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Semester 4 > Case 1 > Flashcards

Case 1 Flashcards

1
Q

European Convention on Human Rights Article 2

A

Right to life

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2
Q

European Convention on Human Rights Article 3

A

inhuman and degrading treatment

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3
Q

European Convention on Human Rights Article 8

A

right to respect for private and family life

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4
Q

True or False: Phospholipid bilayer is impermeable to ions and polar molecules

A

True

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5
Q

What provides permeability to ions and polar mols through phospholipid bilayer?

A

Membrane proteins like channels, pumps, and carriers

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6
Q

What regions form helical transmembrane domains?

A

hydrophobic

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7
Q

Which proteins within tight junctions form the closest connection between cells?

A

Claudins

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8
Q

Aquaporins are highly selective to water. Which aquaporin is important in salivary secretion?

A

Aquaporin 5

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9
Q

Describe the structure of K+ channels

A

4 subunits arranged around a central pore

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10
Q

Describe facilitated diffusion uniport

A

One molecule passing through channel at once in one direction

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11
Q

cotransporter symporter

A

2 molecules passing at once through channels in same direction

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12
Q

exchangers antiporter

A

2 molecules passing in opposite directions at once

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13
Q

Which type of solute carrier families do glucose transporters belong to?

A

SLC2

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14
Q

GLUT1 found in

A

Red cell, brain, kidney, placenta

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15
Q

GLUT 2 found in

A

Liver, intestine

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16
Q

GLUT3 found in

A

Astrocytes, neurones

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17
Q

GLUT 4 found in

A

Adipocytes, muscle

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18
Q

GLUT5 found in

A

Intestine

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19
Q

An important symporter in salivary glands

A

Na+, K+, 2Cl- cotransporter. Inward movement of Na+ drives uptake of Cl- against its gradient.

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20
Q

antiporter:

A

Na+, H+ exchanger,Opposite direction movement

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21
Q

Which ion gradient creates membrane potential

A

K+ gradient

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22
Q

Which subunits make up the Na+, K+ ATPase

A

Alpha and beta

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23
Q

Acinar cells of submandibular glands

A

Serous and mucous acinar cells

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24
Q

Acinar cells of parotid glands

A

Mainly serous acinar cells

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25
Q

Acinar cells of sublingual glands

A

Mainly mucous

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26
Q

Acinar cells of buccal glands

A

mucus

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27
Q

average daily secretion of saliva

A

1L

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28
Q

Saliva contains 2 main secretions

A

serous secretion - contains ptyalin (alpha-amylase) and Mucus secretion - contains mucin for lubricating and surface protective purposes

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29
Q

normal pH of saliva

A

6-7

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30
Q

Primary secretion of saliva by acinar cells

A

contain ptyalin or mucin. Secretion of Na+, Cl-, HCO3-, water added by osmosis. Isotonic, plasma-like secretion.”

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31
Q

Secondary secretion by salivary duct cells

A

reabsorption of NaCl from the duct, some secretion of potassium ions and bicarbonate ions into the duct. Duct cells have low water permeability, so final saliva = HYPOTONIC

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32
Q

what factors are contained within saliva to destroy bacteria

A

thiocyanate ions - bactericidal, lysosomes preolytic enzymes - aid thiocyanate ions and digest food particles.

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33
Q

which brain-stem nuclei control salivary glands

A

parasympathetic nervous signals form superior and inferior salivatory nuclei

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34
Q

Parasympathetic pathway of salivary secretion

A

ACh acts on the muscarinic receptors of the salivary glands. subsequent formation of inositol trisphosphate IP3 leads to increased Ca2+ concentrations within the cell. the second messenger significantly affects salivary volume secretion. Glandular secretion is sustained by acetylcholinesterases, which inhibit the breakdown of ACh.

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35
Q

sympathetic pathway of salivary secretion

A

Binding of the norepinephrine to α-adrenergic receptor results in formation of cAMP, which then leads to phosphorylation of various proteins and activation of different enzymes. Increases in cAMP result in increased salivary enzyme and mucus content.

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36
Q

organisation of GIT wall -inside to outside

A

Mucosa - epithelium, lamina propria, muscularis mucosae, Submucosa - Meissner’s submucosal plexus, Muscularis externa - Inner circular muscle, Auerbach’s Myenteric plexus, longitudinal muscle, serosa/adventitia

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37
Q

what does submucosal plexus control?

A

gastrointestinal secretion and local blood flow.

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38
Q

what does myenteric plexus control?

A

motility and secretes Vasoactive intestinal polypeptide VIP

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39
Q

what do the sensory neurons of enteric nervous system transmit?

A

they transmit the mechanical and chemical conditions of GIT

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40
Q

what do the motor neurons of enteric nervous system transmit?

A

control peristalsis and churning of intestinal contents.

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41
Q

peristalsis require an active ___

A

myenteric plexus

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42
Q

4 stages of swallowing or deglutition

A
  1. Cephalic stage - point where one is thinking about having a meal, 2. Oral stage (voluntary stage), 3. Pharyngeal stage - push food from pharynx to oesophagus, 4. Oesophageal stage - push food from pharynx to the stomach
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43
Q

key things happening during oral stage

A

chewing, salivation and tongue is retracted and push the bolus down into pharynx.

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44
Q

action of incisors

A

cutting food

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45
Q

action of molars

A

grinding food

46
Q

describe the chewing reflex

A
  1. food bolus initiates reflex inhibition of muscles of mastication - jaw drops, 2. jaw drop initiates stretch reflex -rebound contraction, 3. raises jaw and teeth closes, but compress bolus against lining of mouth, inhibiting jaw muscles again
47
Q

what happens during the pharyngeal stage of deglutition?

A
  1. initiation of swallowing reflex - receptors on the platoglossal, palatopharyngeal arches and uvula are stimulated by the passage of the bolus, 2. soft palate is pulled upward to close the posterior nares, to prevent the food reflux into nasopharynx, 3. palatopharyngeal folds pulled medially to form a sagittal slit, allowing food that has been masticated sufficiently to pass with ease into pharynx, 4. vocal cords closed: larynx pulled up and anteriorly neck muscles and epiglottis closed by transverse and oblique aretynoid muscles - preventing food to trachea, 5. upward movement of the larynx enlarges the opening to the oesophagus. at the same time, UES relaxes. 6. Once UES relaxes pharyngeal wall -superior, middle, inferior constrictors- contracts and propels the food by peristalsis into the oesophagus.
48
Q

which muscles make up the UES?

A

cricopharyngeus, inferior pharyngeal constrictor and proximal part of cervical oesophagus

49
Q

innervation of UES

A

Vagus nerve

50
Q

innervation to the muscles that open UES

A

CN V, VII, XII

51
Q

what is at the centre of the swallowing system in the medulla and pons?

A

brainstem Central Pattern Generator (CPG)

52
Q

which nuclei and cranial nerves control the motor response to muscles of swallowing?

A

dorsal vagal motor nucleus and nucleus ambiguus - CN 5,7,9,10,12

53
Q

how many pairs of muscles are required in the entire swallowing process

A

26

54
Q

Sensory receptors in the oropharynx, larynx and oesophagus detect changes and send signals back to the brainstem and the cortex via

A

CN 5, 7, 9, 10 and 12

55
Q

what type of stimulus are the MOST POWERFUL INDUCERS OF A SWALLOW

A

mechanical receptors detect Distension and produce a burning or pain sensation

56
Q

Vagal and spinal afferents send different types of sensations back into the system via

A

Nodose ganglion or inferior ganglion of the vagus afferents, Dorsal root ganglion of the spinal afferents

57
Q

vagus afferents then go via thalamus into cortex via the medulla

A

for spinal afferents - spinothalamic tract is involved in nociception and mechanoception, salivatory nuclei and nuclei controlling breathing are closely situated and work together during swallowing

58
Q

oesophageal stage has primary and secondary peristalsis. what are they?

A

primary - continuation of the peristaltic wave that begins in the pharynx and spreads into the oesophagus during the pharyngeal stage of swallowing - 8 to 10 seconds. Secondary - waves caused by retained food in the oesophagus, initiated partly by intrinsic neural circuits in the myenteric nervous system and partly by reflexes that transmit through vagal afferent fibres to the medulla and back again to the oesophagus through glossopharyngeal and vagal efferent nerve fibres

59
Q

Pharyngeal wall and upper 1/3 oesophagus - what muscle and which nerves control peristalsis?

A

striated muscle - peristalsis controlled by CN IX, X from nucleus ambiguus

60
Q

Lower 2/3 of oesophagus - what muscle and which nerves control peristalsis?

A

Smooth muscle controlled by the vagus nerves acting through connections with the oesophageal myenteric nervous system.

61
Q

pressure in UES

A

100 mmHg

62
Q

pressure in LES

A

20 mmHg

63
Q

intraesophageal pressure?Why?

A

-5 mmHg, helps bolus to be pulled through from the pharynx which is at atmospheric pressure -0mmHg- through the sphincter and into the oesophagus.

The reason why it is negative is because of the lungs and the pleura and there is the mediastinal pleura which pulls against the oesophagus creating

this negative pressure.

64
Q

Pressure in stomach

A

+5 mmHg
doesn’t overcome LES pressure, so reflux is prevented.

65
Q

what two products are secreted by the secretory glands in the GIT?

A

digestive enzymes and mucus

66
Q

what are crypts of Lieberkuhn

A

invaginations of the epithelium into the submucosa - contain specialised secretory cells

67
Q

tubular glands

A

in stomach and upper duodenum, secrete acid and pepsinogen in stomach

68
Q

FOOD –>
Contact with GLANDULAR CELLS –>
GLANDULAR CELL SECRETION
(Hormones) –>
Activation of ENTERIC NERVOUS SYSTEM (<–tactile/chemical stimulation/distnsion of gutwall) –>
Stimulation of MUCOUS CELLS –>
Increased Secretion of DEEP GLANDS

A
69
Q

effect of stimulation of parasympathetic nerves innervating the glands in the GI tract

A

strongly increases the rate of alimentary glandular secretion.

70
Q

Dual effects of stimulation of sympathetic nerves innervating the glands in the GI tract

A
  1. Increase in the amount of secretion (if already parasymp active, then reduces secretion
  2. Constriction of the blood vessels that supply the glands.
71
Q

structural dysphagia

A

Dysphagia caused by an oversized bolus or a narrow lumen

72
Q

propulsive dysphagia

A

Dysphagia due to abnormalities of peristalsis or impaired sphincter relaxation

73
Q

2 types of dysphagia

A

oropharyngeal - caused by Anatomic, neurologic, and muscular defects

oesophageal - motility disorder or a mechanical obstruction

74
Q

1/3 of oropharyngeal dysphagia cases are as a result of unilateral hemispheric strokes

A

larger lesion, greater damage

75
Q

Anterior lesions and lesions in subcortical white matter carry high risk of ….

A

aspiration

76
Q

dysphagia management

A
  • Swallow assessment within 4 hours of arrival in hospital.
  • Nil By Mouth (NBM) if unable to swallow.
  • Intravenous infusion (IV)
  • SALT (Speech and language therapy) assessment.
  • Feeding by alternative route.
  • Nutritional assessment for ALL including weight
77
Q

epidemiology of dysphagia after stroke

A

50% pts

78
Q

Assessment of Dysphagia in Stroke

A

• History
• Clinical observations
• Cognitive screening
• Cranial nerve assessment
• Oral cavity inspection
• Test swallows
• Mealtime observations, posture diet level, self-feeding, respiratory changes
• Videofluoroscopy (barium meal)
• Fiberoptic Endoscopic Examination Swallowing (FEES)
- This is to visualise any residues in the laryngeal inlet.

79
Q

parenteral

A

infusion into the bloodstream via a peripheral vein

80
Q

enteral feeding (preferred route)

A

feeding via a tube placed into the gut.

81
Q

Percutaneous endoscopic gastrostomy (PEG)

A

needs two doctors to insert at endoscopy.
A catheter is placed percutaneously into the stomach under endoscopic control.

82
Q

Under normal circumstances, what causes lower oesophageal sphincter (LOS) to relax?

A

Release of NO, vasoactive intestinal peptide form inhibitory neurones and interruption of normal cholinergic signalling

83
Q

Achalasia

A

the failure of a ring of muscle fibres, such as the lower oesophageal sphincter (LOS), to relax.
results from the degeneration of inhibitory neurons in the oesophageal wall (ganglion cells) in the myenteric plexuses.

Loss of inhibitory innervation in the LOS causes:
The basal sphincter pressure to rise.
Sphincter muscle incapable of normal relaxation.
Oesophageal body smooth muscle aperistalsis.
May result from chronic infections with herpes zoster or measles viruses

84
Q

Primary achalasia

A

Caused by distal oesophageal inhibitory neuronal (ganglion cell) degeneration

85
Q

Secondary achalasia

A

In Chagas disease, in which, Trypanosoma Cruzi infection causes destruction of myenteric plexus, failure of peristalsis and oesophageal dilatation

86
Q

Achalasia is characterised by the triad of..

A

Incomplete LOS relaxation, increased LOS tone and aperistalsis of oesophagus

87
Q

Clinical presentation of achalasia

A

Long history of intermittent dysphagia, characteristically for both liquids and solids from the onset.
Regurgitation of food from the dilated oesophagus occurs, particularly at night, and aspiration pneumonia is a complication.
Weight loss
Difficulty breathing
Chest pain
Heartburn

88
Q

Main symptoms of achalasia

A

Dysphagia for solids and liquids, difficulty in belching, chest pain

89
Q

Diagnostic tests

A

clinical history
endoscopy
radiology
manometry - required for confirmation

90
Q

Manometry

A

passing a catheter through the nose into the oesophagus and allowing the patient to swallow on either saline or a jelly-like substance.
The pressures generated by the muscles in the UOS, the muscles of the oesophagus and the LOS are monitored as the object passes down the oesophagus.

Three primary findings:

  1. Elevated resting LES pressure (above 45mmHg)
  2. Incomplete LES relaxation - this manometric finding distinguishes achalasia from other disorders associated with aperistalsis.
  3. Aperistalsis - in the smooth muscle portion of the oesophagus
91
Q

Treatment of achalasia

A

No treatment can restore muscular activity
Botulinum Toxin:
Endoscopic injection of botulinum toxin (type A) into the lower oesophageal sphincter:
Botulinum toxin inhibits the calcium-dependent release of acetylcholine from nerve terminals, thereby countering the effect of the selective loss of inhibitory neurotransmitters.
initially effective in releiving symptoms in 85% pts, symptoms recur in 50% pts within 6 months

Pneumatic Dilation: Most cost-effective non-surgical treatment option for patients with achalasia. Involves placing a balloon across the LOS, which is then inflated to a pressure adequate to tear the muscle fibres of the sphincter.
Main adverse event: oesophageal perforation

Hellers Myotomy: Surgical myotomy involves carrying out an anterior myotomy across the lower oesophageal sphincter.
o This means cutting the muscles in the anterior part of the LOS, thus allowing food and liquids to pass to the stomach.
Very effective.
Main adverse event: gastro-oesophageal reflux in about 10% of patients.

92
Q

Most usual sites for spillage in those with aspiration pneumonia are

A

apical and posterior segments of the tight lower lobe

93
Q

Clinical signs of aspiration pneumonia

A

Coarse crackles right base lung
Decreased percussion right base lung
Fever
Tachycardia
Tachypnoea
Hypoxia

94
Q

aspiration may cause

A 
chemical pneumonitis: chemical irritation of the lungs
obstruction of the respiratory tract
Bacterial infection (pneumonia): infection of the lower airways may lead to empysema, lung abscess, acute respiratory failure and acute lung injury
95
Q

Which bacteria are usually implicated?
Usually caused by gram-negative enteric pathogens and oral anaerobes

A

Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa

96
Q

4 main endogenous repair mechanisms after stroke

A

1) Neuroplasticity/ Neurogenesis - restoration of the neuronal network, including the migration of the new cells out of the area.
2) Angiogenesis - restoration of the blood supply.
3) Inflammation -neurorepair role of other brain immune cells (microglia), and the expression of growth factors.
4) Glial Scarring - protection of non-injured brain structures.

97
Q

where in the brain does neurogenesis occur

A 
subgranular zone (SGZ) of the dentate gyrus 
subventricular zone (SVZ)
98
Q

process of neurogenesis

A

Neural stem cells proliferate into neural precursor cells.
Precursor cells then do 4 things:
1. Perpetuation
2. Differentiation - into glial cells (astrocytes/ oligodendrocytes/ microglia), neurones
3. Integration - neurones integrate with other parts of the body
4. Migration

99
Q

Neurogenesis in the Subgranular Zone (SGZ) of the dentate gyrus

A

neural stem cells proliferate in the SGZ of the hippocampal dentate gyrus.
differentiate into neurones whilst migrating from the SGZ to the inner granule cell layer in the hippocampal dentate gyrus.
Here the neurones re-establish the function

100
Q

Neurogenesis in the Subventricular Zone (SVZ)

A

In the normal brain, neural progenitors migrate from SVZ to olfactory bulb via Rostral Migratory Steam (RMS).
Following injury, neural progenitors from SVZ leave RMS and migrate laterally towards the damaged area.

101
Q

how do microglia contribute to CNS renewal?

A

resting microglia change their phenotype.
Initially (“primary activation”), they change to a M1 phenotype, where they bring about neurotoxic effects involved in tissue injury.
Then there is “delayed activation”, where the resting microglia change to a M2 phenotype which bring about tissue repair due to immune suppression.

102
Q

Glial scarring

A

Glial scar formed by astrocytes
Neurotoxic - Microglia produce free radicals, nitric acid and arachidonic acid derivatives
Neuroprotective - glial scar forms a barrier between the glial reaction (apoptotic) site and the health tissue surrounding it, thus preventing further damage to the brain

103
Q

what are the 4 main dimensions of quality of Life as defined by Fallowfield (1990)

A

psychological
social
occupational
physical

104
Q

how to measure QoL

A

Unidimensional measures - assess health in terms of one specific aspect of health and can be used on their own or in conjunction with other measures. e.g. McGill Pain questionnaire, hospital anxiety and depression scale, etc.

Multidimensional measures - assess health in the broadest sense, good predictors of mortality.

Composite scale (generic or illness specific) - focus on particular populations, e.g. elderly, children, or on specific illnesses. E.g. SF-36 (Short Form-36), EUROQOL - EQ5D

Standardised or individualised measures - It asks the subjects to rate their own health status but also to define the dimensions along which it should be rated. E.g. of standardised - Barthel index
Individualised - Schedule for Evaluating Individual Quality of Life (SEIQoL)

105
Q

3 things needed for the measures to be useful

A

reliability
validity
sensitivity

106
Q

How can health status be measured?

A

Mortality rates - number of deaths in one year compared with either previous or subsequent years.

Morbidity rates - prevalance rates -how many people within a given population suffer from a particular problem

Measures of functioning - e.g. activity-of-daily-living scales (ADLs)

Subjective health status - ask the individuals to rate their own health.

107
Q

Self-regulatory model

A

Stage 1: Interpretation
Stage 2: Coping approach
Stage 3: Appraisal
look at the pic in Y case 1 notes

108
Q

Removal of nasogastric tube considered as an omission (letting die)

A
109
Q

Principles of biomedical ethics

A
  1. Autonomy
  2. Beneficence
  3. Non-maleficence
  4. Justice
110
Q

Ethical concepts

A

Futility Acts and omissions Double effect Basic care and medical treatment Ordinary and extraordinary treatment

Semester 4 (5 decks)

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