Physiology Ii - Hematology

Front 1

APTT stands for?

measures ?
normal APTT time?

Back 1

- Activated Partial Thromboplastin Time (name doesn't make a whole lot of sense, b/c thromboplastin is TF of extrinsic system)
- measures INTRINSIC and common pathway

expected time 60-120 sec

AI

Front 2

Total Blood Volume (TBV)/ ADULTS:
as a R.o.T. = ???

Back 2

TOTAL BLOOD VOLUME (TBV)/ ADULTS:
~6-8% of body weight OR 60-80 ml / Kg BW

Front 3

FLUID REPLACEMENT THERAPY
how much fluid is needed (without over-infusing)?

How long before blood (fluids) reach tissues?

Back 3

R.o.T: severely dehydrated patients can be given up to the equivalent of
their total blood volume within 1. hour using crystalloids
= ~7% of body weight (or 70ml/kg)

Note: 1hr later, 75% of infused fluid will have moved out of vessels into tissues re-hydrates ECF and ICF

For Maintenance: ~same volume over 24 hours (variable)

Front 4

What layers are visible after blood is centrifuged?

Approx. % by volume?

Back 4

plasma 59%
BUFFY COAT = top layer of white blood cells and platelets, ≈ 1 %
HEMATOCRIT (=PCV) = % of total blood volume occupied by RED BLOOD CELLS, ≈ 40 % (±15% sp. dpd
*formed elements are represent by bottom two layers

Front 5

PCV

Back 5

hematocrit
OR packed cell volume = volume occupied by RBC

Front 6

plasma is made up of?

Back 6

7% proteins (albumin, fibrinogen, globulin,etc)
91.5% water
1.5% other solutes (electrolytes,etc)

Front 7

Plasma Proteins are derived from ?

Back 7

- are derived from liver (albumin, some globulins, fibrinogen) & WBC

Front 8

All formed blood elements
originate from _____; it replenishes itself and differentiates into ________.

Back 8

All formed blood elements
originate from same
pluri-potent stem cell pool ;

it replenishes itself and differentiates into 2 stem
cell lines: Myeloid & Lymphoid

Front 9

Hemopoiesis occurs in _____.



Hemopoiesis is controlled by ______?

Back 9

Hemopoiesis occurs in red bone marrow + lymphoid tissue
(before birth also in spleen, liver, thymus, yolk sac, lymph nodes)

Hemopoiesis is controlled via CSFs (colony stimulating factors), interleukins,
cytokines, thrombopoietin, erythropoietin

Front 10

Which have largest RBC: salamander, camel, ostrich, snake? Smallest?

which are nucleated? what else of nucleus?

Back 10

salamander is largest; camel has smallest

which are nucleated?
amphibians, reptiles, birds <- but RBC nucleus not functional

Front 11

examples of plasma proteins not produced in liver?

Back 11

antibodies and protein hormones

Front 12

how does protein concentration in plasma compare to interstitial fluid?

where in body are caps more permeable to protein?

Back 12

higher than interstitial fluid
(capillary wall not permeable to protein, except in liver)

Front 13

approximate proportion of body weight occupied by blood in cat and dog? also volume per kg BW?

TBV: (just to get idea of range)
In 20kg Dog?
In 5kg Cat?

Back 13

5kg cats 5%
(50ml/kg x 20kg = 1000ml = 1L)

20kg dog is ~9% or 90ml/kg body weight
(90ml/kg x 20kg = 1.8L)

Front 14

approximate proportion of body weight occupied by blood:

in 700kg cold-blood horse?
in bird?

Back 14

c/b horses with 700 kg BW, 7% or 70kg/ml:
~so TBV 49,000 ml or 49L

birds: higher 10%

*cold blooded horse is lightly muscled, and have lower hematocrit than warm/hot blooded horse b/c fewer RBC

Front 15

proportion of blood cells that are RBC?


approx. proportion of blood volume occupied by RBC's?

Back 15

90%

40%

Front 16

If goat has twice as many erythrocytes as dog, why is hematocrit so much lower?

Back 16

RBC of dog more than x2 size

Front 17

compare blood volume between active and inactive animals

Back 17

active animal has larger blood volume e.g. warm blooded horse

Front 18

OSPT stands for?

measures ?
normal OSPT time?

Back 18

OSPT = One Stage Prothrombin Time

-> measures EXTRINSIC and common pathways (expected time < 10 sec!)

OE

Front 19

Plasma Protein (PP) conc in plasma ?

Back 19

rel. stable: 7g / 100ml

Front 20

P.P. increase during ?

what are acute phase proteins?

Back 20

can increase in inflammations (e.g. globulins + fibrinogen, also ferritin <- binds iron, inhibiting microbe iron uptake)
called "acute phase proteins" (> in large animals) = absolute increase
Lab report: PCV normal & PP increased

P.P. can look increased in haemo-concentration / dehydration
= relative increase (all proteins)
Lab report: PCV & PP increased

Front 21

P.P. can be decreased during?

Back 21

can be decreased e.g. in end-stage liver disease (lack of production)
OR after blood loss

Front 22

How many O2 bind to Hb molecule?

How many Fe bind to Hb?

Back 22

Each of four heme groups bind an Fe, the four irons bind an O2 molecule
->so 4 oxygens

Front 23

What blood parameters used to monitor deyhydration?

(give a standard value for each in %)

Back 23

PP (around 7%)
PCV (hemacrit)(around 40%)

Front 24

Approx. life span of RBC in domestic animals?
cat? pig? bird?

Back 24

survival of RBCs is limited to: in most spp. is 4-5 months
cat, pig: 2 months;
birds 5 weeks

- short life span b/c lack DNA, RNA to make new protein

Front 25

Blood cell production in fetus?


Blood cell production in adult?

Back 25

fetus - liver, spleen

adult - bone marrow...particularly flat bones (sternum, ribs, pelvis) !
- if challenged, liver and spleen contribute

Front 26

Mature RBC are approx. ____% hemoglobin

Back 26

Mature RBC are ~33% hemoglobin

Front 27

Name stages of erythropoiesis?

Back 27

(1) Pluripotent stem cell
Erythropoietin stimulates commitment from (2) Myeloid stem cell into (3) CFU/erythrocyte (4) rubriblast (5) reticulocytes. (6) erythrocyte

Front 28

Originate from Myeloid stem cells:

Back 28

* RBCs
* Platelets
* Monocytes
* Granulocytes

Front 29

- takes ___ days from stem cell to reticulocyte

during this time: (3)

What comes before reticulocyte?
What change signifies the formation of a reticulocyte?

Back 29

- takes 4-5 days from stem cell to reticulocyte

during this time:
- cells become smaller
- Hb content increases
- nucleus condenses and extruded

Front 30

extrusion of nucleus correspond with what precursor?

where are found? what changes do they undergo in addition to loss of nucleus? time frame?

Back 30

extrusion of nucleus = reticulocyte

RETICULOCYTES migrate
from b.marrow into CIRCULATION. & mature within 1-2 days to mature RBCs = loss of remaining RNA material which means loss of HB synthesis ability

Front 31

normal Reticulocyte count/blood: ____% ?

Exception?

Back 31

normal Reticulocyte count/blood: 1-2%

Exception: healthy horses and ruminants only release mature RBCs -> NO reticulocytes
circulate in healthy ones

Front 32

Erythropoiesis requires adequate supplies of ? (5)

Back 32

Erythropoiesis requires adequate supplies of: iron, folic acid and Vit B(2,6,12)

Front 33

RETICULOCYTOSIS

(give time frame, etc)
when highest?
how long to see affect?
example of max proportion compared to mature RBC?

Back 33

- elevated lvl of reticulocytes appear in circulation (e.g. up to 25 % in dogs) if blood loss has occurred
- usually change apparent 3-5 days after challange, w/peak after 7 days

Front 34

Can immature RBC in circulation contribute to oxygen carrying capacity?

Back 34

Although immature, these cells contribute to O2 carrying capacity while still increasing their Hb content

Front 35

Removal of aged RBCs occurs where?

Back 35

- rupture during SPLEEN passage
(tight traberculae) and are absorbed by macrophages
- or are selectively removed by Mononuclear – Phagocytic System
(Macrophages in spleen, liver, bone marrow!)
~ so three potential places

Front 36

What parts of RBC do the macroph. recycle?

Back 36

Globin (amino acids)
Protoporphyrin (heme after iron removed)
Iron

note: Protoporphyrin then becomes billirubin

Front 37

Fate of heme group?

Back 37

- Fe removal to become Protoporphyrin
- converted to Bilirubin
- released into circulation, and excreted by liver in bile juice

Front 38

Iron re-cycling: ?

hint: what is name of plasma protein for transport of iron? for storage?

Back 38

- iron is removed from Heme, released into circulation and binds to plasma protein to form TRANSFERRIN = Fe-transport form; iron can either go to liver for storage OR bone marrow where transferrin binds strongly with erythroblastic receptors, Fe is released into myeloblast cells for Hb synthesis
- Transferrin can also release Fe into any other tissue, i.p. liver; Fe then binds to intracellular protein to form FERRITIN = Fe-storage form; is released from storage when needed

Front 39

ferritin

Back 39

protein-iron complex (plasma protein) of macrophages from liver, spleen, and b.marrow

Front 40

transferrin?

Back 40

in blood, iron released (from heme) is transported in the protein-iron complex "transferrin"
to liver for storage OR b.marrow to be reused in hemoglobin synthesis

Front 41

If ferritin stores are full, any excess iron is stored as nearly insoluble _____?
(liver, pancreas, heart) -> can lead to toxic cell damage

Back 41

excess iron is stored as nearly insoluble HEMOSIDERIN

can lead to toxic cell damage
(Hemosiderosis / Iron-Storage-Disease)

Front 42

ERYTHROPOIETIN (EPO)
what does it do?
where made?
where does it go?

Back 42

- controls rate of RBC production
- made in kidney
- when low O2 sensed by RENAL tubular receptors , production of EPO increases
- EPO then goes to b.marrow

Front 43

Name three lab parameters for evaluating erythron and anemia

Back 43

MCV
MCHC
MCH~Mean Corpuscular Hb

Front 44

Anemia

Back 44

Anemia = deficiency in oxygen carrying capacity

Front 45

hemolytic anemia

causes?
regenerative?

Back 45

hemolytic anemia is when RBC destroyed so rapidly that bone marrow is unable to replace them

can be caused fragile RBC due to inherited diseases, etc.

macrocytic-hypochromic, regenerative

Front 46

Characterize dyshemopoietic anemias caused by nutritional deficiencies:

Where is this common?

Back 46

Dyshemopoietic anemia = non-regenerative
Nutritional deficiencies,e.g. LACK of IRON: cells cannot produce sufficient Hb (hypochromic = pale color) and become nonregenerative, MICROCYTIC (small)

Commonly in piglets, b/c milk is low in iron and grow quickly

Front 47

MCHC

what are units?

Back 47

1 of 3 RBC PARAMETERS
MCHC = Mean Corpuscular HEMOGLOBIN Concentration in %
~ describes the Hb content in a deciliter of RBCs
- MCHC = Hb x 100 / Hct = g hemoglobin / dL blood

normochromic = normal conc. of Hb within RBC = 33%
hypochromic = low conc.of Hb, pale in color e.g iron deficiency;immature RBCs
hyperchromic = beyond satur. point, artifact due to hemolytic sample

Front 48

hemorrhagic anemia?

causes?
regenerative?
reticulocyte %?

Back 48

- hemorrhagic anemia is due to blood loss and blood cell loss.
- it is regenerative, so reticulocytes up and blood cells present tend to be macrocytic-hypochromic

Front 49

MCV

Back 49

MCV = Mean Corpuscular Volume (of RBC) in femtoliter
~describes size of 1 RBC!!

MCV (femtoliter per CELL)
= Hct (%) x 10 / RBC (cells/liter)
= Hct% x 10 x 1L / cell <- dividing by fraction so units flip

Front 50

If antibodies not present, the recepient of blood (with different antigen),...

Back 50

If antibodies not present, the recepient slowly develops antibodies after 1st transfusion; initially only mild delayed reaction.

2nd transfusion? gloves are off...

Front 51

What happens to RBC numbers at high altitude?

Back 51

- each RBC transports less O2
- therefore more EPO made, but take couple days RBC to be made

Front 52

5 steps of hEmostasis?

What is primary hemostasis?
What is secondary hemostasis?

Back 52

Hemostasis = sequence of responses that stop bleeding

1. vascular spasm
2. platelet plug formation = primary hemostasis
3. blood clot formation = coagulation = secondary hemostasis
4. healing
5. clot removal = fibrinolysis

Front 53

another word for platelets?

Back 53

thrombocytes

Front 54

BLOOD TYPING

Back 54

= determination of the RBC antigens present in an individual;
done to determine universal donor animals

Front 55

universal donor in dog should be?

Back 55

e.g. DOG: should be negative for DEA 1.1; 1.2 and 7
(because these are the strongly antigenic groups)

Front 56

CROSS MATCHING
Major?

Minor?

Back 56

MAJOR: expose Donor’s RBCs to Recipient’s plasma and observe for agglutination

MINOR: expose Recipient’s RBCs to Donor’s plasma and
observe for agglutination

Front 57

platelets derived from ?

Back 57

Origin: derived from bone marrow megacaryocytes
(pluripotent stem cell – myeloid stem cell – CFU/Meg –
megakaryoblast – megakaryocyte – fragmentation into hundreds of platelets); controlled by hepatic thrombopoietin

Front 58

platelets contain?

Back 58

- contractile proteins (actin, myosin, thrombosthenin)
- ADP, ATP
- Prostaglandins, serotonin, clotting factors, endothelial growth
factors, etc
- Calcium

Front 59

STEP 1 of hemostasis: Vasospasm is caused by?

What is main point of this?

Back 59

is caused by

- Immediate release of ENDOTHELIN from damaged cells
- later: release of THROMBOXANE A2 (= prosta-
glandin derivative important in next step) and serotonin (vasocontrictor) from platelets

- myogenic contraction of damaged smooth muscle cells

-initial step of vasoconstriction to minimize additional blood loss

Front 60

How long can vasospasm last?

Back 60

minutes to hours

Front 61

What releases von Willebrand Factor (vWF)?

Back 61

Damaged endothelial cells!

Front 62

___ promote vasospasm )?
hint: (step 1 of hemostasis)

they are released from?

Back 62

Serotonin and Thromboxane A2

platelets prior to plug form.

Front 63

difference between hemorrhagic and hemalytic anemia?

Back 63

- hemalytic disorders arise when RBC are lysed prematurely

- in hemarrhagic anemia, the RBC are not being lysed, but are lost along with plasma/fluids..

- in both cases, cells being replaced but low hb and increased # of immature RBC lead to anemia

Front 64

Types of dyshemopoietic anemia and examples:

Back 64

All are non-regenerative.
1. Nutr.deficiencies e.g. lack of iron
- weird b/c microcytic
2. Anemia of chronic (imflammatory) disorders = ACD or AID e.g. FeLV, Ehrilichia, cancer, tissue necrosis
3. Chronic renal disease leading to lack of EPO
4. Drug-related suppression, e.g. by estrogene

Front 65

STEP 2: Platelet plug formation
started when...?

~describe the course of events:

Back 65

Endothelial Damage / Exposure of Collagen:
- Damaged endothelial cells release von Willebrand Factor
- vMF binds to exposed collagen fibers and cell membrane (conf. change), serves as receptor for platelets, which degranulate, releasing ADP, serotine, thromboxane A2

Front 66

Characterize dyshemopoietic anemias caused by ACD:

Where is this common?

Back 66

- anemia of CHRONIC (inflammatory) disorders = ACD or AID
- seen in chronic infections, FeLV, Ehlic., inflammations, cancer, tissue necrosis

-release of toxins, e.g. CYTOKINES or Tumor Necrosis Factor, which suppress EPO
- fewer RBCs are released (but remaining are normal)
- typically normocytic/ normo- chromic

Front 67

____ attract more platelets?


they are released from?

Back 67

ADP and Thromboxane A2 released from platelets

(part of positive feedback during form. of plug)

Front 68

When do hemorrhagic (and hemolytic) anemias can become chronic disorders?

Back 68

exhaustion of iron stores after long stimulation

eventually become non-regenerative anemias

eg. GI ulcers, parasites

Front 69

What are consequences of anemia?

Back 69

- REDUCED TISSUE OXYGENATION
- anaerobic metabolism, low ATP, so Na/K pump down, cell function down
- increased lactic acid, metab. acidosis, cardiotoxic

Front 70

How does body compensate for anemia?

Back 70

- increased EPO
- hyperventilation
- vasodilation to vital organs, vasoconstriction to periphery
- HR up, etc

Front 71

What happens when Na/K pump down?

Back 71

intracellular Na - up

extracellular potassium up

because repolarization not occurring properly

Front 72

How does inflammation affect the size of the buffy coat?

Back 72

incr. in WBC, so size of buffer coat increases

Front 73

1 L of blood = ?

Back 73

1 kg

Front 74

A huge increase in the buffy coat can be a sign of what?

Back 74

leukemia

Front 75

If ferritin stores are full, an excess Fe is stored as nearly insoluble ___. This can lead to toxic cell damage.

Back 75

Hemosiderin

Front 76

sequence of responses that stop bleeding called?

Back 76

Hemostasis

~it is fast, localized, and carefully controlled

Front 77

Erythropoisis is controlled by...

Back 77

tissue oxygenation

Front 78

Clinical signs of dehydration: (not asking about blood tests, but rather physical characteristics one might find examining dehydrated animal)

Back 78

* Turgid mucous membranes
* Increased Capillary Refill Time
* Eyes sunken in
* Slow recoil to skin test

Front 79

When Transferrin releases Fe into a tissue, Fe binds to an intracellular protein to form...

Back 79

Ferritin

Front 80

Main function of Erythrocytes (RBCs)

Back 80

exchange of gases, regulation of blood pH

Front 81

Why does erythropoesis shift from all bones to only the marrow of flat bones?

Back 81

B/c as the animal matures, the marrow of long bones fill with fat.

Front 82

Plasma proteins are derived from...

Back 82

liver and WBC

Front 83

Carries fat soluble substances since most of plasma is H2O.

Back 83

Albumin

Front 84

Plasma proteins are essential in maintaining...

Back 84

osmotic pressure

Front 85

Average diameter of a capillary

Back 85

3um

Front 86

Size of RBC

Back 86

7um in diameter

Front 87

ERYTHROPOIESIS is controlled by TISSUE OXYGENATION:

where is low level detected?
Where EPO made?

Back 87

Withdrawal of RBCs -> HYPOXIA -> RENAL tubular receptors -> ERYTHROPOIETIN (EPO) release -> Bone Marrow -> stimulation of Erythropoiesis -> release of new RBCs

Front 88

Part of RBC that is converted to bilirubin, released into circulation, and excreted by the liver in bile juice.

Back 88

Protoporphyrin

Front 89

Part of RBC reused for protein synthesis?

Back 89

Globin

Front 90

RBCs in fish

where made in bony fish?
in cartilaginous fish?

Back 90

* nucleated
* produced in spleen and liver (bony fish)
* produced in circulation in cartilaginous fish

Front 91

what is responsible for recycling most RBC parts?

Back 91

macrophages

Front 92

In healthy animal, every day approx. what % of all RBCs die / are removed and have to be replaced ?

Back 92

1% everyday

Front 93

NSAIDs

Back 93

Non-steroidal anti-inflammatory drug
e.g. ibuprofen and aspirin

prostaglandin synthesis inhibitors,
prostaglandins cause vasospasms and attract platelets

used for anticoagulation to prevent excessive clotting

Front 94

increase in RBC numbers

Back 94

Polycythemia

Front 95

Primary Polycythemia

Back 95

Primary Polycythemia = P. vera (rare)

lack of feedback control -> uncontrolled RBC production (myeloproliferative disorder) -> hematocrit can increase upto 60-70% -> high viscosity -> reduced blood flow but: sight hounds have naturally high PCV values

Front 96

Secondary Polycythemia

how common?
where/when does it occur?
what changes?

Back 96

2^ polycythemia (common)
= physiological response to oxygen deficiency due to e.g. high altitudes, cardiac failure, lung diseases -> Hct increases by a few %; plasma unchanged

Front 97

Transient Polycythemia

Back 97

Splenic contraction due to excitement & exercise seen in horses, cats, sight hounds:
-> elevated PCV, but normal plasma proteins)
NOT pathological!

Front 98

type polythemia that is very common?

Back 98

"Relative Polycythemia” (very common)

is not a true polycythemia, but is caused by:
- dehydration = fluid loss -> all blood components become more concentrated = hemoconcentration -> typically shows as elevated PCV and elevated plasma protein levels

Front 99

Lassie, an elderly *****, suffering from uterine cancer and has become anemic.
What type anemia? Likely cause?

~characterize and describe RBC's:

Back 99

Dyshemopoietic anemia (non-regenerative): specifically of chronic disorders -> release of toxins e.g. tumor necrosis factor (or cytokines) which suppress EPO -> fewer RBCs released but remaining normocytic/ normochromic

Front 100

Concentratoin of RBCs

Back 100

5 million / ul

Front 101

Originate from Lymphoid stem cells:

Back 101

* B-lymphocytes
* T-lymphocytes

Front 102

Conc. of platelets in blood?


Half-life?

Back 102

150.000 – 300.000 / ul


ca 10 days

Front 103

explain how RBC could be hyperchromic?

Back 103

can't be; just artifact when blood is analyzed, elevated b/c of residual hemoglobin floating (from dead cells)

Front 104

Femtolitre

Back 104

unit volume equal to 10^(−15) liter

Front 105

during platelet plug, this glue-like substance to promotes adhesion

Back 105

4. platelets release ADP and Fibronectin -> glue-like substance to promote adhesion

Front 106

Platelet plug: loose plug is formed within _____ to seal off the injury site

Back 106

1-2 minutes

Front 107

Name 3 platelets factors release by platelets that involved in clotting:

Back 107

(III, V and VIII)

Front 108

Why does calcium help with clotting?

Back 108

Most clotting factors negatively charged, so Ca+2 helps bring in.

Front 109

______ lead to formation of a Prothrombin-Activator Complex?


COMMON pathway begins _____?

Back 109

EXTRINSIC and/or INTRINSIC pathway, each produces unique factors important in activating PAC.

COMMON pathway begins activation of Prothrombin to Thrombin via Prothrombin-Activator Complex
(represent merger of ext/intrinsic pathways)

Front 110

factors found in both intrinsic and extrinsic pathways?

Back 110

X, V, Ca

Front 111

Factor XII activates what?
leads to?
which factors involved in cascade?

Back 111

activates an enzymatic cascade of INTRINSIC (inside blood vessel or plasma based) system (kallekrein, factors XI, IX, VIII, X, V, Ca) leading to P.A.C.

note: X, V, Ca found in both

Front 112

which is plasma-based pathway during stage 1 of clot formation?

what happens during this?

Back 112

INTRINSIC SYSTEM (inside blood vessel)

Change in surface charge of
endothelial membranes (neg. charge in cell released) binds and activates Plasma Factor XII, e.g. caused by inflammatory reactions (endotoxins); activated platelets; contact with glass surface (bleeding not necessary!)

Front 113

which is tissue-based pathway during stage 1 of clot formation?

Back 113

EXTRINSIC SYSTEM: comes from outside blood vessel, membrane disrupted

Injured tissue expresses
Tissue Factor

Front 114

What is Tissue Factor?

What is it part of?
What does it activate?

Back 114

Injured tissue Factor (Thromboplastin), of extrinsic pathway, activates an enzymatic cascade (factors VII, X, V, Ca) leading to P.A.C

note: extrinsic comes from outside blood vessel, membrane disrupted

Front 115

Which pathway (intrinsic or extrinsic) of clot form. is faster and more powerful?

Back 115

EXTRINSIC SYSTEM (tissue-based)
is only 15-30 second long.

~in contrast, Intrinsic system (plasma-based) takes 1-6 min

Front 116

Which enzyme of clot formation depends relies of vitamin K?

Name Vit K antagonist..what does it cause?

Back 116

Prothrombin

Coumarin = Vit K antagonist -> impairs liver synthesis of several clotting factors incl. Prothrombin

Front 117

Prothrombin

Back 117

- proenzyme or inactive enzyme precursor, converted by P.A.C. to active thrombin
- is a hepatic alpha globulin
- its liver synthesis is Vit K dependent
- attaches itself to activated platelets

Front 118

Is factor XII a plasma or platelet factor?

Back 118

Plasma Factor, of plasma-based INTRINSIC SYSTEM

activates an enzymatic cascade (kallekrein, factors XI, IX, VIII, X, V, Ca) leading to PAC

Front 119

What kind of factor is Thromboplastin?

identify any related related factors..

Back 119

Tissue Factor, expressed by injured tissue

activates enzymatic cascade of extr.sys. (factors VII, X, V, Ca) leading to PAC

Front 120

What polymerize into long fibers and X-link into meshwork w/i and around the platelet plug?

Bonus: what is time frame?

Back 120

FIBRIN, this meshwork = STABLE CLOT

-> bleeding stops
(within 3-6 min after injury)

Front 121

How is FIBRIN formed?

Back 121

Thrombin hydrolyses FIBRINOGEN (=hepatic soluble protein; already bound to activated platelets) into FIBRIN monomers

Front 122

CLOT RETRACTION

Back 122

W/i the next 30 minutes after stable clot (fibrin meshwork around plug), platelets contract more and pull fibrin threads together
-> clot tightens and pulls edges of injured blood vessel together

Front 123

SERUM vs plasma?

Back 123

SERUM = Plasma minus clotting factors

~blood fluid that remains after hemostasis has occurred is serum

Front 124

Hemostasis: Healing

Back 124

Hemostasis: Step 4
- fibrin meshwork serves as scaffolding for fibroblasts, stim. by platelet derived endothelial GF.
- wound healing / scar formation begins

Front 125

Fibrinolysis

what is it?
time rame?
enzymes involved?

Back 125

Hemostasis: Fibrinolysis = removal of clot (1-2 days after clot formation)

tissue-Plasminogen Activator = tPA
activates hepatic plasma factor Plasminogen to PLASMIN = proteolytic enzyme
- plasmin nibbles at fibrin fibers

Front 126

PLASMIN

Back 126

PLASMIN = proteolytic enzyme

- plasmin hydrolyses fibrin fibers + clotting factors! into FDPs (Fibrin Degradation Products);

Front 127

FDPs are removed by

Back 127

Fibrin Degradation Products are removed by macrophages

Front 128

- _____ inhibit platelets adhesion


- secreted by ??

Back 128

PROSTACYCLIN and Nitric Oxide -> inhibit platelets adhesion

secreted by intact endothelial cells and WBC

Front 129

What limits fibrin formation and positive feedback?

Back 129

Fibrin binds Thrombin -> limits fibrin formation and positive feedback

(remember normally thrombin hydrolyzes fibronogen to form fibrin monomers, as well as +f/b of int/ext.systems)

Front 130

* ANTI-THROMBIN III

* ______from ____ combines with Anti-thrombin III and greatly augments its effectiveness

Back 130

ANTI-THROMBIN III (α globulin) deactivates Thrombin and other clotting factors

Heparin from Mast Cells / Basophils increases A-TIII's effectiveness

Front 131

In vitro anticoagulation

Back 131

Calcium binding agents (e.g. citrate, oxalate, EDTA), heparin

Front 132

In vivo anticoagulation

Back 132

Heparin, Vit K antagonists, prostaglandin synthesis inhibitors (NSAIDs)

Front 133

4 parameters for testing Hemostasis

Back 133

1. Platelets counts
2. (Mucosal) Bleeding Time / in vivo
3. OSPT = 1 Stage Prothrombin Time
4. APTT = Activated Partial Thromboplastin Time

Front 134

(Mucosal) Bleeding Time

what does it test?

Back 134

TESTS PLATELET PLUG FORMATION (not clotting)
*stop time until bleeding stops after standardized small incision into
skin or mucosa (expected time 1-5 min)
-> measures functional ability of platelets and vMF to plug minute injuries

Front 135

OSPT

expected time?
what is added?

Back 135

1 Stage Prothrombin Time:
-> measures EXTRINSIC and COMMON pathways
(expected time < 10 sec)

- measures clot formation in citrated plasma after addition of Tissue Factor, Platelet Factors and calcium

Front 136

APTT

Back 136

APTT = Activated Partial Thrombo- plastin Time
- measures INTRINSIC and common pathway <- measures clot formation after clean venipuncture in citrated plasma and addition of contact activator (diatomaceous earth), Platelets Factors and Calcium
(expected time 60-120 sec)

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heparin

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anticoagulant; decrease clotting ability of blood and help prevent harmful clots from forming.

heparin will not dissolve blood clots already formed, but may prevent clots from becoming larger and causing more serious problems.

(heparin is strong acid and - charged, but physiology processes it involves are unclear)

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Thrombocytopenia

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decreased production (bone marrow; drugs; FeLV) or increased destruction (immune-mediated) or consumption

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von Willebrand’s Disease (Form I,II,III)

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= most common bleeding disorder in animals due to genetic lack / insufficiency of vWF -> platelets fail to adhere to injury sites -> spontaneous bleeding (or ); clinical signs can be mild / severe / fatal; described in ca 60 breeds of dogs with highest
prevalence in Dobermans

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Vit K deficiency / Rodenticide poisoning

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Coumarin = Vit K antagonist -> impairs liver synthesis of several clotting factors incl. Prothrombin

Causes hemorrhagic anemia, regenerative so macrocytic, hypochromic, reticulocytes up, PP down, APTT prolonged, OSPT prolonged

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How much blood can you take from an animal
without endangering it?

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1% of Body Weight
(or 10 ml/kg)

max (and i'm going out a limb here guys) 2% in healthy donor
animals (or 20ml/kg)

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where do RBC get energy?

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GLUCOSE dependent

energy gain depends on anaerobic glycolysis (no mitochondria = no Krebs cycle, no beta oxidation, no ETC)

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Thrombosis

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clotting in an unbroken blood vessel, e.g. due to stasis, atherosclerosis (cholestoral build up), trauma, parasites, tumors if thrombus dislodges -> embolisms = blocking of blood vessels -> ischemia

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give example of Thrombosis

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Aortic Thromboembolism /cats (aka Saddle Thrombus) due to myocardial diseases -> thrombus formation in left atrium -> embolism into aorta -> often lodges at caudal trifurcation, blocking blood supply into iliac arteries

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petechial

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purple spot on the body, caused by a minor hemorrhage

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Ecchymosis

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subcutaneous purpura larger than 1 centimeter or HEMATOME, commonly called a bruise. It's pretty much same as a "petechia". It can be located both in skin as well as in mucous membrane.

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Thrombopoietin

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Hormone produced mainly by liver and kidney that regulates production of platelets by bone marrow; stimulates production and differentiation of megakaryocytes, the bone marrow cells that fragment into large numbers of platelets

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Are Fibrinogen, prothrombin, factor VIII,
von Willebrand factor acute phase proteins?

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Yes b/c increase during inflammation; these are coagulation factors, trapping invading microbes in blood clots.

There are many others like Plasminogen, various globulins, complement factors, ferritin, etc.

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If O2 dissociation curve shift to right?

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If shifts to right, O2 more likely to dissociate e.g. if pH down

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Physio I Review:
CO2 transported in blood mostly as ?

*skip this question until know everything else*

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Bicarbonate HCO3- , 70% of time

w/Hb, 23% of time

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Physio I Review:

Describe path of CO2

*skip this question until know everything else

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-Leaves tissues to ECF, thru capillary wall where enters RBC still as CO2
-CA in RBC, converts W + CO2 --> HCO3- and H+.
- H+ binds to Hb and Cl- uptake drives HCO3- release into plasma