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HYMS Y1 > Block 5 W1 > Flashcards

Block 5 W1 Flashcards

1
Q

What are the advantages and disadvantage of bipedalism?

A

+ frees our hand (increased manual dexterity)
+ elevates our head
+ walk on challenging terrain
- poses biomechanical challenge

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2
Q

Why has the supporting rectangle of humans become smaller than quadrupedal primates?

A

In standing upright, essential that body’s centre of gravity remains directly over the supporting rectangle.

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3
Q

Where did morphological changes necessary for bipedalism occur?

A

Vertebral column and lower limb.

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4
Q

How do chimpanzees move bipedally?

A

Bent knee bent hip gait. Centre of mass = too anterior to base -> energetically costly.

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5
Q

What is the role of the iliofemoral ligament?

A

The tension of the iliofemoral ligament prevents the truck rotating backwards at the hip joint.

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6
Q

What is the role of the cruciate ligament?

A

Keeps upper body and thigh from falling forwards at the knee.

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7
Q

What is the role of the vertebral curves?

A

Cancel out, passing weight directly to the lower limb. Cervical and lumbar lordosis balances body weight over the feet. Shock absorbers.

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8
Q

Why is the human ilium wider than it is high?

A

Reduced height brings the sacroiliac joint closer to the hip joint, reducing stress on the ilium.

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9
Q

Why is the iliac blade curved?

A

It is curved and medially-orientated, which brings the small gluteal muscles into a position where they can act as abductors of the thigh.

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10
Q

What is the role of the abductors of the thigh?

A

Supports the pelvis when the body weight is on one leg and prevents side-to-side swaying of the trunk -> pelvis is kept stable.

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11
Q

Why is the femoral head of humans different?

A

It is larger - adaptation to load bearing.

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12
Q

What does the diagonal position of the femur achieve?

A

It re-centres support directly inferior to the trunk to make bipedal standing more efficient and to enable bipedal walking -> more stable.

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13
Q

Why are the joint surfaces of the knee larger?

A

Load bearing.

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14
Q

How is the knee joint stabilised?

A

By posterior + anterior cruciate ligament and medial + lateral collateral ligaments.

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15
Q

Why does the knee have a locking mechanism?

A

For stability in a fully extended position.

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16
Q

Describe the foot of primates and humans.

A

Primate - transverse arch running mediolaterally.
Humans - two part longitudinal arch to permit medial weight transfer during mid stance, acts as shock absorber and distributes body weight over the sole.

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17
Q

What is torque?

A

When most skeletal muscle contracts, the bones to which they are attached rotate around a joint - rotational force.

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18
Q

What is a lever?

A

A muscle level (moment) arm is the perpendicular distance to the point of rotation from the line of muscle action.

  • force requires long ‘in’ lever and short ‘out’ lever (badger)
  • speed requires short ‘in’ lever and long ‘out’ lever (cheetah).
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19
Q

What are the challenges to bipedal locomotion?

A
  • gravity and efficiency -> gravity acts at CoM of each body segment and may cause gravitational moments depending on how the limb is positioned.
  • stability -> humans CoM = pelvis in midline, anterior to S2. Stability = BoS & CoM.
    So body is technically unstable but won’t fall due to ankle and hip strategy.
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20
Q

What is the gait cycle?

A

Period from heel strike of one limb until the next time that heel hits the ground.

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21
Q

What is the stance phase?

A

First 60% of the cycle from the time the heel strikes until the toe of the same foot begins to lift off the ground.

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22
Q

What is the swing phase?

A

Remaining 40%, limb has lost contact with the ground. Toe off -> heel strike.

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23
Q

Define concentric muscles?

A

Muscle length shortens

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24
Q

Define eccentric muscles?

A

Muscle length increases.

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25
Q

Define step vs. stride.

A

Step - distance from one heel to another (diff feet)

Stride - distance from same heel at the beginning and end of swing phase (same foot).

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26
Q

Describe the walking pattern.

A

One foot is on the ground at all time.

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27
Q

Describe the running pattern.

A

At some point, both feet are off the ground. Absorbing and releasing energy stored in tendons biomechanically makes running a series of controlled leaps.

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28
Q

Describe the nervous system control of locomotion.

A

Receptors in muscles and joints provide info on body position and movement.
Cerebellum - motor correction and adjustments due to sensory and proprioceptive inputs.
Motor learning - improving performance of motor seq. with repitition.
Balance - coordinating muscle systems across the body.

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29
Q

Describe the gait cycle in order.

A
  1. Heel strike
  2. Loading response
  3. Midstance
  4. Terminal stance
  5. Preswing
  6. Terminal swing
    7 Heel strike
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30
Q

Describe heel strike (stance phase).

A
  • Tibalis anterior lowers forefoot to the ground.
  • Gluteus maximus continues deceleration.
  • Intrinsic muscles of foot and long tendons of foot preserve the longitudinal arch of the foot.
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31
Q

Describe loading response (stance phase).

A
  • quadriceps accept the weight
  • triceps surae decelerate mass
  • gluteus medius and minimus + tensor of the fascia lata stabilise the pelvis.
  • intrinsic muscle of foot + long tendons of foot preserve the longitudinal arch of foot.
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32
Q

Describe the midstance (stance phase).

A
  • quadriceps stabilise the knee
  • triceps surae controls dorsiflexion
  • gluteus medius and minimus + tensor of the fascia lata stabilise pelvis.
  • intrinsic muscle + long tendons of foot preserve longitudinal arch of foot.
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33
Q

Describe the terminal stance (stance phase).

A
  • triceps surae accelerates mass
  • gluteus medius and minimus + tensor of the fascia lata stabilise pelvis.
  • intrinsic muscle + long tendons of foot preserve longitudinal arch of foot and fixes the forefoot.
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34
Q

Describe the pre-swing (swing phase).

A
  • hip flexors (rectus femoris) decelerate thigh and prepares for swing.
  • long flexors of digits (flexor hallucis longus) accelerate mass.
  • intrinsic muscle + long tendons of foot preserve longitudinal arch of foot and fixes the forefoot.
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35
Q

Describe the initial swing (swing phase).

A
  • hip flexors (rectus femoris) accelerate thigh and varies cadence.
  • tibialis anterior clears the foot.
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36
Q

Describe the mid-swing (swing phase).

A
  • tibialis anterior clears foot.
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37
Q

Describe the terminal swing (swing phase).

A
  • hip extensors (gluteus maximus) decelerates thigh
  • knee flexors (hamstrings) decelerate leg
  • tibialis anterior positions the foot
  • quadriceps extend knee to place foot and prepares for contact.
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38
Q

How does ageing alter gait?

A

Ageing = decreased muscle bulk and stability.

Reduced stride length.

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39
Q

How does arthritis or other degenerative conditions alter gait?

A

Reduces mobility of joint and causes pain -> limp.

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40
Q

How does flip-flops alter gait?

A
  • shorter steps
  • heel hits ground with less force
  • larger ankle angle
  • shorter stride length
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41
Q

How does high heels alter gait?

A

Shortens achilles tendon and shortens calf.

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42
Q

What is antalgic gait?

A

Any gait that reduces loading on the affected extremity by decreasing stance phase time or joint forces as to avoid pain.
On painful side, shortened stance phase time, lengthened swing phase time and lengthened step length.
e.g. stone in the shoe, diabetic foot.

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43
Q

What is ataxic (cerebellar) gait?

A

Unsteady, uncoordinated, wide base and feet thrown out - can’t stay steady, double tap.
e.g. MS, cerebellar disease.

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44
Q

What is parkinsonian gait?

A

Involuntary short, accelerating steps, tiptoe, trunk forward and legs stiff.
e.g. Parkinson’s disease and conditions affect BG

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45
Q

What is myopathic (waddling) gait?

A

Proximal pelvic girdle muscles weak - pelvis not stabilised thus tilts towards non-weight bearing leg.

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46
Q

What is neuropathic (high stepping) gait?

A

Distal lower extremity affected due to foot dorsiflexors weak - lifts whole leg to avoid toe dragging.

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47
Q

What is trendelenburg gait?

A

Hip paralysis prevents small gluteals functioning - pelvis drops.
To prevent fall, lumbar spine flexes forwards to bring centre of gravity over the foot.

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48
Q

What is cox vara?

A

Decreased angle (< 120) of the femoral head -> mild shortening of lower limb = duck waddle gait.

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49
Q

What is cox valga?

A

Increased angle (> 140) resulting from weakness of abductor muscle. Occurs in cerebral palsy and poliomyelitis.

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50
Q

How does anterior cruciate ligament damage occur?

A

Deceleration or rational forces acting on weight-bearing limb may tear the ligament.

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51
Q

What is pes planus?

A

Flat footed due to overweight.

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52
Q

What are the functions of bone?

A
  • protect organs
  • provide support and rigidity in limbs
  • haematopoiesis in marrow
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53
Q

What is the origin of the skeleton?

A

Derived from neural crest (head) and mesoderm = somites (body).
Neural crest gives rise to bones of head through intramembranous ossification.
Bones of body form though endochondral ossification.

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54
Q

What is neural crest?

A

A membrane within which bones form directly = intramembranous ossification.
Skull bone formed by radiating calcification.

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55
Q

What is the role of somites bone development?

A

Vertebra and base of skull develop from somites.

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56
Q

What are HOX genes?

A

Patterning genes that specify the identity of vertebra.

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57
Q

Describe limb development.

A
  • limb buds develop at 4-5 weeks.
  • patterning genes guide morphogenesis
  • gene on progress zone determine shape and length of the finger and what kind of finger
  • hands develop then cells die from apoptosis between the fingers to form the finger
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58
Q

What is ossification?

A

Cartilage and membrane formed genetically - they are converted to bone -> functional formation.

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59
Q

Describe cartilage formation.

A

Chondroblasts make cartilage by forming chondrocytes by secreting ECM and trapping itself.
Chondrocyte maintains the secretion.
ECM is formed of fibres and ground substance.
Avascular so requires diffusion.

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60
Q

Define lacunae.

A

Cavity within which the chondrocytes reside.

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61
Q

Define interstitial and appositional growth.

A

Interstitial - growth in length

Appositional - growth in diameter.

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62
Q

What is the epiphyseal growth plate?

A

Flow of cartilage cells from epiphysis to metaphysis - cartilage then ossified. Active site of endochondral ossification.

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63
Q

List the different zones of cartilage.

A
  1. zone of resting cartilage
  2. zone of proliferating cartilage
  3. zone of hypertrophic cartilage
  4. zone of calcified cartilage
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64
Q

Describe long bone morphology (compact).

A

Compact -> Haversian/central canal (blood vessels), Volkmann’s canal (vessels), lamellae, lacunae.

65
Q

What is a bone?

A

Bone is a connective tissue comprised of cells, fibres and mineralised ground substance.

66
Q

What are osteoblasts?

A

Deposit bone.
A osteoblasts surround themselves in ECM -> osteocytes.
When mineralised forms osteon.

67
Q

What are osteocytes?

A

Maintain bone and fluid flow between osteocytes.
Signals depending on stress to osteoblasts and osteoclasts for bone growth or removal.
Secretes collagen fibres.

68
Q

What are osteoclasts?

A
  • removes bone
  • multi-nucleated cells
  • ruffled border
  • creates trabeculae based on loading
  • 50 monocyte derived
  • released lysosomal enzymes and acids to digest bone
69
Q

What is a osteon?

A

Circular arrangement of collagen fibres and mineral.

70
Q

How does primary osteon become secondary?

A

Primary osteon is immature -> fracture/death -> secondary osteon.

71
Q

Define trabeculae.

A

Sections of cancellous bone - carved out of the bone.

Maintains strength and stops bone bending.

72
Q

Why is mechanical adaptation of bones necessary?

A

Helps prevent osteoporosis and allows bone healing.

73
Q

Describe the stages of fracture healing.

A
  1. fracture haematoma
  2. subperiosteal and endosteal cell proliferation
  3. callus - woven bone
  4. consolidation - woven to lamellar bone
  5. remodelling by osteoclasts
74
Q

How is bone remodelled?

A

Osteoblasts and osteoclasts remodel bone.
First bone is woven -> collagen fibres random.
Replaced by lamellar bone -> collagen fibres arranged in parallel layers.

75
Q

What is surface remodelling?

A

This adapts the form of bones e.g. skull thus different shapes and sizes.

76
Q

Define osteoporosis.

A

Bone resorption > deposition.
Bone thinning and loss of mechanical integrity.
Trabeculae thinner -> increased risk of fracture

77
Q

What is the nervous system?

A

System of cells, tissues and organs that regulate the body’s response to internal and external stimuli.
Communication via electrochemical impulses.
Responds via action potential and NTs.

78
Q

What is the endocrine system?

A

Responds to stimuli by secreting hormones into circulatory system.
Slow - synthesis of hormone, release and effect.
Long lasting response.

79
Q

How is nervous system divided?

A

CNS - brain and spinal cord

PNS - sensory & motor divisions -> Somatic (voluntary) nervous system + ANS (SympNS + ParaNS)

80
Q

What is the main function of sensory part of nervous system?

A

Responsible for collecting info from internal and external environ.
Integrating, interpreting and assessing.
Creates, encodes and lays down memory.

81
Q

What is the main function of motor part of nervous system?

A

Responsible for producing effects in response to stimuli for homeostasis and modifying behaviour.

82
Q

What are somatic afferents and efferents?

A

External stimuli and voluntary skeletal muscle.

83
Q

What are visceral afferents and efferents?

A

Internal stimuli and involuntary, smooth and cardiac muscles + glands.

84
Q

Define neurone?

A

Functional unit of the nervous system, comprised of cell body (soma), multiple dendrites (input) and axons.

85
Q

Differentiate between cell bodies and axons in CNS and PNS.

A

CNS - cell bodies -> gray matter found in nuclei and cortex. Axons -> white matter and tracts (lemniscus, fasciculus, peduncles).
PNS - cell bodies -> ganglia. Axons -> nerves.

86
Q

Describe the cranial meninges.

A

3 layers of connective tissue:

  • dura mata -> dense, very tough outer layer
  • arachnoid mata -> delicate fibrous layer
  • pia mata -> innermost layer
87
Q

What is meningitis?

A

Cranial meninges inflamed.
Pachymeningitis -> dura mata
Leptomeningitis -> arachnoid mata and pia mata.

88
Q

What are the meningeal spaces?

A

Extradural, subdural and subpial potential spaces.

Subarachnoid space filled with CSF.

89
Q

What is the telencephalon?

A

Cerebral cortex, subcortical white matter, basal ganglia.

90
Q

What is the diencephalon?

A

Thalamus, hypothalamus.

91
Q

What are the ventricles?

A

Cavity where CSF flows though.

92
Q

What does the cerebellum consist of?

A

2 lateral lobes + vermis.

Receives info from spinal cord about touch and proprioception.

93
Q

What does the brainstem consist of?

A

Midbrain
Pons
Medulla

94
Q

At what level does the spinal cord end?

A

L1-L2

95
Q

Describe the difference in white and grey matter in SC vs. brain?

A

SC - grey matter in centre and white matter surrounds.

Brain - grey matter outside forms the cortex and white matter inside.

96
Q

What are plexuses?

A

Network of nerves made of spinal/cranial nerves.
e.g. brachial plexus formed by C6-8 + T1 nerves.
Plexuses receive ventral roots.

97
Q

What does the dorsal and ventral rami supply?

A

Dorsal rami - strip of back

Ventral rami - everything else

98
Q

How are somites divided?

A

Myotomes and dermatomes - areas innervated by a single spinal nerve.
Can work out spinal segment lesion by which particular dermatome.

99
Q

If there is a lesion, why is their mixed sensory and motor problem?

A

Most nerve carry both sensory and motor components.

100
Q

How can peripheral nerve lesions be localised?

A

Pain -> motor, sensory and reflex loss in specific nerve distribution.

101
Q

How can spinal nerve root lesions be localised?

A

Radicular (shooting) pain - motor, sensory and reflex loss in specific root distribution.

102
Q

How can cerebral cortex lesions be localised?

A

Hemiplegia (paralysis), hemisensory loss, aphasia, neglect, hemianopia (loss of vision), dementia, seizure.

103
Q

How can dorsal root ganglion lesions be localised?

A

Sensory loss and reflex loss.

104
Q

How can spinal cord lesion be localised?

A

Neurogenic bladder.

105
Q

What is neuroectoderm?

A

The part of ectoderm that go on to form the nervous system.

106
Q

How does the neural tube form?

A

Boundaries between ectoderm rise and forms neural plate, the boundaries come together and zip up -> neural tube underneath the ectoderm.
Tube has fluid within.

107
Q

What does neural crest cells do?

A

Migrate to other regions e.g. hindbrain into pharyngeal arches. These form:
- bone, muscle, dentine, cranial nerves.

108
Q

What do cranial neural crest cells form?

A
  • neurons and glia of cranial ganglia
  • cartilage and bone
  • connective tissue
109
Q

What do trunk neural crest cells form?

A
  • pigment cells
  • sensory neurons and glia
  • sympathy-adrenal cells
110
Q

What does the neural tube form?

A

Brain and spinal cord

111
Q

What are somites and what do they form?

A

Specialised mesoderm - forms early vertebrae (MSK structures)

112
Q

What does endoderm form?

A

Gut

113
Q

What does notochord form?

A

Precursor to vertebral column.

114
Q

What does the prosencephalon (forebrain) divided into?

A

Telencephalon and diencephalon.

115
Q

What does the mesencephalon go on to form?

A

Midbrain and aquaduct

116
Q

What does the rhombencephalon (hindbrain) divide into?

A

Metencephalon and myelencephalon.

117
Q

What does the telencephalon go on to form?

A

Cerebral hemispheres and lateral ventricles.

118
Q

What does the diencephalon go on to form?

A

Thalami and third ventricles.

119
Q

What does the metencephalon go on to form?

A

Pons, cerebellum and upper part of 4th ventricle

120
Q

What does the myelencephalon go on to form?

A

Medulla and lower part of 4th ventricle

121
Q

What are the flexures of the developing brain?

A
  • cranial flexure -> midbrain bends bringing hindbrain over top of forebrain.
  • cervical flexure -> hindbrain also bends
  • pontine flexure -> hindbrain folds again further pulling midbrain over the forebrain.
122
Q

Describe the growth of the telencephalon.

A

Telencephalon continues to grow over the diencephalon and midbrain. The flexures continue to grow, resulting in the formation of brainstem.
Sulci/gyri forms and telencephalon completely surrounds the diencephalon and midbrain, leaving only the hindbrain.

123
Q

Describe the ventricular system.

A
  • Lateral ventricles occur on each side of hemisphere.
  • Connect in midline and forms 3rd ventricle (in middle of 2 thalami).
  • Connected to 4th ventricle via aqueduct around midbrain.
  • 4th brain occurs around cerebellum/hindbrain.
  • Continues into SC via central canal.
124
Q

What are the structures around the ventricles?

A

Basal ganglia/thalamus has lateral ventricle circling around it.
Caudate nucleus forms flow of lateral ventricle.
Hippocampus and fornix form around top of lateral ventricle.

125
Q

What is the internal capsule?

A

Major tract of fibres passing through diencephalon and basal ganglia and passes through gap between caudate nucleus and putamen.

126
Q

From what does the posterior (dorsal) horn derive from?

A

Alar plate (sensory)

127
Q

From what does the anterior (ventral) horn derive from?

A

Basal plate (motor)

128
Q

Which area does the ANS pass through?

A

Lateral horn

129
Q

Where does the efferent axons develop from?

A

Anterior horn cell bodies and grow out.

130
Q

Where does the afferent axons develop from?

A

Neural crest cells migrate and penetrate into posterior horn.

131
Q

Where do the parasympathetic and sympathetic nerves originate from?

A

P - cranial/sacral

S - thorax/lumbar

132
Q

Where do the cranial nerves originate?

A

Olfactory and optic - extensions of brain
Hypoglossal, oculomotor, tochlear, abducens - ventral root nerves (motor nerves).
Pharyngeal arch: 1 - trigeminal 2 - facial 3 - glossopharyngeal 4 - vagus

133
Q

Describe the components of cancellous bone.

A

40% organic -> type 1 collagen + non-collagenous proteins.

60% inorganic -> calcium hydroxyapatite

134
Q

Describe the bone remodelling cycle.

A

Quiescence -> resorption (osteoclasts release calcium phosphate ions into circulation) -> reversal -> formation (osteoblasts lay down unmineralised osteoid) -> mineralisation -> quiescence.

135
Q

What is the role of bone metabolism?

A

Drives bone remodelling

Maintains level of ionised ca2+ in blood within defined range.

136
Q

What are the signalling mechanisms involved in bone remodelling?

A
  • parathyroid hormone
  • vitamin D
  • calcitonin
  • growth hormone
  • growth factors
  • oestrogen
  • cytokines
137
Q

Describe calcium metabolism.

A

Occurs for bone remodelling and physiological reasons e.g. muscle contractions.
1000g -> 99% skeleton 1% extracellular fluids and soft tissues.

Serum concentration - 2.25-2.6 mmol/L

138
Q

What are the 3 definable fractions of Ca2+?

A
  • ionised Ca2+ -> 50%
  • protein bound Ca2+ -> 40%
  • complexed Ca2+ -> 10%
    Ca2+ levels maintained by PTH, VitD and calcitonin.
139
Q

Describe protein metabolism.

A

600g -> 85% skeleton 15% extracellular fluids as inorganic ions (HPO42-).
Concentrations vary widely by age, diet, pH, hormones.

Serum concentration - 0.9-1.3 mmol/L

140
Q

What are the 3 definable fractions of phosphate?

A
  • ionised phosphate -> 55%
  • protein bound -> 10%
  • complexed phosphates -> 35%
141
Q

Describe the hydroxylation steps of VitD activation.

A
  • synthesised in skin from 7-dehydrocholesterol by UV.
  • 25-hydroxylation in liver makes 25(OH)D3 (main circulating form).
  • 1-hydroxylation in kidney makes 1,25 (OH)2 vitamin D3 (active).

Cholecalciferol

142
Q

What is 1,25 (OH)2 vitamin D3?

A

Principle hormonal form of VitD.

Production is tightly regulated and stimulated by PTH and inhibited by elevated Ca and P.

143
Q

What is the action of 1,25 (OH)2 vitamin D3?

A
  • increases Ca2+ and phosphate absorption from intestine.
  • mobilises Ca2+ and phosphate from bone
  • induces marrow monocytes to differentiate into osteoclasts for bone resorption.
144
Q

What is parathyroid hormone?

A

84 AA polypetide
Half life 20mins
Secreted by parathyroid gland in response to low plasma Ca2+ levels.

145
Q

What are the actions of PTH?

A
  • high levels stimulates osteoclastic bone resorption

- low levels stimulate osteoblastic bone formation

146
Q

What are the effects of PTH?

A
  • decreases renal Ca2+ excretion
  • increases renal production of active D3
  • increased Ca2+ absorption from intestine via VitD
  • increases blood Ca2+ levels.
147
Q

What is parathyroid hormone related protein (PTHrP) and its effects?

A

Product of normal and malignant cells (tumours).
Required for normal development, regulator of proliferator and mineralisation of chondrocytes.
Acts locally.
Acts systemically when secreted in excess.

148
Q

What is calcitonin and its effect?

A

32 AA sequence
Released from C cells in thyroid gland in response to high plasma Ca2+ levels.

Reduces bone resorption by activated calcitonin receptors expressed by osteoclasts.

149
Q

Describe the Ca2+ homeostasis.

A

Decrease

  • induces PTH secretion
  • mobilises Ca2+ from bones
  • decreases renal Ca2+ excretion and increases renal synthesis of VitD
  • enhances Ca2+ mobilisation and absorption.

Increase

  • increases calcitonin levels by inhibiting resorption
  • decreases VitD synthesis.
150
Q

What is the role of oestrogen in bone turnover?

A

Maintains bone mass

  • reduces resorption by inhibiting osteoclastogenesis and function.
  • oestrogen receptors expressed on osteoblasts and osteoclasts
  • high oestrogen stimulates bone formation.
151
Q

What is the role of androgens in bone turnover?

A

Decreased androgen levels linked to lower bone density.

  • correlation between hypogonadism and increased incidence of fractures
  • decreases bone resorption by inhibiting osteoclasts.
152
Q

What are the causes of hypercalcaemia?

A
  • primary hyperparathyroidism
  • malignancy
  • hyperthyroidism
  • immobilisation
  • VitD toxicity
153
Q

What causes hypocalcaemia?

A
  • renal failure
  • VitD deficiency
  • prematurity (immature thyroid gland)
154
Q

What are primary hyperparathyroidism symptoms?

A
  • excess PTH -> osteitis fibrosa cystica (replacement of bone with fibrous tissue)
  • periosteal erosions, fracture, bone pain.
  • kidney stones
155
Q

What is secondary hyperparathyroidism?

A

Physiological response to hypoglycaemia.

156
Q

What causes osteomalacia/rickets?

A

Type 1 collagen made but no mineralisation as less Ca2+.

  • VitD deficiency
  • malabsorption (surgery)
  • renal disease
  • lack of sunlight
  • anticonvulsants inhibits 1,25 (OH)2 vitamin D3 synthesis

Inherited

  • VitD-dependent rickets (VDDR) type 1 (1-hydroxylase deficiency)
  • type 2 (resistance to 1,25 (OH)2 vitamin D3).
157
Q

What are the features of osteomalacia/rickets?

A
  • Diffuse bone pain
  • Muscle weakness
  • Elevated alkaline phosphatase levels (osteoclasts)
  • Decreased mineralisation
  • Long bones -> bowing deformity.
158
Q

Define osteoporosis.

A

Net loss of bone mass due to resorption > formation.

Decreased bone mineral density and deterioration of bone microarchitecture -> increased susceptibility of fracture.

159
Q

What is the treatment of osteoporosis?

A
  • calcium supplementation
  • hormone replacement therapy
  • bisphosphonates -> osteoclast inhibitors (alendronate, residronate)
  • calcitonin
  • selective oestrogen-receptor modulator (SERMs) -> ostrogen agonists (raloxifine)

HYMS Y1 (25 decks)

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