PLATETS AND CLOTTING (maddy)

hemostatis

stopping of bleeding

primary hemostasis

platlet aggregation (the proccess of platlets adhering together and blocking damaged blood vessels to stop bleeding)

Secondary hemostatis

fibrin formation (clot formation)

two types of problems of hemostatis

excessive bleeding and excessive clotting

platelet levels:

150,000-450,000

Thrombocytopenia:

platelets less than 100,000

• blood is too thin, your patient is at risk for bleeding and bruising, and petiche (red spots/ tiny bruises all over body)

thrombocytosis:

platelets greater than 750,000

• blood is too thick, your at risk for clots

medications, illness, and genetic disorders can alter what?

hemostatic factors

three major step of hemostatis?

1. vasoconstriction

2. platelet plug formation

3. blood coagulation

can occur in response to injury or sluggish/stagnant blood flow

thrombus (clot) formation

thrombosis

generation of an occlusive clot (a clot blocking blood flow into artery and veins)

ensures that clots are only formed when necessary and are broken down once the injury has healed, maintaing proper blood flow?

clot dissolution (fibrinolysis)​

give rise to platlets

megakaryocytes

what is thrombopoietin?

made in the liver, and stimulated platelet formation

lifespan for a platelet

7-10 days; platelets live in the spleen

the exposure to collagen and release of the von Willebrand factor

attracts platelets

Abnormal aPTT (activated partial thromboplastin) results =

patient is put on intravenous heperin drip

prothrombin (PT) abnormal results =

if prolonged, need further testing. may be used to moniter warfarin therapy

tPA: tissue plasminogen activator

converts plasminnogen to plasmin

A protien that helps break down clots; CLOT BUSTER (ex. alteplase drug group ends in….ase)

• once a clot is already developed, blood thinners wont work, you need to use a clot buster

unexpected bleeding that occurs despite treatment meant to reduce bleeding risk, often seen on patients on anticoagulant or antiplatelet medications.

paradoxical bleeding

paridoxical effect (ex. when a medication is given and the outcome is the opposite of what is intended or expected)

increased coagulation activity puts you at risk for

bleeding

smoking, high cholesteral, and diabetes

increase platelet activity

some causes of increased platelet number:

the spleen filters blood and removes old or damaged blood cells, including platelets

therfore a splenectomy (surgical removal of the spleen): because platelets live in the spleen there is no place or filteration of the blood which increases platelet numbers.

increased coagulation activity (blood is too thick, excess clotting)

• statis of blood flow

immobile, sedentary (sitting down, not active, someone with a job that sits all day), atrial fibrillation

increase coagulartion factors:

• Estrogen: Women aged 35 years and older may need to consider other alternatives to oral contraceptives​

• Cancer: tumor cells may secrete prothrombotic factors​

• Heart failure – heart fails as a pump. The blood is going to be moving slower/sluggish.​

• Heart valve problems.​

spontaseous bleeding (less than 20,000 per uL)

starts with a nose bleed, or bleeding from the ears

decreased platelet production

• Suppression of bone marrow (aplastic anemia, leukemia, radiation exposure)​

platelts are derived from the bone marrow, so a suppression of the bone marrow will cause issues

decreased platelet survival (7-10days)

antiplatelet antibodies (antibodies that attack or coat your own platelets)

mechanical injury ( an injury to any portion of the body from a blow,crush,cut,or penetrating wound)

impaired platlet activity: bleeding disorders in which the platlets do not form a strong blood clot

Side effects of some drugs:

irreversible acetylation of platelet cyclo-oxygenase decreasing platelet adherence​

• Aspirin: effect lasts for platelet lifespan​

• Other NSAID’s: reversible effect​

renal failure

• toxin build up can cause platelet lysis

inherited disorders

deficiencies in clotting factors: not enoygh protiens in the blood to help it clot properly (prolonged bleeding, frequently bruising, or unexpected bleeding.)

hemophilia (a rare, inherited bleeding disorder that prevents blood from clotting properly)

Von Willebrand disease (VWD) (Prevents blood from clotting properly)

impaired sytheiss (reduced or abnormal production of clotting factors)

• the bodies ability to stop bleeding is comprimised

Liver Disease: The liver produces most clotting factors, so diseases like cirrhosis or hepatitis can reduce their production, leading to bleeding issues.

Vitamin K Deficiency: Vitamin K is essential for the synthesis of several clotting factors. Low levels of vitamin K, due to poor diet, malabsorption, or certain medications, can lead to impaired clotting and increased bleeding risk.

bleeding: Nosebleeds, bruising, bleeding gums, abnormal vagnial bleeding etc.

clotting: DVT, pulmonary embolism

increase clotting: some cancers, athercsclerosis (plaque builds up in the walls of arteries, and ruduces blood flow), atrial fibillation (upper chambers of the heart are beating irregularl)

decreased clotting: luekemia, recent infection, autoimmune disease

Assessment of bleeding and clotting disorders

risk factors of bleeding (what should you do to decrease it?)

electric razor, soft bristled toothbrush, when transfering use a lift sheet, and moniter for bruising and bleeding, document in care plan

S&S of a pulmonary embolism:

unexplained shortness of breath, pain with breathing​

S&S of a blood clot:

warm to the touch, pain, redness, swollen

Lifesytle choices that effect bleeding and clotting disorders assessment

smoking-vasoconstrictor (slows and blocks blood flow)

alcohol abuse-bad for the liver

Anticoagulant drugs: prototype HEPARIN

1. theraputic range for heparin

2. where is heperin given

3. Activates?

1. 60-80 seconds

2. IV or S.C. (S.C rotate around belly button)

3. antithrombin (AT)​ which prevents blood clots from forming

Anticoagulants reduce and prevent blood clots but they are not…..

CLOT BUSTERS

Amticoagulants: prototype;Enoxaparin

A weaker version of heperin, it has a shorter life and less side effects

• given S.C. once or twice per day

• comes in a box of 5 and they have an airbubble at the top of syringe

does enoxaparin require coagulation lab monitering?

No

Enoxaparin has an airbubble in the top of syringe

DO NOT REMOVE AIRBUBBLE, It helps push the medicine into the body so it will not leak out the injection site

What other medications might be contraindicated to use with heparin and enoxaparin?

Aspirin

What does the nurse need to teach the client when they are using these medications?​

They must use an electric razor, a soft bristled toothbrush, and using a lift sheet in a clinical setting. They also need to watch for signs of bleeding and bruising like bleeding gums, or blood in the urine, or any small red spots that may develop of the skin.

thrombolytric agents:

1. CLOT BUSTER is inserted where and how?

2. what can clot buster be used for?

1. Catheter-directed thrombolysis (neck,groin,arm,or behind knee) then place the cstheter through a vein, which the medication will travel to clot and dissolves thrombi

2. ischemic stroke, MI (heart attack)

TIMING OF USE IS IMPORTANT

drug induced thrombocytopenia: risk for bleeding

cause: More than 1,500 medications, also herbal and over-the-counter medications.​

1. How long does it take before this is noticed? What is the sign that generally develops?​

2. what symptoms may occur?

3. What is done to treat this condition?​

1. 1 week, and petechiae will start to develop

2. brusing, bleeding, petechiae, light headedness, fatigue, nausea and vomitting, fever and chils

3. Stop the medication

***COMMON WITH SULFA DRUGS

SIGNS AND SYMPTOMS: Lightheadedness, chills, fever, bleeding symptoms

Petechiae (usually 1 week or 2 after)

Heperin-induced thrombocytopenia: risk for bledding clotting

occurs with Low-molecular-weight heparin or just heparin

slower than drug induced thrombocytopenia, developes 5-10 days after the exposure to the heparin

D-dimers

there is a clot in the body, and that the clot has activated tPA the clot dissolution

pain in legs when walking, but stopping is the pain goes away, but the blood clot is still present?

claudication

platelets full lidespan before completly exiting the body?

60 days

hemophilia (inability to clot), what should you have this?

play sports because there would be too much pressure on the body increasing risk for bleeding and bruising

petechiae

tiny bruises all over body

immune coagulation disorder

thrombocytopenic purpura

thrombotic coagulation diroder:

thrombocytopenic purpura

person may develope DVT on what

heparin; allergic perminantly

Someone on DIC (disseminated intravascular coagulation) is put on

heparin which slows the disease

dietary viamin K

flucuations can affect Warfarin response (ex. salad)

work by blocking a chemical in the body called cyclo-oxygenase (COX), which helps form substances that cause blood clotting.

Aspirin permanently blocks this, while NSAIDs only block it for a short time.

1. Stop Aspirin how many days before surgery

2. stop NSAIDS how many days before surgery

1. 7 days

2. 72 hours (3 days)

extrinsic pathway (factor vll): caused by tissue injury

activated secondary to external trauma, clots blood to stop bleeding

intrinsic pathway responds to spontaneous

• (activate or factor xll): protein in the blood that helps start the process of blood clotting. When activated, it triggers a chain reaction that leads to the formation of a clot to stop bleeding. This activation happens when blood vessels are injured.

internal damage of the vascular endothelium (inside blood vessels and the lymphatic system), clots blood to stop bleeding