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MRC salah pathology > Polytrauma and transfusion > Flashcards

Polytrauma and transfusion Flashcards

1
Q

Define DIC

A

-Pathological consumptive coagulopathy due to widespread activation of coagulation systems.

-This leads to microvascular and macrovascular clotting and the consumption of platelets and clotting factors.

Characterised by:
–> widespread haemorrhage
–> thrombocytopaenia, decreased fibrinogen, increased fibrin degradation products (d-dimer)

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2
Q

What is the function of platelets?

A

-Contribute to haemostatic process in two different ways
-First through adhesive and cohesive functions that lead to formation of a haemostatic plug
-Second, can activate coagulation mechanisms

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3
Q

What is the precursor of platelets? How are platelets formed from bone marrow?

A

Megokaryocytes

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4
Q

What are the stages of haemostasis?

A

1) vasoconstriction
2) formation of temporary platelet plug
3) Activation of clotting cascasde
4) Formation of fibrin plug

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5
Q

Why does this patient have a bleeding tendency?

-Known hepatitis C–> trauma–> blood loss

Splenectomy was done and patient received blood transfusion. Patient develops DIC

A

Because the liver is affected

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6
Q

What are the late manifestations of hepatitis C virus?

A

Cirrhosis
HCC

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7
Q

What activates the intrinsic and extrinsic clotting pathways?

A

-Intrinsic pathway is activated by vessel injury which will lead to activation of factor 12
-Extrinsic pathway is activated by tissue thromboplastin which is released by the damaged cells
-APTT tests for intrinsic pathway
-PT tests for extrinsic pathway and common pathway

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8
Q

Describe hypersensitvitiy reactions by description, mediator, antigen, response time, examples

A

Mnemonic ACID EGG T

1: Anaphylactic
2: Cytotoxic
3. Immune complex
4: delayed type

Igg:
-E
-G
-G
-T cells

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9
Q

What is the lifespan of red blood cells?

A

120 days

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10
Q

What tests would you do before blood transfusion?

A

-ABO
-Rh

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11
Q

What is GXM?

A

Group cross matching: to test donor red cells against recipient serum to detect any potential incompatibility through which antibodies in receipient cause haemolysis to donor cells

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12
Q

Antigen in cross matching

A

ABO

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13
Q

What are the stages of bone healing?

A
  1. Haematoma formation (mass of clotted blood) at fracture site. Tissue in fracture site swells, very painful, obvious inflammation, and bone cells are dying
  2. Fibrocartilaginous callus develops over 3-4 week period. This process involves:
    –> capillary growth in the haematoma
    –> phagocytic cells invading and cleaning up debris in injury site
    –> fibroblasts and osteoblasts migrating into site and beginning reconstruction of bone
    –> fibrocartilaginous callus serves to splint fracture
  3. Bony callous begins forming after 3-4 weeks artery injury and is prominent 2-3 months following injury. Continued migration and multiplying of osteoblasts and osteocytes results in fibrocartinlagenous callus turning to bony callus
  4. Remodelling. Any excess material of the bony callus is removed and compact bone is laid down in order to reconstruct the shaft. Remodelling is the final stage
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14
Q

What is the effect of prolonged immobility on the bone?

A

Loss of bone density, increased risk of osteoporosis

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15
Q

Infected implant, why should it be removed?

A

Biofilm
Septic focus

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16
Q

What is PVL staph aureus?

A

-Panton-valentine leukocidin (PVL) is a cytotoxin produced by SAUR that causes leukocyte destruction and tissue necrosis
-presence of pvl is associated with increased virulence of SAUR and is present in majority of community MRSA cases

17
Q

What is effect of PVL cytotoxin?

A

-Creates pores in membranes of infected cells and is the cause of necrotic lesions involving skin or mucosa, including necrotic haemorrhagic pneumonia

18
Q

What is present inside an abscess?

A

-Central, largely necrotic region rimmed by layer of preserved neutrophils with surrounding zone of dilated vessels and fibroblast proliferation indicative of attempted repair

19
Q

What organisms cause abscess?

A

-Bacterial: SAUR, strep pyogenes
-Non bacterial: fungal, viral, parasitic

20
Q

What test could you use to detect cause of abscess?

A

Gram stain

21
Q

What is the cause of a fever in abscess?

A

-Produced in response to substances called pyrogens (TNF, IL1) that act by stimulating prostaglandin synthesis in the vascular and perivascular cells of the hypothalamus

22
Q

Define cellulitis

A

Spreading bacterial infection that affects dermis and subcut fat, characterised by redness, warmth, swelling and pain

23
Q

What is the difference between abscess and cellulitis?

A

Group A strep secretes fibrinolysin and hyaluronidase. Both of these can break down connective tissue components, speeding the spread of bacteria (hyaluronic acid, fibrin clots)

Coagulase promotes blood clotting by converting fibrinogen to fibrin. This can create a protective barrier around the bacterium, helping them to evade the immune system and antibiotics, and contributing to the formation and persistance of an abscess

24
Q

When would you give antibiotics in abscess?

A

-If not localised (i.e. presence of cellulitis) or cavity is not left open to drain freely

25
Q

What are giant cells?

A

Multinucleated cells derived from fusion of multiple actrivated macrophages to form granuloma

26
Q

What is most common cause of granuloma formation? What stain would you use to confim?

A

Tuberculosis

Ziehl-neelsen (acid fast stain)

27
Q

What changes would you see in lymph node affected with inflammation?

A

Reactive follicular hyperplasia

28
Q

Describe type 1 hypersensitivity reaction

A

-Exogenous antigens
-Mast cell degranulation
-IGE mediated
-Asthma/hayfever

29
Q

Describe type 2 hypersensitivity reaction

A

-Cytotoxic reaction
-IgG, IgM related. Mediated by antibodies reacting against antigens on cell surfaces
-Complement is activated, leading to aggregation of neutrophils and formation of MAC
-Can be autoimmune (self cells) or to exogenous cells (blood transfusion)

30
Q

Describe type 3 hypersensitivity

A

-0Widespread deposition of antibody/antigen complexes in the tissues
-Causes complement activation and local inflammation
-e.g. RA

31
Q

Describe type 4 hypersensitivity

A

-Antigen specific activated t cells. When antigen enters body, T cells activate macrophages causing inflammation
-Takes longer due to length of time to recruit cells to the site of the antigen

MRC salah pathology (11 decks)

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