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MS1 > Week 12 Heam (finally!! Im So Done) > Flashcards

Week 12 Heam (finally!! Im So Done) Flashcards

1
Q

Haemostasis

A

Process of blood clotting
1. Vasoconstriction to reduce blood flow
2. Primary Heamostasis - platelets adherence to injured blood vessel wall, and garage to form a temporary plug
3. Coagulation - formation of a stable blood clot through cascade of biochemical reactions including clotting factors and fibrin

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2
Q

Von williebran factor (vWF)

A

-sticky protein that allows platelets to ahere to damaged endothelium, extends life of factor VIII

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3
Q

Platelet plug formation steps

A

1. Adhesion - certain factors bind to certain subendothelial factors
2. Activation - platelet binding to collagen triggers platelet activation, resulting in shape change, granule secretion, and receptor activation
** 3. Aggregation ** 8 GPllb/IIa on platelets binds to fibrinogen irreversibly, fibrinogen acts as a molecular glue
4.Plug formed by degenerated platelets trapped by fibrinogen

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4
Q

ADP

A

Screwed by activated platelets. Activates its self and platelets in the vincicnty

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5
Q

Thrombaxnae A2

A

Diffuses out of activated platelets, activates itself and other platelets

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6
Q

Thrombin

A

Is formed in the coagulation cascade, enables coagulation to occur and activate platelets

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7
Q

Platelet aggravation

A

Injury to a blood vessel – A blood vessel gets damaged, exposing the underlying collagen.

Platelet activation – Platelets in the blood recognize the injury and become activated, changing shape to stick better.

Release of chemicals – Activated platelets release signaling chemicals (like ADP and thromboxane) that attract more platelets to the site.

Platelet aggregation – New platelets are recruited and stick together, forming a clump (platelet plug) at the injury.

Clot formation – The platelet plug is reinforced with a fibrin mesh, creating a stable blood clot to stop bleeding.

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8
Q

Platelet aggregation

A

Injury to a blood vessel – A blood vessel gets damaged, exposing the underlying collagen.

Platelet activation – Platelets in the blood recognize the injury and become activated, changing shape to stick better.

Release of chemicals – Activated platelets release signaling chemicals (like ADP and thromboxane) that attract more platelets to the site.

Platelet aggregation – New platelets are recruited and stick together, forming a clump (platelet plug) at the injury.

Clot formation – The platelet plug is reinforced with a fibrin mesh, creating a stable blood clot to stop bleeding.

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9
Q

COX inhibitor mechanis,

A

Blocks COX anzymes to reduce synthesis of prostaglandins which play a role in inflamation and pain

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10
Q

ADP receptor antagonist

A

Blocks ADP receptors on platelets preventing activation and aggregation

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11
Q

Phosphodiesterase Inhibitor

A

Inhibits phosphodiesterase enzymes to increase cyclic AMP levels, leading to vasodilation and reduced platelet aggregation.

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12
Q

GPIIb/GPIIIa Inhibitor

A

Blocks the GPIIb/IIIa receptors on platelets, preventing fibrinogen binding and inhibiting platelet aggregation

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13
Q

Contradictions of anti-platelet medications

A

Active bleeding, thrombocytopenia, bleeding disorders.

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14
Q

Tranexamic Acid

A

Tranexamic acid (TXA) is an antifibrinolytic medication used to inhibit fibrinolysis, the process by which the body breaks down blood clots.

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15
Q

Inherited abuses of hypercoagubilty

A

Factor v Leiden mutation
Activated protein c resistance
protein C or S deficiency
Antithrombin deficiency

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16
Q

Primary haemostasis

A

Initial blood vessel response
Platelet adhesion and aggregation to form a temporary plug

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17
Q

Secondary haemostasis

A

Cascade of enzymatic reactions leading to the formation of a stable blood clot via clotting factors

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18
Q

Metastatic carcinoma

A

Cancer that has spread from one part of body to another

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19
Q

Metastatic carcinoma formation

A
  1. Tumour development
    2.Cancer cells invade nearby tissues/ vasculature
  2. Intravasattion of lymph and blood
  3. Extravasation of lymph and blood
  4. Secondary tumour formation
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20
Q

Disseminated intravascular coagulation (DIC)

A

Cody makes wayyy to many clots

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21
Q

Disseminated intravascular coagulation (DIC) formation

A
  1. Underlying cause eg sepsis or trauma
  2. Activation of coagulation cascade
  3. Widespread microthrombi formation
  4. Consumption of coagulation factors
  5. Fibrinolysis and plasmid overactition
  6. Increased bleeding
  7. End organ damage
22
Q

How can bleeding disorders be caused by renal failure

A

Renal failure leads to buildup or ureamic toxins, leading to platelet dysfunctions
Also reduces levels of vWF

23
Q

vWF

A

Protein needed for blood clot

24
Q

Haemophilia pattern of inheritance

A

X linked

25
Q

Clinical features of bleeding disorders

A

Bruising
Purpura
Post op bleeding
Menorrhagia
Heamaturia
Epistaxis

26
Q

Purpura

A

Widespread small or red or purple skin spots caused by bleeding underskin

27
Q

Aspirin mechanism

A

Anti- platelet
Inhibits COX-1, reducing TXA2 production, impairing platelet aggregation

28
Q

Clopidogrel mech

A

In anti-platelet
Blockers ADP receptor on platelets, preventing activation and aggregation

29
Q

Heparin mechanism

A

Anti- coag
Binds to antithrombin III, inhibiting thrombin and Factor Xa, which reduces platelet activation and aggregation, and can also directly impair platelet function.

30
Q

Warfarin

A

Inhibits vitamin K-dependent clotting factors (II, VII, IX, X).

31
Q

Direct oral anticoagulants (DOACs)/New orally active anticoagulants

A

Apixiban = inhibits Xa
Dabigatran= inhibits thrombin, preventing thrombosis formation

32
Q

Tissues Plasminogen Activators (tPA)

A

Thrombolytic Agents
Enzymes that promote conversion of plasminogen into plasmin, dissolving blood clots

33
Q

Indications and Contradictions for anti-platelet medications

A

Indications: Cardiovascular disease, Cerebrovascular disease, PVD
Contradictions: active/recent haemorrhage, Upcoming/recent surgery, serve thrombocytopenia

34
Q

Side effects of Anti-platelet medications

A

Blood loss, GI ulceration or irritation
+ for Ticagrelor specifically:
Dyspnoea, Gout and Bradycardia

35
Q

Side effects of DOACs

A

Bleeding, indigestion, nausea, skin rashes, liver function abnormality, headache

36
Q

Mandatory testing for Blood transfusion

A

HIV, Hepatitis C and B, Syphilis, Human T-lymphotropic virus type I and II

37
Q

Rhesus incompatibility

A

Rh incompatibility is a condition that develops when a pregnant woman has Rh-negative blood and the baby in her womb has Rh-positive blood.

38
Q

Risks and complications of blood transfusions

A

Haemolytic reaction, Allergic reaction, Febrile, Non-haemolytic reaction, infection, iron overload, volume overload.

39
Q

Three Pillars of patient blood management

A

Optimise Hb levels, minimise blood loss, appropriate transfusion

40
Q

Stages of Change

A
  1. Pre-contemplation
  2. Contemplation
  3. Preparation-Action
  4. Maintenance
  5. Relapse
41
Q

Impacts of assumptions on patients

A
  • damages doc patient relation
  • reinforces feelings of helplessness
  • Creats/perpetuates stigma
  • hypocritical
  • doesn’t minimise harm
42
Q

Members of interdisciplinary genetic teams

A

Clinical geneticist - type of doctor
Genetic counsellor - non directive counselling
Phycologist

43
Q

SMART Goals

A

Specific
Measurable
Achievable
Relevant
Time based

44
Q

Branches of law

A

Parliament, executive, courts/judical

45
Q

Key considerations of Negligence Law

A

Duty of Care
Breach of duty
Causation
Damage or loss
Foreseeability

46
Q

Parameters of consent

A

Informed
Capacity
Revocable

47
Q

Cultural factors affecting smoking

A
  • Family Norms
  • Occupation
  • Peer Pressure
  • Media/advertising
  • Cultural beliefs
48
Q

Challenges in Telehealth

A

Tech issues
Privacy/confidentiality
Limited physical exam
Communication barrier
Legal/regulatory

49
Q

Steps to help in Telehealth

A

Confirm audio and video quality
Assess confidentiality
Summarise key points

50
Q

Heamophilla A vs B

A

A= Factor VII deficeincy
B= Factor IX deficiency

51
Q

Disseminated Intravascular Coagulation

A

Systemic activation of coagulation pathways generating fibrin clots throughout the body, with the resulting consumption of platelets & coagulation factors also resulting in bleeding

MS1 (16 decks)

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