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SEM2 2024 > FPB- MST1 > Flashcards

FPB- MST1 Flashcards

1
Q

Define Osteoporosis

A

Decreased bone mass at least 2.5sd below the mean

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2
Q

Define Ostepenia

A

Decreased bone mass

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3
Q

Define Osteomalacia

A

Decreased mineralization of bone (vitamin D deficiency)

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4
Q

Define Osteodystrophy

A

Skeletal changes that occur in chronic renal disease

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5
Q

What are the stages of bone healing

A

Haemotoma, Inflammation, Soft Callus (Fibrocartilaginous), Hard Callus (Woven bone), Remodelling (Lamellar bone)

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6
Q

What is Wolff’s Law?

A

Increased loading on a bone will make it stronger

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7
Q

What are some RF’s of osteoporosis?

A

Low estrogen, physical inactivity, low serum calcium

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8
Q

What is the child version of osteomalecia and some common signs?

A

Rickets
Bowing (genu varus), protrusion of forehead, pigeon chest

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9
Q

What are some mechanisms of osteodystrophy?

A

Low GFR, increasing phosphate retention, which causes hypocalcemia and osteopenia

Decreased activation of vitamin D causing osteomalacia

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10
Q

How is primary fracture healing different from the more common secondary?

A

If ends are close enough together and fixed, then there is no need to form a callus and bone can be formed

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11
Q

What are complications of fracture?

A

Infection, malunion, nerve and vascular damage, fat embolism disrupting blood flow as bone marrow enters bloodstream

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12
Q

What are the stages of muscle injury and repair?

A

Degeneration, inflammation, regeneration and fibrosis

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13
Q

What makes fibrosis occur?

A

Damage to the ECM. If injury only to muscle fibres little fibrosis is needed

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14
Q

Why is creatine kinase not a great measure of muscle injury?

A

Highly variable by individual

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15
Q

What is the gold standard of detecting muscle injury?

A

Decrease in max force

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16
Q

What is sarcomere inhomogeneity?

A

Weak sarcomeres stretched by stronger ones, lengthening not uniform. Weak on descending limb of tension-length
Weak sarcomeres yield or pop

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17
Q

Why does loss of Ca2+ homeostasis cause muscle damage?

A

Cellular necrosis linked with Ca2+ homeostasis, disruption of sarcolemma

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18
Q

What occurs in regeneration?

A

Damaged fibres are degraded, and satellite cells activate and proliferate. Myoblasts derived from satellite fuse into myotubes

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19
Q

What are the function of tendons?

A

Connect muscle to bone, absorb and release energy

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20
Q

What is tendinopathy?

A

Spectrum of changes in damaged diseased tendons, usually from overuse and involving pain and decline in function

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21
Q

What are some risk factors for tendon patholog?

A

Obesity, age, systemic disease, oestrogen deficit, muscle weakness (e.g. runners load), overuse, increase in acitvity, lack of recovery, poor workplace/ergonmics

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22
Q

What is the Beighton scoring system?

A

Measure of joint hypermobility, more than 4 factors required

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23
Q

What is a typical tendinopathy management?

A

Heavy, slow resistance

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24
Q

What is boom bust?

A

In contrast to gradual load, boom bust is when you go to hard at an exercise and then ease off because of pain resulting in a reduction of activity over time

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25
Q

What is permissible pain for exercise?

A

1-4- acceptable
5-7- modify
8-10- rest

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26
Q

Why are ligaments wavy?

A

Bears load from different directions

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27
Q

What are ligaments composed of?

A

Collagen, strong stiff (type 1 strongest)
Elastin, flexible, smaller proportion
Proteoglycans, influence viscoelastic properties

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28
Q

Describe the stress strain curve

A

Toe region- crimped (wavy) fibres straighten
Elastic region- straightened fibres deform but not permanently
Plastic region- permanent deformation, microscopic failure until yield point, then macroscopic failure and rupture

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29
Q

What is stress and strain?

A

Stress is the force per unit, strain is the relative deformation

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30
Q

What is stiffness?

A

Resistance to change in ligament length

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31
Q

How does thickness and length affect stress?

A

Thicker -> small stretch -> higher stiffness
Longer will rupture at increased length but same force, therefore half as stiff

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32
Q

What is viscoelasticity?

A

V- Resistance to flow
E- ability to return to original shape

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33
Q

What is creep?

A

Fixed force, ligament elongate and gradually return to original length

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34
Q

What is stress-relaxation?

A

Stretch to fixed length, force required to maintain length decreases over time

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35
Q

What is strain rate sensitivity?

A

Load fast, stiff, high failure load
Load slow, more compliant

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36
Q

How does ligament injury occur?

A
  1. High stress (contact)
  2. High strain (overuse)
  3. Both (aberrant motion)
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37
Q

How are ligament injuries classified?

A

I- disruption of some collagen fibres, little functional deficit
II- considerable disruption, effusion, increased laxity, moderate functional deficit
III- complete disruption, pop, immediate pain, haeomarthrosis, significant deficit

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38
Q

What are the phases of ligament healing?

A

I- Haemorrhage with inflammation, haeomtoma fills gap, inflammatory cells, vasodilation capillary permeability, rudimentary scar, collagen remodeling begins
II- Matrix and cellular proliferaiton, 6 weeks fibrin clot and granulation tissue fills gap, vascularization, strength of scar improves
III- Remodeling and maturation, decreased vascularity, collagen more organized, tensile strength improves, slightly disorganized and hypercellular ligament

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39
Q

How does ligament structure change upon healing?

A

Different proteoglycan, collagen types
Collagen crosslinks don’t mature
Reduced viscoelastic properties, less stiff more compliant
Reduced failure loads
Inferior creep

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40
Q

What is DDH?

A

Acetabulum cannot contain femur head, potentially due to maternal oestrogen increasing ligamentous laxity. Becomes chronically dislocated.

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41
Q

What are some RF’s of DDH?

A

Breech, incorrect swaddling, hormonal, family history

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42
Q

What are some DDH signs/symptoms?

A

Barlow sign, dislocates hip by adduction and depression of flexed femur

Ortalani sign, elevation and abduction on already dislocated flexed femur, clunk on entry

< 3months, reduced hip abduction, abnormal skin creases
3m<x<1y, reduced hip abduction, leg length discrepancy
>1y, toe walking, trendelenburg

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43
Q

What are the alpha and beta angles?

A

a- Bony acetabulum and ilium ~ >60
b- Labrum and ilium ~ <55

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44
Q

What is Perthes Disease?

A

Blood supply to femoral head disturbed (avascular necrosis), causing softening and collapse of bone and then remodeling to repair

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45
Q

What are signs/symptoms of Perthes?

A

Limping, groin pain, reduced range abduction and internal rotation

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46
Q

How is Perthes classfied?

A

A- normal lateral pillar height
B- >50%
C- <50%

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47
Q

What are some treatment options for Perthes?

A

Casting to maintain hip abductiom
Wheelchair for non-weight bearing

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48
Q

What is SUFE?

A

Femoral head slips on metaphysis due to combination of obesity, growth spurts and endocrine disorders. Neck mostly moves anteriorly and externally rotated

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49
Q

How is SUFE classified?

A

Unstable (unable to WB) or Stable
Acute or Chronic or Acute on Chronic which is sudden displacement of already slipped epiphysis

Can also be mild slip <1/3 of width, moderate <1/2 width or severe >1/2 slip

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50
Q

What are some signs/symptoms of SUFE?

A

Pain (commonly knee), no WB, antalgic gait, out toeing gait
Most reliable, flexed hip will automatically cause external rotation

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51
Q

What are treatment options of SUFE?

A

Emergency surgery, nonWB, osteotomies to reconstruct femur

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52
Q

What are some risk factors of Parkinson’s?

A

Age, pesticides, gender, head injury

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53
Q

What are some protective factors of Parkinson’s?

A

Smoking, coffee

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54
Q

How do we diagnose Parkinson’s?

A

Neuronal loss of substantia nigra
Lewy body build up

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55
Q

What is the pathogenesis of Parkinson’s?

A

Impaired protein trafficking, aggregation
Dysfunction in autophagy
Oxidative stress
Neuroinflammation

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56
Q

What are some cardinal features of Parkinson’s?

A

Bradykinesia (slow movement)
Rigidity
Tremor
Unilateral onset and persistent asymmetry

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57
Q

What are some non-motor symptoms of Parkinson’s?

A

REM sleep behaviour (act out dreams)
Anosmia (lose smell)

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58
Q

What are the four functions of the pain pathway?

A

Transduction
Transmission
Perception ‘Pain’
Descending Modulation

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59
Q

What do transducers do?

A

Ion channels that convert stimulus to electrical activity

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60
Q

What are first and second pains?

A

Immediate to deter from activity
Second delayed throbbing non-specific

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61
Q

What is Complex Regional Pain Syndrome (CRPS)?

A

Pain plus other clinical abnormalities
Swelling, discoloration starting in feet/hands
Persistent burning pain

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62
Q

What does descending modulation do?

A

Reduce or facilitate nociceptive transmission

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63
Q

What is nocebo hyperalgesia?

A

Algesia after defensive encounter promotes expectation of pain

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64
Q

What is the difference between sarcopenia and dynapenia?

A

S- Age related muscle mass loss (and function)
D- Age related muscle strength loss

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65
Q

How can sarcopenia be diagnosed?

A

Need low muscle mass, strength and physical performance
Grip strength, body composition and gait speed

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66
Q

What factors can control muscle mass?

A

Protein synthesis and degradation
Nutrition, hormones, genetics, innervation, blood flow, exercise

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67
Q

Which fibres undergo greatest atrophy?

A

Type II Fast

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68
Q

What neuromuscular functions can change with ageing?

A

Possible demyelination
Widening of endplate
Longer nerve terminals
Fewer side branches

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69
Q

What’s the function of insulin and glucagon and which cells secrete them?

A

I- Glycogenesis, Glycolysis, Triglyceride synthesis, beta cells
G- Glycogenolysis, Gluconeogenesis, alpha cells

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70
Q

What is the marker for insulin levels?

A

C-peptide

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71
Q

What is the pathogenesis of T1DM?

A

Immune death of beta cells, alpha cell dysfunction, post-prandial hyperglucagonemia, hypoglycemic glucagon impairment

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72
Q

What is the pathogenesis of T2DM?

A

Insulin resistance, gradual onset

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73
Q

What are some differences between Typ1 and Type 2 DM?

A

Type 1: ketones common, GAD present, C peptide low, fast progression
Type 2: ketones uncommon, GAD absent, C peptide normal, gradual onset

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74
Q

What are some complications of hypoglycemia and hyperglycemia?

A

Hypo- impaired growth/development, falls, cardiac disease, coma, seizures death (impaired glucose to brain)
Hyper- DKA (diabetic ketoacidosis), Hyperosmolar hyperglycemic state, CVD, stroke, infection

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75
Q

What is PVD (peripheral vascular disease)?

A

Narrowing of arteries, hypertension, hyperlipidemia, venous insufficiency. Hyperglycemia from diabetes can cause narrowing

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76
Q

What is functional decline?

A

Reduced capability to perform self-care, physical or cognitive decline

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77
Q

What is multimorbidity?

A

2 or more chronic conditions simultaneously

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78
Q

What is frailty?

A

Dynamic state of vulnerability that causes a decline in physiologic reserve and recover from stress

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79
Q

What tools are used for screening and assessment of frailty?

A

S- Clinical Frailty Scale 1-9, 1 being very fit, 5 need help with IADLS (instrumental), 9 approaching death

A- Fried Phenotype, 1 point allocated per factor to indicate frailty, weight loss, exhaustion, physical activity, walk time, grip strength

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80
Q

What is carcinogenesis?

A

Normal cells -> cancer cells

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81
Q

What are RF’s for carcinogensis?

A

Age, carcinogens, accumulation of mutations, immunodeficiency

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82
Q

What is a neoplasm?

A

Abnormal mass of tissue from excessive tissue divide

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83
Q

What is the difference between tumour staging and grading?

A

Staging- how much cancer and how far its spread
T0-4, extent of primary tumour
N0-3, spread to lymph nodes
M0,1, metastasis
Grading- aggressiveness
1-4, 1 well differentiated resembling tissue of origin, 4 undifferentiated

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84
Q

What is the most common neoplasm?

A

Carcinomas, from epithelial tissues

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85
Q

How does chemotherapy assist therapy?

A

Cyto-toxic drugs interfere with mitosis, helps other treatments work better

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86
Q

How does radiotherapy assist in treatment?

A

External beam or radiation source, damage cell DNA to stop division

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87
Q

How does hormone therapy assist in treatment?

A

Block production of growth hormones and interfere with action

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88
Q

What defines a mild cognitive impairment?

A

Greater than expected age, does not interfere with ADLs, increased forgetfulness and compensatory tools

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89
Q

What is dementia?

A

Umbrella term for diseases affecting memory and cognitive function
Impaired learning, reasoning, language, personality/behaviour

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90
Q

What are RF’s for cognitive impairment?

A

Age, gender, genetics, Down’s syndrome

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91
Q

What are the common types of dementia?

A

Alzheimer’s- protein/chemical build up, impaired memory, learning, language

Vascular dementia- impaired blood circulation, impaired judgement, gait, instructions

Lewy body dementia- Lewy bodies develop, impaired attention, concentration, hallucinations

Fronto-temporal dementia- protein build up in lobes, change in mood, language, emotional regulation

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92
Q

What is delirium and what are some RFs?

A

Acute disorder of attention and cognition mimicking dementia. Can be hyperactive (agitation, restless), hypoactive (lethargy, withdrawal)

RF- visual and cognitive impairment, severe illness, polypharmacy, dehydration

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93
Q

In CT was is light and dark?

A

Light hyperdense
Dark hypodense

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94
Q

What are pros and cons of CT?

A

P- rapid, non-expensive, excludes large acute pathologies, useful for bone imaging
C- less parenchymal and soft tissue definition, involves radiation

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95
Q

What is CSF produced by?

A

Choroid plexus

96
Q

What is hydrocephalus?

A

Accumulation of CSF in ventricle due to obstruction, failure to absorb or increased production

97
Q

What are the pros and cons of MRI?

A

P- more detailed parenchymal and soft tissue, no ionizing radiation
C- more expensive, more contraindications (metal)

98
Q

How is acute stroke detected?

A

DWI/ADC measures water diffusion]

99
Q

What is the difference between intra-axial and extra-axial tumours?

A

IA- from brain parenchyma
EA- arises from outside brain parenchyma e.g. meningocytes

100
Q

What is the purpose of SWI?

A

Detects diffuse axonal injury

101
Q

What are the three aspects of neuroplasticity?

A

Chemical (neurotransmitters), functional (way neurons work together) and structural (demands of software changes hardware)

102
Q

What are some principles of neuroplasticity?

A

Use it or lose it
Use it and improve it
Salience matters (behaviour must be important to individual)

103
Q

What is MS?

A

An autoimmune inflammatory demyelinating disorder of the CNS

104
Q

What are RFs for MS?

A

HLA-DRB1*1501 genetic marker
Viral Infection
Smoking

105
Q

What is the pathology of MS?

A

CNS inflammation -> Demyelination -> Axonal degeneration. Hallmarks are focal demyelinated plaques, astrocytic scars.
Attack on myelin producing oligodendrocytes.
Leaky BBB allows infiltration of peripheral immune cells.
Axonal damage done by oxidative injury, mitochondrial and ion channel dysfunction

106
Q

What are some typical symptoms of MS?

A

Painful monocular visual loss
Painless diplopia
Cerebellar symptoms: Nystagmus, Vertigo, Ataxia
Spasticity
Bladder Dysfunction
Fatigue
Weakness

107
Q

What is the pathology of a ischemic stroke?

A

Fibrin clot coming from the large arteries of the neck or heart, causing atherosclerosis and blocking blood flow to the brain, causing a cerebral infarction which in turn can cause intracranial hemorrhage

108
Q

What are some methods of secondary prevention for ischemic stroke?

A

Lower BP
Antithrombotics e.g. aspirin
Statins regardless of baseline lipids
Carotid endarterectomy to shell out carotid stenosis

109
Q

What BP do you give thrombolytics?

A

> 220/120

110
Q

What is a transient ischemic attack?

A

High risk presentation that requires emergency attention. Usually last 10 minutes, if it doesn’t return to normal then it is a stroke.

111
Q

What is tPA?

A

Tissue plasminogen activator, converts plasminogen to plasmin which break down clots. Bed rest for 24hr after taking

112
Q

What are some contraindications for tPA?

A

Hemorrhage
Hypodensity (subacute infarct)
GI bleeding
BP >185/105

113
Q

What is symptomatic intracranial haemorrhage a product of?

A

Damaged BBB and reperfusion

114
Q

How often is tPA successful at opening arteries and what’s an alternative?

A

tPA is often not successful, stent retriever thrombectomies are an alternative to allow reperfusion, offering a clear cut benefit for ICA, Middle Cranial 1 and Basilar

115
Q

What is a hemicraniectomy?

A

Large bone flap removed to allow brain to expand

116
Q

How are ICH’s classified?

A

Deep- usually due to hypertension and rupture of deep penetrating arteries
Lobar- superficial, often secondary to amyloid angiopathy, tumour etc.

117
Q

How is stroke recognized?

A

FAST
Face droop
Arm drift
Speech, dysarthria dysphasia
Time call 000

118
Q

What are some risks to the brain during development?

A

Genetic abnormality
Injury in utero
Big head on weak neck
Soft cranium

119
Q

What are some differences in the child brain vs the adult brain?

A

More likely to have diffuse injury
More actively neuroplastic

120
Q

What age group of children recovered the best from traumatic brain injury?

A

Later injuries, <3 years old had the least recovery

121
Q

What are the phases of neuroplasticity following brain injury?

A

Phase 1: cell death, cortical inhibitory pathways reduce
Phase 2: shift to excitatory pathways, new connections made
Phase 3: new synaptic markers, axonal sprouting, remodelling

122
Q

What is a closed and open TBI?

A

Closed, skull not broken
Open, object penetrates

123
Q

What can diagnose TBI?

A

Glascow Coma Scale
Mild 14 to 15 e.g. concussion
Severe 3 to 8
Points for when eyes open, motor response, verbal response
1 point for no response

124
Q

What is important to optimize in TBI?

A

Oxygenation, ventilation and cerebral perfusion to prevent hypoxia

125
Q

What are signs of stroke in children?

A

Headache, seizure, hemiplegic weakness, vision and speech change

126
Q

When is supratentorial and infratentorial tumours common in children?

A

S- 2-3
I- 4-11

127
Q

What are symptoms of brain tumour in children?

A

Headache, vomiting, head tilt, balance and coordination, behavioural changes

128
Q

What is infectious encephalitis and how does it occur?

A

Generalized inflammation of the brain caused by infection, viral, bacterial or fungal. Can be contracted by mosquito or tic

129
Q

What are some symptoms of encephalitis?

A

Fever, seizure, headache, neck stiffness, sensitivity to light or sound

130
Q

What are some symptoms of autoimmune disorders?

A

Confusion, ataxia, sensory changes, nausea, headache

131
Q

What are burrholes, craniotomy and craniectomy?

A

B- drill into skull
CO- create a bone flap
CE- bone flap removed

132
Q

What are types of intracranial haemorrhages?

A

Extradural- between dura and bone, associated with overlying fracture
Subdural- tearing of bridging vein in subdural space (trauma or atrophy)
Intracerebral- hypertension, vasuclopathies or tumour

133
Q

What is a vasospasm?

A

Pathological constriction of blood vessels that may cause ischaemic stroke

134
Q

Describe meningiomas?

A

Most common, benign, arise from arachnoid mater, slow growing

135
Q

How do you treat vasospasm?

A

Triple H therapy hypertension (more blood flow), hypervolemia (more preload), haemodilution (less viscosity). All contribute to cranial perfusion pressure

136
Q

Which cranial nerve does acoustic neuromas impair?

A

Vestibular VIII

137
Q

What is normal intracranial pressure?

A

0-10mmHg, upper limit is 15mmHg

138
Q

How do you manage raised intracranial pressure?

A

Head to 30 degrees improves venous drainage, hyperventilation, CSF drainage, sedation, reduce oedema

139
Q

What is cauda equina syndrome?

A

Cauda equina compressed causing saddle anaesthesia, incontinence, foot drop

140
Q

What is the ASIA scale?

A

Measures neurology of spinal patients
A complete, no motor or sensory to E normal motor and sensory function

141
Q

What are normal cerebellar functions?

A

Integrates sensory information (not visual)
Compares intended action with actual movement
Balance
Coordination
Learning

142
Q

How does vision influence balance and coordination?

A

Cerebellum does not process visual information but visual reflexes react to disturbance in static posture, which can make us feel like we’re moving when we aren’t

143
Q

What are some common tests of cerebellar function?

A

Romberg- compares balance with different feet positions and eye open vs eyes closed
Gait- ataxic, wide-based, arms for balance
Finger-Nose test- tests coordination, whether you overshoot target
Rapid alternating movements- tests dysdiadochokinesia (slow clumsy alternating movement)

144
Q

What is PPC and the aspects of it?

A

Postoperative pulmonary complications
Atelectasis
Pneumonia
Acute Respiratory Distress Syndrome
Pulmonary aspiration

145
Q

What is the definition of an upper abdominal surgery?

A

Incision greater than 5cm above the umbilicus

146
Q

What are the adv and dadv of laparoscopic surgery?

A

Less pain, PPC, faster recovery, minimal surgical trauma, can operate on higher risk patients

Longer time, difficult to remove large pieces

147
Q

How does anaesthesia reduce FRC?

A

Reduced abnominal tone, diaphragm dysfunction, less lung compliance, less phrenic nerve activity

148
Q

What is closing capacity?

A

The maximal lung volume at which airway closure is detected. This means the FRC is too low to keep the lung/alveoli open

149
Q

What are some errors in technique during spirometry?

A

Cough, glottis closure, suboptimal effort, hesitation

150
Q

What is spirometry?

A

Lung function test that measures maximal forced inspiration and expiration

151
Q

What are some test contraindications of spirometry?

A

Coughing blood, unstable cardiovascular, collapsed lung, abdominal surgery

152
Q

What are the criteria for acceptability and repeatability?

A

A: Max 8 trials
R: Two highest FEV1 within 150ml of each other, same for FVC

153
Q

How does obstruction and restriction affect spirometry?

A

O: Reduced FEV1 and FEV1/FVC
R: Reduced FEV1 and FVC, normal or increased FEV1/FVC ratio

154
Q

What is DLCO?

A

Inhale mix of CO and tracer gas, X amount goes in, Y comes out. Gives an idea of diffusion across membrane

155
Q

What is Body Plethysmography?

A

Work out lung volume by measuring box pressure and volume (P1 and V1) and mouth pressure (P2). V2 is FRC

156
Q

What is cardiopulmonary exercise test?

A

Maximal effort, records O2 consumption CO2 output HR RR

157
Q

What are RFs for PPC?

A

> 80
Type of surgery
3 hour surgery
Mobility preop

158
Q

What are the ERAS elements and how do they help recovery?

A

OPEN
Optimize anesthetic
Preop education
Early ambulation
Nutrition optimization

Helps before during and after surgery to reduce risk of PPC, and get lungs working again

159
Q

What are some treatments for DDH?

A

Bracing to maintain contact with acetabulum and surgery

160
Q

What are some treatments for Perthes?

A

Maintain hip abduction with bracing, restrict activity with wheelchair

161
Q

What are some treatments for SUFE?

A

Emergency surgical stabilization, reconstruct femur

162
Q

What are some general treatments for apophysitis?

A

Activity modification, NSAIDS, rest, post, stretching

163
Q

What are some indications for MSK imaging?

A

fracture, dislocation, sprain, neoplasm

164
Q

What are the adv and dadv for Xray?

A

Cheap, quick, easy to interpret

Limited sensitivity and specificity, radiation

165
Q

What two projections are used in Xray?

A

AP and lateral

166
Q

What is fibromyalgia?

A

Severe musculoskeletal pain disorder, pain in all 4 quadrants of the body

167
Q

What is spondyloarthropathy?

A

Inflammatory joint disease with main effect on axial skeleton

168
Q

What are RFs of joint disorders?

A

Age, genetics, joint injury, obesity, occupation

169
Q

What is the pathophysiology of OA?

A

Cartilage erosion, subchondral bone sclerosis, osteophyte formation, joint space narrowing

170
Q

What are some symptoms of OA?

A

Joint pain, morning stiffness, pain on motion

171
Q

How is OA managed?

A

Prevent- e.g. lower obesity
Disease modifying drugs
Treat pain, dysfunction

172
Q

What is the pathophysiolgy of RA?

A

Synovitis, destruction, deformity

173
Q

What are some symptoms of RA?

A

Tiredness, pain, swelling, joint tenderness, effusion

174
Q

What are the radiologic features of hydrocephalus?

A

Ventriculomegaly (enlarged ventricles), periventricular lucency (fan shaped hypodensity), sulcal effacement (mass effect)

175
Q

What are the stages of lung development?

A

Embryonic
Pseudoglandular
Canicular
Saccular
Alveolar

176
Q

What occurs in the embryonic stage of lung development?

A

Lung bud arises from primitive foregut, branching leads to primitive airways

177
Q

What occurs in the pseudoglandular stage of lung development?

A

Secondary and tertiary bronchi, epithelial cell differentiate, develop arteries veins

178
Q

What occurs in the canalicular stage of lung development?

A

Immature bronchioles and alveolar ducts enlarge, blood gas barrier, surfactant

179
Q

What occurs in the saccular stage of lung development?

A

Increase surfactant, alveoli enlarge

180
Q

What occurs in the alveolar stage of lung development?

A

Proliferation to smaller alveoli, high gas exchange capability

181
Q

What are short term consequences of preterm birth?

A

Surfactant too low, respiratory distress, worse gas exchange may need oxygen supplementation

182
Q

How does the cardiorespiratory system compare in adults and children?

A

Horizontal ribs children, angled adult
Primary cartilage children, ossified ribs adult
Larger tongue relative to mouth Floppier epiglottis
Shorter less rigid trachea
Poorly developed cilia
Smaller diameter airway

183
Q

Describe how asthma affects the lungs

A

Smooth muscle tighten on expiration, may result in permanent damage

184
Q

Describe how CF affects the lungs

A

Sticky, dehydrated mucous due to ion channel transport inhibition.
Repeated lung infection and mucous plugging

185
Q

Describe how bronchiectasis affects the lungs

A

Inability to clear mucous, bacterial infection, airways dilated

186
Q

Describe how prematurity associated lung disease affects the lungs

A

Abnormal lung structure from poor development, increased risk of COPD

187
Q

Describe how primary ciliary dyskinesia affects the lungs

A

Dysfunction to cilia, mucous build up airway obstruction

188
Q

Describe how bronchiolitis obliterans affects the lungs

A

Inflammatory lung condition causing scarring which can obstruct airways

189
Q

Describe how neuromuscular weakness affects the lungs

A

Progressive muscle weakness, inefficient cough leads to infection

190
Q

What is obstructive lung disease?

A

Increase in airway resistance and decrease in expiratory flow

191
Q

How is obstructive disease diagnosed?

A

Reduced FEV1 compared to FVC, <70%

192
Q

What are some mechanisms of obstructive lung disease?

A

Smooth muscle constriction, hypertrophy, mucosal inflammation

193
Q

What is COPD?

A

Inflammatory disease caused by inhalation of noxious particles

194
Q

What is the clinical presentation of COPD?

A

Chronic bronchitis (blue bloater)- overweight, oedema, wheezing
Emphysema (pink puffer)- older, thin, dyspnea (breathlessness)

195
Q

Describe COPD pathophysiology

A

Mucous gland hypertrophy and mucous production
Destruction of ciliated epithelial cells
Small airway fibrosis
Increase bronchial smooth muscle
Destruction of capillary bed

196
Q

What are the consequences of COPD pathophysiology?

A

Airflow limitation
Lung hyperinflation, increase residual volume, as harder to expire

197
Q

How is bronchiectasis clinically presented?

A

Recurrent lung infection, chronic cough, chest pain, dyspnea

198
Q

What is the pathophysiology of COPD?

A

Initial infection, inflammation, inability to mucous clear, remodeling more obstructed

199
Q

What is the P wave and how should it look?

A

Depolarization of atria, small bump

200
Q

What is the PR wave and how should it look?

A

Delay of AV node, flat

201
Q

What is the QRS complex and how should it look?

A

Ventricular depolarization, dip then spike up and down

202
Q

What is the T wave and how should it look?

A

Ventricular repolarization, small bump

202
Q

What is the ST segment and how should it look?

A

Beginning of ventricular repolarization, should be flat

203
Q

What heart rates are classified as bradycardia and tachycardia?

A

B- below 60
T- above 100

204
Q

How is atrial fibrillation presented on an ECG?

A

No P waves, narrow QRS

205
Q

How is atrial flutter presented on an ECG?

A

P wave sawtoothed

206
Q

How is ventricular tachycardia presented on an ECG?

A

No P wave, QRS wide and bizarre

207
Q

How is ventricular fibrillation presented on an ECG?

A

No P, QRS or T

208
Q

What is troponin a sign of?

A

Heart muscle damage

209
Q

What is acute coronary syndrome?

A

Manifestation of atherosclerotic coronary plaque erosion including ischaemia and necrosis

210
Q

How is unstable angina clinically presented?

A

Crushing, tight chest pain, dyspnea, pain to jaw/left arm

211
Q

How is ACS managed?

A

Lifestyle
Bypass grafts or stents
Medication (antiplatelet, anticoagulant)

212
Q

What is the gold standard test for coronary artery antamoy?

A

Cardiac catheterization (angiography)

213
Q

Which coronary artery is most affected in coronary artery disease?

A

LCA

214
Q

What is heart failure?

A

Inability of heart to meet demand of tissue

215
Q

What is the difference between systolic and diastolic heart failure?

A

Systolic- ventricles cant pump hard enough
Diastolic- not enough blood fills ventricles

216
Q

What are the stages of prenatal cardiac development?

A

Primitive heart tubes
Embryonic heart division, atria, ventricles, forms septa
Vascular heart connections, complete AV and semilunar valves
Maturation and growth, more defined four chambers, foramen ovale

217
Q
A
218
Q

What are consequences on cardiac system for preterm birth?

A

Immature myocardium, pulmonary hypertension, altered cardiac structure, heart failure

219
Q

What causes congenital heart defects?

A

Genetic conditions, maternal health problems, maternal age

220
Q

What is atrial septal defect and its consequences?

A

Hole between LA RA
O2 blood passes to right side
Enlarged RV, heart failure in later life

221
Q

What is ventricular septal defect and its consequences?

A

Hole between LV RV
Large VSD, increased lung circulation, poor growth, dypsnea

222
Q

What is tetralogy of fallot?

A

VSD
Narrowing of pulmonary valve, Right ventricular hypertrophy
Overriding aorta

223
Q

What is hypoplastic left heart syndrome and its consequences?

A

Left side does not develop, RV becomes pumping chamber

224
Q

What is tricuspid atresia?

A

Tricuspid valve does not develop
Blood diverted from RA to LA

225
Q

What are symptoms of congenital heart conditions?

A

Blue lips, skin
Dyspnea
Respiratory infections

226
Q

How are intrinsic and extrinsic restrictive disorders different?

A

I- lung parenchyma
Parenchymal inflammation, fibrosis
E- pleura, chest wall, neuromuscular etc.
Impacts respiratory pump

227
Q

What are some characteristics of restrictive lung disorders?

A

Reduced lung compliance and volume
Dyspnea
Hypoxemia
Cough, clubbing of nails and crackles

228
Q

How is hypoxaemia different in intrinsic and extrinsic lung disorders?

A

I- Mismatched V/Q ratio

E- hypoventilation, poor respiratory pump

229
Q

How are intrinsic and extrinsic respiratory disorders managed?

A

I- Antifibrotics, immunosuppressant, oxygen therapy

E- Lose weight, surgical management for scoliosis

230
Q

How is intrinsic respiratory disorders caused?

A

Interstitial lung disease- inflammation scarring
Pneumonitis- filling of air spaces with exudate

231
Q

What is idiopathic pulmonary fibrosis?

A

Most common intrinsic lung disease, hypoxia and pulmonary hypertension

232
Q

What is sarcoidosis?

A

Granulomatous inflammation in variety of organs

233
Q

What is occupational lung disease?

A

Inorganic dust exposure causing intrinsic lung disease

234
Q

What are some pleural disorders?

A

Pleural effusion
Pneumothorax, collection of air in pleural cavity
Tumours
Fibrosis

235
Q

What are some chest wall disorders?

A

Deformity
Obesity
Pregnancy
Burns

236
Q
A

SEM2 2024 (4 decks)

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