MSS Flashcards

Question 1

Q

Structure and Function of Joints by Nidhi Sofat

What is a Fibrous joint

*LOB: Classify joints according to the 3 main classes of joint:
fibrous, cartilaginous, synovial

Answer

A

(synarthrosis).
Immobile e.g. skull sutures, tooth socket

Question 2

Q

Structure and Function of Joints by Nidhi Sofat

What is a Cartilaginous joint joint

*LOB: Classify joints according to the 3 main classes of joint:
fibrous, cartilaginous, synovial

Answer

A

(amphiarthrosis).
Slightly mobile e.g. intervertebral disc

Question 3

Q

Structure and Function of Joints by Nidhi Sofat

What is the function of joints?

*LOB: Classify joints according to the 3 main classes of joint:
fibrous, cartilaginous, synovial

Answer

A

Transmit loads.
Allow movement,
yet provide stability

Question 4

Q

Structure and Function of Joints by Nidhi Sofat

What is a Synovial joint

*LOB: Classify joints according to the 3 main classes of joint:
fibrous, cartilaginous, synovial

Answer

A

(diarthrosis).
Freely mobile e. g. limb joints

Question 5

Q

Structure and Function of Joints by Nidhi Sofat

Types of movement allowed by synovial joints

*LOB: Classify joints according to the 3 main classes of joint:
fibrous, cartilaginous, synovial

Answer

A

Planar (sliding) joints e.g. intertarsal joints (foot)

Simple hinge joint e.g. interphalangeal joint (fingers) humero-ulnar (elbow)

Pivot (i. e. rotational) joints

Saddle joints e.g. carpo-metacarpal, base of thumb

Complex hinge with sliding + rotation ie)- the knee

Ball-and-socket e.g. hip, shoulder; maximum mobility, but least stability Abd/adduction Flexion/extension Rotation

Question 6

Q

Structure and Function of Joints by Nidhi Sofat

5 ways to achieve stability

*LOB: Relate the structural elements of different joints to their functions (including intra- and extra-articular elements)

Answer

A

Congruity (matching the shapes of the bone ends)
Fibrous capsule & its thickenings into extra-articular
ligaments
Intra-articular ligaments
Packing to improve congruity, by-
- menisci (semilunar cartilages, knee)
- fat pads (e.g. infrapatellar fat pad of knee)
- Muscles acting across the joint
*

Question 7

Q

Structure and Function of Joints by Nidhi Sofat

Intra-articular structures of the knee

*LOB: Relate the structural elements of different joints to their functions (including intra- and extra-articular elements)

Question 8

Q

Structure and Function of Joints by Nidhi Sofat

Key features of synovial joint

*LOB: Relate the structural elements of different joints to their functions (including intra- and extra-articular elements)

Question 9

Q

Structure and Function of Joints by Nidhi Sofat

What is aggrecan

*LOB: Relate the structural elements of different joints to their functions (including intra- and extra-articular elements)

Answer

A

large proteoglycan
Glycosamino-glycan chain (GAG)
e.g. chondroitin sulphate keratan sulphate, hyaluronan
*

Question 10

Q

Structure and Function of Joints by Nidhi Sofat

What is cartilage? What does it contain?

*LOB: Explain how the components of cartilage contribute to its function

Answer

A

a strong, flexible connective tissue that protects your joints and bones

collagen parallel to surface
Type II collagen fibrils
Aggrecan
Chondrocytes
Hyaluronan

Question 11

Q

Structure and Function of Joints by Nidhi Sofat

What is the function of cartilage and its components?

*LOB: Explain how the components of cartilage contribute to its function

Answer

A

acts as a shock absorber throughout your body and reduces friction

collagen parallel to surface- smooth articulating surface
Type II collagen fibrils - hold it together- resist gel swelling tendency
Aggrecan- huge osmotic pressure inflates cartilage with water (gel swelling pressure
Chondrocytes- secrete the collagen, proteoglycans & hyaluronan
Hyaluronan- tethers the aggrecan

Question 12

Q

Structure and Function of Joints by Nidhi Sofat

Synovial Joint features….

*LOB: Describe the composition, process of formation and role of synovial fluid, and relate this to the pathophysiology of synovial effusion

Answer

A

Articular cartilage is avascular; its nutrients come from the synovial fluid

The synovial fluid gets nutrients from synovial capillaries

Type B cell, synoviocyte,fibroblast-like,Role: to secrete hyaluronan & lubricin

Very superficial, fenestrated capillaries. Role: - produce synovial water-stock it with nutrients for avascular cartilage.

Fenestrations (ultrathin 4nm, water-permeable membranes)- close to surface

An ultrafiltrate of plasma generated by fenestrated capillaries just below synovial surface.

Electrolyte & plasma protein content similar to other interstitial fluids.

Actively secreted molecules lubricin & hyaluronan are added by the synoviocytes.

Lubricin, a glycoprotein, lubricates cartilage under conditions of high load and low velocity (boundary lubrication)

Hyaluronan is a gigantic nonsulphated GAG, Mw 6 million, hydrated radius 100-200 nm (bigger than viruses!). Makes synovial fluid very viscous (syn-ovium = like egg white). Lubricates synovial surface & cartilage under conditions of low load and high velocity (hydrodynamic lubrication - like oil in a car engine).

Question 13

Q

Structure and Function of Joints by Nidhi Sofat

Synovial Fluid

*LOB: Describe the composition, process of formation and role of synovial fluid, and relate this to the pathophysiology of synovial effusion

Answer

A

Volume of fluid is tiny - thickness of fluid film is normally only 10-100 mm.

Volumeincreases 10-100 times in arthritis - called a joint effusion.

Pressure varies with joint angle; subatmospheric in extension, rising above atmospheric on flexion. So fluid enters joint in extension and is driven out of it on flexion.

In arthritic joint effusion, pressure is above atmospheric even in extension and pressure-angle relation is extremely steep. A minimum pressure at a certain angle determines the affected joint’s ‘angle of ease’.

Question 14

Q

Structure and Function of Joints by Nidhi Sofat

Pressure in Synovial Fluid

*LOB: Describe the composition, process of formation and role of synovial fluid, and relate this to the pathophysiology of synovial effusion

Answer

A

**subatmospheric in extension
rising above atmospheric on flexion

Question 15

Q

Structure and Function of Joints by Nidhi Sofat

Why is Hyaluronan important?

*LOB: Describe the composition, process of formation and role of synovial fluid, and relate this to the pathophysiology of synovial effusion

Answer

A

Lubrication of Joints: One of the primary roles of Hyaluronan is to contribute to the lubrication of joints. It forms a gel-like structure within the synovial fluid, providing a slippery surface that reduces friction

Shock Absorption:The viscoelastic nature of Hyaluronan allows it to absorb shock within the joint.

Cushioning: helps distribute the load evenly across the joint surfaces, preventing concentrated pressure points that could lead to damage or discomfort.

Nutrient Transport:

Maintenance of Joint Space Volume: The ability of Hyaluronan to bind with water molecules helps maintain the volume and viscosity of the synovial fluid. This is crucial for creating an optimal environment within the joint, ensuring that it remains properly lubricated and functional. like sponges in water

Question 16

Q

Structure and Function of Joints by Nidhi Sofat

How is synovial fluid synthesised?

*LOB: Describe the composition, process of formation and role of synovial fluid, and relate this to the pathophysiology of synovial effusion

Answer

A

DURING EXTENSION
Joint pressure is lower than capillary pressure
Fluid moves from capillary to joint (ultrafiltrate of blood plasma)

Question 17

Q

Structure and Function of Joints by Nidhi Sofat

How is Synovial Fluid drained?

*LOB: Describe the composition, process of formation and role of synovial fluid, and relate this to the pathophysiology of synovial effusion

Answer

A

DURING FLEXION
During flexion, pressure is raised in the joint
Fluid is driven out of joint
And into subsynovium - lymphatic drainage of H2O and proteins

Question 18

Q

MSS Joint Disease and Arthritis

Synovitis

*LOB: Describe patterns of joint disease using appropriate terminology (e.g. monoarthritis, oligoarthritis, polyarthritis) and identify common causes for these patterns

Answer

A

swelling (inflammation) in the synovial membrane that lines some of your joints

Causes: arthritis and injury.
Places: mainly hands and knees

Question 19

Q

MSS Joint Disease and Arthritis

Tenosynovitis

*LOB: Describe patterns of joint disease using appropriate terminology (e.g. monoarthritis, oligoarthritis, polyarthritis) and identify common causes for these patterns

Answer

A

a broad term describing the inflammation of the fluid-filled synovium within the tendon sheath

Think TENO- tendon synovitis
Symptoms: sharp pain, swelling, contractures

Question 20

Q

MSS Joint Disease and Arthritis

Enthesitis/enthesopathy

*LOB: Describe patterns of joint disease using appropriate terminology (e.g. monoarthritis, oligoarthritis, polyarthritis) and identify common causes for these patterns

Answer

A

First stage in ankylosing spondylitis
Inflamation of the enthesis

Enthesis is the site where a tendon inserts into a bone

Symptoms: pain swelling and inflamation in the peripheral joints

Question 21

Q

MSS Joint Disease and Arthritis

Osteitis

*LOB: Describe patterns of joint disease using appropriate terminology (e.g. monoarthritis, oligoarthritis, polyarthritis) and identify common causes for these patterns

Answer

A

inflammation of the substance of a bone.

NOTE: osteomyelitis is inflammation of the osseous medulla. The term osteitis reflects a more superficial inflammation of the cortex of the bone

Question 22

Q

MSS Joint Disease and Arthritis

Bursitis

*LOB: Describe patterns of joint disease using appropriate terminology (e.g. monoarthritis, oligoarthritis, polyarthritis) and identify common causes for these patterns

Answer

A

inflamation of bursae — that cushion the bones, tendons and muscles near your joints

Pain, swelling, and tenderness near a joint

Temporary, often overuse injury or infection

Question 23

Q

MSS Joint Disease and Arthritis

How to assess patient with arthritis?
History taking

Answer

A

Pain? SOCRATES
Stiffness:
Time of the day
After rest/exercise
Duration
Joint swelling
Physical function limitation

Question 24

Q

MSS Joint disease and arthritis

What are Arthritis associated symptoms?

Answer

A

Associated symptoms
Skin, nail, hair and mucosal changes
Raynaud’s Phenomenon
Ocular and visual
Respiratory and Cardiovascular
GI
Neurological
Urinary
Constitutional symptoms

Question 25

Q

MSS Joint disease and arthritis

Skin changes in arthritis

Answer

A

Atrophic (thin, wrinkled) skin, which is fragile and easy to bruise
Pale, translucent skin on the backs of the hands
Dry skin (xerosis)
Palmar erythema (red palms)
Raynaud phenomenon
Nail changes – brittle nails, onycholysis, nail ridging and splitting, clubbing, ventral pterygium.
Rheumatoid arthritis-related skin diseases

Question 26

Q

MSS Joint disease and arthritis

Raynauds Phenomenon

Question 27

Q

MSS Joint Disease and Arthritis

Oral and Genital ulcers

Answer

A

reactive arthritis, Behçet’s disease, and systemic lupus erythematosus are associated with mouth sores, too

Question 28

Q

MSS joint disease and arthritis

Ocular symptoms in arthritis

Answer

A

Inflammation -> Sclera -> Red eyes, pain, light sensitivity

Inflammation -> Uvea -> (middle layer incl IRIS) -> Red cornea, vision loss (55% Macula damage)

uveitis can cause vision loss

OTHER
Keratoconjunctivitis sicca
Episcleritis (Conjunctiva)
Scleromalacia (non-inflammatory form of anterior necrotising scleritis, Rare bilateral)

Scleromalacia perforans
a rare, severe eye disorder developing an autoimmune damage of episcleral and scleral performing vessels. Type 3 Hypersensitivity

Question 29

Q

MSS Joint disease and arthritis

What are the symptoms and features of inflammatory arthritis

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

Inflammatory
Pain: worse at rest and better on movement
Stiffness: Especially in the morning. Prolonged (>30 minutes)
Swelling:
Erythema
Warmth
Systemic symptoms

Question 30

Q

MSS Joint disease and arthritis

What are the symptoms and features of non- inflammatory arthritis

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

Non-inflammatory
Pain: worse on movement/ weightbearing and relieved by rest
Stiffness: <30 minutes

Question 31

Q

MSS Joint disease and arthritis

What are the main types of arthritis

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

Inflammatory
Rheumatoid arthritis
Psoriatic arthritis
Spondyloarthropathies
Crystal arthritis
Connective tissue diseases
Septic

Non-inflammatory
Degenerative: osteoarthritis
Trauma induced
Chronic pain syndromes

Question 32

Q

MSS Joint disease and arthritis

What are the features of acute monoarthritis?

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

Can occur in infectious arthritis, gout, or trauma (not typical for RA or OA).
Infections should be excluded
Trauma
Crystals: such as calcium pyrophosphate (pseudogout) and monosodium urate (gout)
Hemarthrosis

Question 33

Q

MSS Joint disease and arthritis

What are the features of chronic monoarthrisi?

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

Osteoarthritis
Infections: TB
Tumours

Monoarthritis refers to inflammation that affects a single joint instead of multiple joints. It may manifest in joint pain, swelling, and stiffness. Acute causes include infections, Lyme disease, crystal-induced arthritis, and trauma. Chronic causes include osteoarthritis, rheumatoid arthritis, and spondyloarthritis

Question 34

Q

MSS Joint disease and arthritis

What are the symptoms and features of acute oligoarthritis?

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

can be seen in reactive arthritis
Crystals: such as calcium pyrophosphate (pseudogout) and monosodium urate (gout)
Infections should be excluded

Question 35

Q

MSS Joint disease and arthritis

What are the symptoms and features of chronic oligoarthritis?

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

arthritis of unkown origin
osteoarthritis
Can be seen in both RA (early stages) and OA.
oligoarthritis affects fewer than five joints
most often the large joints like the knees, ankles and elbows
the most common type of juvenile idiopathic arthritis (JIA).

Question 36

Q

MSS Joint disease and arthritis

What are the symptoms and features of acute polyarthritis

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

Autoimmune: JIA, SpA, Psoriatic, RA, CTD
Crystals: such as calcium pyrophosphate (pseudogout) and monosodium urate (gout)
polyarthritis affect five joints or more, and more often smaller joints in the hands and feet.
Infections (especially viral infections) should be excluded
Can be seen in infectious causes, or early RA but not typical for OA.

Question 37

Q

MSS Joint disease and arthritis

What are the symptoms and features of chronic polyarthritis?

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

polyarthritis affect five joints or more, and more often smaller joints in the hands and feet.
Autoimmune: JIA, SpA, Psoriatic, RA
Typical of RA.

Question 38

Q

MSS Joint disease and arthritis

Which are OA and RA?

*LOB: Identify important features of the rheumatological history and differentiate between an inflammatory and non-inflammatory arthritis in relation to the history and examination

Answer

A

Rheumatoid Arthritis (RA):
Chronic Polyarthritis
Chronic Oligoarthritis (less common)

Osteoarthritis (OA):
Chronic Monoarthritis
Chronic Oligoarthritis

Less Common in RA and OA:
Acute Monoarthritis (rare in both)
Acute Oligoarthritis (rare in both)
Acute Polyarthritis (rare in both, but can occur in early RA)

Question 39

Q

MSS Joint disease and arthritis

What is JIA?

*LOB: Describe patterns of joint disease using appropriate terminology (e.g. monoarthritis, oligoarthritis, polyarthritis) and identify common causes for these patterns

Answer

A

Juvenile idiopathic arthritis (JIA) is a form of arthritis in children.

Question 40

Q

MSS Joint disease and arthritis

What is SpA?

*LOB: Describe patterns of joint disease using appropriate terminology (e.g. monoarthritis, oligoarthritis, polyarthritis) and identify common causes for these patterns

Answer

A

Spondyloarthritis (SpA), a family of inflammatory back diseases including ankylosing spondylitis

Question 41

Q

MSS Joint disease and arthritis

What is ReA?

*LOB: Describe patterns of joint disease using appropriate terminology (e.g. monoarthritis, oligoarthritis, polyarthritis) and identify common causes for these patterns

Answer

A

Reactive Arthritis

Question 42

Q

MSS Inflammatory Arthropathies

Arthritis Risk Factors

*LOB: Outline the pathogenesis of rheumatoid arthritis and relate to the clinical presentation of rheumatoid arthritis

Answer

A

FHx:
3 fold increase in 1’ & 2 fold increase in 2’ relatives

Genes:
HLA-DRB1(the strongest). (MHC GENE)
Others: CTLA4, PTPN22,STAT4,TRAF1-C5 (TNF family),PADI4

DEMO Age sex ethnicity

SHx smoking, EtOH, obesity, infections and occupation (sillica)

Question 43

Q

MSS Inflammatory Arthropathies

Arthritis Pathogenesis

*LOB: Outline the pathogenesis of rheumatoid arthritis and relate to the clinical presentation of rheumatoid arthritis

Answer

A

Background
* Epigenetic mod + susceptible gene
* Self-protein citrullination
* Loss of tolerance
* Autoantibodies

Arthritis
* Triggers incl infection, microvasculature, neuroimmune, biomechanic (injury)
* Synovitis
* Sturctural damage
* Applified by co-existing disease like osteroporosis and vascular disease
* RECRUIT AUTOANTIBODIES TO SITE

Question 44

Q

MSS Inflammatory Arthropathies

Key biochemical players in Arthritis

*LOB: Outline the pathogenesis of rheumatoid arthritis and relate to the clinical presentation of rheumatoid arthritis

Answer

A

DAMPS PAMPs and Proteases
Circulating white cells include: Dedrite (CD80/8), Th1 and Th17, B Cell, Plasmablast CD20 (Rheumatoid Factor), Neutrophils (prostaglandins, ROS), Mφ (TLR, TNFα, CXC, IL-6), Chondrocytes and Osteoclasts
Fibroblast-like synoviocyte (IL6, IL1, TNFα TGFΒ PDGF CXC)

Question 45

Q

MSS Inflammatory Arthropathies

Which RA has joint involvement?

*LOB: Outline the pathogenesis of rheumatoid arthritis and relate to the clinical presentation of rheumatoid arthritis

Answer

A

Insidious polyarthritis 70%

Acute polyarthritis 20%

Acute oligo or monoarthritis (not common)

Palindromic rheumatism 10%

Polymyalgic

Question 46

Q

MSS Inflammatory Arthropathies

What joints are affected?

*LOB: Outline the pathogenesis of rheumatoid arthritis and relate to the clinical presentation of rheumatoid arthritis

Answer

A

MCPs, PIPs and MTPs, wrists, ankles and Knees 80%-90%

Hip, elbow 50%

Atlantoaxial joint 10%

Psoriatic Arthritishits DIPS, Rheumatoid hits PIPS and spares DIPS

Question 47

Q

MSS Inflammatory Arthropathies

What joint deformities in arthritis?

*LOB: Outline the pathogenesis of rheumatoid arthritis and relate to the clinical presentation of rheumatoid arthritis

Answer

A

Boutonniere deformity
Swan neck deformity
Ulnar deviation of the fingers
Z-shaped deformity of the thumb (Hitchhiker’s thumb)
Claw toe deformity

Question 48

Q

MSS Inflammatory Arthropathies

What are the extraarticular features in arthritis?

Remember arthritis is systemic so what else happens?

*LOB: Outline the pathogenesis of rheumatoid arthritis and relate to the clinical presentation of rheumatoid arthritis

Answer

A

75% of patients develop one or more extra-articular manifestations within 5 years of the onset of RA
Fatigue and weight loss (early on)
Rheumatoid Nodules (20%) at pressure sites
Normochromic, normocytic anaemia (Iron utilisation is impaired)
Thrombocytosis
Felty’s: RA, splenomegaly, neutropenia, inc infection risk
Pleural effusion: common, usually subclinical
Interstitial lung disease
Pulmonary nodules: rare
Pericarditis is most common cardiac manifestation
Cardiovascular disease
Ocular
Cervical cord compression
Carpal tunnel
peripheral neuropathy
Vasculitis incl nailfold splinter haemmorhages

Question 49

Q

MSS Inflammatory Arthropathies

What tests for arthritis?

*LOB: Outline the pathogenesis of rheumatoid arthritis and relate to the clinical presentation of rheumatoid arthritis

Answer

A

FBC
ESR, CRP
U&E, LFTs
Rheumatoid factor
IgM antibody directed against patients IgG immunoglobulin
High titre in extra-articular disease, nodules and in severe disease
Anti-CCP antibody Anti–cyclic citrullinated peptide (anti-CCP)
Image for joint changes and synovial fluid loss
*

Question 50

Q

MSS Inflammatory Arthropathies

Arthritis Ddx

*LOB:Compare rheumatoid arthritis with other common inflammatory joint diseases such as gout and psoriatic arthritis

Answer

A

Psoriatic arthritis
Reactive arthritis
Arthritis of inflammatory bowel disease
Crystal induced arthritis
Osteoarthritis
Viral polyarthritis: HBV, HCV, or human parvovirus B19 .. etc
Connective tissue diseases: systemic lupus erythematosus (SLE), Sjögren’s syndrome, dermatomyositis .. etc
Polymyalgia rheumatica

Question 51

Q

MSS Inflammatory Arthropathies

What is psoriatic arthrisis?

*LOB:Compare rheumatoid arthritis with other common inflammatory joint diseases such as gout and psoriatic arthritis

Answer

A

Psoriatic arthritis
Personal or family history of psoriasis (>90%)
Seronegative
Mono and oligoarthritis
Asymmetric
Large joints
DIP affected
Lower limbs
Sacroiliitis and axial SpA
Enthesitis are common
Dactylitis 50%
Uveitis

Question 52

Q

MSS Inflammatory Arthropathies

What is RA?

*LOB:Compare rheumatoid arthritis with other common inflammatory joint diseases such as gout and psoriatic arthritis

Answer

A

Rheumatoid arthritis
Seropositive 80%
Polyarthritis
Symmetric
Small joints
DIP spared
Cervical spine
Enthesitis are not common
Dactylitis 5%
Sicca, episcleritis (5%) and scleritis (2%)

Question 53

Q

MSS Inflammatory Arthropathies

What is Crystalline arthritis/ gout?

*LOB:Compare rheumatoid arthritis with other common inflammatory joint diseases such as gout and psoriatic arthritis

Answer

A

Seronegative
High uric acid
Initially monoarthritic – can become polyarticular
Tophi on physical examination
urate crystals in synovial fluids

Question 54

Q

MSS Inflammatory Arthropathies

Arthritis therapy

*LOB:Compare rheumatoid arthritis with other common inflammatory joint diseases such as gout and psoriatic arthritis

Answer

A

Corticosteroids

Conventional synthetic (nonbiologic) disease-modifying antirheumatic drug (sDMARD) therapies: methotrexate, sulfasalazine, hydroxychloroquine, leflunomide

Biologic therapies (bDMARD): TNF inhibitors, interleukin (IL) 6 inhibitors, B-cell depletion therapy, T-cell costimulation blocker, and JAK inhibitors

Question 55

Q

MSS Inflammatory Arthropathies

What is crystalline arthritis/ psuedo gout?

*LOB:Compare rheumatoid arthritis with other common inflammatory joint diseases such as gout and psoriatic arthritis

Answer

A

Calcium pyrophosphate crystals in synovial fluids
Neutrophils phagocytose
Pro-inflammatory
Chondrocalcinosis on radiographs

Pc acute monoarthritis
Risk: Trauma, Age, Metabolism, Genetic

Question 56

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

What are the types of Arthritis?

*LOB: Discuss pathological changes in cartilage and the chondrocyte which lead to cartilage degradation

Answer

A

Acute
Monoarticular (1 joint)
Polyarticular (> 1 joint)

Causes
Infection
Injury

Chronic
Monoarticular (1 joint)
Polyarticular (> 1 joint)

Causes
Immune-mediated
e.g. RA
Cartilage degeneration e.g. OA
Other

Question 57

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

Stages of Athritis cartilage breakdown

*LOB: Discuss pathological changes in cartilage and the chondrocyte which lead to cartilage degradation

Answer

A

Normal
Early fibrillation
Chondrocyte loss
Deep fissuring
Chondrocyte death
Matrix loss

Question 58

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

OA vs RA breakdown

*LOB: Discuss pathological changes in cartilage and the chondrocyte which lead to cartilage degradation

Question 59

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

What contributes to joint pain?

*LOB: Discuss pathological changes in cartilage and the chondrocyte which lead to cartilage degradation

Answer

A

Pain sensitivity
Neurochemical function
Descending modulatory system

Joint Damage
Cartilage quality
Joint laxity
Geometry
Inflamation

Psychosocial
Stress
Emotion
Exercise

Question 60

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

What contributes to joint pain?

*LOB: Discuss the conservative, medical and surgical treatments of osteoarthritis

Answer

A

Pain sensitivity
Neurochemical function
Descending modulatory system

Joint Damage
Cartilage quality
Joint laxity
Geometry
Inflamation

Psychosocial
Stress
Emotion
Exercise

Question 61

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

Which proteinases degrade joint tissue?

*LOB: Discuss pathological changes in cartilage and the chondrocyte which lead to cartilage degradation

Answer

A

two families of metalloproteases – MMPs and the ADAMTSs – are responsible for the degradation of the major components of this tissue.

Question 62

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

Catabolic factors in cartilage

*LOB: Discuss pathological changes in cartilage and the chondrocyte which lead to cartilage degradation

Answer

A

IL-1

IL-17

IL-18

Oncostatin M

TNF

Question 63

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

Anabolic
factors in cartilage

*LOB: Discuss pathological changes in cartilage and the chondrocyte which lead to cartilage degradation

Answer

A

Activin

CTGF

FGF-2

IGF-1

TGF

BMP-2,-4,-6,-7,-9,-13

Remember B for build and G for Growth

Question 64

Q

MSS Cartilage, Chondrocytes and Osteoarthritis

anti-catabolic factors in cartilage

*LOB: Discuss pathological changes in cartilage and the chondrocyte which lead to cartilage degradation

Answer

A

IL-1ra

IL-4

IL-10

IL-13

Answer 61

A

IL-4

IL-6

LIF

Answer 62

A

Injury, Aging, ROS, Mechanical stress,Degraded ECM
Abnormal ECM synthesis, Inflammatory cytokines
LPS, Genetics, Obesity

Fragments of Aggrecan and Collagen activate DDR2 receptors

Fragments of Fibronectin and hyalyronan activate TLR4

Fragments of fibromodulin activate complement

ProMMP can activate for matric breakdown
ADAMTS4,5 release activates for matrix breakdown

Answer 63

A

specific areas in joint
cartilage and bone

Answer 64

A

Joint space narrows
subchondral cysts
cartliage loss
Sclerosis

Answer 65

A

Doppler to show inflamation
Lesions
Ossification

Answer 66

A

Lining cell hyperplasia (border cells thicken)
Increased vascularity (vascular structures/ cells)
Subintimal fibrosis (fibrosis in layers)
Mononuclear cell aggregates (white cells infiltrate)

Answer 67

A

Education, strengthening, lifestyle changes, fitness, weight management, pain killers, insoles, tens, support and brace, heat and cold

Answer 68

A

paracetamol
topical nsaids
Capsaicin
oral nsaids inc COX2 inhibitor
Inter aticular corticosteroid injections
Opiods
steroids

Answer 69

A

arthroscopy, cartilage repair, osteotomy, and knee arthroplasty.

Answer 70

A

Central pain processing ie) duloxetine, amitrityline

Dorsal root ie) cannabidoids and opiates

OA joint ie) effusion, hyaluronic acid, NSAIDs

Answer 71

A

Growth factor to replace cartilage
Invossa gene therapy
Joint distraction
Steroids to control flares
Capsaicin
NSAIDS ?long term effects
Monoclonal Ab against NGF
Autologous chondrocyte implantation for Knee Chondral Defects

Answer 72

A

Integument, or integumentary system: refers to the skin, hair and nails.
Largest and heaviest organ of the body – ~15% of adult weight.

Answer 73

A

Barrier (protection), against:
Dehydration
Infection
Injury / abrasion
Solar radiation
Thermoregulation
Sensation
Repair
Vitamin D production

Answer 74

A

Epidermis
Dermis
Hypodermis

Answer 75

A

Epidermis
Dermis
Hypodermis
Hairs
Glands
Nails
Sense organs

Answer 76

A

Outer epithelial layer
With 4 sublayers
1. Basal layer(Stratum basale)
2. Stratum spinosum (spiny layer)
3. Stratum granulosum (Granular layer)
4. Stratum corneum (cornified layer)

Answer 77

A

Single layer
containing stem cells (constantly proliferate)
attached to dermis via basement membrane

Main cell type keratinocytes

Dynamic - Daughter cells constantly move “up” (distally) through the epidermis, differentiating as they go, until they are shed from the outer surface. This takes ~20-50 days.

Answer 78

A

2nd layer
Thickest of living layers
Lots of Desmosomes (juntions)
Differentiating and moving distally; not dividing.
Cells have many desmosomes (junctions), visible at high magnification as “spines” between the cells. Strong bonds holding the epidermis together.

Answer 79

A

1-4 layers of cells with granules of keratohyalin (pre-keratin)
Lamellar bodies contain lipids (for waterproofing)

Answer 80

A

Outer protective layer
Thicker depending on body site such as palmar thicker
Squamous cells w/o nuclei
Cornified with keratin protein
Tough injury resistance
Non polar lipids between layers

Cornified from Keras - horn (rhino horn)

Answer 81

A

Dendritic shape
DOPA stain shows their form
skin pigment
No melanin – albino mammals

Synthesises melanosomes
and transfers melanosomes (pigment granules) to the basal keratinocytes via dendrites

Do not cross to upper layers of skin
They do not break the basal cell layer

Answer 82

A

the basal layer

Capped for UV protection

Answer 83

A

Mφ like APC
Dendritic shape, form network
Stain pale.

Answer 84

A

Basal cells (somewhat stratum spinosum)
Requires UV (higher in darker skin)
NOT ACTIVE FORM
Converted to active form in liver

UK deficiency high.

Answer 85

A

Dense irregular connx. tissue w/ collagen
Tensile strength
Protection against abrasion
Fibroblasts make collagen. Upreg in wound healing (revise)
Elastin protein for elasticity (loss in UV/age)
Blood and nerve supply
Blood flow reg for thermoreg
**dermis fibroblasts fill gaps w new collagen. **

EPITHELIA NEVER HAVE BLOOD VESSELS

Answer 86

A

Wavy, resistant to shear forces
Such as hands, feet
Rete (ree-tee) Ridges in epidermis
Dermal papillae (finger-like) in dermis

Answer 87

A

aka fascia or subcutis
Fat cells- adipocytes
(not seen on H&E as fat removed, cell border visible)
containing glands, hair follicles, nerves, blood vessels.
Often the thickest layer of skin. Thickness varies with age, body site, nutrition etc.
Function: provides insulation, cushioning and energy storage.

Answer 88

A

Eccrine sweat glands
Sebaceous glands
Apocrine sweat glands

Answer 89

A

normal sweat glands. Watery secretion on to skin surface, cools body by evaporation.

Answer 90

A

secrete oily sebum (“lanolin”) into hair follicle.
Conditioner for hair and skin,
prevents dryness and flaking.
Only from around puberty.

Answer 91

A

secrete into hair follicles.
Found only in armpits and anogenital region.
Oily fluid in humans, function unclear (contains pheromones in some mammals).
Source of body odour after bacterial action.
(Less odour in Asian people – enzyme difference.)
Only after puberty.

Answer 92

A

Note much bigger diameter of apocrine than eccrine sweat glands.
Both are coiled tubes, showing a cluster of circles or ovals of cuboidal epithelium in cross-section.

Answer 93

A

rudimentary in humans over much of body. (Unlike most mammals.)
But keeps the head warm when present
Hair follicles site of acne

Answer 94

A

Nail bed is skin under nail
Nail plate is hard keratin
Nail matrix where nail is formed
The space under nail is hyponychium
3mm growth pmonth

Answer 95

A

Thermoreceptors- dermis
Meissners corpuscle- dermis- touch and vibration
Merkel Cells- light touch- basal epidermis
Nocicpetor free nerve endings- mainly dermis, reach epidermis
Pacinian copuscle- pressure- hypodermis

Answer 96

A

Dehydration- epidermis (keratin holds water)
Infection- epidermis impervious barrier, immune cells
Injury- All layers
UV- epiermis strat corneum and melanin
Thermoreg-hypodermis w fat and blood flow reg.
Sensation- nerves in layers
Repair- epidermis via proliferation but dermis fibroblasts fill gaps w new collagen.
Vit D- epidermis

Answer 97

A

Skin as a vital organ
Normal effects of environment on skin
Adaptations to temperature, friction, sun exposure

Abnormal effects: failure of skin protective functions (introduction)
Irritants, allergies and dermatitis
Cutaneous infections
Ultraviolet damage; burns, ageing and skin lesions including cancer

Skin will die if
Dehydration and shock
Infection
Heat loss and hypothermia (or sometimes hyperthermia due to impaired thermoregulation)
Others: protein loss; electrolyte imbalance; high-output cardiac failure; renal failure.

Answer 98

A

Sweating & vasodilatation in heat; vasoconstriction in cold.Quite fast (minutes)

Hyperkeratosis (callus): thickening of stratum corneum with rubbing or pressure (e.g. feet, guitarist fingers), or (slightly) after ultraviolet exposure. Slow (weeks)

Tanning (melanocyte response) after ultraviolet exposure. Quite slow (days)

Answer 99

A

Drying: Waterproof epidermis + oil from sebaceous glands

Friction, impact: Thick, regenerating epidermis; tough keratin
Wavy epidermal-dermal border against shear forces
Strong collagen fibre network in dermis
Nails

Cold: Subcutaneous fat, hair (head)

Radiation/sunlight: Thick, regenerating epidermis; melanin

Infections: Impervious epidermis; resident immune-system cells

Answer 100

A

Vessel walls relax to increase arterial blood flow and heat loss (when hot)

contract to decrease blood flow (when cold) to the superficial (subpapillary) plexus just below epidermis.

Hence skin goes redder or bluer.

Hairless (glabrous) skin, e.g. palms, also has arteriovenous (AV) shunts or anastomoses between arteries. Shunts likewise open (hot) for additional heat loss, or close (cold).

Answer 101

A

The colour of human skin is due mainly to melanin (dark skin) and haemoglobin (light skin)

Much** normal genetic variation** in the amount of melanin (many genes known)

Melanin protects against DNA damage and thus skin cancer, especially in dark (black & Asiatic) skin: skin cancer incidence only 8-10% that of white people.

Answer 102

A

UV radiation causes DNA breaks in keratinocyte
DNA breaks stimulate MSH: melanocyte-stimulating hormone
MSH leaves the cell to stimulate neighbouring melanocyte
MSH binds with receptor MC1R: melanocortin 1 receptor
The melanocyte via CAMP upreg ↑melanin synthesis & transfer and↑Cell division
Melanocytes then produce melanosomes whcih travel to basal keratinocytes
*Additional protection by epidermal thickening in response to UV.
MC1R gene – often mutated in humans with red or fair hair

Answer 103

A

More extreme form of hyperkeratosis. Reaction to excessive rubbing or scratching/ skin conditions

Answer 104

A

Occurs when too much exposure to a substance.
Can still use it, but reduce amount.
People vary in sensitivity
Any of: Redness, itching, swelling, blistering and/or scaling
NOT ALLERGY

Answer 105

A

Allergy to something that contacts skin - immune system involved
Tiny amount may be sufficient
Varies greatly between people May develop after long or short exposure
Any of: Redness, itching, swelling, blistering and/or weeping
Avoid allergen in future

IS AN ALLERGEN

Answer 106

A

Washing powder
Bleach
White spirit
SODA crystals
Polish
Chalk
Hydrogen peroxide

Answer 107

A

metals
leather shoe polish
Latex

Answer 108

A

(nail fold infection-fungal or bacterial)

Answer 109

A

Fungal example: Tinea capitis (scalp ringworm)

Answer 110

A

Bacterial

(children and elderky with thin skin)

Answer 111

A

Streptococcus

Answer 112

A

Virus example:
Human papilloma virus (HPV) (warts)

Answer 113

A

Is a radiation burn

Inflammation. Can include blisters, = epidermal cell death (severe DNA damage), or peeling (less severe DNA damage)

“Ever sunburnt” associates with increased risk of skin cancer

So does “ever used a UV sunbed below age 35” – by 75%

Answer 114

A

Sun allergy

Answer 115

A

Wrinkles - solar elastosis (loss of elasticity)

Answer 116

A

Benign proliferation of melanocytes

Many or large naevi: risk factor for melanoma skin cancer

Answer 117

A

Involve a genetic component. Also linked to red/fair hair. Often MC1R gene variants
Sun-exposed areas

Answer 118

A

liver spots,
age spots

Answer 119

A

Dysplastic growth of keratinocytes

Answer 120

A

Open question: Ask patient to describe their skin problem

Location/Distribution
Onset/duration
Associated symptoms: Itch, bleeding
Changes/Progression
Triggering factors
Treatments they have tried
Family history
Impact on patient’s life

Answer 121

A

Expose all affected skin areas
Inspect and palpate

Size/Shape/Symmetry
Type of rash/lesion (macular/papular/discoid/plaque)
Colour
Excoriated
Distribution
Palpation- texture, raised/ flat

Nails/Scalp
Dermatoscope (light and magnify)

Answer 122

A

Size/Shape/Symmetry
Type of rash/lesion (macular/papular/discoid/plaque)
Colour
Excoriated
Distribution
Palpation- texture, raised/ flat

NEVER SAY RASH

Answer 123

A

An inflammatory process affecting the skin and due to various factors, both internal and external
Interchangeable with the term ‘dermatitis’
Itchy skin condition

Answer 124

A

The most common form – affects 15% of population
In children – majority onset <5yrs, about 60% will clear by adolescence
Defect in skin barrier function causing skin to become more susceptible to irritation by soap and contact irritants, weather, temperature, etc
Chronic or acute flares
Usually associated with:
allergic rhinitis (hay fever)
Asthma
i.e. atopic tendency
*

Light skin- red patch. Dark skin- violaceous. (violet)

Answer 125

A

Infantile atopic eczema:
Widespread dry scaly skin
Can be weeping
Often cheeks are first area affected
Nappy area spared – moisture-effect

Toddlers/school-age children
More localised (flexural) and thickened, leathery (lichenified) lesions
Scratch marks
Elbows, knees, eyelids, ear creases, neck, scalp

Answer 126

A

Adults
Commonly persistent localised eczema
Recurrent secondary staphylococcal infection
Major factor for irritant contact dermatitis, particularly hands

Answer 127

A

Topical steroid:
mild
moderate
potent
very potent

Other – topical calcineurin inhibitors (Tacrolimus), oral antibiotics, antihistamines

Answer 128

A

Topical steroid:
mild, moderate, potent, very potent
Other – topical calcineurin inhibitors (Tacrolimus), oral antibiotics, antihistamines
Phototherapy
Systemic agents: Azathioprine, Methotrexate, Ciclosporin
Biologics – Dupilumab
Must meet specific criteria based on disease severity/quality of life
Must have trialed other systemic(s)

A referral to a Dermatologist should be made in cases of:
Diagnostic uncertainty
Severe eczema or poor response to topical therapy

Answer 129

A

Complications:
Bacterial co-infection – impetiginisation
Viral co-infection – eczema herpeticum
Post-inflammatory hypopigmentation/hyperpigmentation
Scarring
Striae/skin atrophy from steroid use
Depression/psychosocial impact

Answer 130

A

A chronic inflammatory disorder
Common (1-2% of population)
Focal, well-demarcated, inflamed, oedematous plaques covered with silvery-white scale
Can affect any age
No significant male/female difference
Scaly skin condition

Distribution:
Variety of size and shapes
Symmetrical
Extensor surfaces
Sacrum, scalp, ears, palms, soles
Nails
Environmental, genetic, immunologic factors

Answer 131

A

Disordered maturation of keratinocytes and reduced epidermal transit time from 30 days to 6 days
Leads to hyperproliferation and thickening of the epidermis

Answer 132

A

Topical:
Emollients
Topical steroids
Coal tar
Salicylic acid
Vitamin D analogues (Calcipotriol)
Combination of above
Dithranol

Phototherapy
Systemics: ciclosporin, methotrexate, acitretin
Biologics: Monoclonal antibodies against TNF/IL
Must meet specific criteria based on disease severity/quality of life
Must have trialed other systemic(s)

**Refer to Dermatologist if:
**
Diagnostic uncertainty
Severe psoriasis or poor response to topical therapy

Answer 133

A

EM
Acne lesions
Oily skin (seborrhoea)
Open and closedcomedones(blackheads and whiteheads) – arise when cells lining thesebaceousduct proliferate, and there is increasedsebum production. A comedone is formed by the debris blocking the sebaceous duct andhairfollicle
Papules (small, tender red bumps)
Pustules (white or yellow “squeezable” spots)
Nodules (large painful erythematous lumps)
Pseudocysts (cyst-likefluctuantswellings)
Scarring and post inflammatory hyperpigmentation
Individual acne lesions usually last less than 2 weeks but the deeper papules and nodules maypersistfor months.

Answer 134

A

Bacterial
Highly Infectious
Mainly children

Answer 135

A

. Chronic hives are welts that last for more than six weeks and return often over months or years

Answer 136

A

Intense and usuallywidespreadreddening of the skin . Associated withexfoliation(skin peeling off inscalesor layers.)
Affecting 90% or more of the skin surface.

Causes :
Eczema
Psoriasis
Cutaneous T cell lymphoma- extensive, persistent, lympathadenopathy.
Drug reaction
30% idiopathic

Answer 137

A

ABCDE & MDT approach (HDU/ITU/plastics/dermatology)
Discontinue all unnecessary medications
Monitor fluid balance – loss of fluid from skin results in electrolyte disturbance and dehydration
Maintain skin moisture and body temperature with wet wraps &greasy emollients
Antibiotics if superimposed bacterialinfection
Antihistamines if itch (often severe)
Identify underlying cause and start specific treatment e.g. topical&systemic steroids/ciclosporinforatopic dermatitis orpsoriasis.
*

Answer 138

A

HYPERSENSITIVITY
2 types (both have classic targetoid lesions)
1. Major
mucosal erosionsand blisters,
target lesions,
bullae
Cause: medications

Minor
No erosions/blisters
Targetoid lesions on extremities
Cause: infections

Management:
Stop offending drug
Treat underlying cause
Supportive/symptomatic

Answer 139

A

Medical emergency!

Variants of same condition with sheet like skin and mucosal involvement

Nearly always caused by medication: 80% started 1-3 weeks before presentation
Anyone on medication can develop SJS/TEN unpredictably - 40% caused by antibiotics.

Development a while
Skin pattern nasal vridge to epicanthal folds, under eye.

Answer 140

A

Investigations
SEPSIS 6
Skin biopsy

Management – general measures
ABCDE
Stop the drug
ITU, dermatology, plastics MDT management
Sterile handling of patient – reduce infections
Pain management
Temperature regulation - warm room
Nutrition (NG) & IV fluid management
Non-adherent dressings
Eye, mouth and genital care due to mucosal involvement
Physiotherapy and psychiatric support

Answer 141

A

Autoimmune blistering skin condition

Painful blisters anderosionson the skin andmucousmembranes, most commonly inside the mouth
IgG binds to Desmoglein 3 in the epidermis  keratinocytes separate from eachother and replaced by fluid

Diagnosis: skin biopsy for direct immunofluorescence IgG antibodies on the surface of keratinocytes in epidermis

Management: Symptom control + topicals + Systemic immunosuppression

Answer 142

A

Subepidermal autoimmune disease

Risk factors: neurological conditions, psoriasis, medications
Attack on collagen (BP180) in the basement membraneof theepidermis by IgG +/- IgEimmunoglobulins
Diagnosis: Direct immunofluorescence of askin biopsy linear deposition of IgG antibodies along the basement membrane (between the epidermis and dermis)
Management: emollients, potent topical steroids+ systemic steroids/ doxycycline/ immunosuppressants

Answer 143

A

Ibuprofen is a common ‘over the counter’ NSAID.
Usual dose 200-400mg tds PO.
Standard group of NSAIDs.

Inhibit enzyme cyclo-oxygenase (COX).

Answer 144

A

2 main types of COX enzymes:
COX-1 and COX-2
COX-1 produces prostaglandins which maintain gastric mucosa, platelet-initiated blood clotting
COX-2 generates prostaglandins which promote pain with inflammation.

Answer 145

A

Naproxen, Diclofenac, Indomethacin, Piroxicam, Celecoxib and Etoricoxib.

Answer 146

A

Side effects- headaches, dizziness, abdominal pain, diarrhoea, nausea and indigestion, bleeding, swollen ankles, chest pains, difficulty breathing, rash/sunlight sensitivity, high BP and effects on kidney.

Answer 147

A

Corticosteroids/steroids are synthetic versions of hormones.

Administered orally e.g. prednisolone/dexamethasone, intramuscular/intra-articular methylprednisolone injections , topical creams/gels e.g. Eumovate, intravenous methylprednisolone.

Answer 148

A

Ibuprofen is a common ‘over the counter’ NSAID.
Usual dose 200-400mg tds PO.
Standard group of NSAIDs.

Inhibit enzyme cyclo-oxygenase (COX).

Answer 149

A

Steroids are used sparingly in RA, but can be very beneficial, especially during a flare or when starting a new medication.

Answer 150

A

Relieve pain caused by inflammation rather than reducing the pathological inflammation and the RA degredation

Answer 151

A

class of drugs used in treatment of inflammatory arthritis/other autoimmune conditions
rheumatoid arthritis (RA), psoriatic arthritis (PsA), and spondyloarthritis.
connective tissue diseases such as systemic sclerosis (SSc), systemic lupus erythematosus (SLE), and Sjogren syndrome (SS).
inflammatory myositis, vasculitis, uveitis, inflammatory bowel disease, and psoriasis.
conventional DMARDs
biological DMARDs
*

Answer 152

A

7.5-25mg weekly

PO, SC, IM

BM suppression, effects on liver, GIT upset, rashes, pneumonitis, alopecia, headaches, menstrual cycle abnormalities, mood effects, infections, neoplasia

Answer 153

A

1-1.5G BD

PO

GIT upset, dizziness, cough, joint pain, rashes, allergic reaction, DRESS syndrome

Answer 154

A

200-400mg od

PO
GIT upset, rashes, tinnitus, retinopathy

Answer 155

A

10-20mg od

PO
GIT upset, alopecia, asthenia, weight loss, hepatotoxicity, high BP peripheral neuropathy, effects on blood count

Answer 156

A

1-3mg/kg
check thiopurine methyltransferase (TPMT) level

PO
BM suppression, agranulotosis, nausea, diarrhoea, alopecia, infection, skin sensitivity, rash

Answer 157

A

1.5mg/kg BD with an increase to 2.5mg BD after 6 weeks, if needed

PO
High BP, renal effects, nausea, diarrhoea, gingival hypertrophy, excess hair growth

Answer 158

A

MTX inhibits the enzyme dihydrofolate reductase, thereby depleting the pool of reduced folates
Common treatment for rheumatoid arthritis/inflammatory arthritis and other autoimmune diseases.
1940s developed as a chemotherapeutic agent.
1951 first used in rheumatic disease.

Research studies established the response, efficacy and safety of ‘low dose’ Methotrexate compared to cancer treatment.

Prodrug-active after polyglutamation in cells.
Take up to 27.5 weeks to achieve a steady state.
Therapeutic effect-on average 12 weeks.

80-90% eliminated via kidneys; renal impairment may lead to increased levels and toxicity effects on the bone marrow/other adverse effects.

Administered via oral, SC or IM routes with dose range from 7.5mg weekly to 25mg weekly typically used.

NSAIDs can reduce excretion of MTX, can be used at lower doses.

Answer 159

A

Blocks folate metabolism
Can also bind to folate dependent enzymes

reduces amount of FH4 available for purine and pyrimidine metabolism; amino acid and polyamine synthesis.

Answer 160

A

MTX leads to increased extracellular concentrations of adenosine, which has anti-inflammatory effects.
extracellular dephosphorylation of adenine nucleotides via ecto-5’-nucleotidase.

diminishing leukocyte recruitment

Rodents with no adenosine receptors have no anti-inflammatory effect from MTX (Montesinos et al. Arthritis Rheum 2003)

Other mechanisms: decreased production of proinflammatory by activated T cells, inhibition of methylation, suppression of IL-1β production by mononuclear cells.

Answer 161

A

Sulfasalazine has anti-inflammatory effects by reducing oxidative, nitrative, and nitrosative damage.

Leflunomide inhibits dihydroorotate dehydrogenase with inhibition of pyrimidine synthesis and preventing lymphocyte proliferation.

Hydroxychloroquine is mild agent which inhibits intracellular toll-like receptor TLR9.

Answer 162

A

A group of therapies produced from living cells/their components using biotechnology. They act by targeting different aspects of the immune system which promotes inflammation.

Answer 163

A

Anti TNF therapies e.g. Infliximab (chimeric anti-TNF monoclonal antibody), Adalimumab (humanised anti-TNF monoclonal antibody), Etanercept (TNF fusion protein)

IL-17 inhibitors e.g. Secukinamab (humanized monoclonal antibody to IL-17A, Ixekizumab

JAK inhibitors e.g. Tofacitinib, Updacitinib, Filgotinib

Apremilast (phosphodiesterase 4 [PDE4] inhibitor)

Answer 164

A

It activates signalling pathways: transcription factor activation (nuclear factor-κB), proteases (caspases), and protein kinases (c-Jun N-terminal kinase,MAP kinase).

This activates the target cell and releases cytokines with the initiation of the apoptotic pathway leading to inflammation.

Answer 165

A

Activation of other cells (macrophages, T-cells, B-cells)
Proinflammatory cytokine production (IL-1, IL-6), chemokine production (IL-8, RANTES),
Expression of adhesion molecule (ICAM-1, E-selectin)
Inhibition of regulatory T-cells, RANK-ligand expression upregulation, matrix metalloproteinase production and induction of apoptosis.

Answer 166

A

Dimeric human recombinant fusion protein

Fc of IgG1

Binds TNFα β with high affinity
No apoptosis of TNF expressing cells.

Answer 167

A

CHimeric mouse human mab (70%human)

Fc of IgG1k

Binds TNFα with high affinity
Apoptosis of TNF expressing cells.

Answer 168

A

Humanised IfF1k mAb anti TNF Ab

Binds TNFα β with high affinity
Circulating or cell bound
Apoptosis of TNF expressing cells.

Answer 169

A

Fully humanised IgG1k mAb AntiTNF

Binds TNFα with high affinity
Circulating or cell bound
Apoptosis of TNF expressing cells.

Answer 170

A

Fab fragment of recombinant fully humanised mAn Anti TNF
Fused with 400kDa peg moiety

Binds TNFα β with high affinity
Circulating or cell bound
No apoptosis of TNF expressing cells.
No complement or Ab toxicity

Answer 171

A

Increased risk of infection, reactivation of tuberculosis, shingles, hepatitis B.
Demyelination, drug-induced lupus, increased risk of skin cancer, headaches, rashes, allergies, mood disorders.
Blood abnormalities-leucopenia, anaemia, thrombocytopenia.
Injection site reactions, impaired healing.
Avoid in history of multiple sclerosis, stage III/IV heart failure, lung fibrosis, recent history of cancer.
*

Answer 172

A

Vasculitis
Connx tissue
Inflammatory

Results in Local or organ damage which progresses with morbidity and mortality

Answer 173

A

Psoriatic arthritis: Joint inflammation affecting various parts of the body.
Skin involvement: Psoriasis lesions, which may be widespread or localized.
Nail changes: Psoriatic disease can lead to nail abnormalities.
Psoriatic disease is characterized by chronic inflammation.
Inflammation not limited to the skin and joints but can affect multiple organs.
Association with comorbidities like cardiovascular disease and metabolic syndrome.
Increased risk of developing conditions such as inflammatory bowel disease.
Inflammation beyond the joints, affecting organs like the eyes (uveitis) and tendons (enthesitis).

Answer 174

A

Relative risk in first degree relative with Psoriatic Arthritis
30x more likely for PArhritis
5x more likely for Psoriasis

Answer 175

A

Frozen shoulder and tennis elbow 42%
Rotator Cuff tears RR5

Answer 176

A

Genetic Factors:
1. Familial predisposition
2. Specific genetic markers associated with rheumatic diseases
3. HLA (human leukocyte antigen) associations

B. Environmental Triggers:
1. Infections (viral, bacterial)
2. Environmental toxins
3. Smoking and other lifestyle factors
4. Hormonal influences

C. Immunologic Dysregulation:
1. Autoimmune response
2. Abnormal immune cell function
3. Dysregulated cytokine production
4. Loss of self-tolerance

D. Inflammatory Pathways:
1. Chronic inflammation
2. Tissue damage and repair mechanisms
3. Immune complex deposition
4. Synovial inflammation

Answer 177

A

Musculoskeletal Involvement:
1. Arthritis
2. Joint pain and swelling
3. Osteoporosis
4. Myositis

B. Cutaneous Manifestations:
1. Rash
2. Ulcers
3. Photosensitivity
4. Vasculitis

C. Systemic Involvement:
1. Fever
2. Fatigue
3. Weight loss
4. Lymphadenopathy

D. Organ-Specific Features:
1. Renal involvement
2. Pulmonary manifestations
3. Neurological symptoms
4. Gastrointestinal issues

E. Heterogeneity in Disease Progression:
1. Fluctuating disease activity
2. Remission and relapse patterns
3. Variable response to treatment

Answer 178

A

A. Atherosclerosis and Inflammation:
1. Chronic inflammation contributing to atherosclerotic plaque formation
2. Increased risk of coronary artery disease

B. Endothelial Dysfunction:
1. Vasculitis affecting blood vessels
2. Impaired endothelial function contributing to cardiovascular complications

C. Autoimmune-Mediated Cardiomyopathy:
1. Myocardial inflammation and damage
2. Heart failure as a complication

D. Accelerated Atherosclerosis:
1. Increased cardiovascular risk due to chronic inflammation
2. Premature atherosclerotic events

E. Monitoring and Management:
1. Regular cardiovascular assessment in rheumatic disease patients
2. Cardiovascular risk reduction strategies
3. Collaboration between rheumatologists and cardiologists for comprehensive care.

Answer 179

A

PROTEIN MATRIX (25%)
Organic osteoid
Type 1 collagen
Flexible with tensile strength

MINERAL (75%)
Calcium and Phosphate = Hydroxyapatite
Rigid
High compressional strength
Brittle

CELLS
Osteoblasts
Osteoclasts
Osteocytes
Lining cells
Bone marrow cells

Answer 180

A

CELLS
Osteoblasts- synthesise bone and matrix proteins
Osteoclasts- resorb boe
Osteocytes-mechanosensors
Lining cells-quiescent
Bone marrow cells- middle

Answer 181

A

Osteoblasts- synthesise bone and matrix proteins

Lining cells
Osteocytes
Apoptosis

Answer 182

A

Production of acid
Dissolution of mineral

Production of proteolytic enzymes
Digestion of matrix

Transcellular removal calcium, phosphate, matrix

Answer 183

A

Trabecular
Lower density
High surface area
High remodelling rate
Struts and plates

Cortical
Higher density
Low surface area
Low remodelling rate
Haversian systems

Answer 184

A

Quiescent= Resting
Resoption = osteoclast break
Formation = osteoblast build
Mineralisation = Calcium and Phosphate crystalise in bone

Then back to Q

Answer 185

A

Hormones play a crucial role in bone homeostasis. Parathyroid hormone (PTH) and calcitonin, for example, regulate calcium levels in the blood, influencing bone turnover.

Vitamin D, synthesized in the skin or obtained from diet, is essential for calcium absorption in the gut and bone mineralization.

Answer 186

A

The nervous system indirectly influences bone health through its control of physical activity. Weight-bearing activities and mechanical loading stimulate bone formation, while a lack of activity can lead to bone loss.
Neuropeptides, such as substance P, are involved in the regulation of bone remodeling and can influence bone cell activity.

Answer 187

A

The hypothalamus-pituitary axis plays a role in bone regulation.
Growth hormone (GH) from the pituitary gland stimulates bone growth and maintains bone density.
Sex hormones (estrogen and testosterone) produced by the gonads have a significant impact on bone health.
Estrogen, for example, helps maintain bone density in both men and women.
Adrenal hormones, such as cortisol, can influence bone turnover. Excessive cortisol, as seen in conditions like Cushing’s syndrome, may lead to bone loss.

Answer 188

A

Oestrogen/androgens
Growth hormone/IgF1
Calcitonin
Vitamin D

Answer 189

A

Thyroxine
Glucocorticoids
Parathyroid hormone

Answer 190

A

When bones become osteoporotic and fragile, the cortical bone (the outer shell) thins and the struts within the trabecular bone (inner mesh) also narrow and become less strong.

as ‘fragility fractures’

Eventually the architecture within the trabecular structure breaks down, leading to loss of bone strength and an increased risk fracture.

Answer 191

A

Measures Bone Mineral Density BMD

Bone mass and bone mineral density are synonymous

Quantity not quality

The scan uses low dose radiation; is painless and silent and involves lying on a bed for a few minutes.

Answer 192

A

Osteoporosis is a systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, leading to a high risk of fracture. 1
Often called a ‘silent disease’: people may not be aware that they have it until they break a bone

Answer 193

A

Normal T score does not exclude OP
Artefacts falsely elevate BMD – eg spine OA or fracture
Bone fragility can be due to poor bone architecture

Low T score is not always due to osteoporosis
Osteomalacia (undermineralised bone) also causes low BMD

Answer 194

A

Age: The risk of osteoporosis increases with age, as bone density tends to decrease over time.
Gender: Women are at a higher risk of osteoporosis than men, especially after menopause when estrogen levels decline.
Family history: If you have a family history of osteoporosis, you may be more likely to develop the condition.
Race and ethnicity: Caucasian and Asian women are at a higher risk, but people of all ethnicities can develop osteoporosis.
Hormonal changes: Low estrogen levels in women, especially after menopause, and low testosterone levels in men can contribute to bone loss.
Body weight: Being underweight or having a small body frame can increase the risk of osteoporosis and fractures.
Dietary factors: A diet low in calcium and vitamin D can contribute to weaker bones. These nutrients are essential for maintaining bone health.
Physical inactivity: Lack of weight-bearing exercise or physical activity can lead to bone loss. Regular exercise helps in maintaining bone density and strength.
Smoking: Smoking has been linked to lower bone density and an increased risk of fractures.
Excessive alcohol consumption: Heavy alcohol intake can interfere with the body’s ability to absorb calcium, leading to bone loss.
Certain medications: Long-term use of certain medications, such as glucocorticoids (corticosteroids), anticonvulsants, and some cancer treatments, can increase the risk of osteoporosis.
Medical conditions: Some medical conditions, such as rheumatoid arthritis, inflammatory bowel disease, and hormonal disorders, can contribute to bone loss.
Low body mass index (BMI): Having a BMI below the normal range may be associated with lower bone density and an increased risk of fractures.

Answer 195

A

Asymptomatic Stage: Osteoporosis often progresses without symptoms until a fracture occurs.
Fractures: Fragility fractures, especially in the spine, hip, and wrist, are common. Spinal fractures can lead to height loss, kyphosis (curvature of the spine), and back pain.
Pain: Chronic back pain may occur due to vertebral compression fractures.

Answer 196

A

Bone Density Testing:
Dual-Energy X-ray Absorptiometry (DEXA) scan measures bone mineral density (BMD) at the hip and spine.
T-scores compare BMD to that of a healthy young adult, while Z-scores compare to age-matched peers.
Fracture Risk Assessment:
FRAX tool assesses the 10-year probability of major osteoporotic fractures based on clinical risk factors.
Medical History and Physical Examination:
Evaluation of risk factors, family history, and presence of previous fractures.
Laboratory Tests:
Blood tests to assess calcium, vitamin D, and hormone levels.
*

Answer 197

A

Bone metastases
Myeloma screen
CXR
Need history and Ix

70% of vertebral fractures are not diagnosed
BUT not asymptomatic
Back pain is often not investigated

Once diagnosed - Start osteoporosis treatment quickly to prevent further fractures occurring

Answer 198

A

The T-score compares an individual’s bone mineral density to that of a healthy young adult of the same gender.
It is expressed in standard deviations (SD) from the average peak bone mass.
Normal: T-score above -1 SD
Osteopenia (Low Bone Mass): T-score between -1 and -2.5 SD
Osteoporosis: T-score -2.5 SD or lower
Severe Osteoporosis: T-score -2.5 SD or lower with a history of fractures

Answer 199

A

The Z-score compares an individual’s bone mineral density to that of an age-matched and sex-matched reference population.
Z-score results are used to assess bone density in the context of age.
A Z-score significantly below the expected range for age may indicate factors other than normal aging affecting bone density, such as underlying medical conditions.

Answer 200

A

Present
Often asymptomatic until fractures occur
Fragility fractures (fractures resulting from minor trauma or even normal activities)
Common sites: spine, hip, wrist
May lead to loss of height, stooped posture, back pain

Diagnosis:
Medical History and Physical Examination:
Fracture history
Risk factors (age, gender, family history, lifestyle, medications)
Bone Density Testing:
Dual-energy X-ray absorptiometry (DXA or DEXA scan)
Measures bone mineral density (BMD)
T-score compares patient’s BMD to that of a young, healthy adult
Laboratory Tests:
Blood tests to rule out secondary causes (e.g., vitamin D levels, thyroid function)
Imaging Studies:
X-rays to detect fractures
Vertebral fracture assessment (VFA) for spine evaluation
Fracture Risk Assessment:
FRAX tool: Calculates 10-year probability of major osteoporotic fracture or hip fracture
Incorporates clinical risk factors with BMD results
Additional Tests:
Bone turnover markers (blood or urine tests) to assess bone metabolism
Genetic testing in certain cases to identify rare genetic causes

Answer 201

A

Teriparatide daily subcut
For 2 yrs
Romosozumab mthly subcut

Women only
NICE approved in 2022
For 1 yr

The most effective drugs have antifracture efficacy at all 3 sites

Answer 202

A

Act on osteoclasts

Reduce bone resorption

Bisphosphonates – inhibit farnesyl pyrophosphate synthase
Denosumab - RANK ligand inhibitor

The most effective drugs have antifracture efficacy at all 3 sites

Answer 203

A

Osteoporosis drugs have varied half life in bone

Bisphosphonates
Long half life in bone
Concept of ‘drug pause’ after 5-10 years for mild osteoporosis

Non-bisphosphonates
have short half life in bone (quick onset, quick offset)
High fracture risk if treatment stopped or paused
Denosumab (risk of multiple vertebral fractures)
Anabolics – teriparatide/romosozumab
Don’t pause treatment when eg in hospital
At end of treatment, need follow on treatment plan, no gap

The most effective drugs have antifracture efficacy at all 3 sites

Answer 204

A

Elderly – reduced dietary calcium absorption
On steroids cause a negative calcium balance
On parenteral antiresorptives
Reduces Osteoclastic bone resorption
Less calcium released by osteoclasts from skeleton

The most effective drugs have antifracture efficacy at all 3 sites

Answer 205

A

Inspection
No wasting or fasciculation
Tone
Hypertonia
Power
Weakness
Reflexes
Hyperreflexia
Extensor plantar responses (Babinski’s sign positive)
Clonus

Answer 206

A

Inspection
wasting or fasciculation
Tone
Hyportonia
Power
Weakness
Reflexes
Hyporeflexia or areflexia
Flexor plantar responses (Babinski’s sign negative)
No clonus

Answer 207

A

Root Lesion
Disc Herniation

Answer 208

A

Plexus Lesion
Brachial Neuritis

Answer 209

A

Single nerve
(median nerve palsy, facial palsy)

Answer 210

A

Several induvidual nevres
Assymetric
Vasculitis

Answer 211

A

umerous peripheral nerves at the same time
distal
symmetrical
motor and sensory

Answer 212

A

Dorsal root ganglia
Purely sensory neuropathy
Paraneoplastic syndrome

Answer 213

A

Myelin sheeth pathology
Guillian Barre syndrome

Answer 214

A

Axonal degeneration
(diabetes)

Answer 215

A

Motor ± Sensory ± Autonomic
Distal pattern of weakness
LMN lesion (wasting, fasciculation,
hypotonia, hyporeflexia, flexor planter
response)
Gloves and stocks pattern of sensory loss
High-steppage gait

Answer 216

A

Motor (Normal reflexes and Normal sensory exam)
Proximal pattern of weakness (Difficulty in combing Hair,
standing from a Chair, climbing a Stair).
Waddling gait.
Positive Gower sign.

Answer 217

A

Motor (Normal reflexes usually and normal sensory exam)
Proximal pattern of weakness (Difficulty in combing Hair,
standing from a Chair, climbing a Stair)
Fatigable weakness
Ptosis, complex ophthalmoplegia, blurring of vision.
Dysarthria, dysphagia, dyspnea

Answer 218

A

Claw not benediction

Answer 219

A

wrist drop

Answer 220

A

Hx (alcohol, diabetes etc…)
FBC, LFTs, GGT and U+E’s TFTs Glucose or HBA1C
Plasma B12 and folate HIV
serum protein
electrophoresis and
immunoelectrophoresis
ESR, CRP (vasculitic
screens if indicated e.g.
ANA, ANCA, ENA etc…)
Urinalysis CXR
Nerve conduction
studies and
electromyography

Answer 221

A

Gowers SIgn present

Answer 222

A

Electromyography (EMG) and nerve conduction studies (NCSs) are valuable diagnostic tools that help neurologists locate and determine the causes of diseases that affect muscles and peripheral nerves

While EMG and NCSs are different tests, they’re often used together because the information gained from each test.

EMG used to diagnose myopathies
to differentiate between myopathy and neuropathy
to detect widespread denervation that would be present in motor neuronopathies such as motor neuron disease.

Answer 223

A

Spinal Cord Injury (SCI)
Spinal Cord Compression
Transverse Myelitis
Cauda Equina Syndrome

Answer 224

A

Herniated Disc
Radicular Pain (Sciatica)
Foraminal Stenosis
Nerve Root Avulsion

Answer 225

A

Brachial Plexus Injury
Lumbosacral Plexopathy
Thoracic Outlet Syndrome
Diabetic Amyotrophy

Answer 226

A

Peripheral Neuropathy
Carpal Tunnel Syndrome
Guillain-Barré Syndrome
Charcot-Marie-Tooth Disease
Neuropathy due to Chemotherapy

Answer 227

A

Myasthenia Gravis
Lambert-Eaton Myasthenic Syndrome (LEMS)
Botulism
Congenital Myasthenic Syndromes

Answer 228

A

Myasthenia Gravis
Lambert-Eaton Myasthenic Syndrome (LEMS)
Botulism
Congenital Myasthenic Syndromes

Answer 229

A

dense and solid and surrounds the marrow space

Osteon- fundamental functional unit of compact bone.
containing concentric rings of bone matrix called lamellae, which surround a central canal

central canalof blood vessels and nerve, lymphatic vessels, providing nutrients and oxygen to the bone cells (osteocytes)

Canaliculi are tiny channels that radiate from the central canal to the lacunae (small spaces) where osteocytes are located. These channels allow for the exchange of nutrients, gases, and waste products

Lacunae are small, fluid-filled spaces within the bone matrix that house osteocytes—mature bone cells.

Answer 230

A

Fibrous Layer: The outer layer of the periosteum is made up of dense, irregular connective tissue. This fibrous layer serves as a protective barrier, helping to shield the bone from external forces and providing structural support. It also contains blood vessels, nerves, and lymphatic vessels that supply the bone with nutrients and oxygen.

Osteogenic Layer: The inner layer of the periosteum, known as the osteogenic layer, is rich in cells involved in bone formation and repair. These cells include osteoblasts, which are responsible for producing new bone tissue, and osteogenic cells, which are undifferentiated stem cells that can differentiate into osteoblasts. The osteogenic layer plays a crucial role in the growth and repair of bones.

In children this is responsible for bone diameter increasing.

Answer 231

A

Bone Repair and Growth: The osteogenic layer of the periosteum is involved in bone repair and growth. Osteoblasts in this layer contribute to the formation of new bone tissue during processes such as bone remodeling, fracture healing, and bone development in growing individuals.

Attachment for Ligaments and Tendons:Ligaments (connecting bone to bone) and tendons (connecting muscle to bone) often attach to the periosteum. This attachment helps stabilize the bones and facilitates movement.

Answer 232

A

The two main cells are:

Osteoclasts (chew)
They break down and reabsorb bone tissue by secreting enzymes and acids that dissolve the mineralized matrix.
Osteoclasts are larger, multinucleated cells with a ruffled border. The ruffled border increases the cell’s surface area

Osteoblasts (build)
They secrete organic components of the bone matrix, including collagen, and actively participate in the mineralization of bone
*Osteoblasts have a cuboidal or columnar shape with abundant rough endoplasmic reticulum and Golgi apparatus. *

Answer 233

A

Calcitonin:
Inhibits osteoclast, stimulates osteoblast

PTH
Stimulates osteoblasts indirectly, Directly stimulates osteoclast
PTH helps regulate calcium levels

Oestrogen
Stimulates osteoblast, Inhibits osteoclast

Vitamin D
Promotes the absorption of calcium and phosphate at osteoblasts
Indirectly inhibits osteoclast

Mechanical Stress (Weight-Bearing Activity):
stimulates osteoblast activity, indirectly inhibit osteoclast

Cytokines (e.g., Interleukin-1 and Tumor Necrosis Factor-alpha):
May inhibit osteoblast activity. stimulates osteoclasts

Answer 234

A

Collagen: provides flexibility and tensile strength

Osteoblasts: bone-forming cells. produce collagen and other proteins

Osteocytes: maintain the daily metabolism of bone tissue producing and maintaining the extracellular matrix.

Osteoid: primarily composed of collagen fibers, glycoproteins, and proteoglycans. It provides a scaffold for mineralization and gives bones their flexibility.

Answer 235

A

Hydroxyapatite: crystalline structure composed of calcium and phosphate ions. provides bones with hardness and compressive strength.

Mineral Salts: mineral salts, including calcium carbonate and magnesium hydroxide.

Answer 236

A

bONE = type ONE collagen

Answer 237

A

multiple components to reduce stress and increase strcutre

Answer 238

A

identical structure
collagen and minerals stick
identical collagen fibrils
macroscopic/cellular level of organisation is different.

Trabecular bone has a porous, lattice-like structure, while cortical bone is dense and compact.
Trabecular bone is found at the ends of long bones, in the interior of flat bones, and in the spine, while cortical bone forms the outer layer of all bones and the diaphysis of long bones.

Answer 239

A

1. haematoma and tissue destruction
vessels torn, bone at fracture end dies due to the lack of blood supply

2. inflammation
inflammatory mediators released, proliferation of cells from endosteum, growth of new capillaries

3. callus
soft woven material with immature fibroblast chondrogenic, osteogenic cells and osteoclasts. Neogenesis b/n ends, periosteum reforms

4. consolidation
continuing osteoblastic and osteoclastic activity, woven bone transformed to lamellar bone. Bony matrix appearing

5. remodelling
fracture bridged by solid bone continuous reshaping of bone haversian system restored

Answer 240

A

Subcutaneous
low blood (talus, scaphoid) the healing phase is longer and remodelling is long.

Remodelling can take up to 2 years

4-6weeks in a small bone in a healthy child before use again.

HEAL when the bone is structurally sound to function. (NOT ALWaYS remodelled)

Answer 241

A

BONES RESPOND TO STRENGTH
Trabecular oganisation to respond to density for higher load stress
Osteocytes know “up and down”
They respond to direction of load.

Answer 242

A

patient survival reusucitate etc
limb survival vascularity
compartment syndrome
functional survival fracture union
muscle/tenson units nerve
infection prevention
soft tissue coverage

Answer 243

A

*antibiotics
*anti-tetanus
*a splint
*a photograph
*a barrier dressing *an operation

Answer 244

A

“raised pressure in a closed fascial compartment that exceeds capillary perfusion pressure”

Faschia does not allow osmotic transfer
So raised pressure can only go to capillaries
If it overwhelmes capillary load (arterial bleed into comparment)
It collapses venous outflow
Arterial continues
Venous continues to collapse
INCREASE PRESSURE
PAIN PAIN PAIN
Pulse can still be present, but if pulse lost >6 hours and ischaemia. limb loss
* Passive stretch gives pain (cramp is minor but similar mechanism of stretch)

Answer 245

A

*nothing
*splint
*plaster of paris

Answer 246

A

*external fixator
*internal plating *intramedullary nailing
*joint replacement

Answer 247

A

reduces infection rate

Answer 248

A

no wait for fracture healing

Answer 249

A

longest part
atrophy of joints and muscle
aim: normal function asap
* physiotherapy when splintage is removed to enable full joint function
* encourage proprioception

Answer 250

A

age
co-morbidities
vascular disease
diabetes
drugs
smoking
associated injuries (iss)
surgical skill / experience
local resource

Answer 251

A

Rarely pt fault
Smoking and alcohol
Diabetes
NSAIDs impair healing as stops the cascade early
fear of using the limb- trabecular stimulatio

Answer 252

A

pathological increase of osteoblasts- rigid “petrified” bones

Answer 253

A

Abnormal lateral curvature of the spine.

Answer 254

A

Shortening or stiffness of the neck muscles, leading to limited neck movement.

Brevi- short, Collis- Collar. Short Collar. Stiff Neck

Answer 255

A

Absence of one or more limbs.

Answer 256

A

Ectrodactyly refers to missing digits or portions of limbs, while polydactyly refers to extra digits.

Answer 257

A

Developmental anomaly characterized by a split or cleft in the hand or foot.

Answer 258

A

Genetic disorder resulting in dwarfism due to impaired bone growth.

Answer 259

A

Keratinocytes: Predominant cell type in the epidermis responsible for producing keratin, a structural protein.
Melanocytes: Cells that produce melanin, responsible for skin pigmentation.
Langerhans cells: Dendritic cells involved in immune responses.
Merkel cells: Sensory cells associated with touch sensation.

Answer 260

A

Keratinocytes originate from basal cells in the stratum basale, where they undergo mitosis.
As keratinocytes mature, they move upward through the epidermal layers: stratum spinosum, stratum granulosum, and stratum corneum.
In the stratum corneum, keratinocytes are fully keratinized and eventually shed from the skin surface.

Answer 261

A

Epidermal Barrier: The outermost layer of the skin, the stratum corneum, acts as a physical barrier, preventing the entry of pathogens and harmful substances
.
Sebum Production: Sebaceous glands secrete sebum, which helps lubricate the skin and maintains its waterproof barrier function.

Immune Response: Langerhans cells and other immune cells in the skin mount an immune response against pathogens.

pH Regulation: The slightly acidic pH of the skin inhibits the growth of harmful bacteria.

Answer 262

A

Spinal Cord: Injury or compression causing sensory, motor, or autonomic dysfunction.
Nerve Root: Radiculopathy from compression, leading to pain and sensory/motor deficits.
Plexus: Brachial or lumbar plexopathy causing arm or leg weakness, numbness, or pain.
Peripheral Nerves: Neuropathy or Guillain-Barré syndrome causing limb tingling, numbness, or weakness.
Neuromuscular Junction: Myasthenia gravis or Lambert-Eaton syndrome resulting in muscle weakness.
Muscle: Muscular dystrophy or myositis causing progressive muscle weakness and degeneration.

Answer 263

A

Facial nerve (CN VII); Unilateral facial paralysis, inability to close eye, loss of forehead wrinkles, loss of taste on anterior 2/3 of tongue; Idiopathic, possibly viral (HSV), Lyme disease

Answer 264

A

Radial nerve; Wrist drop, loss of sensation over dorsal hand, weakness in extension of wrist and fingers; Humeral fracture, prolonged compression (e.g., ‘Saturday night palsy’)

Answer 265

A

Ulnar nerve; Claw hand deformity, loss of sensation over medial 1.5 fingers, weakness in finger abduction/adduction; Elbow injury (e.g., cubital tunnel syndrome), wrist injury

Answer 266

A

Median nerve; Ape hand deformity, loss of thumb opposition, weakness in flexion of lateral fingers, sensory loss over lateral 3.5 fingers; Carpal tunnel syndrome, forearm fractures

Answer 267

A

Common peroneal (fibular) nerve; Foot drop, loss of sensation over lateral leg and dorsum of foot, difficulty dorsiflexing and everting foot; Fibular head fracture, prolonged leg crossing

Answer 268

A

Sciatic nerve; Weakness in knee flexion, foot drop, sensory loss over posterior thigh, leg, and foot; Hip dislocation, herniated disc, intramuscular injection injury

Answer 269

A

Long thoracic nerve; Winged scapula, difficulty raising arm above head; Trauma to shoulder, surgical injury, repetitive overhead activities

Answer 270

A

Axillary nerve; Deltoid muscle atrophy, loss of abduction of shoulder, sensory loss over deltoid region; Shoulder dislocation, surgical neck fracture of humerus

Answer 271

A

Femoral nerve; Weakness in hip flexion and knee extension, sensory loss over anterior thigh and medial leg; Pelvic fracture, retroperitoneal hematoma

Answer 272

A

Obturator nerve; Weakness in thigh adduction, sensory loss over medial thigh; Pelvic surgery, pelvic trauma

Answer 273

A

Oculomotor nerve (CN III); Ptosis, ‘down and out’ eye position, dilated pupil, loss of pupillary reflex; Aneurysm, diabetes, trauma

Answer 274

A

Trochlear nerve (CN IV); Vertical diplopia, difficulty looking down and in, head tilt to compensate; Trauma, congenital, microvascular disease

Answer 275

A

Abducens nerve (CN VI); Horizontal diplopia, inability to abduct eye, medial deviation of eye; Increased intracranial pressure, trauma, microvascular disease

Answer 276

A

Lateral medulla; Ipsilateral facial pain and temperature loss, contralateral body pain and temperature loss, dysphagia, hoarseness, vertigo, ataxia; Posterior inferior cerebellar artery (PICA) stroke

Answer 277

A

Medial medulla; Contralateral hemiparesis, contralateral loss of proprioception and vibration, ipsilateral tongue deviation; Anterior spinal artery stroke

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