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PBL Y2 S4 > Case 1 - Oeosphageal cancer > Flashcards

Case 1 - Oeosphageal cancer Flashcards

1
Q

What 3 ligaments stabilise the TMJ?

A

Lateral (temperomandibular) ligament
Stylomandibular ligament
Sphenomandibular ligament

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2
Q

What are the attachments of the temporalis?

A

O = Temporal fossa
I= coronoid process of mandible

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3
Q

What are the attachments of the masseter?

A

O: zygomatic arch and bone
I: lateral surface of mandible, including the ramus

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4
Q

What are the attachments of the lateral pterygoid?

A

O: superior head= roof of temporal fossa, inferior head =lateral pterygoid plate of sphenoid
I: Neck of mandible

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5
Q

What are the attachments of the medial pterygoid?

A

O: superficial head= maxillary tuberosity and palatine bone, deep head= lateral pterygoid plate of sphenoid
I: ramus of mandible (near angle) on medial side

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6
Q

What are the 2 groups of pharyngeal muscles and their role?

A

Circular muscles: contract sequentially from superior to inferior to propel food into the oeosphagus
Longitudinal muscles: act to shorten and widen the pharynx and elevate larynx during swallowing

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7
Q

Give the names of the circular pharyngeal muscles

A

Superior, middle and inferior pharyngeal constrictors

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8
Q

Give the names of the longitudinal pharyngeal muscles

A

Stylopharyngeus
Palatopharyngeus
Salpingopharyngeus

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9
Q

What is the oesophagus lined by and why?

A

Non-keratinised stratified squamous epithelium = resists abrasion

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10
Q

Where are the 2 plexuses found in the oesophagus? Give their roles

A

Meissner’s (submucosal) plexus: found in the submucosa, controls the size of blood vessels and secretion of gastric juice
Myenteric plexus: found between circular (inner) and longitudinal (outer) layers of muscle in muscularis propria, when activated it casuses relaxation

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11
Q

What muscle type is found in the oesophagus?

A

First 1/3 = skeletal
Middle 1/3 = skeletal and smooth
last 1/3 = smooth

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12
Q

Compare the roles of different teeth for eating

A

Incisors = slice and cut
Canines = tear and rip
Premolars = grind and crush
Molars = mostly grinding (some crush)

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13
Q

What muscles predominantly produce the protrusion and retraction of jaw during chewing?

A

Protraction = lateral pterygoid, some by medial pterygoid
Retraction = temporalis

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14
Q

What muscles act as the depressors of the mandible? Give their innervation

A
  • Lateral pterygoid = V3
  • Anterior belly of digastric = V3
  • Mylohyoid = V3
  • Geniohyoid = cervical plexus
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15
Q

Describe the chewing reflex of the jaw

A

Presence of a bolus pushing against the roof and back of the mouth initiates a reflex inhibition of the muscles of mastication to open the mouth.
In turn, depression of the mandible activates muscle spindles (stretch receptors) which sends afferent signal via trigeminal nerve
This activates the elevators of the mandible to close the mouth

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16
Q

Which muscles act as the elevators of the mandible?

A
  • Temporalis
  • Masseter
  • Medial pterygoid
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17
Q

What are the 3 phases of swallowing?

A

Phase 1 = oral phase
Phase 2 = pharyngeal phase
Phase 3 = oesophageal phase

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18
Q

Describe what happens in the oral phase of swallowing

A

1: mastication
2: salivation for chemical digestion of food to increase SA and to lubricate bolus
3: Tongue forms a downward slope by elevating the tip (extrinsic muscles) and forming a central tunnel (intrinsic muscles) to push food into the oropharynx

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19
Q

Describe briefly what happens in the pharyngeal phase of swallowing

A
  • Stimulation of afferent CN IX fibres (palatopharyngeal and palatoglossal arches) by bolus to activate nucleus solitarius and CN X
  • Ensure bolus doesnt enter nasopharynx or larynx
  • Push bolus into pharynx
  • UES relaxes
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20
Q

What mechanisms are in place to ensure the bolus doesnt enter the nasopharynx?

A
  • Contraction of the uvula (CN IX)
  • Levator levi palatini contracts to lift the soft palate (CN X)
  • Tensor veli palatini tenses the soft palate and attenuates LLP’s action (CN V)
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21
Q

What mechanisms are in place to ensure the bolus doesnt enter the larynx?

A
  • Contraction of lateral cricoarytenoids and oblique/ transverse arytenoids to adduct the vocal cords (so cannot breath at this point)
  • Retroversion of epiglottis to block larynx
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22
Q

What mechanisms push the bolus into the pharynx?

A
  • Contraction of the palatopharyngeus and palatoglossus (muscles around the arches) pulls the arches together
  • Longitudinal muscles elevate the pharynx and larynx
  • Inner circular muscles are responsible for pharyngeal peristalsis
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23
Q

What causes relaxation of the upper esophageal sphincter? (3 factors)

A

1- relaxation of the cricopharyngeus (most important!!) via CN X
2 - Contraction of suprahyoid and thyrohyoid to pull the hyoid and larynx upwards
3- Pressure of the bolus to distend the UES

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24
Q

Describe what happens in the oesophageal phase of swallowing

A

1: primary peristalsis: continuation of pharyngeal peristalsis, i.e. relaxes the LES
2: secondary peristalsis: if the bolus gets stuck, it activates stretch receptors so the muscle above the bolus contracts and the muscle below relaxes (local reflex)

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25
Q

Describe the type of secretion of the parotid gland, and where it enters the oral cavity

A

Serous secretion, enters via the parotid duct around the 2nd upper molar

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26
Q

Describe the type of secretion of the submandibular gland, and where it enters the oral cavity

A

Mixed secretion, i.e. both serous and mucous. Enters via submandibular duct in the lingual frenulum

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27
Q

Describe the type of secretion of the sublingual gland, and where it enters the oral cavity

A

Mucous secretion, some serous but minor. Via sublingual ducts (10-20x) into floor of oral cavity

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28
Q

Compare the saliva produced by serous and mucus cells

A

Serous = watery and enzyme-rich
Mucus = glycoprotein, mucous rich so is thick

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29
Q

Give examples of the intrinsic saliva glands and what they secrete

A

Buccal, labial, lingual, palatine = primary mucus saliva at a constant rate

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30
Q

Describe the innervation (inc nuclei involved) of the extrinsic salivary glands

A

PARASYMPATHETIC (inc. saliva production)
Facial nerve: superior salivary nucleus to the submandibular ganglion, then post-symp fibres innervate submandibular and sublingual glands

Glossopharyngeal: inferior salivary nucleus to the otic ganglion, then post-symp fibres innervate the parotid gland

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31
Q

What can increase saliva secretion?

A

Chemoreceptors (e.g. acidic food) or mechanoreceptors (chewing) = act on superior and inferior salivary nucleus
Sight, smell and thought of food

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32
Q

How does the sympathetic NS influence the saliva?

A

Sympathetic T1-T4 = deep petrosal nerve, makes a more protein-rich and viscous saliva (thicker)

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33
Q

Compare the osmolality of primary and secondary secretions

A

Primary = isotonic (same as blood plasma)
Secondary= hypotonic (less than blood plasma)

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34
Q

Describe the main movements of ions that forms the primary secretion in the acinar cells

A
  • Na+/K+ ATPase creates a gradient, so NKCC1 allows Na+, K+, 2Cl- to enter via concentration gradient, but K+ is recycled back after
  • Cl- accumulates then leaves via Cl- channels
  • Na+ drawn in via paracellular route down electrochemical gradient
  • AQP5 expressed on apical + basolateral membranes so H2O enters via osmosis
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35
Q

Describe the modification of primary secretion into secondary secretion by the duct cells

A
  • Na+ reabsorbed by ENaC (passive) and leaves basolaterally by Na+/K+ ATPase
  • Positive charge on basolateral side draws Cl- in via Cl- channels
  • Apical Cl-/ HCO3- exchangers for the HCO3- generated intracellularly via carbonic anhydrase (so Cl- into blood and HCO3- in lumen)
  • Basolateral exchangers swap Na+ for H+ (so H+ enters blood and Na+ back out via ATPase)
    = Impermeable to water, so creates a dilute and hypotonic saliva
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36
Q

What may be present in the saliva for the antimicrobial defence?

A

IgA, lysozymes, cystatins, defensins

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37
Q

What centre is responsible for the neural control of swallowing?

A

Central Programme Generator (CPG) in the medulla - it excites/ inhibits muscles of swallowing

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38
Q

What nerves are involved in the neural control of swallowing?

A

CN V, VII, IX, X, XII

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39
Q

Damage to which nucleus in the brainstem results in severe dysphagia?

A

Nucleus ambiguus

40
Q

What are the normal pressures throughout the oesophagus?

A

UES = 100 mmHg (high pressure)
Intraoesophageal = -5 mmHg (negative so bolus can be pulled into oesophagus)
LES = 20 mmHg
Intragastric = +5 mmHg

41
Q

What is oropharyngeal dysphagia? What are the signs and risks?

A

Abnormal bolus transfer to oesophagus, so there’s difficulty initiating a swallow, e.g. stroke (neurologic) or myasthenia gravis (muscular)

Signs = drooling, food seeping out of mouth
Risk of aspiration or regurgitation into nasal cavity

42
Q

What is oesophageal dysphagia?

A

Abnormal bolus transport through the oesophagus; the food stops after initiation of a swallow. Caused by a motility disorder or obstruction (e.g. in primary disease like achalasia)

43
Q

What are some causes of dysphagia?

A

Neurological: stroke (>50% of patients), dementia, TBI, Guillian-Barre
Progressive: Parkinsons, Huntingtons, age
Obstructive: oesophageal structure, cleft lip (doesnt create enough pressure to push bolus down if cant shut mouth)
Muscular: achalasia and sarcopenia

44
Q

Describe how the brain recovers from dysphagia following a stroke

A

There is compensation, so if the dominant side is damaged, the non-dominant side develops (increases plasticity) = there is compensatory reorganisation to improve swallowing

45
Q

How does age cause dysphagia?

A

Ageing leads to loss of connective tissue elasticity and decreased muscle mass, so there is less strength and ROM. Also have reduced saliva production

46
Q

What is achalasia? Give some signs and symptoms

A

Failure of the oesophageal sphincter to relax (onset >25 yrs).
Dysphagia, chest pain, coughing, weight loss, heart burn, reflux

47
Q

What is the gold-standard for achalasia diagnosis? List the findings that need to be present for a diagnosis

A

Monometry, with presence of 3 findings:
- Elevated resting LES pressure: >45 mmHg
- Incomplete LES relaxation
- Aperistalsis: loss of peristalsis in smooth muscle portion

48
Q

What are the 3 types of achalasia characterised by peristaltic movement?

A

Type I: no persistalsis
Type II: asynchronous peristalsis
Type III: high pressure, vigorous peristalsis

49
Q

How can achalasia be treated?

A
  • Botulinum toxin A (inhibit Ca2+ release)
  • Pneumatic dilation (inflate balloon across LES)
  • Hellers myotomy (incision across LES so it can’t contract)
  • POEM (incision but less invasive than HM)
50
Q

What are some implications of dysphagia?

A
  • Aspiration pneumonia: leading cause of mortality, has a 40% increased risk of death
  • Malnutrition
  • Dehydration
  • Poor outcome; high mortality
  • Depression
51
Q

What other exams can be done to assess achalasia? What findings may be present?

A

Endoscopy: may reveal dilated oesophagus with residual material and candida infection may be present
Radiology: barrium swallow (diagnostic acccuracy 95%) - dilated oesophagus with beak-like narrowing, may be sigmoid shape if severe

52
Q

What is involved in a bedside swallow screen?

A

Cognitive screen, one-step commands (i.e. poke your tongue out) and then oral-motor exam - use tongue depressor for resistance, ask to cough etc.
90mL water - ask to drink sequentially until finished (feel their throat). Watch them afterwards for 1 minute

53
Q

What signs may be present after drinking 90ml water in a patient with dysphagia?

A
  • Signs of struggle
  • Coughing
  • Choking
  • Wet, gurgly voice
54
Q

What can the bedside swallow screen be supplemented with?

A
  • Videoflouroscopy: dynamic images of swallowing
  • Fiberoptic endoscopic examination (FES): tube with a camera through the nose to base of tongue, pharynx and larynx. Checks for any residue in the laryngeal inlet
55
Q

What is transcranial magnetic stimulation?

A

Stimulates brain, visualises the pathway involved - should have a lateralised (symmetrical) swallowing system

56
Q

What is conventional manometry?

A

Takes pressure recordings in the oesophagus following catheterisation. As someone swallows it picks up pressures from the pharynx, UES and LES and tells you if they are opening

57
Q

What is high resolution manometry? Which plots are the most accurate and why?

A

More precise measurement, uses spatiotemporal or topographic plots.
Spatiotemporal are more accurate & give location and pressure data

58
Q

How might dysphagia be managed?

A
  • Use postures or manouvres to decrease pharyngeal residue and enhance airway protection, i.e. lying down or chin up
  • Oesophageal dilation for oesophageal dysphagia
  • Soft diet or nil by the mouth with IV infusion (if unable to swallow)
  • If severe - gastrotomy and enteral feeding (NG or PEG tubes)
59
Q

When would enteral feeding be considered?

A
  • BMI < 18.5
  • Unintentional weight loss >10% in 3-6 months
  • BMI <20 with unintentional weight loss >5% in 3-6 months
  • People at risk of malnutrition, i.e. eaten nothing or little for 5 days, or poor absorptive capacity
60
Q

What is a PEG and when would it be used?

A

Percutaneous endoscopic gastrostomy: tube into stomach, used if need enteral nutrition for long periods (i.e. >30d) and can last months to years.

61
Q

What is a complication of a PEG?

A

‘Buried bumper syndrome’ - ring around the bumper is overgrown, so can’t put food down it. Happens if you dont rotate the tube regularly (should every day). Need to remove as there is a risk of perforation

62
Q

What is a PEG-J and when would it be used?

A

Adds a jejunal extension (J-tube) to a PEG so it goes into SI not the stomach. This is used in patients that cant tolerate PEG to overcome vomiting and reflux

63
Q

What is a nasogastric tube and when would it be used?

A

Goes through nose down to stomach, can give fluids, medications and liquid food through it. Used for shorter time periods if unable to intake adequate amounts

64
Q

What is a complication of nasogastric tubes?

A

Aspiration pneumonia - inhalation of stomach contents can cause lower respiratory tract infections, occurs in debilitated patients with abnormal reflexes. Can lead to pneumonia (bacterial infection)

65
Q

What are the 4 types of altered diets?

A

Type 1: dysphagia pureed = pudding-like texture, no chewing required just bolus control
Type 2: mechanically altered dysphagia = moist, semi-solid foods, some chewing required
Type 3: dysphagia advanced = soft-solids, requires more chewing ability
Type 4: regular = no modifications

66
Q

What is Barrett’s oesophagus?

A

Type of metaplasia where a portion of the normal distal stratified squamous epithelial lining has ben replaced by metaplastic columnar epithelium

67
Q

Where is Barrett’s oesophagus visible?

A

Endoscopically visible >1cm above the gastro-epithelial junction (GOJ) - the GOJ is where the epithelium usually changes

68
Q

What are the symptoms of Barrett’s oesophagus?

A

Heartburn, regurgitation of food, nausea, upper abdominal pain, metallic taste in mouth, chronic sore throat

69
Q

What condition is Barrett’s oesophagus associated with and why?

A

Gastro-oesophageal reflux disease (GORD) - causes reflux of acid and gastric contents into the oesophagus. overtime, the oesophagus changes from squamous epithelium to columnar. The lining of the oesophagus may resemble the stomach - ‘intestinal metaplasia’

70
Q

What are some risk factors for Barrett’s oesophagus?

A

Age, male (3x increased risk), family history, obesity, smoking, hiatus hernia

71
Q

Describe the progression of Barrett’s oesophagus into cancer

A

1- Barrett’s oesophagus, 1 in 10 will develop:
2- low grade dysplasia
3- high grade dysplasia = 40% risk of developing cancer in 5 years
4- oesophageal adenocarcinoma

72
Q

Explain the use of cytosponge TFF3

A

Used to diagnose Barrett’s: swallow capsule with a sponge inside, attached to a piece of thread. The capsule dissolves after 7 mins and sponge is released. It is retrieved and collects cells on its way out, the cells are then examined with stain TFF3.
If cells show changes - need endoscopy to confirm

73
Q

How might an endoscopy differ between a healthy patient and one with Barretts?

A

Endoscopy at GOJ:
Healthy = white-ish coloured lining
Barrett’s = pink coloured lining

74
Q

How might Barrett’s oesophagus with dysplasia be treated?

A
  • Endoscopic mucosal resection: remove polyps or growths from the lining of oesophagus or stomach, i.e. pre-cancerous cells or small areas of cancer
  • Radiofrequency ablation: burn away abnormal cells under sedation - flat areas only (EMR removes raised areas)
75
Q

How might Barrett’s oesophagus without dysplasia be treated?

A

Cannot remove Barrett’s oesophagus so it doesnt decrease risk of cancer, however can:
- Give proton pump inhibitors, e.g. omeprazole, to reduce stomach acid production and reduce reflux
- lifestyle changes, e.g. reduce alcohol, stop smoking, weight loss

76
Q

What surgery can be done if lifestyle changes and medication isnt helping Barrett’s oesophagus?

A

Laparoscopic Nissen fundoplication - upper part of stomach is wrapped and stapled around lower oesophagus

77
Q

What are unidimensional measures for QoL?

A

Assess health in terms of one specific aspect, for example:
- General health questionnaire (assesses mood)
- McGill pain questionnaire

78
Q

What are multi-dimensional measured of QoL?

A

Assesses health in the broadest sense; respondents make a judgement about their health from best to worst, i.e. WHO QoL-100

79
Q

What are individual QoL measures?

A

Assess subjective health status, i.e. ask them to rate their own health. This uses dimensions along which it should be rated, for example: Schedule for Evaluating Individual QoL - individual selects 5 areas of their lives, then weigh each in importance and then how satisfied they are currently

80
Q

Compare absolute vs relative poverty

A

Absolute: poverty level relative to a fixed standard of living, rather than to the rest of the population

Relative: compares each households income to the median of their country, where those with <60% of the median income are classified as poor (<40% = severe poverty)

81
Q

What is a statement of intent?

A

Statement made by the GP, which states that the patient will probably die within 14 days so refers to palliative care. It means that death can be registered without automatically having to refer the death to the coroner (provided the patient has been seen by a doctor within the last 28 days - thus a SOI is valid for 28d)

82
Q

When can you withdraw treatment from a patient? What type of euthanasia is this?

A

If it is no longer in a patient’s best interest or of ‘overall benefit’. This is ‘non-voluntary passive euthanasia’ and is permissible for treatment of clinical benefit, i.e. as long as you’re surer they’re of no benefit then you can withhold them (although basic care does not stop)

83
Q

What is the doctorine of double effect?

A

If doing something morally good has a bad side-effect, then it is acceptable to do it providing the bad side effect was not intended.
IF they intended harm = murder

84
Q

What is manslaughter gross negligence?

A

Failure to meet the appropriate standard of care, resulting in death, through action or omission sufficiently negligent to amount to a crime

85
Q

When would assistance of suicide be prosecuted?

A
  • If the victim is under 18
  • If the victim did not have capacity
  • If the victim hadn’t made a decision
  • If the victim was under that doctors care
86
Q

When is prosecution less likely with assistance of suicide?

A
  • If motivated by compassion
  • If only of minor assistance
  • If involved attempted dissuasion
  • If reluctantly done
  • If compliant to police investigation
87
Q

What is active voluntary euthanasia?

A

‘Assisted suicide’: requested by the patient but administered by another, e.g. a drug to kill them. Illegal but may not be prosecuted if occurs abroad

88
Q

What is passive voluntary euthanasia?

A

Elective cessation of treatment, i.e. patient requests/ consents to refuse treatment (i.e. refuse chemotherapy even though it will save them). This is legal (non-contentious) and can be facilitated by ADRT

89
Q

What is active non-voluntary euthanasia?

A

When the patient hasnt expressed to be euthanised but are killed = usually murder or manslaughter

90
Q

What is passive non-voluntary euthanasia?

A

Withdrawal of treatment for people who lack the capacity / unable to make a decision themselves. if treatment is of NO clinical benefit then may be permissable, otherwise they are vulnerable to negligence/ manslaughter

91
Q

How can health status be measured?

A
  • Mortality rates: No. of deaths in one year compared to previous
  • Morbidity rates: prevalence rates, i.e. how many people in a given population suffer from a specific problem
  • Measure of functioning, i.e. ADL scales
  • Subjective health status - ask them to rate their own health
92
Q

What is the self-regulatory model?

A

Framework for how individual symptoms and emotions experienced during a health threat or diagnosis influence perception of illness and guides subsequent coping behaviour. The model suggests individuals search to understand their illness by understanding what it is, what it means, its causes, consequences, how long it will last and whether it can be cured

93
Q

How can poverty affect health?

A
  • 25% of disadvantaged groups have depression
  • Babies from disadvantaged groups have a lower birth weight which may affect cogntiive development (=cognitive delay)
  • Poor diet + processed foods = obesity and poor nutrition
  • Children from deprived areas are more likely to have chronic disease
  • People from more deprived areas are 3x more likely to have mental health problems and 13x more likely to die from non-accidental injury
94
Q

What cell types are present in the stomach and what do they produce?

A

Goblet cells: alkaline mucus
Parietal cells: secrete gastric acid and intrinsic factor
Mucous cells: secrete mucus and pepsinogens
Chief cells: secrete pepsin and gastric lipase
G cells: secrete gastrin
D cells: secrete somatostatin

95
Q

Where are the highest numbers of colon cancer seen in the UK?

A

North West of England

96
Q

What determines the degree of permeability of tight junctions?

A

Claudin family of proteins

97
Q

What are the consequences of dysphagia of:
1- oral phase
2- pharyngeal phase

A

1: aspiration pneumonia

2: nasal regurgitation

PBL Y2 S4 (9 decks)

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