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Flashcards in MOD Deck (186)
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60

How do plasma cells appear histologically?

Clock face nuclei (clumped peripheral chromatin)
White halo of golgi

61

How do eosinophils appear histologically?

Bilobed nuclei in red staining cytoplasm (sunburnt face with sunglasses)

62

What are the types of giant cells?

Langerhans - TB - ordered crescent of nuclei peripherally
Foreign body type - FB! - disordered nuclei, evidence of debris
Toutons - fat - ordered crescent of nuclei with foamy appearance outside of cell

63

What causes giant cell formation?

Frustrated macrophages unable to phagocytose pathogen / debris joins with others.

64

How does chronic inflammation cause fibrosis? In what conditions does this occur?

Mediator production by macrophages cause fibroblast recruitment resulting in collagen production. This causes fibrosis.
This impairs function.
Found in cirrhosis, repeated choleocystitis, fibrotic lung disease

65

When does chronic inflammation result in up-regulation of function?

Graves disease

66

What is a granuloma?

A focal discrete collection of immobile macrophages (epitheloid macrophages) surrounded by lymphocytes.

67

What causes granuloma formation?

Persistent low grade irritation that cant be removed - e.g TB or idiopathic like wegners granulomatoisis and chrones disease

68

What are the different classifications of stem cells

Unipotent
Multipotent
Pluripotent
Totipotent

69

How can cell division be classified?

Labile - actively dividing, no entry to g0
Stable - divides when signalled but usually at rest
Permanent - unable to divide fixed in g0

70

What factors upregulate cell division? Give examples

Growth factors
Pdgf
Egf
Gh
Oestrogen

71

What factors downregulate cell division?

Adhesion molecules in neighbouring cells and basement membrane (contact inhibition)

72

When would a tissue repair by fibrous repair not regeneration?

Necrosis of permanent cells
Loss of collagen framework of necrosed labile or stable cells

73

What are the three stages of fibrous repair?

Cell migration
Angiogenesis
Extracellular matrix production

74

What are the cells involved in fibrous repair? What do they do?

Inflammatory cells - phagocytosis and mediator release
Endothelial cells for angiogenesis
Fibroblasts and myofibroblasts for matrix production and wound closure.

75

What occurs in the angiogenesis phase of fibrous repair?

Growth factors (eg VEGF) trigger preexisting vessels to sprout new vessels
- endothelial proteolysis of basement membrane
- migration of endothelial cells by chemotaxis
- endothelial proliferation
- maturation and remodelling with recruitment of pericytes

76

Explain the rabbit ear chamber model of fibrous repair

- blood clot forms with acute inflammation progressing to chronic inflammation
- clot replaced with granulation tissue with anginogenesis, (myo)fibroblast infiltration, ECM production and decline in immune cell levels
- granulation tissue matures - cell populations decline, collagen increases, myofibroblasts reduce volume.

77

Differentiate healing by primary and secondary intention

Primary - edges in apposition, little granulation tissue formation, epidermis regenerates over injury, minimal scarring, there is risk of abcess formation if infection trapped under regenerating epidermis

Secondary - edges not in apposition, clot forms creating an eschar, granulation tissue forms from bottom up forming large scar and wound contraction

78

What local factors could influence wound healing?

Movement/joint
Size of wound
Blood supply
Infection
Radiation
Foreign materials

79

What systemic factors could influence wound healing?

Age
Comorbidities - diabetes, CHF, PVD, connective tissue disease, immunosuppressive disease
Medications - steroids, hormones
Dietary deficiency - proteins, vitamins, essential amino acids

80

What are the complications of insufficient wound healing?

Dehiscence
Herniation
Ulceration

81

What are the complications of excessive wound healing

Scarring
Keloids
Cirrhosis
Fibrosis
Strictures
Contractures

82

What is the initial response to blood vessel damage?

Vasoconstriction and venoconstriction

83

How does a platelet plug form?

- Platelets adhere to connective tissue vessel walls activating them
- Release of calcium from ER
- Activation of GPIIb/IIIa receptors which bind to fibrinogen creating cross links to other active platelets
- Release of vesicles containing ADP and TXA2
- ADP inhibits adenyl cyclase reducing cAMP reducing inhibition of calcium release
-TXA increases IP3 increasing calcium release

84

How is inappropriate platelet activation inhibited?

Release of prostacyclin by endothelium which activates adenyl cyclase increasing cAMP reducing calcium release

85

How can coagulation be activated?

Intrinsic pathway - damaged endothelial cells activating factor XII-XIIa
Extrinsic pathway - release of tissue factor causes factor VII-VIIa - very fast activation.

86

What is the common pathway of coagulation

X-Xa
Prothrombin - thrombin
Fibrinogen - fibrin and XIII-XIIIa

87

What are some controls of the coagulation cascade?

Antithrombin III - binds thrombin inactivating it
Protein C - binds thrombin becoming APC
APC - deactivates factors Va and VIIIa
Fibrinolysis - plasmin converted to plasminogen breaking down fibrin
Thrombomodulin - increases activation of PC to APC

88

What is a thrombosis?

A solid mass of blood in the circulatory system

89

What raises risk of thrombosis?

Virchows triad
Abnormal vessel wall (athroma, injury, inflammation)
Abnormal coagulability (stagnation, turbulence)
Abnormal blood flow (smoker, post partum, post op, disease)