Resp Flashcards
1
Q
What is the pathway of airway
A
Nasal or oral cavities >pharynx>trachea>primary bronchi>secondary>tertiary>bronchioles>alveoli
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)
3
Q
What is fR
A
Respiratory frequency - breaths per min (usually 12-15 at rest)
4
Q
What is Ve
A
Minute ventilation - usually 5-8L/min
Tidal volume x frequency
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
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
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
8
Q
Describe the dorsal respiratory groups
A
In the medulla oblongata
Composed of mainly inspiratory neurones
Controls generation of basic rhythms
9
Q
Describe the ventral respiratory groups
A
In the medulla oblongata
Contain inspiratory and expiratory neurones
Primarily active during exercise and stress
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
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
12
Q
What can respiratory rhythms be affected by
A
Lung receptors and chemoreceptors
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
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
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
16
Q
What does hypocapnia cause
A
Little change in ventilation
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
18
Q
What does hyperoxia cause
A
Small decrease in ventilation
19
Q
What can happen in COPD
A
Chronic elevation of CO2
Desensitisation of central chemoreceptors
Giving high flow oxygen can depress breathing
20
Q
What happens to breathing during sleep
A
Decreases
Patients often develop resp failure in their sleep
21
Q
What happens in obstructive sleep apnoea
A
Upper airways narrowed
Allowed upper airway to collapse during sleep
Can cause extreme tiredness
22
Q
What drugs affect respiration
A
Depress - opioids, almost all anaesthetics, sedatives e.g. benzodiazepines, ethanol
Stimulate - doxapram, beta agonists
23
Q
Daltons law
A
Each gas exerts a pressure in a mixture
24
Q
Henry’s law
A
Concentration of a gas dissolved in a liquid is proportional to it’s partial pressure
25
What is important about different gases with the same partial pressures?
Will have different concentrations in solution due to different solubility constants
26
Which factors affect O2 affinity for haemoglobin
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
27
What happen if the iron in haemoglobin is oxidised
Becomes methaemoglobin which does not bind oxygen
ferrous --> ferric
metHb reductase reduces it back to Hb
28
What is special about foetal haemoglobin
It has a higher affinity for oxygen so can take oxygen from maternal blood
29
What are the three ways CO2 is transported
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
30
How to measure Hb saturation
Absorption spectrometry as oxygenated is red and deoxygenated is blue
31
What factors affect oxygen delivery to tissues
```
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
```
32
What effect does hyperventilation have
Less CO2, little impact on O2
33
What effect does hypoventilation have
Less O2, more CO2
34
What is type 1 resp failure
Low PaO2 and normal PaCO2 due to V/Q mismatch
35
What is type 2 resp failure
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
36
What is the V/Q ratio
Amount of air reaching lungs to the amount of blood reaching the lungs. Generally higher in the apex than the base due to gravity
37
What happens in VQ mismatch
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
38
What are the different types of oxygen delivery methods
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
39
What is the Venturi effect
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
40
What happens in restrictive disorders
```
More fibrous tissue (more rigid)
Lower compliance (needs high pressure to inflate)
More elastic recoil (deflates easily)
```
41
What happens in obstructive disorders
```
Lower elastic tissue (more floppy)
Higher compliance (inflates at low pressure)
Less elastic recoil (harder to deflate)
```
42
Describe surfactant
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
43
What is important for premature babies
Surfactant produced from 30 weeks onward so babies lungs can fail to inflate leading to resp distress syndrome
44
What are the principal buffers in the plasma
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
45
What is acidaemia and alkalaemia
Acidaemia - H+ >44nM
Alkalaemia - H+ <36nM
46
What are causes of acid - base disturbance
Respiratory - changes in CO2 due to lung function
Metabolic - changes in plasma HCO3 due to kidney function
47
What is the difference between actual bicarbonate and standard bicarbonate
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
48
What is an increased anion gap indicate
Lactate, 3-hydrobutyrate
Metabolic acidaemia
49
What is base excess
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
50
How to decided if a patient had acidaemia or alkalaemia
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
Common causes if respiratory acidaemia
```
Impaired gas exchange
Hypoventilation
Lung disease, COPD
Drugs
Muscle paralysis
```
52
Common causes if respiratory alkalaemia
Hyperventilation from:
Salicylate poisoning
Resp centre stimulation
Hysteria, anxiety
Cerebral diseases such as viral infection/head injury
53
Common causes if metabolic acidaemia
```
Acidic metabolic products
Loss of HCO3
Chronic diarrhoea
Increase buffering demand (keto/lactic acidaemia)
Acid indigestion
```
54
Common causes if metabolic alkalaemia
Bicarbonate ingestion
| Severe vomiting
55
What are obstructive lung disorders
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
What is FEV1
Forced expiratory volume in one second
57
What is FVC
Forced vital capacity - max forced expiration volume
58
What is the ratio between FVC and FEV
Used to differentiate obstructive and restrictive disorders
| In obstructive, vital capacity is normal but it takes longer to breathe out
59
What happens to FEV/FVC ratio in severe obstructive disorders
May be normal as FVC is also reduced due to airway collapse when breathing out fast to measure FEV
60
What are the changes to peak flow in restrictive disorders
Decreased FEV and FVC so normal ratio
61
What investigations do we use to differentiate between restrictive disorders
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
What are examples of intrapulmonary restriction
```
Silicosis
Drug induced lung fibrosis
Asbestosis
Rheumatoid lung
Pigeon fancier lung
Infant resp distress syndrome
```
63
What are examples of extrapulmonary restriction
Nerves to resp muscles inhibited e.g. high cervical dislocation
Impaired neuromuscular junction
Impaired muscles
Pleural thickening
Skeletal abnormalities
64
What is the TLCO and KCO in intra- and extra-pulmonary restriction
TLCO is reduced in both
In extra KCO is high
In intra KCO is reduced because alveoli are abnormal
65
What is bronchiolitis
Inflammation of the bronchioles - a feature of chronic bronchitis
Often in children
66
Describe localised airway obstruction
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
Describe diffuse obstructive airways disease
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
Describe chronic bronchitis
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
Describe emphysema
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
What are the types of asthma
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
What is bronchiectasis
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
Cystic fibrosis
Multi system disorder due to impaired ion transport which leads to viscous mucus
73
What are the types of pneumonia
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
Describe acute respiratory distress syndrome
Hypoxia, non-cardiogenic pulmonary oedema, diffuse bilateral infiltrates on x-ray
Causes- direct - pneumonia, aspiration, ventilation
Indirect - sepsis, trauma, pancreatitis, acute hepatic failure
75
What is the treatment for TB
RIPE
Rifampicin, Isoniazid, Pyramidizine, Ethambutol
All 4 for 2 months
Then rifampicin and isoniazid for 4 more months
76
Describe squamous cell carcinoma
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
Describe adenocarcinoma
30-40% and increasing
Evidence of glandular growth pattern e.g. mucus production
Usually originates in peripheral tissue
78
Small cell carcinoma
Very poorly differentiated
Evidence of neuroendocrine differentiation
Often metastatic at presentation and present late
Strongly associated with smoking
79
Describe mesothelioma
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
Symptoms of lung cancer
```
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
Describe B2 agonists
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
Describe anticholinergics
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
Xanthines
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
Corticosteroids
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
Leukotriene antagonist
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
Mast cells stabilisers
Cromoglicate
Stabilises mast cells, reduced release of histamine, prevent airway inflammation
Treatment of asthma, conjunctivitis, allergic rhinitis
Local irritation, transient bronchospasm
87
Drugs which cause bronchospasm
Beta antagonists - propranolol
NSAIDs
88
Mechanism of NSAIDs
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
Drugs which suppress respiration
Benzodiazepines, opioids
90
Drugs which cause interstitial lung disease
Amiodarone
91
What is VD (volume of distribution)
Total amount of drug in body/drug plasma concentration
92
What are parenteral drugs
Administered somehow other than alimentary canal
93
Mechanisms of resistance
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
Beta lactams
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
Glycopeptides
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
Aminoglycosides
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
Tetracyclines
Tetracycline
Bacteriostatic
Especially Chlamydia
Inhibit binding of tRNA - protein synthesis inhibited
Diarrhoea, nausea, teeth discolouration
Avoid in children and pregnant/lactating women
98
Macrolides
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
Lincosamides
Clindamycin
Bacteriostatic against gram positive and aerobes
Bind to 50S subunit - protein synthesis inhibited
Diarrhoea, colitis
100
THFA inhibitors
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
RNA synthesis inhibitors
Rifampicin
TB (in combination)
Binds to DNA dependent RNA polymerase. Inhibits initiation
Drug interactions
Inactivates oral contraceptive
Hepatitis, nausea, body fluids go orange
102
DNA synthesis inhibitors
Fluoroquinolone
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
Amantadine
Influenza A
Interferes with viral protein channels and effects uncoating
Insomnia, depression, especially in the elderly
104
Enfuvirtide/maraviroc
HIV
Maraviroc affects chemokine co-receptor 5 on CD4 cells
Enfuvirtide affects gp41 attachment
Injection site reactions
105
Aciclovir
Herpes simplex
Treatment and prophylaxis
Viral DNA synthesis halted, premature chain termination, viral DNA polymerase irreversibly inactivated
Resistance can occur
106
Ribavirin
Severe RSV in babies also lassa, Marburg, ebola
Guanosine analogue, inhibits viral nucleic acid replication
Respiratory depression, reticulocytotic, teratogenic
107
Zidovudine
HIV
Reverse transcriptase inhibitor
Nucleoside inhibitors
Incorporated into viral DNA, premature chain termination
Bone marrow, renal and hepatic toxicity
Resistance widespread
108
Nevirapine, efacrine, etravarine
HIV
Bind to non-substrate binding site of reverse transcriptase therefore inhibiting it
Rash, nausea, hepatitis, pancreatitis
109
Ritonavir
HIV
Protease inhibitors
Prevents cleavage of protein products
Severe side effects
110
Oseltamivir (tamiflu), zanamivir
Influenza A and B
Inhibits neuraminidase preventing release of viral particles
Resistance can develop
111
Interferons
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
Polyenes
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
Azoles
Clotrimazole, fluconazole
Thrush (candida)
Acts by inhibiting demethylase enzyme required for ergosterol synthesis
114
Echinocandins
Caspofungin, anidulafungin, micafungin
Candida and aspergillus
Target beta glycan synthases, inhibit cell wall construction
115
Flucytosine
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
Terbinafine
Fungal nail infections
Inhibits equalene epoxidase required in ergosterol synthesis
GI upset
117
Griseofulvin
Fungal skin and nail infections
Natural product if penicillium species z incorporated into new keratin
118
Idiopathic pulmonary fibrosis
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
Hypersensitivity pneumonitis
Type III
Ab, Ag complex in lung
Pigeon fanciers lung, farmers lung, mushroom lung
Most resolve when agent of exposure is removed
120
P = DKa/d
```
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
Carcinoid tumours
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
What are the lymph nodes numbered less than 9?
In the mediastinum
| If these are involved be tumor is less treatable and often not curable
123
What are the ways of measuring blood O2
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
What is physiological dead space
Alveolar dead space (alveoli with lack of blood supply, rate in youth) + anatomical dead space (conducting airways where no has exchange takes place)
