Hemostasis, Hemorrhagic disorders and thrombosis

Question 1

Single blood supply vs dual blood supply, which one has what kind of infarct?

Answer 1

single = white

dual = red

Question 2

What does Thrombin do?

1) what factor is it again?
2) what does it do?

Answer 2

2A

convert fibrinogen to fibrin at the last step of the cascade

activates platelets

activate receptors on inflammatory cells and endothelium

Question 3

Someone presents with a swollen leg, but not the other. After a blood culture you notice an elevation of IgE. What is your diagnosis?

what is it the most common thing?

Answer 3

Filariasis – helminths infection (Wuchereria)

it’s the most common round worm infection

Question 4

thrombocytopenia

1) what is the mechanism
2) what is the platelet count like
3) is there platelet adhesion?
4) is there platelet aggregation?

Answer 4

Loss or impaired production of platelets

Low

Yes

Yes

Question 5

You wan’t to stop someone from clotting too much, what are you going to give them?

additionally, these people can also overdose on this during suicides

what physiologically happens?

Answer 5

aspirin.

no platelet aggregation

Question 6

Glanzmann’s Thrombasthenia:

1) what is the mechanism
2) what is the platelet count like
3) is there platelet adhesion?
4) is there platelet aggregation?

Answer 6

Abnormal GpIIb-IIIa

Normal

Yes

No

Question 7

What kind of thrombi is associated with strokes?

what about heart attacks?

Answer 7

white thrombi

Question 8

why are our lungs edematous in heart failure?

Answer 8

as your left ventricle stops pumping, there’s a congestion happening.

immediately upstream of the left chamber is the lungs! so pulmonary circulation is congestion

so they start leaking fluid into the pleural parenchyma and the pleural space?

Question 9

when would alterations in blood flow occur that can result in higher risk of thrombosis? (5 things)

1) when could this occur normally? what can it lead to?
2) what can this #1 lead to?
3) what are 2 pathological region?
4) what about the heart, what can happen after a heart attack?
5) what about someone with generalized heart problems?

Answer 9

Normal bifurcations

internal obstruction (atherosclerotic plaque formation)

Dilated vessels / aneurysm or hemorrhoids.. hemorrhoids are dilated static vascular channels.

external compression –> if we have a heart attack, the myocardial wall doesn’t contract.. this coronary artery is pushed against by dead myocardium –> obstruct

AFIB –> it just kind of vibrates a little bit rather than full on contract so you can have an increased risk of thrombosis

Question 10

What are the three factors influencing infarcts?

explain each

Answer 10

anatomy of vascular supply –> availability of alternative blood supply is the most important determinant if occlusion will cause damage (single or dual blood supply).. single = usually tissue death, dual = less likely for infarction

rate of occlusion –> slow developing are less likely for infarction because of collateral pathways for perfusion form.

tissue vulnerability to hypoxia –> neurons undergo irreversible damage in 3-4 minutes. myocardial cells –> 20-30 mn.

Question 11

when do you think that someone has a primary hypercoaguable problem?

Answer 11

they have an initial event: DVT, PE, they’re young, strong family history

Question 12

What are the hallmarks related to heart failure and edema?

Answer 12

soft tissue pitting edema

pulmonary edema

Question 13

Alterations in blood flow and increased risk of thrombosis?

Answer 13

laminar flow is normal, but it changes to turbulent flow which is very bad

you swish and swirl the blood and factors associated with creating a platelet plug, which results in endothelial damage

Question 14

What is the name for the fatal pulmonary embolus? why is it fatal?

smaller emboli travel where and present with what?

Answer 14

Saddle Embolus –> super big –> instantaneous right heart failure

more peripherally of the lung, present with SOB

Question 15

Explain an amniotic fluid embolism

1) what happens
2) what does the mother go through?
3) what do you see histologically?

Answer 15

amniotic fluid is introduced into the mothers blood stream.

anaphylactic reaction –> the mother goes into shock, sudden dyspnea, cyanosis (because it’s foreign components)

squamous cells, hair, fat, mucus in the vessels.

Question 16

Weible Palade Bodies are found where?

if there’s a tumor and you see it on a slide, what kind of tumor is it?

what do they look like?

what do they release?

Answer 16

endothelial cell

vascular tumor

cucumbers

VWF + P-Selectin

Question 17

What are the different types of emboli?

Answer 17

Thromboemboli (blood clot)

Fat/marrow emboli

Air emboli

Septic emboli

Amniotic fluid emboli

Question 18

What is Bernard Soulier Syndrome?

what’s going to be the clinical presentation?

what’s going on under the microscope?

what’s the mnemonic?

Answer 18

Lac of Gp1b receptor on the platelet –> can’t bind to VWF

they have bleeding problems

mild thrombocytopenia with ENLARGED platelets

Bernard Soulier are Big Suckers

Question 19

What happens if you damage endothelium? what three things tell you that the endothelium has gone from antithrombotic to prothrombotic?

Answer 19

it gets deranged and switches from antithrombotic to prothrombotic

decreases NO activity, increases activation of adhesion molecules

downregulates thrombomodulin (so no protein C, so no anticoagulation)

tPA is inhibited (tissue plasminogen activator) –> this is due to the secretion of Plasminogen activator inhibitors (PAI)

Question 20

Edema is most likely what kind of fluid?

If you have inflammation, what kind of fluid do you have?

Answer 20

transudate

exudate

Question 21

You have a normal PTT but an abnormal PT. what factor is affected?

Answer 21

7

Question 22

Heparin-induced thrombocytopenia

1) What kind of disease process is this? be specific! why is this important?
2) what is the normal process for people with giving heparin?
3) what about abnormal?
4) why is it called thrombocytopenia if that’s not how it works?

Answer 22

hypercoaguability –> Secondary (acquired) physicians do this on accident

1) we give someone heparin, and this binds to PF4… this causes coagulation.. which is normal

HOWEVER in some patients it freaks out their immune system, produces IgG –> starts cross linking it with Fc receptors on platelets –> the platelets release more PF4 –> cycles

so you are cycling and using more and more platelets so excessive coagulation.

you end up having low amounts of platelets because it’s taking it out of the total pool. using everything up

Question 23

What does the extrinsic pathway involve?

what “time” is it associated with?

why is it called the extrinsic pathway?

Answer 23

7 –> 10 –> thrombin –> fibrinogen –> fibrin clot

Prothrombin (PT)

IT NEEDS to be activated by a factor extrinsic to the blood –> Tissue factor

Question 24

What is shock?

what are the 5 types?

Answer 24

Body needs more oxygen than it actually can get

cardiogenic shock –> heart isn’t pumping adequately

hypovolemic shock –> not enough volume in your vessels

systemic inflammatory response syndrome –> body is very high maintenance

neurogenic –> decreased vascular resistance due to autonomic disruption

anaphylactic –> IgE mediated decrease in vascular resistance

Question 25

What is the APCR test?

Answer 25

active protein C resistance test 1) normal patient, add snake venom for it to clot. then you add more and more concentrations of protein C and it takes longer and longer to clot 2) if you do the same with someone with this problem, they will not respond to more and more... it'll clot

Question 26

What is the highest risk of acquired (secondary) cause of hypercoaguability that gives people a high risk of thrombosis? what about women that are under the age of 30?

Answer 26

prolonged bed rest or immobilization this is why people are giving anticoagulants to patients on bed rest, we don't have... compression socks, etc. Oral contraceptive pills --> estrogen increases risk of thrombosis

Question 27

Some factors of the coagulation pathway are produced in inactive forms. what activates them to active forms and what are they called? why do they need this? considering what's in this pathway, what is vitamin K needed for

Answer 27

2,7,9,10, protein C, protein S Vitamin K Vitamin K is needed to make the precursor able to bind calcium, without calcium, those factors are useless --> so these have to use a vitamin K dependent system of carboxylation. since 2,7,9,10 are all for coagulation, protein C and S are for anticoagulation, so it's important for both!

Question 28

What is Virchow's Triad? which feed into each other and why?

Answer 28

risk factors for thrombosis 1) endothelial injury 2) hypercoaguability 3) abnormal blood flow abnormal blood flow and endothelial injury because turbulent flow leads to scraping of the endothelium from the platelet factors

Question 29

An individual presents with the following symptoms: mucosal bleeding, coughing up blood, bleeding time is up. after bloodwork you find they have a deficiency in GP2B3A. what is happening and what is this condition called?

Answer 29

can't cross link with fibrinogen or aggregate platelets Glanzmann Thrombasthenia

Question 30

Why is the healthy endothelium described as a potent antithrombotic mediator? 4 major reasons*****

Answer 30

Endothelium 1) just being there and intact covers up tissue factor (needed to activate extrinsic) 2) inhibits platelets by releasing prostacyclin, NO, and Adenosine diphosphatase (remember ADP is released to increase aggregation of platelets) 3) anticoagulation --> thrombin sees a normal endothelial cell, it'll bind to the endothelial thrombomodulin... this will create active protein C 4) fibrinolysis via t-PA

Question 31

Explain White Infarct 1) where does it occur 2) what kind of tissue 3) what kind of circulation and give examples

Answer 31

arterial occlusion in solid organs --> super dense tissue --> limits the seepage of blood from adjoining capillary beds end-arterial circulation --> heart, spleen, kidney

Question 32

We have activation that has happened, what happens during aggregation? what is the final result

Answer 32

the conformational change in Gp2b-3a complex allows for binding of fibrinogen and cross linking to occur to allow for aggregation a WEAK platelet plug

Question 33

Someone is diagnosed with antiphospholipid antibody syndrome what explains why they are having frequent miscarriages? what false-positive test would they have that could throw physicians off? what's the difference between primary and secondary AAS?

Answer 33

antibody-mediated interference with the growth and differentiation of trophoblasts --> so failure of placentation syphilis primary --> presents independent secondary --> presents with lupus too.

Question 34

1) what is the most common area for thrombosis? 2) where does it present? 3) what does the pt present with?

Answer 34

Deep Vein Thrombosis --> "DVT" typically occurs in the lower extremity 1) swelling and redness on the back of the leg, pain even. they can say it feels like they've torn a muscle

Question 35

What are the three fate of thrombi?

Answer 35

Propagation --> thrombus can grow Emboli Dissolution (dissolving a clot) organization/recanalization

Question 36

Secondary Hemostasis involves what? what are we forming?

Answer 36

the coagulation cascade! a fibrin clot --> you're making sure that the weak plug is stabilized

Question 37

Why does rate of occlusion matter? what is more likely to lead to an infarct?

Answer 37

if occlusion occurs slowly enough, COLLATERAL circulation can make up for the vascular obstruction extremely fast occlusion

Question 38

If you have a diagnosis of hemosiderosis, what are you going to see on a histological slide? what are these called? why are they called this? how do you know that it's what it is?

Answer 38

remember, hemosiderosis is red blood cells going through with the edema --> but what happens is you have macrophages ingest these and they become "laden with pigment" --> called "hemosiderin-laden macrophages" --> "heart failure cells" --> most commonly associated with heart failure we use an iron stain (makes sense because blood has iron in it)

Question 39

what is the underlying mechanism or the vast majority of infarcts? what still possible but less likely? where would these happen? what kind of infarct would this be called?

Answer 39

arterial thrombosis or arterial embolism venous thrombosis --> more likely in organs with single efferent vein (testis --> testicular torsion, and ovary) --> Red infarct

Question 40

"mural thrombi" means what?

Answer 40

thrombi occurring in heart chambers or in the aortic lumen

Question 41

What's a normal platelet count? what's a normal bleeding time? why would we do a bone marrow biopsy on someone to check for platelet problems?

Answer 41

150,000 to 400,000 per microliter 2-7 minutes megakaryocytic produce platelets, so we see if we don't have them in the bone marrow to check for platelet problems

Question 42

Von Willebrand disease 1) what is the mechanism 2) what is the platelet count like 3) is there platelet adhesion? 4) is there platelet aggregation?

Answer 42

Inherited lack of vWF Normal No Yes

Question 43

Red vs White thrombi?

Answer 43

Red thrombi --> venous, red blood cell rich, and occur in STASIS! White --> PLATELET RICH because they occur in arteries! they're occurring in high shear stress and ATHEROSCLEROSIS

Question 44

Increasing age, people seem to hyper coagulate. why?

Answer 44

reduced endothelial PGI2 (which remember prevents platelet aggregation)

Question 45

A 90 year old patient comes into the ER and docs do chest compressions for 30 minutes before calling it. what embolis could you see post mortem?

Answer 45

Fat emboli (you broke the ribs)

Question 46

When congestion is chronic, what happens? what is this called? What can it also lead to?

Answer 46

Fluid that was coming out now increases to fluid + blood cells --> Hemosiderosis can lead to tissue damage

Question 47

What's the difference between thrombus and embolis?

Answer 47

thrombus is an occlusion embolis is a traveling occlusion waiting to cause trouble where it lands

Question 48

***Septic Emboli? 1) what is it? 2) what is it MOST OFTEN SEEN IN? 3) what is this complication? 4) what 3 signs would you see associated with this?

Answer 48

blood borne infective material occurs in endocarditis --> heart valve is infected. through infective vegetations. you need to be aware of the peripheral manifestations of endocarditis Janeway lestions (purpura on the hands and feet) Retinal micro emboli --> ROTH spots Splinter hemorrhages in the nail bed!

Question 49

Primary hemostasis: We have the platelets bound to the VWF via GP1B, then what? what two things change? why does this need to happen? what initiates the secretion of stuff? what three things are released by this? what does each do?

Answer 49

they have to undergo activation the platelets change shape --> increase surface area and become NEGATIVELY CHARGED!! in the process we have these GP2b3a receptors that change to allow for aggregation to occur. THROMBIN is what initiates secretion. Thrombin allows for degranulation of mediators that are going to be necessary to move this process forward. 1) ADP --> induces platelets to aggregate at the site of injury via GP2b3a and then links to others using fibrinogen 2) Thromboxane A2 --> derivative of platelet cyclooxygenase --> more aggregation 3) fibrinogen --> important linker molecule that links platelets

Question 50

What test is utilized to show that you have a problem with VWF?

Answer 50

Ristocetin test --> usually this would lead to an aggregation of platelets but since you don't have VWF it would be an abnormal test

Question 51

Edema mechanisms (there are two)

Answer 51

increase in hydrostatic pressure --> (if you retained water, or congestion)... Bursting pipe! so it's leaking reduced plasma oncotic pressure --> loses fluid through equilibrium across a semipermeable membrane.. --> oncotic proteins are lost so you can't pull as much water in anymore so more is lost

Question 52

What are the 3 clinical features of disorders of primary hemostasis? what are examples of each?

Answer 52

1) mucosal bleeding --> epistaxis, hemoptysis (coughing up blood), hematuria, menorrhagia 2) skin bleeding --> Petechiae (pinpoint bleeding), Purpura (larger bleeding 3mm or larger), Ecchymoses (greater than 1cm) 3) easy bruising

Question 53

Heparin Induced Thrombocytopenia presents with what?

Answer 53

microvascular thrombosis seen in hands and feet. you'll see black feet and hands

Question 54

Pathogenesis of septic shock? 1) what first happens? 2) what releases because of this response? what is ultimately activated? 3) from here, endothelial cells go rampant. what is it doing? (3 things) 4) what does this ultimately lead to?

Answer 54

first: inflammatory response... there are PAMPS on the pathogenic bacteria that interact with TLRs of innate immune cells they say "OH SHIT" and release IL-1, IL-12, IL-18, IFN-gamma, TNF it activates complement ---------- from there endothelial cells are activated to have exudative edema and vasodilation through releasing NO, decreasing resistance they go procoagulant --> increase factor 12, increase TF, decrease antithrombin and protein C ------ Hypotension, Hypovolemia, thrombosis --> decreased tissue oxygenation

Question 55

what is our bodies most powerful endogenous anticoagulants? what does it do?

Answer 55

Protein C - inactivates the coagulation cascade by inhibiting factors V and VIII

Question 56

1) A kid presents to your office with an extremely swollen knee. You notice that it is boggy and it's only confined within the space between the femur and the tibia/fibula. the kid states that this same problem has KEPT HAPPENING for years to the point where he's having a hard time walking. what is your diagnosis? 2) what is it a problem with?

Answer 56

Hemarthrosis --> combined hemophilia It's a problem with hemophiliacs --> Factor 8 the bone is eroded over time so kids have to have crutches because of crippling arthritis due to joint bleeds.

Question 57

why are we getting edema in heart failure? what is the explanation as to why our soft tissue are edematous? what organ is involved?

Answer 57

there's a failure of the heart to accurately perfuse the body when the kidneys under perfuse (less blood going to it) they react by holding onto water by activating the RAAS system --> to retain DILUTE WATER because of that, they increase the volume --> increase the intravascular volume... but because it's dilute, it'll be leaky because there's not as much protein

Question 58

Kwashiorkor's relates to edema how? what specifically do they not have?

Answer 58

Protein deficiency --> decrease in oncotic pressure --> leaky deficiency in albumin

Question 59

what's the difference between hyperemia and congestion?

Answer 59

hyperemia is regulated through the precapillary sphincter --> this is responsible for maintaining proper pressure into the capillary bed (REGULATED) if there's a backup of venous blood, this is congestion and it goes back into capillary bed because there's no regulation from the precapillary sphincter

Question 60

What's the dominant histologic characteristic of infarction in most tissues? what about brain infarction what about in in the cardiac valve with vegetations?

Answer 60

ischemic coagulative necrosis liquefactive necrosis septic infarctions --> infected cardiac valve vegetations embolise --> result in an abscess increasing the inflammatory response

Question 61

Say we have prothrombin... and there's a genetic mutation in the 3'UTR of this gene. (G20210A) what can it lead to?

Answer 61

a Primary Hypercoaguable state (genetic) it upregulates prothrombin and increases the risk for venous thrombosis 3x.

Question 62

what is the final result of septic shock? what is this from (3 things) what can this septic shock lead to and why? (4 things)

Answer 62

hypoxic tissue injury from the hypotension, hypovolemia, and thrombosis as septic shock progresses, you get heart failure --> because of lowered cardiac output you can under perfuse the kidney so renal failure, lung failure eventually coma

Question 63

Liver Failure has what mechanisms leading to edema/ascites (2 of them)

Answer 63

we get edema --> liver is responsible for producing albumin, so no albumin means more leaky fluid. we get ascites --> occurring because of increased portal hypertension in the hepatic portal vein.. this causes congestion and you get ascites

Question 64

You have an autopsy to do, how do you know if the thrombus seen was the cause of death or not? what do you see? explain this.

Answer 64

if you see Lines of Zahn (alternating fibrin, blood, fibrin, blood), you the thrombus occurred during active blood flow. this means that was present when the patient was still alive --> this would mean it was almost definitely the cause of death.

Question 65

There's a disruption in the tissue, what's the first thing that happens during hemostasis? (technically two things) what does this allow?

Answer 65

Neural stimulations fire, and endothelial cells themselves release endothelin this results in a quick transient vasoconstriction! reduces blood flow from the area and reduces surface area so you can have easier platelet stuff

Question 66

What does Prothrombin do?

Answer 66

It is the precursor to thrombin from Va --> from here it's the most important coagulation factor that (mostly leads to clotting) 1) converts fibrinogen to fibrin 2) activates platelets 3) pro-flammatory effects that contribute to tissue repair and angiogenesis 4) anticoagulant effects

Question 67

What is Homocysteines role in thrombosis? what deficiency can increase its likelihood for problems?

Answer 67

elevated levels of it contribute to arterial and venous thrombosis cystathione B-synthetase --> leads to marked elevations

Question 68

What are the different dermatologic manifestations that are common in hemostasis disorders

Answer 68

Petechiae --> small, less than 3mm Purpura --> larger Ecchymosis --> palpable

Question 69

what three things are associated with decreased oncotic pressure?

Answer 69

malnutrition liver failure kidney disease with nephrotic syndrome

Question 70

What is Factor 1 called? what is Factor 1a? What is Factor 2 called? 2a?

Answer 70

Fibrinogen Fibrin Prothrombin Thrombin

Question 71

Explain Red Infarct 1) where does it occur and what's an example 2) what kind of tissue 3) what kind of circulation and give examples

Answer 71

venous occlusion --> testicular torsion loose, spongy tissue dual circulation --> lung and small intestine, liver, hand and forearm.

Question 72

Antiphospholipid antibody syndrome? 1) what kind of disease process is it? be specific 2) what is it? 3) what can it present with (otherwise it's independent) 4) what dramatic clinical manifestations does it present with? 5) what subtle manifestations does it present with? 6) what is the suspected antibody target?

Answer 72

hypercoaguability syndrome (acquired) 1) antibodies are directed against particular plasma proteins that bind to phospholipids --> so you get thrombus formation. present in association with Lupus erethematosus or independent when thrombus occurs it can be really dramatic --> necrotic digits, DVT, pulmonary emboli, cardiac disease, stroke subtle manifestations --> repeated miscarriage B2 glycoprotein I

Question 73

You have a normal PT but an abnormal PTT 1) what factors are associated with the bleeding 2) what factor is NOT associated with the bleeding?

Answer 73

11, 9, 8 12

Question 74

What is Factor 8 called? what happens if you have a deficiency in factor 8? what pathway is this associated with?

Answer 74

Antihemophilic A factor (AHF) Hemophilia A Intrinsic Pathway

Question 75

What is the most common heritable hypercoagulopathy? what is the mechanism?

Answer 75

Factor V Leiden Mutation Mechanism --> mutation in factorV that makes it resistant to cleavage by protein C (remember, c inactivates 5 and 8)

Question 76

1) What's the problem with naming it a fat embolism? 2) when would this happen? 3) what symptoms would you see and what is this collectively called?

Answer 76

It's not fat, it's bone marrow, which contains fat (more as you get older) if you break your bone, trauma, marrow can get introduced into circulation which gives you an embolis. this is called a fat embolism syndrome: they can have respiratory distress, mental status changes, strokes

Question 77

What does a DVT put you at an increased risk of? where does this go?

Answer 77

Embolus --> the thrombus dislodges and gives you an embolus this embolus will go to your lungs --> the lungs is the first place that the embolis can lodge (pulmonary embolis)

Question 78

Hyperemia is what? example Congestion is what? what is pathologic?

Answer 78

physiologic arterial process where necessary blood is brought to an area that needs it most --> running to class gives you blood to the right muscles not enough blood is LEAVING the system so pooling of blood --> pathologic --> fluid leaves out.

Question 79

What is "organization and recanalization" of a thrombi?

Answer 79

you block a vessel long enough you're going to regrow stuff --> organization. This doesn't help vascular flow, but you can have.... (scar tissue fish) recanalization --> formation of neovascularized spaces --> small vascularized channels that once was a thrombus.

Question 80

What do we use for therapeutic fibrinolysis? what is it used to treat and within how long is it okay to use? why wouldn't it be okay to use it after that point?

Answer 80

Exogenous tPA embolic stroke, 6 hours if you wait till the brain is damaged by ischemia and you reperfuse, they'll hemorrhage!

Question 81

Renal Failure causes edema how? explain both

Answer 81

1) activate the RAAS system, increase Na and water retention --> increased volume but not increasing protein --> leaky 2) nephrotic syndrome --> glomeruli are damaged so can't filter. when they're damaged, proteins get spilled and you have proteinuria. this gives you decreased oncotic pressure and therefore EDEMA!

Question 82

Primary hemostasis: So we have the exposed sub-endothelial collagen. we've already vasoconstricted transiently. what's the next step of hemostasis? where does VWF come from?

Answer 82

Weibel Palade bodies uncoil to release Von Willibrand Factor.. so VWF binds there and acts as a linker molecule for platelets to bind to Platelets come to the spot and use GP1B to bind to VWF (GP1B is ON the platelet) VWF comes from Weible-Palade Bodies of the endothelial cell.

Question 83

Lymphedema is most commonly seen where?

Answer 83

in someone with breast cancer surgery --> they have axillary lymph nodes removed when you remove it, there's not a place to remove the fluid that's backing up, so people have one swollen arm, but not the other.

Question 84

What if you have both PTT and PT times affected?

Answer 84

MULTIPLE factors deficiencies or something along the COMMON pathway.

Question 85

Chronic hepatic congestion gives you what? what's backing up ahead of this problem? what specific pathology is this called? what does it look like? why do they look like this? what kind of necrosis is it?

Answer 85

Congestion of the central vein so you have sluggish flow out right heart we get nutmeg liver --> alternating light dark pattern (dark is dying hepatocytes) they're dying because we aren't getting new blood. centrolobular necrosis --> center of the lobule contains cells that are going to die first since the outside cells are close to the arterial supply still

Question 86

Why might oral contraceptive pills account for hypercoaguability states? is this primary or secondary hypercoaguability?

Answer 86

secondary (acquired) increased hepatic synthesis of coagulation factors and reduced anticoagulant synthesis from the hormone ingestion.

Question 87

What is a normal PT time? what's a normal PTT time? to activate a PT time, what do you have to add? to activate a PTT time, what do you have to add?

Answer 87

10-14 seconds 32-45 seconds Tissue factor Calcium and a negative surface

Question 88

what is the most common inherited coagulation disorder? what genetics is it? what happens? pt presentation? what factor is associated with this and what does that mean is going to happen with the PT/PTT time? what's the treatment?

Answer 88

VWF disease Autosomal dominant no VSF, so problem with adhesion mild mucosa and skin bleeding factor 8, so PTT is going to be elevated Desmopressin --> increases release of VSF from the weibel palate bodies.

Question 89

Bernard-Soulier Disease 1) what is the mechanism 2) what is the platelet count like 3) is there platelet adhesion? 4) is there platelet aggregation?

Answer 89

Abnormal Gp1b Low-normal No Yes

Question 90

A patient comes in with one swollen leg, but not the other, what could cause this?

Answer 90

lymphatic obstruction called lymphedema lymphedema --> form of edema that is localized, especially the extremities.

Question 91

Coumadin is considered what? what does it do? what is it also called?

Answer 91

Coumadin blocks the formation of active vitamin K so it doesn't activate 2,7,9,10 so it's an anticoagulant Warfarin

Question 92

Healthy 23 year old female is giving birth.. suddenly she goes into shock and is turning blue. The baby comes out just fine and there are no problems. What happened to the mom?

Answer 92

amniotic fluid embolism --> she went into anaphylactic shock due to amniotic fluid introduced into her blood stream.

Question 93

Red thrombi or white thrombi , which one is more likely to lead to an infarct and why?

Answer 93

white, because it's part of the arterial supply, because they block the oxygenated blood from leaving to the end organ

Question 94

Cardiac catheterization can have one human error, what is it? when else could you see this type of problem?

Answer 94

air embolism --> introduction of air the bends from scuba diving --> nitrogen falls out of circulation wherever its at rather than out of the lungs when you come up slowly

Question 95

What is a severe complication involving disorders of primary hemostasis?

Answer 95

intracranial bleeding with severe thrombocytopenia.

Question 96

Why do edema and effusions happen?

Answer 96

hydrostatic pressure needs to push fluid out colloidal needs to help fluid come back in when something deranges you have edema

Question 97

what does the intrinsic pathway involve? what "time" is it associated with?

Answer 97

12 --> 11 --> 9 --> 8 --> 10 --> thrombin --> fibrinogen --> fibrin clot partial Thromboplastin time (PTT)

Question 98

What's the difference between edema and effusions? examples of each?

Answer 98

they're both abnormal accumulation of fluid edema --> interstitial space (soft tissue swelling) effusion --> in a potential space (pleural space, peritoneal space, pericardial space, joint space

Question 99

The last step in hemostasis is what? what does it (2 things) what specifically deals with fibrinolysis what activates this?

Answer 99

stopping hemostasis blood flow washes away activated clotting factors we have Plasmin --> breaks apart fibrin.. this is the body's endogenous fibrin dissolver t-PA --> tissue plasminogen activator --> "the clot buster"