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mpharm year 3 sem 2 > week 10 > Flashcards

week 10 Flashcards

1
Q

are autoimmune disease more common in men or women?

A

women (top 10 causes of death)

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2
Q

how do self tolerance mechanisms work to prevent autoimmune diseases?

A

immune system is able to differentiate self reactive from non-self reactive lymphocytes and therefore get rid of lymphocytes which recognise self antigens (this causes autoimmune diseases)

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3
Q

name 7 organ specific autoimmune diseases

A

o Type one diabetes
o Multiple sclerosis
o Crohn’s disease
- Psoriasis
o Graves’ disease
o Hashimoto’s thyroiditis
o Addison’s disease

o Goodpasture’s syndrome
o Autoimmune haemolytic anaemia

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4
Q

name 3 systemic autoimmune diseases

A

o Rheumatoid arthritis
o Scleroderma
o Systemic lupus erythematosus

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5
Q

describe how tissue damage in rhematoid arthritis occurs

A

antibodies to IgE and citrullinated peptides activate macrophages and promote inflammatory response in the joint

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6
Q

name 3 conventional treatments for rheumatoid arthritis and what they do?

A
  • methotrexate
  • sulfasalazine
  • hydroxychloroquine

found to improve symptoms and decrease joint damage

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7
Q

name 2 biological treatments for rheumatoid arthritis

A
  • anti- TNF-a inhibitors (infliximab)
  • reagent against cell surface molecules (rituximab)
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8
Q

describe the mechanisms of tissue damage involved in systemic Lupus Erythematosus

A

characterised by high titres of autoantibodies, particularly against nuclear antigens which generate an immune complex mediated inflammation in the kidneys, skin, joints and CV system

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9
Q

name 2 conventional treatment options for reducing the incidence of flares and 1 for treatment of flares in systemic Lupus Erythematosus

A

reducing incidence of flairs
- methotrexate
- hydroxychloroquine

treatment of flairs
- corticosteroids

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10
Q

name 3 biological treatment options for Systemic Lupus Erythematosus

A
  • rituximab
  • Epratuzumab
  • belimumab
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11
Q

describe the mechanisms of tissue damage involved in multiple sclerosis

A

disease due to nerve cell demyelination
promoted by myelin-specific T cells, which are able to cross the blood-brain-barrier
resultant inflammation triggers magnified response involving macrophages and cytokines

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12
Q

name one conventional treatment for during symptomatic attacks in multiple sclerosis

A

methylprednisolone

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13
Q

name one conventional treatment for reducing relapse and disease progression in multiple sclerosis

A

glatiramer acetate

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14
Q

name one biological treatment for multiple sclerosis and describe how it works

A

natalizumab- prevents immune system cells from exiting the bloodstream to cross the blood-brain-barrier thereby preventing relapse and cognitive decline

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15
Q

describe the mechanism of tissue damage in type one diabetes

A

participating immune system components include auto-reactive CD4+ T helper cells and CD8+ T cytotoxic cells and also auto-antibody producing B cells

effector T cell recognises peptides from a B cell specific protein and kills the B cell

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16
Q

describe the mechanisms of tissue damage involved in inflammatory bowel disease

A

there is a role for genetic and environmental factors in disease development but symptoms caused by balance between pro- and anti- inflammatory cytokines

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17
Q

state 2 treatment options for inflammatory bowel disease

A

surgery- used in ulcerative colitis
drug treatment- immune supression

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18
Q

what is chronic bronchitis?

A

prolonged inflammation of the bronchial airways which leads to cough and mucus production

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19
Q

what is pleuritis?

A

inflammation of the pleural membranes- can have many causes influencing pulmonary embolism and viral/ bacterial infections

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20
Q

what is bronchiectasis?

A

permanent dilation of the bronchi- often equal of insufficiently treated lung disease that develops into pathological pattern of dilated bronchi- heightens susceptibility to further lung infection

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21
Q

describe the pathology of bronchiectasis

A

Permanent enlargement of the airways. Weakening of the elastic and muscular component of the bronchial walls. Excessive inflammatory response.

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22
Q

name 4 causes of brochiectasis

A

-cycstic fibrosis
- lung infections (bacterial, TB, viral)
- impaired immune system
- aspergillosis (hypersensitivity to the fungus aspergillius)

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23
Q

describe a method which can be used to diagnose bronchiectasis, what are we looking for?

A

CT scan
‘tree in bud appearance’- bronchial wall thickening

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24
Q

state treatment options for mild (1), moderate/ persistent (3) and for severe (5) bronchiectasis

A

mild- airway clearance techniques
moderate/ persistant- inhaled steroid, antibiotics, airway clearance techniques
severe- inhaled steroids, antibiotics, airway clearance techniques, long term oxygen, surgery

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25
describe the inflammatory response involved in pneumonia and what is pneumonia?
pneumonia= inflammation of the alveoli when infection reaches alveoli- inflammatory response occurs- alveoli fill with fluid, white blood cells, proteins and red blood cells this leads to compromised gaseous exchange
26
when does consolidation occur in the lungs?
when the air spaces of the lungs are filled with something other than air
27
state 3 treatments for pneumonia
mild- moderate= treat infectious agent ie antibiotics rest, fluids, steam baths more severe- oxygen therapy
28
what can inflammatory injury to the alveolar/ capillary barrier cause?
acute respiratory distress syndrome
29
how does a problem with chloride channels cause cystic fibrosis?
in normal lung Cl- ions to pass out of the cell with sodium ions and water. In CF lungs, when the CFTR (cystic fibrosis transmembrane conductance regulator) is blocked, the chloride ions can’t leave the cellular compartment. Mucus retention and chronic infection.
30
state 3 treatment options for cystic fibrosis
- oral antibiotics - prednisolone - azithromycin other than these just symptomatic control really
31
what is interstitial lung disease?
when the connective tissue of the lung is compromised interstitium= fluid filled space between cells containing collagen and elastin
32
name 3 treatment options for interstitial lung disease
- corticosteroids (IV for during exacerbations, oral prednisolone for more manageable times) - methotrexate - N-acetylcyctine (mucolytic, modulates inflammation)
33
what is idiopathic pulmonary fibrosis?
scarring on lungs- makes breathing more difficult
34
what kind of cells are present in a patient with idiopathic pulmonary fibrosis ?
influx of fibroblasts, macrophages, myofibroblasts
35
why would we not use corticosteroids in idiopathic pulmonary fibrosis?
ineffective- all corticosteroids and anti-inflammatory treatments
36
name 2 treatments suitable for idiopathic pulmonary fibrosis
- nintedanib - pirfenidone (oral antifibrotic)
37
what mab (biological treatment) can be used in interstitial lung disease?
rituximab
38
what is rituximab effective on?
CD20 on B cells
39
why is it possible to treat asthma with helminths? (theoretically in mice)
they induce an anti-inflammatory response and so help to relax and prevent airway remodelling in asthma
40
what actually is a cough?
deep inspiration followed by build up of intra-thoracic pressure against a closed glottis glottis then opens and rapid expulsion of air- followed by sound
41
name 3 causes of persistent coughs
asthma rhino sinusitis (with post nasal drip) GERD can also be associated with drug causes (ACEi), lung cancer, chronic infections etc
42
treatment of coughs originating above the larynx
- can often be helped with application of medicine which forms a soothing coating over the throat ie lozenges and thick sugar based syrups this is called a demulcent
43
treatment of coughs originating below the larynx
steam inhalation menthol, eucalyptus- stimulate secretion of a thin layer of mucus to protect the inflamed area
44
name 4 drugs which cause suppression of coughs (centrally)
codeine, methadone - activate mu opioid receptors dextromethorphan and pholcodeine act via sigma opioid receptors
45
why is methadone useful in lung cancer patients?
helps with pain relief and sleep due to sedating effects also suppresses cough via mu opioid receptors
46
how is ATP related to cough suppression?
ATP is released into the extracellular space during airway inflammation, where it binds to corresponding P2 receptors to mediate the cough reflex and participate in the formation of cough hypersensitivity. The underlying mechanism may be related to TRPV4-mediated activation of Aδ afferent vagal fibers
47
how do mycolytics such as N-acetylcysteine and carbocystine work to suppress coughing?
they break apart the di-sulphide bonds in the mucins- this decreases viscosity of mucus- making it easier to clear
48
what is dornase alpha and how does it work?
mucolytic enzyme used in cystic fibrosis- works by breaking DNA polymers found in the thickened mucus- making it less viscous and easier to clear
49
why are surfactants so important to alveoli?
they lower surface tension on alveoli- reduced inner pressure within alveolar- without them the small alveoli would collapse and gas exchange would be severely compromised also prevent too much fluid coming from capillaries into the lungs- like a sealant
50
what is infant respiratory distress syndrome?
Alveoli collapse leaving larger spaces that get filled with cellular debris. This Diffuse Alveolar Damage (DAD) - layer of dead cells, proteins and surfactant on the surface of the alveoli (so-called hyaline membranes). Gaseous exchange is severely compromised.
51
how do we treat infant respiratory distress syndrome?
Pre-treatment of the mother before she gives birth with glucocorticoids can enhance surfactant secretion and prevent many cases. Treatment with 40% oxygen therapy, mechanical ventilation, fluids and artificial surfactants are used to combat the symptoms. Artificial surfactants for intratracheal application include: colfosceril palmitate, poractant-α and beractant
52
describe the difference between obstructive and central apnoea
obstructive- collapsible airways, narrow airways central- neurological disfunction/ imbalance no inspiration
53
name 2 respiratory stimulants
doxapram aminophylline
54
name 3 treatment options for pulmonary oedema
oxygen (for acute, significant PO) ACE inhibitor surgery
55
describe the difference between type 1 and type 2 respiratory failure and how they are treated
type 1= low oxygen (hypoxemia), CO2 normal- treat with high flow oxygen (~90%) type 2= low/normal oxygen, HIGH CO2- hypoxemia and hypercapnia- give low flow oxygen (~25%)- can't give too much too quick- pt will stop breathing as their body will think it has enough oxygen and doesn't need to breath (this is because their breathing is being driven by oxygen requirement and not by how much CO2 they need to get rid of)
56
name the 4 stages of the decision making process
stage one- gather relevant facts stage two- prioritise and ascribe values stage three- generate options stage four- choose an option
57
what is metabolic acidosis?
low pH - originating from body/ blood
58
what is metabolic alkalosis?
high pH- originating from body/ blood
59
what is respiratory acidosis?
low pH- originating in the lungs
60
what is respiratory alkalosis?
high pH- originating in the lungs
61
ROME?
Respiratory Opposite= high pH, low CO2- vice versa Metabolic Equivalent= high pH, high CO2- vice versa
62
name 4 causes of respiratory acidosis
- poor breathing- drug related-ie heroine - an obstruction - mechanical ventilation - pulmonary oedema
63
name 5 causes of metabolic acidosis
- diabetic ketoacidosis - severe diarrhoea - renal failure - salicylate overdose - shock
64
name 7 metabolic acidosis symptoms
- headache - decreased BP - hyperkalaemia - warm, flushed skin - nausea, vomiting, diarrhoea - changes in LOC (increased confusion and drowsiness) - muscle twitching
65
name 9 symptoms of respiratory acidosis
- hypoventilation- hypoxia - rapid, shallow breathing - decreased BP - dyspnoea - headache - hyperkalaemia - dysrhythmias (increased potassium) - drowsiness, dizziness, disorientation - muscle weakness, hyperreflexia
66
name 7 causes of respiratory alkalosis
- hyperventilation - anxiety - high altitudes - pregnancy - fever - hypoxia - initial stages of pulmonary emboli
67
name 3 causes of metabolic alkalosis
- loss of gastric juices (vomiting, loss of H+ ions) - potassium wasting diuretics - over use of antacids
68
name 5 symptoms of respiratory alkalosis
- Seizures - Deep, rapid breathing - Hyperventilation - tachycardia - Low or normal BP - Hypokalaemia - Numbness and tingling in extremities - Lethargy and confusion - Light headedness - Nausea, vomiting
69
name 5 symptoms of metabolic alkalosis
- Restlessness followed by lethargy - Dysrhythmias (tachycardia) - Compensatory hypoventilation - Confusion (decrease LOC, dizzy, irritable) - Nausea, vomiting, diarrhoea - Tremors, muscle cramps, tingling of fingers and toes - Hypokalaemia
70
name 4 mabs and what they are effective on in Rheumatoid arthritis
- Anti-TNF-a: e.g., infliximab - Anti-IL-6: e.g., sirukumab - Anti-IL-6 receptor: e.g., tocilizumab - Anti-CD20: e.g. rituximab
71
what does infliximab act on?
anti TNF alpha
72
what does sirukumab act on?
anti IL-6
73
what does tocilizumab act on?
anti IL-6
74
what does rituximab act on?
anti- CD20
75
name 3 mabs and what they are effective on in Systemic Lupus Erythematosus
- Anti-CD20: e.g. rituximab - Anti-BAFF: e.g., belimumab - Anti-CD22: e.g., epratuzumab
76
what does belimumab act on?
anti BAFF which is a B cell activating factor
77
what does epratuzumab act on?
anti CD22
78
name 3 mabs and what they are effective on in Multiple Sclerosis
- natalizumab -Anti-a4-integrin - rituximab- Anti-CD20 - opicinumab: LINGO 1- under investigation/some effects
79
what does natalizumab act on?
anti a4 integrin
80
name 2 mabs and what they are effective on in Type one Diabetes
- otelixizumab - Anti-CD3 - rituximab –Anti-CD20 both generally not sustainable effects
81
what does otelixizumab act on?
Anti-CD3
82
name 2 mabs and what they are effective on in Inflammatory Bowel Disease
- infliximab/ adalimumab- Anti-TNF-a - natalizumab -Anti-a4-integrin
83
name 4 mabs and what they are effective on in Asthma
- omalizumab- Anti-IgE - mepolizumab- Anti-IL-5 - dupilumab- Anti-IL-4Ra - lebrikizumab- Anti-IL-13
84
state 5 counselling points for doxycycline
- take on an empty stomach (1 hour before or 2 hours after food) - take standing or sitting upright - avoid milk, iron, zinc, antacids - photosensitivity- use sun cream and cover up - complete the course
85
state 3 counselling points for prednisolone
- take all tablets in the morning (mimics natural cortisol levels, can keep pt awake if taken at night) - common side effects- GI upset - take after food to reduce likelihood of this
86
Ventolin/ MDI counselling (non steroid)
- Sit up - Shake - Cap off - Deep breath out - Seal around the mouth - Press and inhale - Remove inhaler and hold breath about 10 secs - Relax for 1 min - Then whole routine again for second puff – if required - Cap back on- cleanliness - Clean regularly, remove canister and wash with warm water, dry thoroughly and store safely - Should also explain that this is a reliever- when to use (when feeling breathless)- what to do if it doesn’t help- GP/OOH
87
what is the maximum daily dose of salbutamol?
800mcg - note an accuhaler is 200mcg per dose - this is double a normal MDI
88
steroid inhaler counselling
- normal take the cap off, shake etc all apply here too - Applies to any steroid, or combination inhaler - Rinse out mouth or brush teeth after dose - Take it regularly – explain there will be no immediate benefit or relief - If the patient was previously on only a steroid inhaler and has now been switched to a combination inhaler- ensure they are aware they have to stop lone steroid inhaler- can bring it into the pharmacy to be disposed of
89
name 5 side effects of tiotropium
o dry mouth- is it enough to advise to take regular sips of water or chewing gum or do we need to change to something like o Constipation o Blurred vision- because it increases intraocular pressure o Tachycardia o Urinary problems
90
what is a pulmonary embolism?
a DVT that has moved from (presumably the leg) to the RHS of the heart and then into the pulmonary artery causing a blockage
91
how do we diagnose a PE?
look at all signs and symptoms, risk factors and a chest Xray but ultimately a CTPA (picture before and after inserting dye into artery shows if there is a blockage- prevents the dye moving around) is what we use to diagnose
92
name 7 risk factors for developing a pulmonary embolism
- recent long haul flight - recent surgery - recent period of immobility - high BMI - hormone therapy (combined pill or HRT) - malignancy - pregnancy
93
name the 4 treatments we would use in treating a PE
- thrombosis- alteplase - oxygen therpay- if they hypoxic - very likely - pain relief - start with paracetamol - anticoagulation- apixaban
94
what is the alteplase dose we use in PE treatment?
10mg initially, over 1-2 mins then 90mg over 2 hours
95
why do we need to be careful with certain pain meds in PE?- what are these?
opioids these can cause respiratory depression- already issues related they can be used just need close monitoring for adverse reactions
96
which factor does apixaban inhibit?
factor 10a
97
what is the apixaban dose used in PE treatment?
10mg twice daily for 7 days then 5mg twice daily there after
98
how long do we treat PE with apixaban?
3 months then review- if clot is completely gone then we can stop- if not continue and review in a further 3 months
99
in what situation would we not use alteplase in a PE?
if the patient is well otherwise- use when the patient is hemodynamic unstable- ie- low BP, high HR, HIGH respiratory rate, bilateral PE (one on either side)
100
state 6 apixaban counselling points for PE
- dose will be changing after 7 days- super important - side effects - bruising- see pharmacist or GP- bleeding- what to do if bleeding (any bleeding they cannot stop- nose bleed more than 10 mins)- A&E - avoid NSAIDs - let other HCPs know- dentist etc - avoid pregnancy- conversation about contraception - if missed dose- take when remember but not more than daily dose

mpharm year 3 sem 2 (11 decks)

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