hallmarks of nonregenerative anemia 1. No reticulocytosis 2. Maybe decr MCV & decr MCHC (Fe deficiency)
Which CBC hallmark would show no reticulocytosis: nonregenerative or regenerative anemia Nonregenerative anemia
Agglutination 1. Aggregation into clumps or masses 2. Doesn't separate when diluted with saline 3. Due to antigen-antibody complex
Coagulation 1. Forming of blood clot due to coag cascade 2. Doesn't sep when diluated with saline
Rouleaux 1. Roll of RBCs looks like coin stack 2. Occurs when incr fibrinogen concern or other changes in plasma proteins 3. Disppears when blood diluted with saline
Primitive RBCs made in _____, definitive RBCs made in _____ yolk sac; liver & later spleen and bone marrow
Primitive hematopoiesis 1. 1st phase of blood cell prod 2. makes blood elements during earliest stage of embryogenesis 3. takes place in visceral yolk sac
Hemangioblasts 1. mesodermal cells committed to starting and supporting hematopoiesis 2. arise as undifferentiated cells at primitive-streak stage and commit to making a particular cell lineage b4 blood island formation
Blood islands 1. Multiple hemangioblast aggregates 2. contains central core of unattached inner hemangioblasts (hematopoietic progenitors) surrounded by rim of spindle-shaped outer hemangioblasts (endothelial progenitors)
Definitive Hematopoiesis 1. Stage 2 in blood cell prod 2. Mainly arises from AGM (aorta-gonad-mesonephros region) which is main source of mesenchyme-derived HSCs (hematopoietic stem cells)
List (in oder) the HSCs (hematopoietic stem cells) migration pattern 1. Embryonic liver 2. Embryonic thymus 3. Fetal spleen 4. Bone Marrow
Primitive RBCs have greater affinity for oxygen than maternal RBCs.... but what animal is the exception Domestic cats
Where do hematopoietic stem cells arise from First embryonic yolk sac then fetal para-aortic splanchnopleura from which liver and bone marrow are seeded
____ is most potent endogenous neg regulator of hematopoiesis TGF-B
List the first 4 steps in erythropoiesis 1. Hematopoietic stem cell (HSC) 2. Multipotential progenitor (MP) 3. Common myeloid progenitor (CMP) 4. Megakaryocyte/erythroid progenitor (MEP)
List the steps 4-8 in erythropoiesis Burst forming unit erythroid (BFU-E) -> colony forming unit erythroid (CFU-E) -> Rubriblast -> prorubricyte/basophilic rubricyte (BR)
List the last 4 steps (9-12) in erythropoiesis Polychromatophyilic rubricyte (PR) -> metarubricyte (MR) -> reticulocyte ® -> RBC
Rubriblast Earliest precursor that can be recognized as erythroid cell
Prorubricyte similar to rubriblast except ____ It lacks nucleous
Metarubricytes have most _____ Hemoglobin
What is the main hormonal regulator of erythropoiesis & what induces its expression EPO (erythropoietin); low oxygen tension ie hypoxia
IL-3 role in erythropoiesis 1. acts on HSC and progenitor cells to induce prolif and self renewal
What mainly makes EPO Peritubular interstitial fibroblasts of kidney in adult animals
Alpha hemolysis 1. Dark green 2. Caused by hydrogen peroxide made by bacteria oxidizing hemoglobin to green methemglobin
Beta hemolysis 1. Aka complete lysis 2. Yellow or transparent 3. Streptolysin causes the complete lysis
Streptolysin 1. Enzyme made by bacteria -> complete RBC lysis; 2 types 2. Type O: oxygen sensitive cytotoxin 3. Type S: Oxygen stable cytotoxin
Streptolysin O 1. Oxygen sensitive cytotoxin 2. Interacts w/ choelsterol in membrane of euk cells (mainly RBCs, macrophages, platelets)
Streptolysin S 1. Oxygen stable cytotoxin 2. Mainly affects immune cells (leukocytes and lymphocytes)
Lancefield grouping Method of grouping catalase-neg, coagulase-neg bacteria based on their carb comp of bacteria antigens found on cell walls; used to organize families of strep
Gamma hemolysis Organism doesn't induce hemolysis
What bacteria are hemolytic E. coli (alpha); Strep (beta)
Urticaria 1. Supf version of angioedema (dermal swelling) 2. Transient vascular reaction in the superficial dermis consisting of edema 3. Manifested clinically as wheals
What is the pathophysiology of type II hypersensitivity Antibodies against self antigens
acantholysis Disruption of intercellular junctions between keratinocytes
Crust is defined as dry transudate: T or F F
Which condition is a bacterial skin disease? A. Demodicosis B. Dermatophilosis C. Dermatophytosis D. Dirofilariasis Dermatophilosis
What is inflamed in panniculitis Subcutaneous adipose tissues
What is a primary mechanism for the anti-inflammatory effects of glucocorticoids Inhibition of phospholipase A2 (PLA2)
What is the active growth phase of hair Anagen
Consider that an injection of a local anesthetic abolishes pain sensation but does not abolish touch sensation. What would be an expected component of the best explanation of this effect? Action potential conduction is more affected in C-fibers than in A-delta fibers
The pruriceptive system of vertebrate skin is richly (>75%) innervated by which of the following receptor types? Multimodal C-fibers
Most common mediator involved in acute pruritus? Histamine
Created by: NinaP183
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