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Year 1 > Respiratory Sytem > Flashcards

Respiratory Sytem Flashcards

1
Q

What is the respiratory system?

A

Tract that delivers O2 and removes co2 via gas exchange

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2
Q

What is the upper respiratory system?

A

nose, nasal cavity, pharynx and larynx

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3
Q

What is the lower respiratory system?

A

trachea, bronchi, bronchioles and lungs

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4
Q

Why is the respiratory system divided?

A

clinical determinant of the impact of infection on breathing mechanisms

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5
Q

What is sinusitis?

A

Infection of sinuses- tenders around cheeks, eyes forehead, high temp, teeth pain and blocked nose

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6
Q

What is tonsilitis?

A

Symptom of Bacterial/viral infection- sore throat, bad breath, cough

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7
Q

What is pharyngitis?

A

Symptom of viral influenza or bacterial strep throat- sore throat, bad breath, swollen gland

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8
Q

What are the LRT infections?

A

Tracheitis, bronchitis, bronchiolitis, pleurisy and pneumonia

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9
Q

What is the cause of tracheitis?

A

Gram+ streptoccocus- deep severe cough, stridor(high pitch) fever, and respiratory distress ike dysapnea (shortness of breath)

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10
Q

What are the two types of bronchitis?

A

Acute bronchitis and chronic bronchitis

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11
Q

What is acute bronchitis?

A

3 week viral infection, higher susceptibility when smoking with similar symptoms to a cold:
runny nose
a dry cough which progresses onto a mucus cough
dysapnea
fatigue
fever
wheezing

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12
Q

What is the chronic bronchitis?

A

8+ weeks/ more than 3 months, common with smokers, asthma or emphysema (holes in alveoli)

Build-up of mucus in bronchi leads to blockage
Mucus cough, wheezing
chest pain
blue tinge (low o2)

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13
Q

What is pleurisy?

A

Inflammation of pleura caused by a tumour, viral/bacterial infection or tumour

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14
Q

What is the cause of pleurisy?

A

Sharp chest pain when breathing
Crunchy sound (stethescope)
dysapnea when trying to limit chest pain

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15
Q

How are infections in the respiratory tracts treated?

A

Gram + bacteria- antibiotics
Viral infections- antiviral medication rarely but generally treat symptoms

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16
Q

What are recommendations for RT infections?

A

Drink fluids to clear mucus and raise head while sleeping
Take NSAIDs for pain
Gargle salt water for sore throat
Lemon and honey to soothe cough

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17
Q

What is the cause of pneumonia?

A

Contagious bacterial infection: pneumococcus, mycoplasma pneumoniae, legionella penumoniae
Viral infection- influenza, cold
Fungi- penumocystis for immunocompromised

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18
Q

What level is the sternal angle?

A

T4/T5, where bifurcation of trachea also occurs

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19
Q

What are the respiratory muscles in inspiration?

A

Elevation of ribs anteroposteriorly- external intercostal and scalene
Elevation of sternum- sternocleoidomasotid muscle
Contraction and flattening of diaphragm

These increase lung and thoracic volume and decrease intrathroacic pressure

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20
Q

What muscle is involved in forced inspiration?

A

Serratus muscle elevates the ribs when shoulders are in fixed position

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21
Q

What are the respiratory muscles in expiration?

A

Passive expiration- internal intercostal contract to depress the ribs
Diaphragm relaxes and rises
Intentional expiration:
External oblique- contralateral rotation
Internal oblique- ipsilateral rotation
This raises the diaphragm further to decrease thoracic and lung volume and increase intrathoracic pressure

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22
Q

Which side of the lung accommodates for the heart?

A

Cardiac notch on the left lung

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23
Q

What is the histology of the nose?

A

Pseudostratified columnar epithelia to secrete mucus which warms and humidifies air to prevent respiratory tract damage. The epithelia support the olfactory fibres for scent.

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24
Q

What are the apertures of the nose?

A

Anterior nostrils and posterior chonae

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25
Q

What is the cribiform plate?

A

Perforations in the ethmoid bone

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26
Q

What are mitral cells and location?

A

Neurons in the olfactory bulb which interact with other neurons for olfaction

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27
Q

What cells support the olfactory bulb?

A

Pseudostratified columnar epithelia

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28
Q

What are the bony shelves in the nose and where do they project

A

Superior, middle and inferior Conchae which project medially from the lateral wall of the nasal cavity

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29
Q

What are the broad openings in the nose?

A

Superior, middle and inferior meatus inferior to the conchae.

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30
Q

What are the paranasal sinuses?

A

Frontal, ethmoid, sphenoid and maxillary sinus.

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31
Q

Function of the sinus?

A

Unknown but may assist in air filtration

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32
Q

What does the sphenoethmoidal recess drain?

A

Sphenoid sinus

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33
Q

What does the superior meatus drain?

A

Posterior ethmoidal sinus

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34
Q

What does the middle meatus drain?

A

Frontal sinus, maxillary sinus and anterior and inferior ethmoidal sinus

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35
Q

What does the inferior meatus drain?

A

nasolacrimal duct to drain excess fluid-
crying causes runny nose

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36
Q

What is the vascularisation of the nose?

A

Kiessalbeck’s plexus of the anastomosis of 5 arteries
Superior ethmoidal- near the frontal bone
Inferior ethmoidal- near the middle ethmoidal bone
Sphenopalantine artery- near the sphenoid bone
Greater palantine- near the teeth
Superior labia- near the lips

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37
Q

Why does epitaxis occur?

A

Nose is highly vascularised, damage of one blood vessel leads to quick and severe bleeding from all blood vessels.

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38
Q

What are the 3 components of the pharynx?

A

Nasopharynx- base of skull to the soft palate and uvula
Oropharynx- Soft palate to epiglottis
Laryngopharynx- superior margin epiglottis to the circoid cartilage

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39
Q

What is posterior to the pharynx?

A

Nasal cavity, oral cavity and larynx.

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40
Q

What is the function of the eustachian tube?

A

Protect and aerate middle ear and equalise pressure in the middle ear in response to external pressure

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41
Q

Who is at risk of eustachian tube blockage?

A

Children- narrower tubes prone to inflammation
Smokers- damaged cilia that allows mucus to enter and cause blockage and inflammation
Overweight people- fatty deposits may block the eustachian tube

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42
Q

What are the tonsils?

A

Collections of lumphoid tissue containing dendritic cells and lymphocytes for pathogen defense

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43
Q

What structures are present nasopharynx?

A

Conchae, meatus, eustachian tube and two tonsils:
Adenoid/Pharyngeal tonsil-connective tissue attaches it to the ethmoid bone and is lined with pseudostratified epithelia
Tubal tonsils- inferior to the eustachian tube

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44
Q

What are the structures in the oropharynx?

A

Superiorly- hard palate –> soft palate

Uvula attached to soft palate

Palatine tonsil- superior to the tongue. It invaginates to form crypts. Lined with stratified squamous non keratinising epithelia

Tongue

Lingual tonsil on posterior tongue that invaginates to form crypts filled with bacteria. Stratified squamous non keratinising epithelia

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45
Q

What is the laryngeal inlet?

A

The opening in the pharynx for the beginning of the larynx. It is posterior to the epiglottis and superior to the arytenoid cartilage (vocal folds). Bordered laterally by the aryepiglottic folds.

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46
Q

What is anterior, posterior, superior and inferior to the larynx?

A

Anterior- Thyroid cartilage
Posterior- Oesophagus
Superior- Laryngeal inlet
Inferior- Cricoid cartilage

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47
Q

Where does the larynx run from?

A

Muscular tube from C3 to C6/7 for phonation.

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48
Q

What are the divisions of the larynx?

A

Supraglottis- Above the vocal folds, contains
epiglottis to regulate food movement
Aryepiglottic folds- connects epiglottis and arytenoids
Arytenoids- joint for movement of vocal folds
False vocal folds- protection of the vocal folds

Glottis- contains vocal folds for phonation

Infraglottis- adjusts vocal fold tension

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49
Q

How can the larynx prevent regurgitation?

A

Applying pressure to the cricoid cartilage

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50
Q

What is the vascularisation of the larynx?

A

Superior and inferior laryngeal artery Superior and inferior laryngeal veins

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51
Q

What is the function of the interarytenoid notch?

A

Adduction (closure) of the vocal folds

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52
Q

What is the glottis?

A

Contains vocal folds for phonation. The opening is the rima glottidis

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53
Q

What is the function of the cuneiform cartilage?

A

Support the vocal folds and the epiglottis

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54
Q

What does abduction cause in the vocal folds?

A

Opening

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55
Q

What does adduction cause in the vocal folds?

A

Closure

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56
Q

What muscles cause abduction?

A

Lateral cricoarytenoid muscle

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57
Q

What muscles cause adduction?

A

Posterior cricoarytenoid muscle
Oblique arytenoid muscle
Transverse arytenoid muscle

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58
Q

What is the origin, insertion and innervation of the posterior cricoarytenoid muscle?

A

Origin: Posterior lamina of cricoid cartilage
Insertion: Posterior muscular process of cricoid cartilage
Innervation: recurrent laryngeal nerve (branch of vagus)

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59
Q

What is the origin, insertion and innervation of the lateral cricoarytenoid muscle?

A

Origin: Upper margin of cricoid cartilage
Insertion: Anterior muscular process of cricoid cartilage
Innervation: recurrent laryngeal nerve (branch of vagus)

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60
Q

What is the origin, insertion and innervation of the oblique arytenoid muscle?

A

Origin: Muscular process of arytrnoif
Insertion: Adjacent contralateral muscular process
Innervation: reccurrent laryngeal nerve

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61
Q

What is the origin, insertion and innervation of the transverse arytenoid muscle?

A

Origin: posterior muscular process of the arytenoid cartilage
Insertion: Adjacent lateral
Innervation: reccurrent laryngeal nerve

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62
Q

What muscle causes high pitch phonation?

A

Cricothyroid muscle- only tesnor muscle involved in phonation

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63
Q

What muscle causes the low pitch phonation?

A

Thyroarytenoid which includes vocalis

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64
Q

What is the origin and insertion of the cricothyroid muscle?

A

Origin: Anterior lateral cricoid cartilage
Insertion: Inferior lamina of cricoid cartilage
Innervation: Superior external laryngeal nerve

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65
Q

What is the origin, insertion and innervation of the thyroarytenoid muscle?

A

Origin: Inferior surface of thyroid cartilage
Insertion: Anterolateral arytenoid cartilage
Innervation: recurrent laryngeal nerve

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66
Q

What is dysphonia and causes?

A

Abnormal voice
-> tumour
->damage to the recurrent laryngeal nerve during surgery that can cause unilateral paralysis of a hoarse voice or bilateral paralysis of no voice

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67
Q

What is the trachea?

A

10-15cm airway tract from C6- T4/T5. Outermost layer is the adventitia formed of connective tissue containing fibroblasts.

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68
Q

What anatomical structure is related to trachea bifurcation?

A

Sternal angle at T4/T5

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69
Q

Why is trachea flexibility important?

A

Swallowing in the posterior oesophagus, achieved by the trachealis muscle and the cartilaginous rings.

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70
Q

What are the 3 body cavities?

A

Pleura- Lungs
Pericardium- Heart
Peritoneal- Abdominal Cavity

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71
Q

What is the lining of the body cavities?

A

Mesothelium- simple squamous epithelia for filtration

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72
Q

What is cardiogenic mesoderm?

A

Precursor to the cardiac muscle for heart formation on the cranial end. Due to ventral folding, it moves towards the midline.

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73
Q

What is the septum transversum?

A

Precursor to the diaphragm and lies laterally to the cardiogenic mesoderm on the cranial end

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74
Q

What are the features of the septum transversum?

A

Dorsally incomplete that creates pericardioperitoneal canals to allow communication between the cavities.

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75
Q

What is the cloacal membrane?

A

Anus precursor- Ectoderm and mesoderm that forms a ring on the caudal end.

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76
Q

What is the oropharyngeal membrane?

A

Mouth precursory- ectoderm and mesoderm that lies on cranial end

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77
Q

What is the notochord?

A

Precursor to the brain and spinal cord, formed from invagination of the mesoderm medially.

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78
Q

How is the foregut, midgut and hindgut formed?

A

In the yolk sac, ventral folding like a drawstring creates cranial end foregut, medial midgut and caudal end hindgut.

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79
Q

What is allantosis?

A

Outpouch of the yolk sac for urinary waste and gas exchange

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80
Q

What is the mesentery?

A

Creates attachment for the peritoneal cavity to the abdominal wall dorsally(posterior)

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81
Q

What is the sphlancic mesoderm?

A

Inner- Aligns with yolk sac

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82
Q

What is the somatic mesoderm?

A

Outer mesoderm- Continous with inner amnion membrane of the amniotic cavity

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83
Q

What happens during development to the diaphragm?

A

Initially at C3-C5, along with phrenic nerve but moves inferiorly to end at L3 and the level of ribs 7-12

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84
Q

What does the endoderm form?

A

The Lungs and GI tract

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85
Q

What is the lining of the lung bud and the attachment?

A

Lined with pericardium
Ventrally attached to gut wall
Cranial position to septum transversum

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86
Q

How do lung buds develop bronchi?

A

Budding

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87
Q

Describe the formation of the musculotendinous diaphragm

A

Fusion of the pleuroperitoneal membrane with the septum transversum transversely. Myoblast cells in the mesoderm migrate.

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88
Q

Describe the separation of the pleural and pericardial cavity

A

Week 5-7
W5: Medial folding of the pleuropericardial folds along with the phrenic nerve contained in the walls.
W6: Continues to fold medially and lungs extend ventrally
W7: Pleuropericardial folds fuse to create distinct pleural cavity and pericardial cavity

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89
Q

Why does congenital diaphragmatic herniation occur?

A

Incomplete closure of the pleuroperitoneal membrane. Herniation (opening) creates an opening in the diaphragm
Insufficient migration of myoblast cells creates easily palpable diaphragm.

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90
Q

What is the outcome of congenital diaphragmatic herniation?

A

Lung hypoplasia- underdeveloped lungs. Due to pressure from abdominal organs.

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91
Q

What is the function of respiration?

A

maintain po2 and pCO2 levels and maintain ph of the plasmaa

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92
Q

What is internal respiration?

A

Gas exchange across metabolising tissues

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93
Q

What is the change in O2 levels in the blood during internal respiration?

A

Decreases from 100 mmHg to 40mmHg

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94
Q

What is the change in CO2 levels in the blood during internal respiration?

A

Increases from 40mmHg to 45mmHg

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95
Q

What is external respiraton?

A

Gas exchange across lung membrane

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96
Q

What is the change in CO2 levels in the blood during external respiration?

A

Decreases from 45mmHg to 40mmHg

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97
Q

What is the change in O2 levels in blood during external respiration?

A

Increases from 40mmHg to 100mmHg

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98
Q

What is the kPa for hypoxia?

A

8kPa

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99
Q

How is alveolar po2 and pco2 maintained?

A

Gas exchange.

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100
Q

What is hypercapnia?

A

High CO2 caused by Hypoventilation

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101
Q

What is hypocapnia?

A

Low CO2 caused by Hyperventilation

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102
Q

How is ph regulated?

A

Kidneys through HCO3- in the carbonate acid buffer system

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103
Q

What is the central control of respiration?

A

Nucleus tractus solitaris in the medulla

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104
Q

What are the two peripheral chemoreceptors?

A

Carotid body- bifurcation of the capillaries in the neck- innervated by the glossopharyngeal nerve
Aortic body- near the aortic arch- innervated by the vagus nerve

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105
Q

Function of chemoreceptors?

A

Flow dependent and are in areas rich in high flowing blood to detect pO2 levels and minimally pCO2

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106
Q

Location of carotid body

A

Each side of the neck, at the bifurcation of the common carotid artery

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107
Q

What are the 3 mechanoreceptors?

A

Neurons found in the airways and the lungs
-Myelinated Rapidly adapting stretch receptors
-Myelinated Slow adapting stretch receptors
-Unmyelinated C fibres

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108
Q

Location of aortic body?

A

Along aortic arch

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109
Q

Location and function of rapidly stretch adapting receptor?

A

Airways to lungs
respond to changes in lung or airway volume, possibly caused by tumours or inflation

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110
Q

Location and function slow adapting receptor?

A

Smooth muscle of airways -> lungs
responds to changes in lung or airway volume possibly caused by tumours or inflation

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111
Q

Difference between rapidly adapting and slow adapting receptors?

A

RAR respond briefly but quickly to stimuli
SAR maintain firing rate of impulses in response to stimuli.

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112
Q

Location and function of c fibres?

A

Airways-> alveolar walls
Chemosensitive to inflammatory mediators like cytokines or bradykinins in the airways -> lungs

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113
Q

Location and function of central chemoreceptor?

A

Changes in pCO2 levels in the ECF of the blood brain barrier between arterial blood supply and cerebral spinal fluid

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114
Q

Mechanism of action of central chemoreceptor?

A

Movement of CO2 through ECF into the CSF is detect by chemoreceptors which send impulses to the nucleus tractus solitaris in the medulla
increase ventilation during hypercapnia
decrease ventilation during hypocapnia

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115
Q

How is the ph of cerebrospinal fluid detected?

A

Central chemoreceptors

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116
Q

How is the ph of cerebrospinal fluid maintained?

A

Chloroid plexus cells that increase the movement of HCO3- to decrease ph of CSF.

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117
Q

What occurs in the inspiration phase?

A

Irritation of Chemoreceptors/Mechanoreceptors
Impulse down vagus afferent nerve to the nucleus tractus solitaris in the medulla
Contraction of lateral arytenoid muscle for adduction of vocal folds for air entry
Elevation of ribs- scalene and external intercostal muscle
Elevation of sternum- sternocleoidomastoid muscle
Diaphragm contracts and flattens
Decrease in intrathoracic pressure

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118
Q

What is the compression phase?

A

Abductor muscles posterior cricoarytenoid, transverse/oblique arytenoid contract to close vocal folds
Expiration occurs against closed glottis which increases intrathoracic pressure

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119
Q

What is the expulsion phase?

A

Thyroarytenoid contracts to release vocal fold tension
Internal intercostal muscle contracts to depress ribs
Abdominal muscles contracts to force diaphragm more superiorly to increase intrathoracic pressure
Posterior cricoarytenoid contracts briefly to abduct vocal folds
Lateral cricoarytenoid contracts to adduct vocal folds wider
Air containing irritant is expelled

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120
Q

How do opiods affect cough mechanism?

A

Inhibits cough reflex by targeting the central control pathway and the vagal efferent nerves.

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121
Q

What is the effect of opiod receptors?

A

Endorphin ligands bind and induce calming and analgesic effect, part of the reward system

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122
Q

What are the 3 opiod receptors?

A

Mu, kappa and delta

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123
Q

Effect of mu opioid receptor?

A

Mood, pain and reward

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124
Q

Effect of kappa receptors?

A

Mood, reward and pain

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125
Q

Effect of delta receptors?

A

Mood

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126
Q

What do opioid agonists do?

A

Occupy opioid receptor site longer and continuously attaches to produces slower long lasting effect

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127
Q

What is the laryngeal inlet?

A

The opening in the pharynx for the beginning of the larynx

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128
Q

What is the faces?

A

Opening at the back of the oropharynx

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129
Q

What is superior to the vocal fold?

A

Vestibular fold

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130
Q

What is the nasal vestibule?

A

Most anterior of the nasal cavity enclosed by cartilage. Lined with stratified squamous keratinising epithelia like the skin

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131
Q

What are help seeking behaviours?

A

An attempt to mitigate pain or distress, actively seeking help if it affects their physical or mental capabilities

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132
Q

What are the stages of the help seeking process?

A

1) Awareness of problem
2) Expressing need for support
3) Gaining understanding of resources and availability of support
4)Willingness to seek and disclose help

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133
Q

What triggers help seeking behaviour?

A

Occupation, literacy level, history of serious illness in family and suicidal ideation

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134
Q

What inhibits help seeking behaviour?

A

Communication diffculty in expressing distress
shame
culture of stigma
self-reliance
anticipation that help is inaccessible

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135
Q

Examples of help seeking behaviours?

A

Going to a social worker, going to see a GP.

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136
Q

What is skewed data?

A

Assymetrical distriubtion around the mean

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137
Q

What are the characteristics of a right skew?

A

More values on the left- positive value
Higher mean than median
IQR and mode is unafffected
Box plot- line in the middle representing median favours the left 1st quartile

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138
Q

What are the characteristics of a left skew?

A

More values on the right- negative value
Higher median, lower mean
IQR and mode is unaffected
Box plot- line in the middle representing the median favours the right 3rd quartile

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139
Q

What is standard deviation?

A

Spread of data around the mean, mu

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140
Q

How does the curve change with standard deviation?

A

Wider curve- higher standard deviation
Narrower curve- lower standard deviation
Area under the graph does not change

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141
Q

What is 95% confidence interval?

A

Probability that parameter (a number in a population) will fall within the set of values

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142
Q

What are opiate receptors?

A

G protein coupled receptor with 7 transmembrane alpha helices, stimulated by binding of artificial or endogenous opioid

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143
Q

Location of opiate receptors?

A

Medulla, pons, pulmonary mucosa in the lungs, smooth muscle of the trachea and bronchi and the gut.

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144
Q

What do opioids do?

A

Inhibit central sympathetic outflow to the vagus nerve, decreasing inspiration rate and peristalsis.

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145
Q

Effect of opioids?

A

Nausea, vomiting, lower heart rate, blood pressure and lower respiration. Lower blood pressure in use with opioids leads to increased intracranial pressure

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146
Q

Contraindications for opioids

A

Respiratory failure, bradycardia, comatose patients

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147
Q

Indications

A

Myocardial infarction, tacycardia, chronic and severe pain

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148
Q

What class is naloxone?

A

Opioid antagonist

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149
Q

Mechanism of opioid antagonists

A

Competitive inhibition and blockage of mu receptors with opioids

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150
Q

What class is morphine and diamorphine?

A

Opioid analgesic

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151
Q

What is minute volume?

A

Volume of air entering and leaving the lungs in one minute

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152
Q

What is tidal volume?

A

Air taken in and out with each breath in the lungs

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153
Q

What is ventilation?

A

Movement of air in and out of the lungs

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154
Q

What are the two types of ventilation?

A

Pulmonary ventilation and Alveolar ventilation

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155
Q

How can ventilation be measured?

A

Spirometer

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156
Q

What is respiratory rate?

A

No of breaths per minute

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157
Q

How does respiratory rate change with age?

A

Decreases; infant 30-50, child 20-30
adult 12-20

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158
Q

What are the 2 respiratory tracts?

A

Conducting and respiratory

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159
Q

Function of conducting airways?

A

Filter, warm and humidify air to prevent airway damage. Includes nose -> terminal bronchioles

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160
Q

Function of respiratory airways?

A

Gas exchange. Includes respiratory bronchioles, alveolar ducts, alveolar sacs and the alveoli

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161
Q

What is dead space?

A

Air in the airways that does not participate in gas exchange

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162
Q

What is anatomical dead space?

A

Area in the aiways that does not participate in gas exchange

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163
Q

What is physiological dead space?

A

Damage to the respiratory airways involved in gas exchange such as emphysema where damaged alveolar areas become dead space

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164
Q

What does the helium dilation method measure?

A

Residual volume and FRV. Patient breathes in a closed air circuit mixture of helium and oxygen conc(C1). Helium should be 12-14% and O2 30% to prevent respiratory distress- and allow resting state breathing to be measured. Helium enters the lungs and is insoluble so eventually helium in spirometer tank and lungs equilibriate to produce C2.

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165
Q

How do we calculate residual volume using the helium dilation method?

A

C1 X V1= C2 (V1 + V2)

C1 is the initial tank conc. V1 is the initial lung volume.
C2 is the equilibrated tank conc. V2 is the equilibrated lung volume.

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166
Q

What is plethysmography used for?

A

Record pressure of organs like the functional residual volume. Patient sits in a container and pants through an external tube while open and once while shut. This creates oscillations in the airways and pressure which is recorded by signal transducers. it can diagnose emphysema and COPD and asthma due to higher residual volume as an indicator

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167
Q

Why does high RV/FRV occur?

A

Inefficient respiratory movement
More work needed for breathing
Respiratory muscles have longer resting length

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168
Q

What is COPD?

A

Chronic obstructive pulmonary disorder which is lung conditions that cause breathing difficulties.
Emphysema- damage to alveolar air sacs
Chronic bronchitis- 8+ weeks of airway inflammation
associated with breathlessness, wheezing, mucusal chesty cough and frequent infections

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169
Q

What causes COPD?

A

Damage to the lungs, such as a genetic susceptibility or smoking

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170
Q

What does high vital capaicty indicate?

A

Exercise tolerance or underlying pulmonary disease like asthma

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171
Q

Can PEFR diagnose asthma?

A

No, it measures airflow obstruction generally which may be associated with other conditions

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172
Q

What is a better indicator for total lung capacity:
Residual volume or Total vital capacity?

A

Total vital capacity only identifies moderate and severe lung obstruction.
Residual volume distinguishes between mild to moderate lung obstruction.

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173
Q

How can lung hyperinflation be determined?

A

Residual volume and FRV of high values using helium dilation method or plethysmography.

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174
Q

How to measure RV/FRV?

A

Helium dilation method or plethysmography

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175
Q

How can we measure airflow obstruction?

A

Peak flow meter

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176
Q

What causes an increase in lung capacity?

A

Higher weight, male sex

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177
Q

How does aging affect lung capacity?

A

No effect on total lung capacity but decrease in ERV and Vt
After age 30, elastic recoil is weaker.
More hyperinflation so RV and FRV increases

178
Q

How does alcohol affect the lungs?

A

Damages cilia and lung cells and suppress immune response which protect lungs

179
Q

What does FEV1 measure?

A

Forced expiratory volume of air in one breath. Should be at least 75%. Decreases with COPD.

180
Q

What is COPD?

A

Difficulty in expelling air containing CO2 due to obstruction. This causes low FEV1 (forced expiratory volume in one second).Because air can’t be expelled, lung hyperinflation so high residual and FRV.

181
Q

WHat are examples of obstructive pulmonary disease?

A

Emphysema: degeneration of the alveolar air sac which increases dead space in the lungs and reduces release of air.

Asthma: chronic inflammatory disease where constricted bronchi smooth muscle reduces airflow. It is a overactive th2 centered response by T helper cell 2 that may recruit eosinophils and may be allergy induced sometimes. 1.1% of respiratory mortality

Cystic fibrosis: mucus build-up restricts airways

Bronchiectasis- scarring of the bronchi caused by damaged that causes inability to clear mucus which builds up

182
Q

What is the consequence of ph with COPD?

A

Build up of non-expelled CO2 will cause acidosis to occur. Acidosis results in rapid short breaths, dyspnea, headache and fatigue (due to hypoxia) and hyperreflexia (muscle cramping due to hyperkalemia.)

183
Q

What is the breathing of a person with COPD?

A

->Dyspnea
-> Slow exhalation which is wheezy and shallow because airflow is limited.

184
Q

What is restrictive pulmonary disease?

A

Difficulty expanding the lungs either intrinsically or extrinsically which limits the volume of air inhaled.

185
Q

What is intrinsic restrictive disease?

A

Difficulty expanding the lungs intrinsically.

Pulmonary fibrosis- Irritants like smoke, metal dust or asbestos damage the lungs and cause scar tissue formation by overproduction of fibroblasts by epithelia 4.6% of mortality of respiratory disease

Pneumonia- infection of alveoli which fill with fluid/pus and reduces O2 uptake. 25.3% of respiratory mortality.

Tuberculosis: Bacterial infection which creates lung lesions that may induce fibrosis or rupture the pleura.

186
Q

What are examples of extrinsic restrictive pulmonary disease?

A

Difficulty expanding the lungs externally.
Tumors- infection which breaks down lung tissue. 31% of respiratory mortality
Pleurisy- inflammation of pleura membrane
Rib fractures
Obesity- fatty deposits prevent full inhalation

187
Q

What are the indications of obstruction on lung measures?

A

Lower FEV1 than FVC
Volume lower than normal
Expiration is limited more than inspiration.

188
Q

What are the indications of restriction on lung measures?

A

Significantly lowest FVC than normal and obstructive disease. It decreases in proprotion to FEV1 because inspiration is limited more than expiration

189
Q

Difference between obstructive and restrictive disease?

A

Obstructive: Expiration and FEV1 is significantly lower. Higher Vc and inspiratory flow. Less air flows.
Restrictive: Inspiration and Vc is significantly lower. Higher air flow.

190
Q

Why do we measure VC?

A

Indicator for diagnosis and treatment efficacy

191
Q

How is VC affected in obstructive disease?

A

Not decreased in purely obstructive disease

192
Q

How is VC affected in restrictive disease?

A

Decreases

193
Q

What is tidal volume?

A

Volume of air taken in and out in one breath.

194
Q

What is ventilation?

A

Flow of air in and out of the lungs

195
Q

What is respiratory rate?

A

No. of breaths per minute

196
Q

What is minute volume?

A

Volume of air moving in and out of the longs in one minute

197
Q

What is vital capacity?

A

Maximum volume of air in and out of the lungs in one breath.

198
Q

What is the inspiratory reserve volume?

A

Volume of air that can be inspired beyond resting breathing.

199
Q

What is the expiratory reserve volume?

A

Volume of air that can be expired beyond resting breathing.

200
Q

What is the residual volume?

A

Volume in the lungs remaining after maximum expiration to keep alveoli inflated

201
Q

What is the functional residual capacity?

A

Volume of air remaining in the lungs after passive expiration

202
Q

What is the inspiratory capacity?

A

Volume of air inspired during resting breathing

203
Q

What is spirometry used for?

A

Spirometer measures most lung volumes like tidal volume, inspiratory reserve volume and exspiratory reserve volume. It cannot measure residual volume or functional reserve volume

204
Q

How does spirometry measure lung volume values?

A

Patient breathes into a tube which increases air volume in the drum. This alters the counterbalance weight attached to the pen that records reading.

205
Q

Why can’t we use a spirometer to measure residual volume?

A

It is impossible to fully empty the lungs of air

206
Q

What does plethysmography measure?

A

Plethysmography measures the residual volume and the functional reserve volume.

207
Q

What does peak flow meter measure?

A

Peak flow meter measures airflow obstruction. Green zone: 80 to 100 percent of your usual flow rate.
Yellow zone: 50 to 80 percent of your usual flow rate. Airways starting to narrow.
Red: less than 50 percent- severe narrowing

208
Q

Why is higher lung capacity problematic?

A

Higher lung capacity means the lungs are hyperinflated, which is indicative of pulmonary disease. Hyperinflation means there is a greater Residual Volume and Functional Reserve volume.

209
Q

Why is high RV/FRV problematic?

A

Lungs are hyperinflated because the respiratory movements are inefficient at fully expelling air or taking it in and resting length between breathing is longer.

210
Q

How does smoking affect the airways?

A

Smoking is an irritant
->stimulates overproduction of fibroblasts by alveoli that leads to fibrosis which limits gas exchange in the lungs.
->acts on macrophages to recruit monocytes, neutrophils and T cells.
->Causes emphysema: Smoking induced neutrophil recruitment will release proteases that cause hypersecretion of mucus from goblet cells and damage cilia cells to prevent movement of mucus.
->The proteases secreted by neutrophils and T killer cells will cause destruction of the alveolar wall due to the cigarette smoke present. Causes emphysema

211
Q

How does smoking affect the airways?

A

Smoking is an irritant
->stimulates overproduction of fibroblasts by alveoli that leads to fibrosis which limits gas exchange in the lungs.
->acts on macrophages to recruit monocytes, neutrophils and T cells.
->Causes emphysema: Smoking induced neutrophil recruitment will release proteases that cause hypersecretion of mucus from goblet cells and damage cilia cells to prevent movement of mucus.
->The proteases secreted by neutrophils and T killer cells will cause destruction of the alveolar wall due to the cigarette smoke present. Causes emphysema

212
Q

How does gas exchange occur?

A

Pressure gradient

213
Q

What is ventilation reliant on?

A

Intrathoracic pressure

214
Q

What is Boyle’s law?

A

Volume and pressure are inversely proportional.

215
Q

What is Avagadro’s constant?

A

Gases at the same pressure and temp have same number of moles at 6.02 x 10(23)

216
Q

What is Graham’s Law?

A

Diffusion rate decreases with higher molecular weight

217
Q

What is Henry’s Law?

A

Mass of dissolved substance = Solubility coefficient x partial pressure

218
Q

What is Charles’ Law?

A

Temperature and Pressure are proportional

219
Q

What is Dalton’s Law?

A

Total partial pressure is the sum of the individual partial pressures

220
Q

What is PaO2?

A

Blood pO2

221
Q

What is CaO2?

A

Total Arterial O2 levels

222
Q

What is SaO2?

A

Amount of O2 bound to haemoglobin

223
Q

What is the Haldane effect?

A

CO2 has a higher affinity to deoxyhaemoglobin than oxyhaemoglobin. This facilitates CO2 uptake in tissues

224
Q

Where is the movement of oxygen?

A

Oxygen leaves arteries; uptake by veins

225
Q

Where is the movement of CO2?

A

CO2 uptake by arteries; leaves veins

226
Q

What is pulmonary circulation?

A

Closed circuit blood circulation between the heart and the lungs. Includes the pulmonary artery and the pulmonary vein

227
Q

How does haemoglobin’s affinity for O2 increase?

A

Low temp, Low H+, Low CO2, Low BPG

228
Q

How does haemoglobin’s affinity for O2 decrease?

A

High Temp, high H+, high CO2, high BPG

229
Q

What are sources of Carbon monoxide?

A

Endogenously: Haemolysis of RBC because haem group contains endogenous CO
Environmental: smoking, vehicle exhaust, pollution, asbestos, gas fire

230
Q

How is CO2 transported in the blood?

A

In order: Carbonic Acid H2CO3, Carboxaminohaemoglobin and Dissolved CO2

231
Q

What is the Bohr effect?

A

CO2 decreases haemoglobin’s affinity for O2

232
Q

Why does the chloride shift occur?

A

HCO3- is exchanged for CL- intracellularly to maintain electrolyte balance

233
Q

What is the composition of atmospheric air compared to the alveoli?

A

CO2 Increases from 0.3 mmHg to 40mmHg
O2 decreases from 159mmhg to 105mmhg
N2 decreases from 607 mmhg to 568mmhg
H20 is variable but in the alveolar it is 47mmHg

234
Q

Why is nitrogen important in O2 uptake?

A

It is insoluble and exerts pressure to keep alveoli inflated

235
Q

How does O2 composition change during pulmonary circulation?

A

Decreases from the arteries; Increases in the veins
40mmHg> 105mmg

236
Q

How does CO2 composition change during pulmonary circulation?

A

Increases into the arteries; decreases from the veins
47 mmHg / 40 mmhG

237
Q

Symptoms of carbon monoxide poisoning?

A

Hallucinations, tiredness, fatigue, headaches

238
Q

What are the ranges for ph?

A

pH should be maintained at 7.4
7.35 is low ph
7.45 is high pH

239
Q

What is the H+/K+ ATPase?

A

Enzyme which increases cell uptake of H+ via ATP hydrolysis to exudate K+ into the interstitial space

240
Q

What is acidosis?

A

pH below 7.35
Respiratory acidosis: CO2
Hypercapnia; retention of CO2 due to problems expelling like restrictive disease or retaining in obstructive
Metabolic acidosis: High H+
Diabetic ketoacidosis: Insulin amount is insufficient to free glycogen stores. Acidic Ketone bodies in excess.
Renal failure

241
Q

What are the effects of acidosis?

A

Bradycardia and hyperreflexia: Hyperkalaemia due to high H+ uptake /high K+ exudation to tissue which impacts 3Na+ out/ 2K+ in. Hyperkalaemia reduces Na+ activation, increases refractory period of AP and lowers neuron resting potential.
Bradycardia

Rapid short breaths, wheezing, dysnpea, respiratory distress

242
Q

How does the body mitigate acidosis?

A

Increasing ventilation or increasing renal excretion. It can use buffers like HCO3-.

243
Q

What is alkalosis?

A

pH is above 7.45.
Respiratory: loss of CO2
Hypocapnia: excessive ventilation, associated with hypoxia.

Metabolic: loss of H+
Vomiting
Increased urinary loss of H+ via vomiting, diuretics, overactive kidneys

244
Q

What are the effects of alkalosis?

A

Tacycardia, normal to high BP and muscle weakness and Paraesthesia (pins and needles) -> Hypokalemia as H+ is too low for H+/K+ ATPase to exudate K into tissue fluid. Resting potential increases. Low extracellular K+ disrupts muscle contraction

245
Q

How does the body mitigate alkalosis?

A

Decreasing renal excretion of H+, increasing excretion of HCO3-, decreasing ventilation.

246
Q

What are the components of the mucosal membrane?

A

-Lamina propia- below the epithelia and conncts it to smooth muscle to regulate contraction. It has immune cells for pathogen defense such as leukocytes, lymphocytes and mast cells
-Pseudostratified columnar epithelia
Olfactory- for olfaction
Bowman’s gland- secretions keep the olfactory moist

247
Q

What are the 3 types of cells present in the psuedostratified columnar epithelia in the nose?

A

Goblet cells- secretes mucus.
Cilia cells- coordinated beating of the cilia transports mucus down the airways
Basal cells- for adhesion and cell renewal

248
Q

How can the mucociliary epithelia be disrupted?

A

-Smoking damages cilia which prevent cilia beating, leading to mucus build-up in the airways
-Cystic fibrosis causes mucus build-up due to deficiency in CFTR gene which encodes for CL- transport that affects water content of mucus. This causes it to harden and damage airways.

249
Q

Where does histology of airways change?

A

In the terminal bronchioles from columnar epithelia containing goblet cells to the cuboidal epithelia containing clara cells

250
Q

What are clara cells?

A

They secrete non mucous secretions and are non-ciliated. Involved in pathogen defence and proliferation of epithelia.

251
Q

What are the components of the primary bronchi?

A

pseudostratified columnar epithelia. Hyaline cartilage and smooth muscle with a thin lamina propia. Lamina propia connects the epithelia to the smooth muscle for regulation of contraction. It contains immune cells like macrophages and mast cells but mostly connective tissue like fibroblasts

252
Q

What are the components of the secondary bronchi?

A

Pseudostratified ciliated columnar epithelia. Plates of hyaline cartilage and no smooth muscle. It is smaller than primary bronchi.

253
Q

What are the components of the tertiary bronchi?

A

Tall pseudostratified Columnar epithelia containing goblet cells. Contains smooth muscle which causes mucosa to fold and has seromucous glands to facilitate movement.

254
Q

What are the components of the terminal bronchi?

A

Ciliated columnar epithelia which transitions to cuboidal epithelia with clara cells. Clara cells secrete substances for pathogen defence like goblet cells, but it is not ciliated and not mucus. It is the progenitor for ciliated epithelia. Vagus nerve stimulates contraction of terminal bronchioles to constrict.

255
Q

What are the components of the respiratory bronchi?

A

Sacs extending from the wall of the terminal bronchioles. Beginning of the respiratory airways. It contains cuboidal epithelia with clara cells.

256
Q

What are the alveolar ducts?

A

Collect air from the respiratory bronchioles and disperse it throughout the alvoelar sacs

257
Q

What are the alveolar sacs?

A

Collections of multiple alveoli

258
Q

What cells are present in the alveoli?

A

Macrophages, and pneumocytes (alveolar epithelia)

259
Q

What are type 1 pneumocytes?

A

Simple squamous epithelia which cover most of the pulmonary surface. It fuses with pulmonary endothelium to form occluding junctions to control barrier for substance exchange.

260
Q

What are type 2 pneumocytes?

A

Simple cuboidal epithelia which is most numerous. It secretes the pulmonary surfactant phosphatidylcholine that reduces surface pressure of alveoli to prevent bursting due to varying size

261
Q

What are the chemical barriers to pathogen entry in the airways?

A

->low ph of the skin, gastric acid and vagina. This either denatures pathogen proteins or creates a hostile environment.
->Lysozymes- fungicidal and bactericidal properties present in sebum perspiration and urine, mucus.
->Mucus
->Defensins produced by epithelial cells. Alpha defensins are found in macrophages, neutrophils and intestinal paneth cells. Beta defensins create channels that disrupt the microbial membrane

262
Q

What are the physical barriers to pathogen entry in the airways?

A
263
Q

What are the structural reflexes to pathogen entry in the airways?

A

Cough reflex and sneezing reflex

264
Q

Describe the sneezing reflex

A

Irritation of nasal mucous membrane. Detected by olfactory receptor/trigeminal nerve terminals in nasal mucosa. Transmits impulse down trigeminal/olfactory nerve to the nucleus tractus solitaris in the medulla and the reticular formation in the brainstem. This acts on efferent fibres like the trigeminal and facial efferent to contort face, vagus and intercostal nerves for forced expiration and glossopharyngeal to elevate the pharynx and larynx. Activates tracheal muscle for constriction of trachea and internal intercostal muscles Initially glottis is closed but sneezing is with an open glottis to expel air through the mouth and the nose, containing the mucosal debris

265
Q

What are the biological barriers to pathogen entry in the airways?

A

Microbes present in the nasopharynx, vagina, GI tract, skin and mouth.
They outcompete pathogens for attachment sites, nutrients, stimulate the immune system, or may perform direct antagonism like microbes in the vagina, secrete lactic acid, an antimicrobial peptide to inhibit pathogenic activity

266
Q

Where is the the lungs located?

A

The lung is located in the thoracic cavity, lateral to the mediastinum, and enclosed within a pleural cavity.

267
Q

How are the lung lobes seperated?

A

Visceral pleura

268
Q

What is the lung hilum?

A

Hilum is the lung root where anatomical structures enter the lungs. It is the reflection of the parietal pleura off different directions in the thoracic cavity that joins with the visceral pleura to form the hilum.

269
Q

Where is the heart located?

A

Middle mediastinum. It runs inferolateral towards the left with 1/3 of the lying to the right and 2/3 lying to the left.

270
Q

What structures are present in the superior mediastinum?

A

Artery: aortic arch-> brachiocephalic artery, left and right common carotid and left and right subclavian artery
Veins: Brachiocephalic vein which gives rise to the right subclavian vein left subclavian vein which drains the left superior intercostal and the left and right supreme intercostal
Thoracic duct, oesophagus, trachea

271
Q

What structures are present in the anterior mediastinum?

A

Lymph nodes, sternopericardial ligaments, Connective tissue, thymus (in infants) and Fibrofatty (adults)
Artery: aortic arch-> brachiocephalic artery, left and right common carotid and left and right subclavian artery
Veins: Brachiocephalic vein which gives rise to the right subclavian vein left subclavian vein which drains the left superior intercostal and the left and right supreme intercostal

272
Q

What structures are present in the middle mediastinum?

A

Veins: Deep cardiac plexus of vagal nerve, phrenic nerve and recurrent laryngeal nerve cardiac branches

273
Q

What structures are present in the posterior mediastinum?

A

Thoracic duct, lymph nodes, oesophagus
Veins: vagal nerve of oesophagi

274
Q

What is the auscultation of the lung apex?

A

At clavicle between ant ribs 1-2/post 2/3

275
Q

What is the auscultation of the anterior border?

A

Sternal line ant ribs 2-3/ post ribs 3-4

276
Q

What is the ausculatation of the superior border?

A

midclavicular line ant between 3rd and 4th rib

277
Q

What is the auscultation of the middle lobe?

A

Mid axillary line between the 5th and 6th rib

278
Q

What is the auscultation of the inferior border?

A

Between Ant ribs 7 and 8/ post ribs 8 and 9

279
Q

What are the two components of the pleural cavity?

A

Costomediastinal recess and the costadiaphragmatic recess

280
Q

How to differentiate between the right and left lung hilum?

A

Bronchus anterior to pulmonary artery.
Bronchus superior to pulmonary artery

281
Q

What are the atria?

A

Thin walled chambers that establish cardiac pace at 40bpm.

282
Q

What is the atria?

A

Atria are thin walled chambers which establish cardiac pace at 60bpm and primarily fill the ventricles with blood

283
Q

Where is the micuspid valve located?

A

Atrioventricular valve between the L atria and L ventricle

284
Q

Where is the tricuspid valve located?

A

Atrioventricular valve between R atria and R ventricle.

285
Q

Where do we auscultate for the bicuspid valve?

A
286
Q

Where do we auscultate for the tricuspid valve?

A
287
Q

What are the ventricles?

A

Thick-walled chambers which establish cardiac pace at 40bpm. Contains papillary muscles close to the valves which contract chordae tendinae to prevent backflow of blood.

288
Q

What is the difference between the left and right ventricle?

A

Right ventricle contains a muscular column called the moderator band associated with papillary muscles to prevent overdistension of the ventricles with blood.
Left ventricle has more prominent trabeculae carnae

289
Q

Why can’t we ausculate cardiac valves directly?

A
290
Q

Where do you auscultate for the aortic valve?

A
291
Q

Where do you auscultate for the pulmonary valve?

A
292
Q

What is the innervation of the heart?

A
293
Q

What are the layers of the pericardial sac?

A

Inner endocardium- simple endothelial cells with a subendocardial layer continuous with the myocardium
Myocardium- thickest layer formed of cardiac myocytes with intercalated discs for electrical conduction, synchronised contraction and scaffolding
Visceral epicardium- adipose, mesocardium and connective tissue layer to cushion the heart. Reflections of this form the parietal pericardium which

294
Q

How do the sinuses form?

A
295
Q

What is the coronary artery?

A
296
Q

What are the branches of the right coronary artery?

A
297
Q

What are the branches of the left coronary artery?

A
298
Q

What is the coronary sinus?

A
299
Q

What are the branches of the right coronary vein?

A
300
Q

What are the branches of the left coronary vein?

A
301
Q

What is vasculogenesis?

A
302
Q

What is angiogenesis?

A
303
Q

What does the truncos arteriosus give rise to?

A
304
Q

What are the subunits in myosin?

A

There are two heavy polypeptide chains which coil to form an alpha double helix
4 light polypeptide chains in total. Two light polypeptide chains on each myosin head. One is the regulatory light chain which regulates myosin head movement. There is an alkali light chain.

305
Q

Why is the myosin light chain phosphorylated?

A

It increases Ca2+ conc for muscle contraction

306
Q

What are the domains of myosin?

A

The heads of myosin contain myosin ATPase for the hydrolysis of ATP during muscle contraction to break actin-myosin cross bridge

The hinge region is the lever to transduce force generated by myosin head to the entire molecule

The double helix tail connects to other myosin molecules and regulate motor activity

307
Q

What are the components of actin?

A

Two helical strands of spherical a-globular protein. Between the strands is the tube-shaped protein tropomyosin which regulates the interaction between actin and myosin by covering the myosin binding site on actin filament which shortens the muscle. It unmasks the binding site when it moves deeper into the actin grove
Attached to tropomyosin at regular intervals is the troponin regulatory complex which is the Ca2+ binding site. It has 3 isoforms
Troponin T- connects and binds troponin complex to tropmyosin
Troponin C- Ca2+ binding site for contraction
Troponin I: regulates and inhibits actin interaction with myosin

308
Q

What are the isoforms and function of troponin complex?

A

Troponin complex regulates muscle contraction and has 3 isoforms:
Troponin T- connects and binds troponin complex to tropomyosin
Troponin C- Ca2+ binding site for contraction
Troponin I: regulates and inhibits actin interaction with myosin

309
Q

What occurs following Ca2+ entry into the cell cytosol?

A

Ca2+ binds to troponin C of the troponin regulatory complex. The troponin complex triggers a conformational change to undergo in tropomyosin which unmasks the region in actin globular protein where myosin head will bind

Myosin head is in the cocked position prior to cross bridge formation. It releases ADP and Pi and binds to active site on actin globular protein. In a power stroke it pulls actin inward to cause muscle contraction.
To release from actin and break the cross bridge, ATP binds to myosin and is hydrolysed by ATPase.

310
Q

What is lusitropy?

A

Lusitropy is rate of muscle relaxation following muscle contraction

311
Q

What are the transporters involved in lusitropy?

A

Lusitropy uses two transporters:
Na+/Ca2+ exchanger which exudates Ca2+ for the high influx EC Na+
SERCA (sarcoendoplasmic reticulum calcium ATPase) which regulates Ca2+ release from sarcoplasmic reticulum

312
Q

What is dromotropy?

A

The rate of impulse conduction through the AV node

313
Q

What is chronotropy?

A

Heart rate/ number of times the heart beats per minute (bpm)

314
Q

What are cardaic glycosides used for?

A

Treat heart failure by increasing inotropy and chronotropy and prolong refractory period

315
Q

Which cells do cardiac glycosides influence and how?

A

It directly inhibits the Na+/K+ pump in cardiac myocytes. Accumulation of intracellular Na+ disrupts the Na+/Ca2+ exchanger. This causes accumulation of intracellular Na+ which disrupts Na+/Ca2+ exchanger which exudates Ca2+ for EC Na+. Ca2+ accumulates in the cell and binds to troponin C complex for heart muscle contraction.

316
Q

What is excitation-coupling?

A

Action potential triggers synchronised contraction of the atrial and ventricular myocytes via intercalated discs.

317
Q

How does the autonomic nervous system affect heart rate?

A

Induces secretion of adrenaline/noradrenaline for calcium-induced-calcium release

318
Q

How is the SAN affected by the autonomic nervous system?

A

SAN generates action potentials, induced by the sympathetic release of noradrenaline. This binds to B1/B2 adrenergic g protein coupled receptor on the SAN.
Activates adenyl cyclase -> cAMP formation-> protein kinase activation for phosphorylation-activation of

Funny channels: allow influx of Na+
T-type calcium channels- low voltage activated Ca2+ channels which allow entry of Ca2+.

The influx of Na+ and Ca2+ causes depolarisation of SAN which fires impulses that travel to the sarcolemma of cardiac myocytes.

319
Q

Where is Ca2+ stored in cardaic myocytes?

A

Ca2+ is contained in Sarcoplasmic reticulum, regulated by the pump SERCA. SERCA may be inhibited by the enzyme phspholamban.

320
Q

Where is Ca2+ stored in cardiac myocytes?

A

Ca2+ is contained in Sarcoplasmic reticulum, regulated by the pump SERCA. SERCA may be inhibited by the enzyme phospholamban.

321
Q

How does parasympathetic stimulation affect the SAN?

A

Acetylcholine binds to muscarinic M2 receptors on the SAN node. These cause disassociation of alpha subunit bound to GTP. This associates with the G protein inwardly rectifier channel which allows influx of K+ into the SAN. This repolarises the membrane to become more negative and inactivates T-type calcium channels that become activate at 50mV. Blocked entry of Ca2+ prevents heart contraction.
Leads to reduce dromotropy, inotropy, chronotropy, lusitropy.

322
Q

How long is the cardiac cycle?

A

Cardiac cycle is initiated by SAN impulses. It lasts 0.8s at 75bpm.

323
Q

What occurs during diastole?

A

Mitral valve is open. AV is open. Passive ventricular filling and atria contract to eject final amount of blood..

324
Q

What is the pressure in the heart chambers during diastole?

A
325
Q

What occurs during end diastolic volume?

A

EDV is amount of blood 135ml before the ventricles contract. Ventricular pressure builds for 50 m/s

326
Q

What occurs during end diastolic volume?

A

EDV is 135ml. Mitral valves close so both SL valves are closed. Ventricular pressure builds for 50 m/s

327
Q

What is isovolumic ventricular contraction?

A

Initial ventricular contraction causes left ventricular pressure to rise about the right ventricular pressure which closes the mitral valve.

328
Q

What is ventricular ejection?

A

R ventricle pressure of 25mmHg exceeds pulmonary artery of 10mmHg; pulmonary valve opens, and pulmonary artery fills with blood. Pressure builds in pulmonary artery to 25mmHg.

Left side: L ventricle pressure of 120mmHg exceeds aorta of 80mmhg; aortic valve opens, and aorta fills with blood. Aortic pressure builds to 120mmHg.
Blood is ejected through outflow tracks

329
Q

What is end systolic volume?

A

Volume in blood at the end of systole which is 65ml

330
Q

What is isovolumic ventricular relaxation?

A

R ventricle pressure decreases as it relaxes
L ventricle pressure decreases as it relaxes
This causes blood to leak back into ventricles so the semilunar valve to close as blood leaks though

331
Q

When do mitral valve and aortic valve closes?

A

Mitral valve is open during passive ventricular diastole and filling and atrial contraction. It closes at the end diastolic volume.
During isovolumic contraction, both semilunar valves are closed.
During ventricular ejection, aortic valve opens. It closes during isovolumic relaxation when ventricles relax.

332
Q

What is cardiac output?

A

Cardiac output is the amount of blood pumped out of the heart per minute.
Cardiac output= stroke volume x heart rate.

333
Q

Why does cardiac output increase?

A

Initial increase in CO is due to
both higher stroke volume and heart rate. However, there is a limitation to stroke volume so extreme increase in CO is due to heart rate increase.

334
Q

What is stroke volume?

A

Stroke volume is the volume of blood pumped out of the ventricles. It is calculated by
Stroke volume= end diastolic volume - end systolic volume
Stroke volume is proprotional to end diastolic volume.

335
Q

How does stroke volume increase?

A

Parasympathetic stimulation -> slower heart rate and inotropy -> Longer filling time, more venuous filling

336
Q

What causes decrease in stroke volume?

A

Sympathetic stimulation which increases heart rate -> less venous filling- lower filling time
Associated with higher stroke volume Higher stroke volume

337
Q

What is the ejection fraction?

A

Ejection fraction is how much end diastolic volume blood is pumped out of the ventricles. It is a measure of ventricular performance as a percentage:
Stroke volume / end diastolic volume

338
Q

What is the implications of ejection fraction?

A

Normal ejection fraction is between 55%-75%. Below this indicates issues with ventricular performance that is insufficient to supply the body with oxygenated blood. May cause hypoxia and is a indicator of heart disease of myopathy.

339
Q

How does Ca2+ affect sarcomere length?

A

More Ca2+ decreases length of sarcomere
Less Ca2+ increases sarcomere length

340
Q

How does end systolic volume increase?

A

End systolic volume increases with
afterload- peripheral vascular resistance in the heart against ventricular contraction.
parasympathetic stimulation
shorter filling time
less venous return

341
Q

What is atrial reflex?

A

Atrial reflex is when atrial pressure causes heart rate to increase.

342
Q

How does heart rate increase?

A

Heart rate increases with more venous return, atrial reflex and sympathetic stimulation.

343
Q

What is an action potential?

A

An action potential is the change in membrane potential that travels as an impulse across the membrane of a cell. In ventricular cells such as cardiac myocytes, it triggers release of Ca2+ intracellular vesicles to cause heart contraction.

344
Q

What is electrical coupling?

A

Electrical coupling ensures heart electrical activity is synchronised with a unidirectional spread. The gap junctions allow adjacent cells to share a cytosol to facillitate ion movement down the electrochemical gradient.

345
Q

What is equilibrium potential?

A

Equlibrium potential is the membrane potential diference in exact equilibrium with an ion conc gradient. It has the symbol Ek.

346
Q

What is equilibrium potential?

A

Equilibrium potential is the membrane potential difference in exact equilibrium with an ion conc gradient. It has the symbol Ek.

347
Q

What are the phases of an action potential?

A

Phase 4: Baseline at -70 to -90mv driven by opening of rectifier K+channels and some influx of Na+
Brings membrane potential closer to the negative K+ equilibrium potential (Ek). There is some influx of Na+. Rectifier channels are channels rectifier that passes current into the cell more easily than outwards by allowing K+ to move more easily into the cell.)

Phase 0-Depolarisation/Rapid upstroke driven by opening of Na+ channels
Depolarisation occurs. This triggers voltage gated Na+ channels to open. Influx of Na+ depolarises the cell and triggers opening of more Na+ channels and influx of Na+ in a positive feedback cycle. This increases membrane potential. Opened Na+ channels during depolarisation inactivate and close almost instantly after opening due to negative membrane potential. The current produced is toward the electrode.

Phase 1- Notch/ Early rapid repolarisation/depolarisation

Na+ channels inactivate.
Transient (temporarily) open K+ channels repolarise the cell and K+ is exudated from the cell to establish a new membrane potential for the plateau phase. More K+ current repolarise moreand exude K+ to estbalish lower membrane potential during the plateau. Less K+ repolarise less and exudate less K+ which means there is a higher membrane potential during the plateu

Phase 2- Plateau caused by balance between Ca2+ entry and K+ exudation.
Ca2+ channels in T-tubules are close to sarcoplasmic reticulum and move through a channel inside ryanodine receptors on sarcoplasmic reticulum membrane to bind to ryandoine receptors. This triggers Voltage gated Ca2+ channels to open and influx of CA2+ that binds to ryanodine receptors on sarcoplasmic reticulum. This triggers further release of Ca2+ which binds to troponin C that initates movement of tropomyosin away from mysoin binding site to cause cell contraction.
Ca2+ enters the cell. There is a balance between entry of C2+ and exudation of K+

Phase 3- Final Repolarisation driven by Ca+ activation
Ca2+ channels close and there is delayed K+ effluxs to repolarise the cell back towards a negative membrane potential via K+ exudation. Na+ channels recover as this occurs.

348
Q

What is the veolicty of depolarisation in the heart chambers?

A

Atrial pathways have a speed of 0.3m/s
AV node is 0.05m/s
Purkinje fibres have veolcity of 4.m/s
Ventircles have volcity of 1 m/s

349
Q

What is the speed of depolarisation?

A

R atria 0.07s-> left atria 0.09s
Reaches AV node at 0.03 but travels down at 0.16s due to delay
Ventircles 0.19-0.22s

350
Q

How does heart contraction occur?

A

Impulses are generated by pacemaker cells in the SAN of the upper right atria that stimulate atrial contraction. This impulse travels down the atrial septum to the AVN node . -> AV Bundle of His -> Bundle branches –> Purkinje fibres. At the Purkinje fibres, it activates the myocardium of the left and right ventircles to cause ventricular contraction from the apex.

351
Q

Where are pacemaker cells?

A

SAN is located in the right atria and contains pacemaker cells. Pacemaker cells are located mainly in the SAN, which is in the upper wall of the right atria. They have natural automaticity to generate own AP spontaneously because of their unstable membrane potential. The rate of depolarisation of pacemaker cells determines heart rhythm. Usually there is a slow depolarisation to reach the threshold potential to establish a slow heart rhythm. There is no plateau phase with equal Ca2+ and K+ influx.

352
Q

What is the action potential phases in the SAN?

A

Phase 4- Resting potential/ slow depolarisaton
This occurs between the end of an AP and the start of the new. The resting is transient as there is an immediate slow depolarisation of pacemaker cells by hyperpolarisation activated cyclic nucleotide gated channels (HCN) These channels are permeable to both K+ and Na+. It allows entery of Na+ entry into the cells when memrbane potential is lower than -50mv to increase it.

Phase 0- Spontaneous depolarisation
Depolarisaton raises membrane pontential to -40mv, causing voltage gated Ca2+ chnnaels to open and influx of Ca2+ to create rapid upstroke. HCN inactivates and at the peak of the upstroke, CA2+ inactivates and K+ opens

Phase 3- Exudation of K+ by open K+ channels which repolarises the membrane to cause downstroke.

No plateau stake because Ca2+ channel opening is not sustained. When downstroke reaches -50mv, HCN is reactivated

353
Q

How does sympathetic activation affect heart rate?

A

Noradrenaline acts on B1 adrenoreceptors in the SAN and AVN of the cardiac myocytes.. Afferent vagal fibres transmit this to the Cardioaccelaratory centre in the medulla. This innervates sympathetic fibres in the sympathetic chain ganglioon of the spinal cord. The ganglion is a collection of neuronal cell bodies with sympathetic chains that have a cardiac fibre to accelerate inotropy and chronotropy in the SAN.

354
Q

How does parasympathetic activation affect heart rate?

A

Acetlycholine acts on M2 muscarinic receptors in the SAN, This travels via afferent vagal nerve to the cardioinhibiory centre in the medulla. It responds by innervating efferent parasympathetic fibres to decrease chronotropy and inotropy.

355
Q

What nervous response causes increase in heart rate?

A

the parasympathetic system dominates to produce rrsting rate of 60bpm. Initial increase in heat rate is caused by reductionin parasympathetic flow. Further increase is caused by increase in sympathetic outflow.

356
Q

Where is adrenaline synthesised?

A

Adrenaline is synthesised in the chromaffin cells in the medulla of the adrenal gland. It increases chronotropy and inotropy and acts on B1 adrenergic receptors in the heart. It is competitively inhibited by Beta blockers like adrenolol.

357
Q

Where is adrenaline synthesised?

A

Adrenaline is synthesised in the chromaffin cells in the medulla of the adrenal gland. It increases chronotropy and inotropy and acts on B1 adrenergic receptors in the heart. It is competitively inhibited by Beta blockers like adrenolol.

358
Q

How to interpret stages of ECG?

A

Baseline- SAN activity and atrial activation at 80-100 AP per min at rest
P wave- atrial depolarisation caused by stimuli from fibres spreading across atrial surfaces to reach AV node. This is towards the chest lead that causes upward inflection

PR interval- Time taken for excitation to spread from SA to the ventricles Delay at the AV node to cause atrial contraction. Then, there is conduction of AV node and AV bundle of His

QRS complex- impulse spreads through ventricles to cause ventricular contraction and begin atrial contraction
Q wave initial ventricular depolarisation caused by stimuli impulse spreading along interventricular septum-> AV bundle -> Bundle of Purkinje -> moderator band -> papillary muscles in R ventricular from the Bundle of His. This is away from the chest electrode

R wave ventricular depolarisation towards Lead II which creates upwards positive wave
S wave depolarisation spreads from ventricular apex to go superiorly away from lead II to generate a small downward inflection
T wave ventricular repolarisation which creates small, curved inflection

359
Q

What are the intervals in ECG?

A

Normal ECG PR interval is 0.12-0.20 .
Normal QRS interval is 0.12s

360
Q

What is ECG used for?

A

ECG is used to trace electrical activity of impulses in cardiac tissue through various angles. We can use it to identify and locate pathology. Commonly, ECG is measured using 3 leads or 12 leads.

361
Q

What is an ECG lead?

A

An ECG lead is a graphical description/image of electrical activity in the heart, generated by analysing the electrical currents produced by electrodes

362
Q

What do the chest leads show?

A

V1- 4th intercostal space on right sternal margin- Septal view
V2-4th intercostal space on left sternal margin
V3- midway betwen V2 and V4
V4- mid clavicular line
V5 anterior axillary line
V6- mid axillary line

363
Q

What is the avL lead?

A

avL lead is on the left arm to provide a superolateral view of left heart such as the left ventricle outflow tract. Variable polarity of the p wave.

364
Q

What is the avR lead?

A

aVR is on the right arm to provide a lead with a superlateral view of the heart, such as the right ventricle outflow tract and basal interventricular septum. P wave is always negative.

365
Q

What does the Lead I show?

A

Lead I is an exploring electrode which records the electrical difference between the right and left. It produces a high lateral view of the heart. Current towards the avR produces negative deflection, current towards the avL produces a positive upward.

366
Q

What is avF lead show?

A

avF is on the left leg to produce lead of the inferior view of the heart such as the left ventricle. P wave is always negative.

367
Q

What is cardiac output?

A

Measure of ventricular performance- healthy is 5L/min
Heart rate x stroke volume

368
Q

What is flow?

A

Flow is synonymous with cardiac output.
Flow is the volume of fluid passing in a given time period. (Cm3/s)

369
Q

What is velocity?

A

Velocity is the rate of particle flow.

370
Q

What is circumtional area?

A

Radius is half the diameter of the vessel. We can use radius to determine the area of a vessel.
pi x r2

371
Q

How to calculate flow?

A

Flow(cm3/s)= cross sectional area (cm) x velocity (cm/s)
Flow= pressure/resistance

372
Q

How does velocity change in vessel?

A

Velocity of blood flow is highest in the centre of each section in the vessel. Velocity decreases more superiorly/inferiorly closer to the vessel walls due to the resistance.

373
Q

What is bruit?

A

Bruit is the audible turbulent flow of blood within arteries clogged with atherosclerotic plaque.

374
Q

What is resistance?

A

Resistance is the opposition to flow.

375
Q

What is pressure?

A

Difference between mean arterial pressure - central venous pressure?

376
Q

What is the relationship between flow and pressure?

A

Flow increases non-linearly with higher pressure. They have a non-linear relationship due to this equation.
Pressure is= cardiac output x resistance

377
Q

What is the equation of flow affecting factors?

A

Pouiselle’s Law?
Flow= Change in pressure x radius (to the power of 4)/ 8 x viscosity x length

378
Q

What are the factors affecting flow?

A

Radius: Increases flow by a factor of 4
Viscosity- Decreases flow. In hypoxic conditions, more RBC produced called polycythaemia to carry more O2 which will decrease flow.
Length- longer vessel will have a greater resistance -> higher BP-> low flow/ high velocity
Shorter vessel will have less resistance-> low BP-> higher flow/ low velocity

379
Q

What is the relationship between flow and resistance?

A

Resistance decreases flow however resistance increaases blood pressure which increases flow.

380
Q

What is the average heart beat?

A

Average HR is average 70bpm

381
Q

How is flow controlled locally?

A

Vascular tone controls local flow. This is affected by metabolic products.

382
Q

Which factors increase vasodilation?

A

-acidity such as H+ and hypercapnia (CO2) is harmful so increased blood flow removes it
-> Nitric oxidate. Triggers vasodilation in response to blood vessel damage to increase blood flow of inflammatory mediators
->K+ is a vasodilator for repolarisation of the membrane

383
Q

Which factors increase vasoconstriction?

A

hypoxia- direct blood to important organs
Alkaline/ high Ph above 7.7
HCO3- increases vasoconstriction

384
Q

How is BP controlled in the short term?

A

Nerve endings called baroreceptors respond to high BP that causes stretch in the myocardium via stretch-triggered opening of voltage gated Na+ channels which transmit impulses to the medulla.

385
Q

What brain structure controls BP?

A

->Cardioacceleratory centre
->Cardioinhibitory centre
Vasomotor centre has two divisions which acts on the tunica media of the smooth muscle
C1: stimulates vasoconstrciton
A1: stimulates vasodilation

386
Q

Where are the baroreceptors located?

A

Aortic sinus-> innervates vagus nerve
Carotid sinus-> innervates glossopharyngeal nerve

387
Q

How is hypertension regulated?

A

Baroreceptors increase firing of the afferent sympathetic vagus/glossopharyngeal fibres to the vasomotor centre.
Cardioinhibitory centre reduces sympathetic innervation of adrenaline and noradrenaline release to act on B1 and B2 receptors. It stimulates the A1 segment of the vasomotor to act on the tunica media of blood vessels to decrease afterload. It prevents renin release for Na+ and Cl- reabsorption for water retention, therefore more urinary loss.
Increase vasodilation
Decreases vascular resistance, cardiac output, stroke volume (inotropy)

388
Q

How is hypotension regulated?

A

Little firing by baroreceptors down the afferent fibres to the medulla oblaganta. This triggers the cardioacceleratory centre to inhibit the cardioinhibitory centre and increases release of adrenaline and noradrenaline to act on B1 and B2 receptors to increase SAN and AVN depolarisation. It also stimulates the vasomotor motor C1 segment to act on the systemic blood vessels of the tunica media and cause vasoconstriction. Renin also acts on B1 receptors in the kidney to cause release of angiotensin for vasoconstriction.
This causes vasoconstriction, cardiac output, and angiotensin promotes release of aldosterone and ADH which increases Na+ and CL- reabsorption for water retention to increase blood volume and therefore blood pressure.

389
Q

What is the juxtaglomerular apparatus?

A

It is three components:
->vascular component of the afferent and efferent arterioles and the extraglomerular mesangial cells. Extraglomerular mesangial cells are pericytes present in the arterioles outside glomerulus that regulate blood flow.
->A plaque of epithelial tissue called macula densa in the DCT which detect Na+ conc.

390
Q

What are pericytes?

A

Cells present in the vasculature that regulate blood flow through vascular tone

391
Q

What is the mechanism of renin-angiotensin-aldosterone system?

A

Macula Densa detects low Na+ and Cl- and in response releases paracrine signals to release renin. It is released into the bloodstream and binds to B1 receptors of the kidneys and cleaves angiotensinogen-> angiotensin I. Angiotensin I travels in the bloodstream and is a potent vasoconstrictor by acting on the tunica media of the blood vessels. It reaches the lungs where ACE and causes angiotensin I-> Angiotensin II. Angiotensin II moves through the heart aorta throughout the body to act on the adrenal medulla. It stimulates release of aldosterone which binds to renal receptors in the DCT. DCT has principal cells which are stimulated by aldosterone to increase expression of Na+ channels and K+ channels present in the luminal side. This allows influx of Na+ into the principal cells which establishes a gradient for Na+/K+ ATPase to move Na+ into the bloodstream and K+ into the lumen of the cell for excretion into the urine. Hydrostatic pressure decreases. ADH binds to G protein coupled receptors and alters expression of insertion of aquaporin receptors for water absorption. This increases blood volume, BP and heart rate.

392
Q

What is the role of the macula densa?

A

Detects Na+/Cl- levels in the body and releases renin in response.

393
Q

What is the role of aldosterone?

A

Increases Na+/Cl- reabsorption by binding to principal cells in the DCT. It causes insertion of Na+ and K+ channels in the laminal surface which establishes a gradient via Na+/K+ ATPase for Na+ out into the bloodstream and K+ into the lumen. This increases osmolality which reduces hydrostatic pressure.

394
Q

What is the role of ADH?

A

ADH binds to G protein coupled receptors and alters expression of insertion of aquaporin receptors for water absorption.

395
Q

Which system induces lower blood pressure?

A

Natriuretic peptide system.

396
Q

Which system induces high blood pressure?

A

Renin-angiotensin-aldosterone system.

397
Q

What is the mechanism of natriuretic peptide system?

A

Natriuretic peptide system is the secretion of peptide hormones by the cardiac myocytes when the myocardium is stretched. There are two types of natriuretic peptide cells in the heart:
->Atrial natriuretic peptide (ANP) that respond to atrial stretch. In the inactive state, it is pro-ANP and when there is atrial stretch, releases the CORIN protein to transfer the N-terminal and become ANP.
->B-type natriuretic (BNP) peptide cells that respond to ventricular stretch. In the inactive state, it is pro-BNP which releases FURIN enzyme to become active BNP.

Both ANP and BNP cause the release of the natriuretic peptide cGMP/cyclic guanosine monophosphate.

cGMP causes vasodilation and is a diuretic which increases urinary secretion of water and Na+ and CL- via increasing GFR rate. Therefore, cGMP inhibits aldosterone secretion and renin. . cGMP inhibits aldosterone and ADH.

Aldosterone causes fibrosis of myocardium; natriuretic peptides cause antifibrosis which is helpful for patients with heart failure that have difficulty contracting.

398
Q

What is the role of cGMP?

A

cGMP causes vasodilation and is a diuretic which increases urinary secretion of water and Na+ and CL- via increasing GFR rate. Therefore, cGMP inhibits aldosterone secretion and renin. . cGMP inhibits aldosterone and ADH.

Aldosterone causes fibrosis of myocardium; natriuretic peptides cause antifibrosis which is helpful for patients with heart failure that have difficulty contracting.

399
Q

When are beta blockers prescribed?

A

Beta blockers are antagonists for beta receptors activated by the sympathetic system. Therefore, it reduces vasoconstriction and lowers BP and HR. It ends i the suffix -lol eg atenolol. It is not widely used because of its inability to lower central arterial pressure in the heart, brain and kidneys.

400
Q

What is pericardial effusion?

A

Pericardial effusion is when extra fluid gathers in the space between the pericardial sac and the heart which generates pressure ON the heart that limits its ablity to contract.

401
Q

What is the coronary sulcus?

A

The coronary sulcus is the atrioventricular groove.

402
Q

Where does the right coronary artery originate from and its tributaries?

A

Right coronary artery arises from the right cusp of the aortic sinus.
Right marginal artery- supplies right ventricle and heart septum
Right posterior interventricular artery- supplies the posteiror 1/3 of the interventricular septum and inferior part of the heart

The right PIV artery may anastomose with the left anterior descending artery in some people

403
Q

Where does the left coronary artery originate from and its tributaries?

A

Left coronary artery arises from the space between the left cusp of the aortic sinus.
Circumflex artery- supplies the left atria and posterior-lateral ventricle.
Left marginal artery supplies the apex of the left ventricle
Left anterior descending artery- supplies Left atrium and ventricle, part of the right ventricle anterior 2/3 of the interventricular septum, atrioventricular bundle and SAN in (40%)
-> diagonal branch supplies anterior surface of left ventricle

404
Q

What is the infundibulum?

A

The funnel leading to the pulmonary artery

405
Q

What is heart dominance determined by?

A

Dominance in the heart is determined by the posterior descending artery. Most people are right dominant with a right posterior interventricular artery.
Left dominance is less common but where the left circumflex artery will give a posterior descending artery.

Codominance is when both the right coronary artery and left circumflex artery supply the posterior interventricular artery.

406
Q

What is the blood supply to the SAN and its origin?

A

Sinoatrial nodal artery- supplies SAN and originates either directly from right coronary artery or left circumflex

407
Q

What is the blood supply to the AVN and its origin?

A

Atrioventricular nodal artery- supplies AVN- in 80-90% of people it is the right coronary artery and less commonly it is the left circumflex

408
Q

What happens to the blood flow in the left coronary artery when systole begins?

A

Briefly has zero blood flow.

409
Q

What is atherosclerosis?

A

Atherosclerosis is when there is build-up of fat in the coronary arteries which reduces blood flow. This can lead to a blood clot forming becomes stuck in this plaque and forms a thrombosis.

410
Q

What is the difference between cardiac and skeletal muscle?

A

Cardiac muscle is shorter, branched via intercalated discs and is uninucleate or

411
Q

What is the similarities between cardiac and skeletal muscle?

A

Both are striated.

412
Q

How do the boundaries in the sarcomere change during contraction?

A

During contraction, I band and H zone shorten significantly. There is no change in A band

413
Q

What are pacemaker cells?

A

Pacemaker cells are cells that depolarise to generate electrical impulses. They are present in the SAN, AVN, Bundle of His and purkinje which form the electrical condcution system in the heart to induce contraction

414
Q

What is Bachmann’s bundle?

A

Bachmann’s bundle is the interatrial pathway for conduction from the SAN.

415
Q

What are the phases of action potentials in the SAN?

A

Phase 0 is Pre-potential is slow depolarisation caused by slow Na+ influx.
Phase 1- Ca2+ inflx for depolarisation
Phase 3 exudation of K+n for repolarisation

416
Q

What is the difference in action potentials between cardiac muscle and neurons?

A

Cardiac cells have a longer duration of action potentials than neurons. Neurons take 1ms; cardiac myocytes is 2-5ms.

417
Q

What is the direction of flow by blood vessels?

A

Arteries carry blood away from the heart
Veins carry blood to the heart.

418
Q

What is a capillary bed?

A

A capillary bed is an interconnecting network of capillaries which is the main site of exchange of substances occurs between the capillary blood stream and tissue fluid.

419
Q

Why does flow change in a capillary bed?

A

Capillaries have a larger cross-sectional area due to their branching and larger radius which decreases flow. This is beneficial for the exchange of substances in perfusion.

420
Q

What is the tunica intima?

A

Tunica intima is the innermost layer formed of endothelial cells. It has a subendothelial layer below formed of elastic fibres and connective tissue such as fibroblasts and collagen. This can be the site to cause thrombogenesis. The internal elastic lamina is the elastic fibre sheet which separates the tunica intima from the tunica media.

421
Q

What diseases can arise from the tunica intima?

A

Ehlers Danlos syndrome will affect the internal elastic lamina of the tunica intima.

422
Q

What initiates thrombogenesis in the blood vessels?

A

Damage to the endothelial lining and exposure of blood to the collagenous lining in the tunica intima leads to thrombogenesis

423
Q

What is the tunica media?

A

Tunica media is the middle layer of mainly elastic fibres, connective tissue, ground substance and smooth muscle. It is sympathetically innervated to influence hypertension or hypotension of the blood vasodilation and constriction.External elastic lamina is a sheet which separates the tunica media and tunica externa.

424
Q

What issues can arise from the tunica media?

A

Issues with sympathetic innervation can lead to neurogenic shock.

425
Q

What is in the tunica externa?

A

The tunica externa/adventitia is the outer sheath of the vessels consisting of macrophages, collagen and elastic fibres, nerva vasorum and vasa vasorum. It supports and holds the vessel in place

426
Q

What are the types of vasa vasorum?

A

There are two types of vasa vasorum:
vasa vasorum internae-> directly from the main branch
vasa vasorum externae-> branch of the main artery which is within the main vessel wall

427
Q

Why are arterial diseases more common than venous?

A

Veins have a wider lumen than arteries, despite having the same diameter. This means the vasa vasorum in the tunica adventitia is closer and able to supply more nutrients. This explains why arterial diseases are more common

428
Q

What are the vasa vasorum?

A

These are small arteries in the outer tunica adventitia layer that remove metabolic waste and supply nutrients. The tunica intima and tunica media layer contain connective tissue and other cells which require nutrient supply and waste removal. This role is supplied by the vasa vasorum.

429
Q

What are the types of arteries?

A

There are two different types of arteries:
Elastic conducting arteries and muscular arteries?

430
Q

What are the elastic conducting arteries?

A

Elastic conducting arteries- largest artery with a diameter of 1.5cm and length of 1cm. They are directly branching from the outflow tract of the aorta and the pulmonary artery. Therefore, they have a lot of elastic fibre and collagen in their tunica media layer to expand and absorb systolic pressure. It also recoils to release it and maintain a constant pressure gradient with the constant pumping of the heart.

431
Q

What are the muscular arteries?

A

It has a diameter of 0.6cm/6mm and receives blood from elastic conducting arteries to suppply to tissues and organs. They have a lot of smooth muscle in their tunica media layer to regulate blood flow to the supplied tissue/organs via vasodilation and vasoconstriction. Examples of this includes the brachial artery and the femoral.

432
Q

What are the arterioles?

A

Arterioles connect arteries to the capillary bed and have a wider lumen which greatly reduces blood pressure in order to direct flow. They have the same layers as arteries however, they have much thinner layers. Both arteries and arterioles have the thickest layers to withstand pressure

433
Q

What are the metarterioles?

A

Metarterioles are branches from the terminal arteriole which directly supply blood from arterioles to capillaries. They have the same layers however, smooth muscle in the tunica media layer is arranged in rings called sphincter muscles to regulate blood flow into the capillary bed to decrease pressure.

434
Q

What is the role of the pre-capillary sphincters?

A

Rings of circular smooth muscle called the pre-capillary sphincters surround the opening of the metarteriole to the capillary bed. Pre-capillary sphincters regulate blood flow in and out of the capillaries by opening and closing.

435
Q

What is vascular shunt?

A

When surrounding tissue requires O2, pre-capillary sphincters open to allow blood to enter the capillary bed for exchange. When capillary beds in other parts of the body require gas exchange such as the muscles during exercise, the pre-capillary sphincters will close. Blood supply from the metarterioles will flow directly through thoroughfare channels to the venules. This is known as vascular shunt- the redirection of blood flow.

436
Q

What is a thoroughfare channel?

A

Channel which directly connects the metarterioles to the postcapillary venules

437
Q

What is vasomotion?

A

Vasomotion is blood flow in the capillaries; this is generally irregular and pulsating. Vasomotion is regulated in response to levels of O2 vs CO2, H+ and lactic acid. When O2 levels are low, and CO2, Lactic acid and H+ levels are high, there will be a greater rate of vasomotion for exchange to occur

438
Q

What is pinocytosis?

A

Pinocytosis is cell drinking-uptake fluid containing proteins, lipids and white blood cells for pathogen defence via vesicle budding

439
Q

What are the features of the capillaries?

A

Capillaries contain invaginations in the endothelial layer called caveolae which they can uptake substanes through via transcytosis. Capillaries have only a tunica intima layer for a short diffusion path.

440
Q

What are the 3 types of capillaries?

A

Continuous, fenestrated and sinusoid

441
Q

What are the continuous capillaries?

A

It has an intact basement membrane with tight junctions in the endothelial layers. Depending on location, the tight junctions may have intercellular clefts/gaps that allow small molecules to pass through. Continuous capillaries in the brain do not have any intercellular gaps; they highly restrict exchange via astrocyte extensions of end feet
Outside the brain, continuous capillaries have intercellular celfts for movement of water, glucose and other hydrophobic molecules for endocytosis and exocytosis.

Year 1 (191 decks)

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