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Year 1 - Semester 2 > Resp > Flashcards

Resp Flashcards

1
Q

What is the pathway of airway

A

Nasal or oral cavities >pharynx>trachea>primary bronchi>secondary>tertiary>bronchioles>alveoli

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2
Q

What is Vt

A

Tidal volume - volume of gas breathed in or out in one breath (usually 0.4-0.8L at rest)

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3
Q

What is fR

A

Respiratory frequency - breaths per min (usually 12-15 at rest)

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4
Q

What is Ve

A

Minute ventilation - usually 5-8L/min

Tidal volume x frequency

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5
Q

What are the capacities of the lungs

A

Tidal volume - normal breathing

Inspiratory reserve volume - Max you can breathe in on top of your normal inhalation

Inspiratory capacity is tidal volume + inspiratory reserve volume - Max you can breathe in after a normal exhalation

Vital capacity is the inspiratory capacity + expiratory reserve volume - max someone can exhale after a max inhalation

Functional residual capacity is the residual volume + expiratory reserve volume - amount left in the lungs after a normal exhalation

Residual - air left in lungs after max exhalation

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6
Q

What happens in inspiration

A

Diaphragm and external intercostals contract, expanding the rib cage and decreasing pleural pressure allowing air to flow in down the pressure gradient

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7
Q

What happens in expiration

A

During normal breathing, the natural elastic recoil of lung tissue causes lungs to decrease in size

During forced breathing, internal/innermost intercostals and abdominal muscles contract, which pushed the diaphragm up and compresses the ribs, reducing the size of the thoracic cavity

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8
Q

Describe the dorsal respiratory groups

A

In the medulla oblongata

Composed of mainly inspiratory neurones

Controls generation of basic rhythms

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9
Q

Describe the ventral respiratory groups

A

In the medulla oblongata
Contain inspiratory and expiratory neurones

Primarily active during exercise and stress

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10
Q

Describe the pontine respiratory groups

A

In the pons

Contains inspiratory and expiratory neurones

Pneumotaxic center (PNC) involved in inhibiting neurones from the medulla. Sectioning the upper pons results in slow, gasping breaths

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11
Q

Describe the generation of breathing rhythm

A

Discharge from inspiratory neurones activates resp muscles via spinal motor nerves
Expiratory neurones fire and inhibit the inspiratory neurones and passive expiration occurs

If forceful expiration is needed, expiratory neurone activity also activates expiratory muscles

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12
Q

What can respiratory rhythms be affected by

A

Lung receptors and chemoreceptors

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13
Q

What are the types of lung receptors

A 
Rapidly adapting (irritant) receptors
These are sub epithelial mechanoreceptors in the trachea and bronchi simulated by irritants or mechanical factors, such as smoke, dust and  chemicals such as histamine. They cause coughing, mucus production and bronchoconstriction. Afferent fibres are myelinated
Slowly adapting (stretch) receptors 
These are mechanoreceptors located close to airway smooth muscle which are stimulated by stretching of airway walls. This helps prevent over-inflation by initiating expiratory rhythms. This has an important role in the hering-brueemr reflex (prolonged inspiration causes prolonged expiration). Also myelinated afferent fibres

C fibres - unmyelinated nerve endings stimulated by oedema and various inflammatory mediators. Cause rapid, shallow breathing and dyspnoea

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14
Q

How do chemoreceptors work

A

CO2 crosses the blood brain barrier and reacts with H2O to form H2CO3 which is then converted to HCO3 and H

This hydrogen ion is detected by the medulla and the response is generally slow

Located in the corotid sinus (IX glossopharyngeal nerve)
And aortic arch (X vagus nerve)
Both respond rapidly to pO2 but those in carotid are more responsive

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15
Q

What does hypercapnia cause

A

Linear increase in minute ventilation

Response to hypercapnia is increased by hypoxia and decreased by hyperoxia

Interaction mediated by peripheral chemoreceptors

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16
Q

What does hypocapnia cause

A

Little change in ventilation

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17
Q

What does hypoxia cause

A

Curvilinear increase in ventilation
Little change until pO2 drops below about 8kPa

Mediated by peripheral chemoreceptors
Almost exclusively by carotid body

Increased by hypercapnia

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18
Q

What does hyperoxia cause

A

Small decrease in ventilation

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19
Q

What can happen in COPD

A

Chronic elevation of CO2

Desensitisation of central chemoreceptors

Giving high flow oxygen can depress breathing

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20
Q

What happens to breathing during sleep

A

Decreases

Patients often develop resp failure in their sleep

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21
Q

What happens in obstructive sleep apnoea

A

Upper airways narrowed
Allowed upper airway to collapse during sleep
Can cause extreme tiredness

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22
Q

What drugs affect respiration

A

Depress - opioids, almost all anaesthetics, sedatives e.g. benzodiazepines, ethanol

Stimulate - doxapram, beta agonists

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23
Q

Daltons law

A

Each gas exerts a pressure in a mixture

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24
Q

Henry’s law

A

Concentration of a gas dissolved in a liquid is proportional to it’s partial pressure

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25
Q

What is important about different gases with the same partial pressures?

A

Will have different concentrations in solution due to different solubility constants

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26
Q

Which factors affect O2 affinity for haemoglobin

A

O2 binding - cooperativity

H+ - Bohr effect - increasing h+ decreases oxygen affinity

[CO2] - Haldane effect - increasing co2 decreases oxygen affinity

Temperature - increasing temperature decreases oxygen affinity

Carbon monoxide - binds with affinity 200x greater than oxygen. Also affects other oxygen binding sites - oxygen poorly released

2,3 biphosphoglycerate - lowers O2 affinity

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27
Q

What happen if the iron in haemoglobin is oxidised

A

Becomes methaemoglobin which does not bind oxygen
ferrous –> ferric
metHb reductase reduces it back to Hb

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28
Q

What is special about foetal haemoglobin

A

It has a higher affinity for oxygen so can take oxygen from maternal blood

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29
Q

What are the three ways CO2 is transported

A

60% is mediated by HCO3 - from carbonic acid which is formed from CO2 and H2O by carbonic anhydrase

(Further ionisation to CO3 is negligible as the pKa is too high)

30% is carried by carbamino groups - mostly haemoglobin

10% is dissolved in blood

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30
Q

How to measure Hb saturation

A

Absorption spectrometry as oxygenated is red and deoxygenated is blue

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31
Q

What factors affect oxygen delivery to tissues

A 
Partial pressure of oxygen in the air
How well air can travel into lungs
How well oxygen diffuses across the alveolar lining 
Haemoglobin concentration
Cardiac output
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32
Q

What effect does hyperventilation have

A

Less CO2, little impact on O2

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33
Q

What effect does hypoventilation have

A

Less O2, more CO2

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34
Q

What is type 1 resp failure

A

Low PaO2 and normal PaCO2 due to V/Q mismatch

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35
Q

What is type 2 resp failure

A

Low PaO2, High PaCO2 due to hypoventilation

Won’t breathe- typically overdose of drugs such as opioids, benzodiazepines, analgesics

Can’t breathe - broken mechanism such as nerves not working or bisected, muscles not working (muscular dystrophy), chest can’t move (scoliosis), gas can’t get in or out

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36
Q

What is the V/Q ratio

A

Amount of air reaching lungs to the amount of blood reaching the lungs. Generally higher in the apex than the base due to gravity

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37
Q

What happens in VQ mismatch

A

Typically happens locally so other parts of the lung can compensate.
Initially, CO2 in the area is high but it stimulates ventilation and mixes with areas of the lung with normal V/Q and therefore CO2 in blood is normal

This is not the case for oxygen as normal blood is already saturated with oxygen so when this blood mixes with blood with low O2, the result is low O2

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38
Q

What are the different types of oxygen delivery methods

A

Variable performance - amount inspired is dependent on the patients breathing

Fixed performance - high flow Venturi - different valves allow jet of oxygen - constant controlled delivery

Max performance - non-rebreather mask - reservoir bag fills when patients inspiratory flow rate is lower than the delivered O2 flow rate. Patient preferentially inhales O2

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39
Q

What is the Venturi effect

A

Drop in pressure induced by the increase in velocity of something flowing through a narrow nozzle pulls air from environment in. The size of the nozzle determines the dilution of the O2 and therefore the oxygen concentration delivered to the patient

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40
Q

What happens in restrictive disorders

A 
More fibrous tissue (more rigid)
Lower compliance (needs high pressure to inflate)
More elastic recoil (deflates easily)
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41
Q

What happens in obstructive disorders

A 
Lower elastic tissue (more floppy)
Higher compliance (inflates at low pressure)
Less elastic recoil (harder to deflate)
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42
Q

Describe surfactant

A

Produced by type 2 alveolar cells (pneumocyte), composed of 90% lipids and proteins
Reduced surface tension
In expanded alveoli, the surfactant molecules are spread out evenly and have no effect on surface tension
When they are small, the surfactant is tightly packed and reduces surface tension

Aid expansion of lungs and decreases effort needed for inspiration

Stabilise alveoli to prevent collapse during expiration

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43
Q

What is important for premature babies

A

Surfactant produced from 30 weeks onward so babies lungs can fail to inflate leading to resp distress syndrome

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44
Q

What are the principal buffers in the plasma

A

Phosphate - important urinary buffer for H+ excretion
Buffers intracellular fluid

Protein - present in large amounts
Buffers intracellular fluid and plasma
Haemoglobin buffer in RBCs

Bicarbonate - primary extracellular buffer (plasma)

Ammonia - formed from glutamine
Allowed excretion of H+ as NH4+ in acidaemia
Not present in plasma

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45
Q

What is acidaemia and alkalaemia

A

Acidaemia - H+ >44nM

Alkalaemia - H+ <36nM

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46
Q

What are causes of acid - base disturbance

A

Respiratory - changes in CO2 due to lung function

Metabolic - changes in plasma HCO3 due to kidney function

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47
Q

What is the difference between actual bicarbonate and standard bicarbonate

A

Actual - calculated from actual H+ and pCO2 values

Standard - calculated from actual H+ and a normal pCO2 of 5.3kPa.

standard is only affected by metabolic effects. If normal then no metabolic component
If CO2 is high then partly respiratory

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48
Q

What is an increased anion gap indicate

A

Lactate, 3-hydrobutyrate

Metabolic acidaemia

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49
Q

What is base excess

A

Amount of base needed to be removed from a litre of blood at normal pCO2 in order to bring H+ back to normal
Measured at normal CO2 (so only metabolic component considered)
Normal value is 0 (-2 to 2)
Big negative indicates metabolic acidosis

If base excess and standard bicarbonate are normal and pCO2 is high, then acidaemia is purely respiratory

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50
Q

How to decided if a patient had acidaemia or alkalaemia

A

Look at H+

Then look at PaCO2 - if abnormal then respiratory effect
If the change could have caused the change in H+ then there is primary respiratory disturbance
If it could have opposed the change in H+ then respiratory compensation has occured

Then look at HCO3 - if abnormal then metabolic effect
If it could have caused H+ change then primary metabolic disturbance
If it opposed the H+ change then metabolic compensation has occured

51
Q

Common causes if respiratory acidaemia

A 
Impaired gas exchange
Hypoventilation
Lung disease, COPD
Drugs
Muscle paralysis
52
Q

Common causes if respiratory alkalaemia

A

Hyperventilation from:

Salicylate poisoning
Resp centre stimulation
Hysteria, anxiety
Cerebral diseases such as viral infection/head injury

53
Q

Common causes if metabolic acidaemia

A 
Acidic metabolic products
Loss of HCO3
Chronic diarrhoea
Increase buffering demand (keto/lactic acidaemia)
Acid indigestion
54
Q

Common causes if metabolic alkalaemia

A

Bicarbonate ingestion

Severe vomiting

55
Q

What are obstructive lung disorders

A

Cause narrowing of airway

This can be caused by:

Increased mucus production - produced by vagal parasympathetic activity

Anatomical features - loss of alveolar attachments which hold open the airways
Reduced elastic recoil

Autonomic and NANC (non-adrenergic, non-cholinergic) - parasympathetic innervation, carried by the vagus nerve causes release of acetylcholine at M3 muscarinic receptors, causing bronchoconstriction and mucus secretion

B2 agonists such as adrenaline and noradrenaline cause bronchoconstriction

NANC nerves, also carried by the vagus nerve, cause bronchodilation through NO and vasoactive intestinal polypeptide and bronchoconstriction through substance P and neurokinins

Inflammation - mast cells release histamines, leukotrienes and prostaglandins

56
Q

What is FEV1

A

Forced expiratory volume in one second

57
Q

What is FVC

A

Forced vital capacity - max forced expiration volume

58
Q

What is the ratio between FVC and FEV

A

Used to differentiate obstructive and restrictive disorders

In obstructive, vital capacity is normal but it takes longer to breathe out

59
Q

What happens to FEV/FVC ratio in severe obstructive disorders

A

May be normal as FVC is also reduced due to airway collapse when breathing out fast to measure FEV

60
Q

What are the changes to peak flow in restrictive disorders

A

Decreased FEV and FVC so normal ratio

61
Q

What investigations do we use to differentiate between restrictive disorders

A

Gas exchange tested using carbon monoxide because it has high affinity for Hb - easy to measure

Alveolar volume tested using helium as it’s not taken up by Hb and easy to measure
Two measurements:

TLCO - total gas exchange capacity - how much gas (normally oxygen but CO in the test) is able to cross the alveolar wall into the blood

KCO - TLCO divided by the total alveolar volume - tests efficiency of alveoli such as thickening of alveolar wall

62
Q

What are examples of intrapulmonary restriction

A 
Silicosis
Drug induced lung fibrosis
Asbestosis
Rheumatoid lung
Pigeon fancier lung
Infant resp distress syndrome
63
Q

What are examples of extrapulmonary restriction

A

Nerves to resp muscles inhibited e.g. high cervical dislocation

Impaired neuromuscular junction
Impaired muscles
Pleural thickening
Skeletal abnormalities

64
Q

What is the TLCO and KCO in intra- and extra-pulmonary restriction

A

TLCO is reduced in both

In extra KCO is high

In intra KCO is reduced because alveoli are abnormal

65
Q

What is bronchiolitis

A

Inflammation of the bronchioles - a feature of chronic bronchitis
Often in children

66
Q

Describe localised airway obstruction

A

Lesion outside (e.g. lymph node), lesion inside wall (e.g. tumour), foreign object in lumen

Can cause distal over inflation or collapse
Normal pulmonary function tests
May be distal lipid or infective pneumonia

67
Q

Describe diffuse obstructive airways disease

A

Reversible and intermittent or irreversible and permeant, centred on bronchi and bronchioles

Many airways involved
Obstructive pulmonary function tests

Can be from emphysema, asthma, chronic bronchitis, bronchiectasis

COPD us a spectrum of emphysema and chronic bronchitis

68
Q

Describe chronic bronchitis

A

Persistent cough for 3 consecutive months over 2 consecutive years

Caused by smoking, pollution

Cause hypercapnia, hypoxia, pulmonary hypertension- eventually cor pulmonale - hypertrophy of right ventricle, often due to pulmonary hypertension

Termed blue bloater - cyanosis and oedema from right heart failure

69
Q

Describe emphysema

A

Abnormal and permanent enlargement of the air spaces that are distal to the terminal bronchioles (alveoli)

Accompanied by destruction of alveolar walls without obvious fibrosis

Types:

Centrilobular - strongly associated with smoking, seen in those with pneumoconiosis. Resp bronchiolitis often present. Most common in upper lobes and resp bronchioles

Panlobular - usually in lower lobes, associated with alpha 1 antitrypsin deficiency - markedly accelerated in smokers

Paraseptal - distention adjacent to plural surfaces - associates with scarring

Irregular - associated with scarring

Called pink puffers

Puffer because hyperinflation causes barrel chest and hyperventilation

Normal PCO2 and PO2 but hypoxic during exercise due to inefficient gas exchange - pink

Chronic breathlessness

Elevated FRC, VC and TLC.

Weight loss and ventricular failure

70
Q

What are the types of asthma

A

Extrinsic - definite external cause - type 1 sensitivity reaction typically starting in childhood

Intrinsic - no external cause starting in adulthood. Cannot be improved

Atopic - allergies

Non-atopic - associated with recurrent infections. Not immune mediated

Aspirin induced - associated with recurrent rhinitis, uticaria and nasal polyps

Occupational - caused by allergens at work

Allergic bronchopulmonary aspergillosis - response to spores. Type 1 and 3 hypersensitivity reactions

71
Q

What is bronchiectasis

A

Localised, irreversible dilation of part of the bronchial tree caused by destruction of muscle and elastic tissue. Classified as an obstructive disorder along with emphysema, asthma, cystic fibrosis.
Involved bronchi are dilated, inflamed and easily collapsible

Usually results from bacterial infections

Cough and lots of sputum

Finger clubbing

72
Q

Cystic fibrosis

A

Multi system disorder due to impaired ion transport which leads to viscous mucus

73
Q

What are the types of pneumonia

A

Bronchopneumonia - patchy, widespread, most common
Acute supparitive inflammation
Often in elderly e.g. heart failure, renal failure, stroke, COPD

Lobar pneumonia - rust coloured sputum
Consolidation of an entire lobe or portion
Grey/red hepatisation (dense like liver)
Congestion, resolution

74
Q

Describe acute respiratory distress syndrome

A

Hypoxia, non-cardiogenic pulmonary oedema, diffuse bilateral infiltrates on x-ray

Causes- direct - pneumonia, aspiration, ventilation
Indirect - sepsis, trauma, pancreatitis, acute hepatic failure

75
Q

What is the treatment for TB

A

RIPE

Rifampicin, Isoniazid, Pyramidizine, Ethambutol

All 4 for 2 months

Then rifampicin and isoniazid for 4 more months

76
Q

Describe squamous cell carcinoma

A

40-50% of lung cancers

Show squamous differentiation

Usually starts near a central bronchus, hollow cavity with associated necrosis at centre

Metaplastic squamous epithelia > squamous dysplasia > squamous carcinoma in situ > invasive squamous cell carcinoma

77
Q

Describe adenocarcinoma

A

30-40% and increasing
Evidence of glandular growth pattern e.g. mucus production
Usually originates in peripheral tissue

78
Q

Small cell carcinoma

A

Very poorly differentiated
Evidence of neuroendocrine differentiation
Often metastatic at presentation and present late
Strongly associated with smoking

79
Q

Describe mesothelioma

A

Commonly in pleura
Cause if often asbestos
presents as pleural effusion, chest wall pain
Often 40 years between exposure and diagnosis
Survival rates are very poor

80
Q

Symptoms of lung cancer

A 
Cough, dyspnoea, haemoptysis
Weight loss
Chest/shoulder pain
Hoarseness and fatigue
Slow to clear pneumonia
Finger clubbing
Liver, bone, brain metastases
Pleural effusion
Hypercalcaemia, Cushing's
81
Q

Describe B2 agonists

A

Salbutamol, terbutaline (short acting), salmeterol, formoterol (long acting)

Relax smooth muscle by activating G protein coupled receptors, activating adenylyl cyclase which in turn increases cyclic AMP production
Causes vasodilation and inhibits the release of histamine etc from mast cells. Also increases K intake

Used for COPD, asthma and hyperkalemia

Hypothermia, tachycardia, palpitations, skeletal muscle tremors

82
Q

Describe anticholinergics

A

Ipotropium (short acting), tiotropium (long acting)

Inhibit muscarinic receptors (M1/M2/M3)

Therefore relaxing smooth muscle and inhibiting mucus secretion. Also inhibits PNS impulses by selectively blocking M2 receptors. Decreases spasms

Treatment of asthma, COPD, allergic rhinitis

Reduced secretion - dry throat, mouth
Reduced SM contraction - urinary retention, constipation
Reduced vagal tone - headachesz nausea

Inhaling rather than oral reduces side effects

83
Q

Xanthines

A

Theophylline, aminophylline

Inhibits phosphodiesterases therefore increasing cAMP, therefore relaxes smooth muscle

May also block receptor for adenosine, preventing airway narrowing

Treatment of COPD

Side effects - tachycardia, palpitations, nausea

Plasma concentrations should be monitoring

84
Q

Corticosteroids

A

Prednisolone (oral), beclomethasone (inhaled), hydrocortisone (topical)

Endogenously produced in adrenal cortices

Treatment of COPD, asthma, rheumatoid arthritis, IBD

Hyperglycaemia, osteoporosis, proximal myopathy, skin thinning, weight gain, altered body fat distribution, hypertension, growth suppression in children, viral/fungal susceptibility increased

85
Q

Leukotriene antagonist

A

Monteleukast

Reduced airway narrowing and mucus production usually caused by leukotrienes
Treatment of exercise induced asthma , seasonal allergic rhinitis

Abdominal pain, thirst, headache, hyperkinesia, hypersensitivity, increased infection risk, muscle aches, liver damage

86
Q

Mast cells stabilisers

A

Cromoglicate

Stabilises mast cells, reduced release of histamine, prevent airway inflammation

Treatment of asthma, conjunctivitis, allergic rhinitis

Local irritation, transient bronchospasm

87
Q

Drugs which cause bronchospasm

A

Beta antagonists - propranolol

NSAIDs

88
Q

Mechanism of NSAIDs

A

Phospholipid are converted to arachnidonic acid by phospholipase A2

Then either 5-lipoxygenase makes leukotrienes or cyclooxygenase makes prostaglandins and thromboxane

NSAIDs inhibit cyclooxygenase so more leukotrienes produced which causes mucus production and bronchoconstriction

89
Q

Drugs which suppress respiration

A

Benzodiazepines, opioids

90
Q

Drugs which cause interstitial lung disease

A

Amiodarone

91
Q

What is VD (volume of distribution)

A

Total amount of drug in body/drug plasma concentration

92
Q

What are parenteral drugs

A

Administered somehow other than alimentary canal

93
Q

Mechanisms of resistance

A

Target site alteration so drug affinity is reduced

Reduced access - drug removed or cannot enter cell

Inactivation - such as beta lactamase for penicillin

Metabolic bypass by producing additional targets

94
Q

Beta lactams

A

Penicillin - group A strep, meningococci

Cephalosporin - broader spectrum - not enterococci

Carbapenems - broad spectrum

Target peptidoglycan cell wall
Binds to transpeptidases (penicillin-binding protein) responsible for polysaccharide cross-link formation

Hypersensitivity rash, diarrhoea, must reduce dose in kidney failure, anaphylaxis, allergy

95
Q

Glycopeptides

A

Vancomycin

For gram positive - useful vs MRSA

Binds to terminal D-ala-D-ala of peptide chain, prevents incorporation of new subunits into cell wall

Nephrotoxicity

96
Q

Aminoglycosides

A

Gentamicin

Good Vs gram negative
Not good Vs anaerobes
Broad spectrum

Inhibit binding of 30S subunit to mRNA - protein synthesis inhibited

Ototoxicity and nephrotoxicity

97
Q

Tetracyclines

A

Tetracycline

Bacteriostatic
Especially Chlamydia

Inhibit binding of tRNA - protein synthesis inhibited

Diarrhoea, nausea, teeth discolouration
Avoid in children and pregnant/lactating women

98
Q

Macrolides

A

Erythromycin
Clarylithromycin

Narrow spectrum - gram positive

Prevent peptidyl transferase from adding the growing peptide attached to tRNA to the next amino acid

GI upset
Thrombophlebitis

99
Q

Lincosamides

A

Clindamycin

Bacteriostatic against gram positive and aerobes

Bind to 50S subunit - protein synthesis inhibited

Diarrhoea, colitis

100
Q

THFA inhibitors

A

Sulphonamide, trimethoprim

Trimethoprim most commonly used in UTI

Selectively toxic to bacteria as humans don’t make folic acid

Together they are bactericidal

Do not give trimethoprim during pregnancy

101
Q

RNA synthesis inhibitors

A

Rifampicin

TB (in combination)

Binds to DNA dependent RNA polymerase. Inhibits initiation

Drug interactions
Inactivates oral contraceptive
Hepatitis, nausea, body fluids go orange

102
Q

DNA synthesis inhibitors

Fluoroquinolone

A

Ciprofloxacin

Broad spectrum

Quinolones bind to DNA gyrase and topoisomerase so DNA coiling is inhibited

Neurotoxicity, confusion, fits, cartilage defects (not in pregnant women or children), photosensitivity, association with C diff infection

103
Q

Amantadine

A

Influenza A
Interferes with viral protein channels and effects uncoating

Insomnia, depression, especially in the elderly

104
Q

Enfuvirtide/maraviroc

A

HIV

Maraviroc affects chemokine co-receptor 5 on CD4 cells

Enfuvirtide affects gp41 attachment

Injection site reactions

105
Q

Aciclovir

A

Herpes simplex

Treatment and prophylaxis

Viral DNA synthesis halted, premature chain termination, viral DNA polymerase irreversibly inactivated

Resistance can occur

106
Q

Ribavirin

A

Severe RSV in babies also lassa, Marburg, ebola

Guanosine analogue, inhibits viral nucleic acid replication

Respiratory depression, reticulocytotic, teratogenic

107
Q

Zidovudine

A

HIV

Reverse transcriptase inhibitor
Nucleoside inhibitors
Incorporated into viral DNA, premature chain termination

Bone marrow, renal and hepatic toxicity

Resistance widespread

108
Q

Nevirapine, efacrine, etravarine

A

HIV

Bind to non-substrate binding site of reverse transcriptase therefore inhibiting it

Rash, nausea, hepatitis, pancreatitis

109
Q

Ritonavir

A

HIV

Protease inhibitors
Prevents cleavage of protein products

Severe side effects

110
Q

Oseltamivir (tamiflu), zanamivir

A

Influenza A and B

Inhibits neuraminidase preventing release of viral particles

Resistance can develop

111
Q

Interferons

A

Chronic hep B and C

Immunomodulators
Produced in the body in response to infections

Affect production of cellular proteins which act at different stages of viral cycle

112
Q

Polyenes

A

Amphotericin B, Nystatin

S. nodosis, s. noursei

Binds to sterols in the cytoplasmic membrane, affects membrane permeability, leakage of intracellular ions followed by water

113
Q

Azoles

A

Clotrimazole, fluconazole

Thrush (candida)

Acts by inhibiting demethylase enzyme required for ergosterol synthesis

114
Q

Echinocandins

A

Caspofungin, anidulafungin, micafungin

Candida and aspergillus

Target beta glycan synthases, inhibit cell wall construction

115
Q

Flucytosine

A

Systemic severe yeast infections

Usually used with amphotericin B

Interferes with DNA synthesis, analogue of cytosine

GI tract, hepatic and gone marrow toxicity

Monitoring serum levels needed

116
Q

Terbinafine

A

Fungal nail infections

Inhibits equalene epoxidase required in ergosterol synthesis

GI upset

117
Q

Griseofulvin

A

Fungal skin and nail infections

Natural product if penicillium species z incorporated into new keratin

118
Q

Idiopathic pulmonary fibrosis

A

Abnormal proliferation of collagen
Subpleural thickening which spreads throughout the lung
Some areas are uninvolved and some have fibrosis
Mixed inflammatory cells and increase in alveolar macrophages

119
Q

Hypersensitivity pneumonitis

A

Type III

Ab, Ag complex in lung

Pigeon fanciers lung, farmers lung, mushroom lung

Most resolve when agent of exposure is removed

120
Q

P = DKa/d

A 
P= permeation rate 
D= diffusion constant (diffusion when dissolved)
K= partition constant (tendency to dissolve)
a = membrane area
d= membrane thickness

Oxygen is smaller so diffuses faster - higher D
CO2 is less polar so much higher K
CO2 diffuses much faster

121
Q

Carcinoid tumours

A

Typical - higher survival rate
<2 mitoses per 2mm^2
No necrosis

Atypical - lower survival rate
>2 but <10 mitoses per 2mm^2
Focal necrosis

More than 10 is classified as something else

122
Q

What are the lymph nodes numbered less than 9?

A

In the mediastinum

If these are involved be tumor is less treatable and often not curable

123
Q

What are the ways of measuring blood O2

A

Sats monitor - very easy - reliable as long as Hb is normal
Absorption spectrometry

Arterial blood gases - invasive and more complicated
Radial it femoral artery
Measures PaO2, PaCO2, H+, bicarbonate, some do others such as electrolytes

124
Q

What is physiological dead space

A

Alveolar dead space (alveoli with lack of blood supply, rate in youth) + anatomical dead space (conducting airways where no has exchange takes place)

Year 1 - Semester 2 (3 decks)

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