Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBBS - Year 1 > Pathology - Monoarticular joint pain > Flashcards

Pathology - Monoarticular joint pain Flashcards

1
Q

Why did we need bones

A 
Mechanical support 
Transmission of forces generated by muscle 
Protection of vital organs 
Mineral homeostasis 
Production of blood cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Trabecular vs cortical bone

A

T is more metabolically active and makes up 8-% of weight bearing bones, C makes up 80% of long bones exposed to large torsional forces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Methods of bone formation

A

Intramembranous ossification

Endochondral ossification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Intramembranous ossification

A

Bone develops directly from sheets of mesenchymal tissue

Begins in utero and continues until adolescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why isn’t skull and clavicles fully ossified at birth

A

Allows passes through birth canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the last bones to ossify

A

Flat bones of the face

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Endochondral ossification

A

Bone develops by replacing hyaline cartilage – cartilage acts as template
Takes much longer than intramembranous ossification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which bones form via endochondral ossification

A

Bones at base of skull and long bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Haversian systems

A

Origination of compact bone in parallel systems, run lengthwise down long bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do Haversian systems consist of

A

Lamellae, concentric rings of bone surrounding haversian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Haversian canal

A

Nerves
Blood vessels
Lymphatic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How are Haversian systems connected

A

By Volkmann canals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are Haversian systems created by

A

Osteoblasts – secrete matrix and become trapped in lacuna —> osteocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Osteon

A

Packet of bone on which the collagen fibres are aligned

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Points of weakness in the bone

A

Cement lines – collagen poor lines between osteons
Lacunae
Osteocyte canaliculi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where does vascular insufficiency occur from

A

Mechanical injury to blood vessels
Thromboembolism blocking vessels
External pressure collapsing vessels
Venous occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Osteonecrosis

A

Ischaemic necrosis of bone and bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of osteonecrosis

A

Trauma or fracture (most common)
Steroids
Siickle cell anaemia
‘The bends’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

‘The bends’

A

Nitrogen released from fatty bone marrow forms a gas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Osteomyelitis

A

Infection of bone or bone marrow – often in children
Usually bacterial – hematogenous spread
Lytic focus (sequestrum) and surrounding sclerosis (involucrum) on x-ray is v. characteristic
Diagnosis is generally made by blood culture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is osteomyelitis usually caused by

A

Staph. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical features of osteomyelitis

A

Bone pain

Systemic signs of infection e.g fever and leucocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Signs of infl

A 
Rubor - redness 
Calor - heat 
Tumor - swelling 
Dolor - pain 
Function Laesa - loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Causes of infl

A

Infections
Tissue necrosis
Foreign bodies
Immune reactions (hypersensitivity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why are hypersensitivities difficult to cure

A

The stimuli for the inflammatory responses cannot always be eliminated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

When does acute infl arises

A

In response to tissue necrosis (to clear necrotic debris) or infection (to eliminate pathogens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Development of acute infl

A

Within mins – hrs and lasts for several hrs – few days

28
Q

What does acute infl allow

A

Inflammatory cells, plasma proteins and fluid to exit blood vessels and to enter the interstitial space

29
Q

What is acute infl characterised by

A

Presence of oedema and neutrophils in tissue

30
Q

Which external factors can trigger infl

A

Microbes - virulence factors and PAMPs
Allergens
Irritants
Toxic compounds

31
Q

Which internal factors can trigger infl

A

DAMPs – intracellular proteins released when a csm is injured or when a cell dies

32
Q

Virulence factors

A

Molecules that help pathogens to colonise tissues and cause infection

33
Q

PAMPs

A

Small molecules w/ conserved patterns that are shared amongst many diff pathogens e.g. bacterial wall components like peptidoglycan, lipopolysaccharide and lipoteichoic acid and fungal wall components. May also include viral DNA or RNA – intracellular pathogens.

34
Q

What are PAMPs and DAMPs recognised by

A

Pattern Recognition Receptors (PRP) – cell surface receptors on leukocytes (macrophages, dendritic cells, mast cells) that activate them and begin infl process

35
Q

What do PRP activate

A

Multiprotein complex (inflammasome) —->I nduces production of IL1 —-> recruits leucocytes —–> inducing infl

36
Q

5 R’s of infl

A 
Recognition (of the injurious agent)
Recruitment (of leucocytes)
Removal of the agent 
Regulation of the response 
Resolution of the damage
37
Q

Mediators of infl

A 
Hageman factors (Factor XII)
Complement system 
Mast cells 
Arachnidonic acid metabolites 
Toll-like receptors
38
Q

Factor XII

A

Inactive pro-inflammatory protein produced by the liver

Contact activation – activated by contact w/ pathogens or artificial surfaces

39
Q

What does the complement system result in

A

Formation of C3 convertase —> activates leucocytes using anaphylatoxins, phagocytosis and forms membrane attack complex (causes water to flood in, destroying the pathogen)

40
Q

Pathways in complement system

A

Classical
Alternative
Mannose-binding lectin pathway

41
Q

Classical pathway of complement system

A

Antigen binds to IgG or IgM —-> Activates C1

42
Q

Alternative pathway of complement system

A

Activated by microbial components directly

43
Q

Mannose-binding lectin pathway

A

MBL binds to mannose in bacterial surface

44
Q

Functions of complement system

A

Formation of anaphylatoxins, opsonisation
Cell lysis (MAC),
Immunoglobulin clearance

45
Q

What are mast cells activated by

A

Complement proteins C3a + C5a
Tissue trauma
Crosslinking of cell surface IgE by antigen

46
Q

Immediate response of mast cels

A

Via release of preformed histamine granules – causes vasodilation of arterioles and increased vascular permeability

47
Q

Arichidonic acid metabolite

A

Steroids – reduce transcription of phospholipase A2

Aspirin and other NSAIDs act as COX inhibitors

48
Q

Where are toll-like receptors present

A

Cells of the innate immune system including macrophages and dendritic cells and adaptive immune system

49
Q

What does toll-like receptor activation up regulate

A

Nuclear Factor Kappa Beta—–> activates immune response genes producing cytokines which can amplify reaction

50
Q

Rubor and Calor

A

Due to vasodilation, causing increased blood flow

Relaxation of arteriolar smooth muscle

51
Q

What are rubor and calor mediated by

A

Histamine
Prostaglandins,
Bradykinin
Nitric oxide

52
Q

What do pyrogens cause

A

Macrophages to release IL-1 and tumour necrosis factor —-> increases COX activity in hypothalamus

53
Q

What is tumor caused by

A

Leakage of fluid from post-capillary venules into interstitial space (exudate)

54
Q

What is tumour mediated by

A

Histamine (endothelial cell contraction) and tissue damage (endothelial cell disruption)

55
Q

Exudate

A

Extravascular fluid w. high protein conc. and contains cellular debris

56
Q

Transudate

A

Fluid w/ low protein content, little to no cellular material and low spp gravity – osmotic/hydrostatic imbalance

57
Q

Oedema

A

Excess of fluid in the interstitial tissue or serous cavities, can be exudate or a transudate

58
Q

Pus

A

Purulent exudate, rich in neutrophils contains debris of dead cells and in many cases microbes

59
Q

Neutrophil arrival and function

A 
Margination 
Rolling 
Adhesion 
Transmigration and chemotaxis 
Phagocytosis 
Destruction of phagocytosed material 
Resolution
60
Q

Margination of neutrophils

A

Vasodilation slows blood-flow in post-capillary venules, cells marginate from centre of flow to periphery

61
Q

Rolling of neutrophils

A

Selectins cause neutrophil to slow down and to roll along the endothelial surface

62
Q

Adhesion of neutrophils

A

Uses integrins

63
Q

Transmigration and chemotaxis of neutrophils

A

Activation of actin

64
Q

Destruction of phagocytose material in neutrophils

A

HOCL generated by oxidative burst in phagolysosomes destroys phagocytosed microbes. O2 dependent killing is the most effective mechanism

65
Q

Resolution of neutrophils

A

Neutrophils undergo apoptosis

66
Q

When do macrophages peak

A

2 – 3 days after inflammation begins

67
Q

What sequence does macrophages follow

A

The margination, rolling, adhesion and transmigration sequence

MBBS - Year 1 (93 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions