Brainscape's Knowledge GenomeTM

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


See full index

Pathophys 2 > Conditions for 16/01/23 > Flashcards

Conditions for 16/01/23 Flashcards

1
Q

OA aetiology

A
  • Increased age (takes years to develop)
  • Incongruent Jts
  • Relationship between stress on articulate cartilage + ability of cartilage to withstand stress
    Obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

OA clinical features

A
  • P starts insidiously + increases slowly over few months
  • Aggravated by exertion
  • Relieved by rest
  • Stiffness usually worse after rest
  • Swelling, crepitus, deformity, tenderness, muscle wastage, reduced ROM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

OA X-ray findings

A
  • Osteophyte formation
  • Jt space narrowing
  • Subchondral sclerosis (thickening of bone in affected Jt)
  • Cysts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

OA pathophysiology

A
  • Softening of cartilaginous surfaces
  • Become frayed
  • Eventually worn away  exposes underlying bone in areas of great stress
  • Bone can develop cysts
  • Surrounding trabeculae can become thickened
  • Ossification produces bony growths
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

OA cautions

A

Exercise
Posture
Knees, hips, hands, spine

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

OA management

A
  • Pharmacological
  • Braces/support
  • Supplements
  • Surgery
  • Osteopathy- increased ROM, flexibility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lumbar spondylosis aetiology

A
  • No specific cause
  • Associated with ageing, degeneration of Jts, ligaments, discs, natural wear and tear
    Degeneration of intervertebral discs in Jts in lower back- wear + tear
    Risks- OA, poor posture, obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Lumbar spondylosis clinical features

A
  • P in low back
  • Often worse when standing or walking, relieved when sitting or bending forward
  • P spread to thighs
  • Tight hamstrings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Lumbar spondylosis X-ray finding

A
  • Reactive sclerosis
  • Narrowing of intervertebral disc space e
  • Deviation or step off signs of SPs
  • Degeneration of facet Jt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Lumbar spondylosis pathophysiology

A
  • Occurs as result of new bone formation in areas where annular ligament is stressed
    Degen of intervertebral discs + Its in low back
    Forms bony spurs, narrowing disc space, which can put pressure on N and cause P
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cautions lumbar spondylosis

A
  • Avoid sitting for more than 30 mins at a time
  • Eating diet high in sugar, processed and refined foods (inflammatory)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lumbar spondylosis management

A
  • Pain relieves
  • NSAIDs
  • Muscle relaxants
    PT- exercises to improve strength + flexibility
    Surgery- alleviate pressure on nerves, remove bony spurs
    Chronic- requires follow up care
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lumbar facet degeneration aetiology

A
  • Alternate spinal conditions which change the way facets align
  • OA leading cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lumbar facet degeneration clinical features

A
  • P or tenderness in low back
  • Stiffness in surrounding structures
  • Difficulty with certain movements, e.g. standing up straight or getting up from a chair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lumbar facet degeneration X-ray

A
  • Narrowing of disc space
  • Subchondral sclerosis
  • Osteophytes
    Not specific to facet irritation, not all will show these changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lumbar facet degeneration pathophysiology

A
  • Facet Jt comprises posterior element of ‘three-Jt complex’
  • Intervertebral disc is anterior part
  • As disc degenerates more load will shift posteriorly and facet Jt OA will subsequently develop
  • Rarely occurs without disc degeneration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Lumbar facet degeneration cautions

A

Advances age or osteoporosis- increase risk of fracture
Pregnancy- certain treatment not safe

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

Lumbar facet degeneration management

A
  • Physio and pharmacology (NSAIDs) first line treatment
  • Facet Jt injection, medial branch block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Spondylolithesis aetiology

A

Failure of facet and laminae locking mechanism
Degenerative- wear and tear
Dysplastic- congenital
Isthmic- fracture to pars interarticularis (bone that covers upper + lower facet)- cause forward slip to L5/S1
Pathologic- slip due to weakness of bones

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

Spondylolithesis clinical features

A
  • Usually painless
  • L4/5/S1
  • Intermittent back ache, may be exacerbated by exercise or strain
  • Step deformity
  • Normal ROM in younger Pts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Spondylolithesis X-ray findings

A

Slippage of vertebra from spinal column
Shows if congenital or acquired
CT/MRI for surrounding structures

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

Spondylolithesis pathophysiology

A
  • Normal laminae and facet locking mechanism fails
  • Causes forward slippage (listheis) of vertebral body
    L4/5/S1 most common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Spondylolithesis cautions

A

Cauda equina- numbness in saddle, los =s of bowel or bladder control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Spondylolithesis management

A

Conservative- NSAIDs, steroid injection
Surgery if grade 3/4, spinal fusion of veterbra to above, laminectomy

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

Herniated nucleus pulposus aetiology

A
  • Failure of annulus fibrosis integrity
  • Makes content pf nucleus protrude into spinal canal
  • Trauma, contact sport
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Herniated nucleus pulposus clinical features

A
  • Low back P
  • Radiculopathy (likely down back of leg, sciatic L4-S3)
    Tingling sensation, muscle weakness, bladder control incontinence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Herniated nucleus pulposus further investigations

A
  • Suspected during history/physical exam
  • Confirmed from MRI or CT scan- determines location and size
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Herniated nucleus pulpous cautions

A
  • Compression on nerve root may cause severe motor deficit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Herniated nucleus pulpous management

A
  • Microdiscectomy- small incision made to remove disc fragment that is impinging nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Spinal stenosis aetiology

A
  • Age related- discs become drier and shrink
  • Arthritis
    Herniated disc
    Tumours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Spinal stenosis clinical features

A
  • Lsp- sciatica like symptoms
  • Csp- major body weakness, full body paralysis is possible
  • Pins and needles, numbness, weakness
  • C2 and above is facial symptoms
  • C3 or below is paralysis
  • Male most common
  • Over 50s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Stenosis X-ray

A
  • Narrowed disc space
  • Fracture
  • Bone spurs
  • OA (spondylosis)
    CT- degree and location
    MRI- spinal canal and neural structures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Stenosis cautions

A

Surgery should be avoided if suffering with osteoporosis, pregnancy, bleeding disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Stenosis pathophysiology

A
  • Narrowing of spinal column that causes pressure on cord or foramina (where N exits)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Stenosis management

A
  • NSAIDs
  • Opioids- e.g. oxycodone
  • Physical therapy- build strength, maintain flexibility
  • Laminectomy- surgery which removes lamina od affected spinal bone, eases pressure on nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Arachnoiditis aetiology

A
  • No exact cause
  • Rare condition
  • Arachnoid can become inflamed because of complications of spinal surgery, direct injury to spine, infection, chronic compression of spinal nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Arachnoiditis clinical features

A
  • Headaches
  • Shooting P
  • Tingling, numbness and weakness in your legs
  • Difficulty sitting for too long
  • Muscle cramps, spasms
    Difficulty with balance + coordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Arachnoiditis further investigation

A
  • Difficult to diagnose
  • Diagnosis based on MRI or CT scan- nerve root thickening, inflammatory mass
    MRI preferred imaging test to show changes to arachnoid matter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Arachnoiditis pathology

A
  • Inflammation of arachnoid matter (middle layer of meninges)
  • Rare but serious condition
    Results in scarring + thickening of membrane which can lead to compression of nerve roots + spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Arachnoiditis management

A
  • Pain management
  • Physical therapy
  • Stretching, ROM exercises
  • Adaptation- mobility, comfort
    Medication- corticosteroid, opioids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Spinal infection aetiology (osteomyelitis)

A
  • Bacterial or fungal in other part of body that has been carried into spine via bloodstream
    Most commonly staphylococcus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Spinal infection clinical features

A
  • Point tenderness
  • Local P
  • Referred P- deep muscle, Jt, throbbing sensation
  • Systematic signs of infection- feeling faint, nausea, vomiting
    Weakness, numbness, tingling in arms or legs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Infection further investigations

A
  • Blood work- WBC count, erythrocyte sedimentation rate + C-reactive protein count- elevated with spinal infection
  • Imaging tests to pin point exact location (MRI or CT)
    Spinal fluid extraction to identify bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Infection pathology

A

Caused by spread of microorganism, such as bacteria to bones and soft tissues of spine
Causes inflammation and damage to bones
Leading to formation of abscesses and/or sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Management of infection

A

ABS or anti fungal therapy
PT- manage P and weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Multiple sclerosis aetiology

A
  • Unknown
  • Considered immune mediated disease
  • Immune system destroys myelin
  • Genetic (gene on chromosome 6p21) and environmental factors contribute
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Multiple scelerosis clinical features

A
  • Depend on location and severity
  • Some can lose ability to walk or ambulate
  • Some may experience periods of remission without new symptoms
  • Numbness or weakness in limbs, typically unilateral
  • Tingling
  • Lack of coordination
  • Blurry vision, vertigo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Multiple sclerosis further investigation

A

Diagnosis of exclusion
Evoked potentials- measure electrical activity in brain in response to visual, auditory or somatosensory stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Multiple sclerosis pathology

A
  • Immune system attacks myelin sheath and causes communication problems between brain and rest of body
  • Can eventually cause permanent damage or deterioration of nerve fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Cautions of multiple sclerosis

A
  • May also develop muscle stiffness/spasm, weakness or paralysis, problems with bladder
    Wide range of symptoms therefore difficult to predict
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Management of multiple sclerosis

A
  • Interferon beta medication- interfere with diseases that attack body and decrease inflammation and increase nerve growth
    PT- rehab, help with mobility, balance + coordination
    Occupational therapy- help with daily living
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Bone info

A

Bone turnover= removal + replacement of old bone
Cortex- outer shell of bone
Matrix- soft + light inner structure
Phosphorus + calcium protect cortex
Vitamin D controls levels of calcium + phosphorus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Rickets aetiology

A

Lack of vitamin D or calcium
Lack of sunlight exposure, poor diet
Most common in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Rickets clinical features

A
  • Thickening of ankles, wrists and knees
  • Bowed legs
  • Poor growth
  • Dental problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Rickets X-ray

A
  • Fraying- indistinct margins of metaphysis
  • Splaying- widening of metaphyseal ends
  • X-ray of wrists and ankles usually confirm diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Rickets pathology

A

Usually from extreme,e prolonged vitamin D deficiency- failure in mineralisation of bones, softness + weakness
Rare inherited problems can cause rickets
Can cause hormone imbalance of parathyroid hormone, leading to increased bone resorption

57
Q

Cautions of rickets

A

Treatable, delay can cause serious complications such as irreversible bone deformities

58
Q

Management of rickets

A
  • Increase child’s intake of vitamin D and calcium
    PT- maintain ROM and strength
59
Q

Paget’s disease aetiology

A
  • Unknown
  • Suggest combination of genetic and environmental factors
  • Several genes appear to be linked
    Abnormal bone remodelling
    More common in adults
60
Q

Paget’s clinical features

A
  • Most people have no symptoms
  • Most common complain is bone P
  • Pelvis- hip P
  • Skull- overgrowth of bone hearing loss or headaches
  • Spine- nerve root compression, P and tingling
  • Legs- weaknening  bending
61
Q

Paget’s X-ray

A
  • Areas of bone breakdown
  • Enlargement of bone and deformities that are characteristic of disease (e.g. bowing of long bones)
62
Q

Paget’s pathology

A
  • Interference of bodys normal recycling process
  • Causes body to generate new bone faster than normal, rapid remodelling produces bone that’s weaker than normal bone, leading to P, deformities and fractures
  • Over time bone become fragile
  • Pelvis, skull, spine and legs most affected
  • Risk increases with age
63
Q

Cautions of Pagets

A

Long term treatment

64
Q

Paget’s management

A
  • Osteoporosis drugs (bisphosphonates)
  • Typically administered through injection, can be taken orally (however can irritate stomach)
65
Q

Hyperthyroidism aetiology

A
  • Inefficiency in parathyroid gland
  • Primary due to- noncancerous growth (adenoma|) on gland, enlargement (hyperplasia) of parathyroid gland, cancerous tumour (very rare cause)
  • Secondary- anything condition leading to severe calcium/vit D deficiency, chronic kidney failure
    Tertiary- chronic secondary hyperthyroidism
66
Q

Hyperthyroidism clinical features

A
  • Primary often described before signs and symptoms occur
  • Severe- Weak bones that break easily (osteoporosis)
  • Kidney stones
  • Excessive urination
  • Fatigue
  • Nausea, vomiting, loss of appetite
67
Q

Hyperthyroidism further investigation

A

Blood tests- elevated calcium levels
X-ray bone density loss, bone cysts in rare cases

68
Q

Hyperthyroidism pathology

A

Parathyroid gland produces PTH in response to low calcium levels, PTH increases calcium absorption in gut, activates osteoclasts to break down bone, releasing calcium into blood stream
- Where parathyroid gland over produces parathyroid hormone in bloodstream
- Parathyroid healps maintain right balance of calcium in blood stream and tissues
- Especillay important for nerve and muscle function as well as bone health
- Primary- enlargement of parathyroid gland casues overproduction of parathyroid hormone
- Secondary- result of another disease

69
Q

Cautions of hyperthyroidism

A

Avoid high calcium diet- such as dairy
Avoid Vit D supplements

70
Q

Hyperthyroidism management

A

Primary- surgery to remove parathyroid gland
Secondary- treat underlying condition, phosphate binders
Severe- IV fluids, diuretics, steroids used to remove excess calcium from blood + reduce symptoms
Regular monitoring of blood tests to confirm normalisation of calcium levels

71
Q

Hypothyroidism aetiology

A
  • Acquired- Removal or injury to parathyroid gland
  • Autoimmune disease- attacks parathyroid gland
    Idiopathic- no cause
72
Q

Hypothyroidism clinical features

A
  • Twitching facial muscles
  • Muscle P or cramps
  • Fatigue or weakness
  • memory loss
73
Q

Hypothyroidism further investigation

A

Blood test
X-ray- increased bone density + calcification of soft tissue
Urine analysis

74
Q

Hypothyroidism pathology

A
  • Uncommon
  • Body produces abnormally low levels of parathyroid hormone
  • Difficulty regulating calcium and phosphorus
    Low blood calcium leads to formation of membrane and muscle spams, nerve damage
75
Q

Cautions of hypothyroidism

A

Avoid low calcium diets
Cautions of vit D and calcium supplements if HX of kidney stones/renal failure as this increases risk

76
Q

Hypothyroidism management

A
  • Supplements can bring calcium and phosphorus levels to normal range
    Regular blood tests to check levels
77
Q

Parkinson’s aetiology

A
  • Breakdown of neurons
  • Mainly due to loss of neurons that produce dopamine in brain
  • When dopamine levels decrease, it causes atypical brain activity, leadsing to impaired movement and other symptoms of Parkinson’s
78
Q

Parkinson’s acronym

A

TRAP
Tremor, rigidity, akinesia/bradikinesia (stopping starting/stopping), posture
1. resting tremor first sign
2. bradikinesia (generalised slowness of movement)- difficulty with daily activities
3. muscle rigidity- muscle tone increases

79
Q

Parkinson’s clinical features

A
  • Symptoms start slowly
  • First symptoms barely noticeable
  • Tremors are common
  • Early stage- little expression on face, arms may not swing when walking, speech may become slurred
  • Loss of automatic movements
  • Swoop posture
    Man, aged 70
80
Q

Parkinson’s further investigation

A
  • No specific test to diagnose
  • Neurologist will diagnose Parkinson’s based on medical history, review signs and symptoms, and a neurological and physical examination
    Normal X-ray
81
Q

Parkinson’s pathology

A
  • Progressive disorder which affects nervous system and parts of body controlled by the nerves
  • Genes and environmental factors
    Basal ganglia in middle of brain responsible for movements such as walking and looking around
    Substantia nigra in basal ganglia produces NT dopamine
    Dopamine essential for basal ganglia function
    Parkinson’s= decrease in dopamine
82
Q

Parkinson’s management

A
  • Medication- levodopa- absorbed by nerve cells in brain and turned into dopamine, which transmits messages between parts of the brain and nerves that control movement
    PT- improve mobility, manage non-motor symptoms, improve QOL
83
Q

Gout aetiology

A
  • Obesity
  • Kidney disease
  • Drinking too much alcohol
    Build up of uric acid in Jts- leads to formation of crystals which deposit in Jts and cause inflammation
84
Q

Gout clinical features

A
  • Acute attacks 1-2 weeks
  • Spontaneous- may be precipitated by minor trauma, operation, excessive alcohol
  • Most common site- metatarsopharyngeal Jt of hallux, ankle, olecranon bursa + finger Jt
  • Skin looks red, shiny, swollen, hot and tender
85
Q

Gout further investigation

A
  • Dual-energy computerised tomography (DECT)- detects urate crystals in Jts
  • Blood tests- uric acid levels
  • X-ray to rule out other potentials- normal on acute attacks
    Chronic shows tophi- large lumps of crystals in JTs
86
Q

Gout pathology

A
  • Characterised by presence of crystals in Jt, bursa and tendons
  • Consequences of these deposits may be inert + asymptomatic may include acute inflammatory reaction, may result in slow destruction of tissue
87
Q

Cautions of gout

A

Long term management
Serious complications lead to Jt damage and kidney stones

88
Q

Gout management

A
  • NSAIDs
  • Colchicine- anti-inflammatory drug that effectively reduces gout P
  • Corticosteroids- e.g. prednisone, controls inflammation and P
    PT- ROM, strength, avoid Jt damage
    Reduce purine intake
    Combination of meds and lifestyle changes needed to prevent future gout attacks
89
Q

Pseudo-gout aetiology

A
  • Presence of calcium pyrophosphate dihydrate crystals within affected Jt
  • Appear in nearly half the population older than 85
  • Not all develop pseudogout
    Predisposed- Jt damage, OA, hyperthyroidism
90
Q

Pseudo-gout clinical features

A
  • Most commonly affects knees
  • Swollen, warm and severely painful- sudden + severe
    Accompanied by fever and chills
91
Q

Pseudo-gout further investigation

A
  • Arthrocentesis- withdraw sample of fluid with needle
  • X-ray can reveal Jt damage + crystal deposits in Jt cartilage
    Jt fluid analysis and blood tests confirm diagnosis- detect calcium pyrophosphate dehydrate in Jt fluid
92
Q

Pseudo-gout pathology

A
  • Form of arthritis
  • Aka calcium pyrophosphate deposition disease (CPPD)
  • Crystal deposits form in Jt (different to usual gout)
    Calcium pyrophosphate crustals cause inflammation
93
Q

Cautions of pseudo gout

A

Risk increases with age
Chronic therefore requires long term treatment

94
Q

Management of pseudo gout

A
  • Colchicine daily as preventative measure
  • Corticosteroids
  • NSAIDs- relive P, reduce inflammation
    Lifestyle- lose weight
    Surgery may be needed to remove crystals
95
Q

Reactive arthritis aetiology

A
  • Bacteria spreads it
  • Chlamydia, salmonella, shigella
96
Q

Reactive arthritis clinical features

A
  • Usually targets knees, ankles and feet
  • Signs and symptoms often occur 1-4 weeks after exposure to triggering infection
  • P and stiffness
  • Eye inflammation (conjunctivitis)
  • Urinary problems
  • Swollen toes or fingers
  • Low back P which rends to be worse in the morning
97
Q

Further investigations of reactive arthritis

A

Changes in Jts typically not as severe as OA- X-ray
Osteopenia- no osteophytes or Jt space narrowing
Blood tests- to determine cause of infection

98
Q

Reactive arthritis pathology

A
  • Jt P and swelling triggered by an infection in another part of the body- most often intestines, genitals and urinary tract
  • Numerous bacteria can cause reactive arthritis
    Immune system overreacts to infection, causing inflammation
99
Q

Reactive arthritis management

A
  • DMARDs- disease-modifying anti-rheumatic drugs
  • NSAIDs
    Manage underlying condition
    If lasts longer than 6 months management approach is different
100
Q

Osteomalacia

A

Softening + weakness of bones

101
Q

Symptoms of osteomalacia

A

Bone P in legs, groin, upper thighs and knees
Muscle weakness/stiffness
Fractures which can lead to full breaks

Affects anyone with Vitamin D deficiency

102
Q

Osteomalacia aetiology

A

Vit D deficiency, essential for absorption of calcium and formation of strong bones
Inadequate light exposure, dietary intake

103
Q

Osteomalacia clinical features

A

Muscle weakness + P, particularly in low back, hips, thighs, pelvis
Bone P
Difficulty standing from seated
Tenderness to touch over bone

104
Q

Osteomalacia x-ray

A

Bone demineralisation
Early stages may be norma
Blood tests- identify fit D, phosphorus, calcium deficiency

105
Q

Osteomalacia patho

A

Decreased vitamin D
Decreased absorption of calcium in gut and decreased bone mineralisation
Bones become less dense
Unable to support weight of body, muscle weakness + P
Vitamin D affects muscle function- cramping, weakness and P

106
Q

Osteomalacia cautions

A

Hx of kidney stones or hyperglycaemia
Medication which interacts with vitamin D

107
Q

Osteomalacia management

A

VItamin D supplements
Adequate sun exposure
Regular exercise, healthy diet

108
Q

Polymyalgia rhematica aetilogy

A

Unknown
Thought to be autoimmune
Most common in women over 50s

109
Q

Polymyalgia clinical features

A

muscle P and stiffness in neck, shoulders and hip
Fatigue, fever, weight loss
Stiffness usually worse in mornings or after periods of rest

110
Q

Polymyalgia further investigations

A

Erythrocyte sedimentation rate + c-reactive proteins to confirm diagnosis and monitor effectiveness of treatment

111
Q

Polymyalgia patho

A

Chronic inflammation of muscles and tendons

112
Q

Polymyalgia causions

A

Chronic condition requiring long term treatment

113
Q

Polymyalgia management

A

Corticosteroids to reduce inflammation + P
Treatment typically at a high dose, gradually tapered over several months
PT- maintain Jt ROM and strength
Some Px can develop giant cell arthritis- requires prompt diagnosis and treatment

114
Q

Osteoporosis aetiology

A

Unknown
Thought to be result of genetic + teratogens
Female, over 50s
smoking, excessive alcohol

115
Q

Osteoporosis x-ray

A

X-ray cannot detect until significant amount of bone density has been lost
Decreased size of bone, fractures, decreased space between bones

116
Q

Osteoporosis further investigation

A

Dual-energy x-ray absorptiometry- measures bone density
Ultrasound bone density testing

117
Q

Osteoporosis patho

A

Interruption of new bone formation and old bone reabsorption is disrupted, leading to rapid loss of bone density
Bone density decreases with age

118
Q

Osteoporosis features

A

Silent- unaware until fracture
Symptoms of advanced- back P from collapsed vertebra, reduced height, stoop posture, fractures from little to no trauma

119
Q

Osteoporosis management

A

Bisphosphonates- medication can slow bone loss and increase density
Regular exercise
Calcium and vit D supplements
Regular check ups to monitor

120
Q

RA aetiology

A

Cause unknown
Foreign antigen sets off chain reaction
HLA-DR4 gene
Smoking, exposure to toxins

121
Q

RA presentation

A

Symmetrical
Morning stiffness
Women affected 3x more than men
Early stage- swelling, stiffness, warmth, tenderness
Progression- restriction
Later stage- deformity, ulnar deviation, values knees, claw toes

122
Q

RA further investigations

A

X-ray- Jt space narrowing, erosion
May take time to see changes on x-ray
Blood tests- C-reactive proteins, erythrocyte sedimentation rate

123
Q

RA cations

A

Some medication has serious side effects, e.g. increased risk of infection
Higher risk of CV disease, important to monitor risk factors such as high blood pressure

124
Q

RA patho

A

Stage 1- preclinical- well before signs arise, immune pathology begins. increased erythrocyte, c-reactive proteins, rheumatoid factors
2- synovitis- inflammation of synovial membrane, P and swelling in Jts, potentially reversible
3- destruction- persistent Jt inflammation causes destruction, articular cartilage erodes
4- deformity- combination of articular destruction, capsular stretching + tendon rupture leading to progressive instability + deformity

125
Q

RA management

A

DMARDs
PT- maintain Jt function and prevent muscle weakness

126
Q

Reactive arthritis aetiology

A

After infection (urinary, GI, genitals)
Most caused by salmonella, shigella, chlamydia

127
Q

Reactive arthritis clinical features

A

Jt P, swelling
Particularly in knees, ankles and feet
Some may develop skin rash called keratoderma blenorrhagica

128
Q

Reactive arthritis further investigations

A

No osteophyte or Jt space narrowing
Osteopenia

129
Q

Reactive arthritis patho

A

Immune response to infection
Overreacts causing inflammation in Jts and other parts of body

130
Q

Reactive arthritis cautions

A

Any age, more common in young/middle aged

131
Q

Reactive arthritis management

A

Manage underlying infection
ABs
Improvement once infection treated
NSAIDs reduce inflammation + P
PT for increasing ROM, strength
DMARDs- prevents Jt damage

132
Q

Spina bifida aetiology

A

Combination of genetic and environmental e.g. lack of folate acid during pregnancy, exposure to radiation

133
Q

Spina bifida detail

A

Neuralisation- produces CNS
Ectoderm thickens, forming neural plate
Neural plate folds inwards forming neural fold + crest
Day 22- neural crest fuses forming neural tube
Anterior end becomes brain + rest becomes spinal cord
Closure reliant on adequate folic acid- failure= spina bifida

134
Q

Clinical features of spina bifida

A

Depends on size and location
Weakness/paralysis of legs
Scoliosis
Hairy patch

135
Q

Further investigation for spina bifida

A

Abnormalities of vertebra, defects of spinal column, scoliosis, absence of curve
MRI detects brain and spinal cord impairment

136
Q

Cautions of spina bifida

A

Avoid medication that closure to failure of neural tube closure during embryonic development
Careful handling of baby

137
Q

Spina bifida management

A

Surgery to cover exposed neural tissue

138
Q

Types of spina bifida

A

Occulta- vertebral fail to close properly, bones don’t fuse, predisposing back P

Meningocele- neural tube closes but meninges frequently herniate through vertebra

Myelomeningecele- neural tube failed to close leading to exposure of neural tissue- can’t carry nerve impulse= paralysis

Pathophys 2 (5 decks)

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