clinical relevance / extra pbl Flashcards

1
Q

which airway is an aspirated object more likely to end up

A

right - it is less angulated

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2
Q

ECG signs of sinus invertus

A

R axis deviation; Positive QRS complexes (with upright P and T waves) in aVR; Lead I: inversion of all complexes, aka ‘global negativity’; Absent R-wave progression in the chest leads

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3
Q

what are the main defense mechanisms against inhaled pathogens

A

mucociliary escalator

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4
Q

disease affecting cilia (4)

A

primary cilia diskinesia; cartagenous syndrome; CF; young’s syndrome (yellow nails, pleural effusion)

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5
Q

4 components of the immune response to an infection and how to they work

A

cytotoxic T cells (respond to MHC1 and release perforin);
Natural killer cells (responds to downreg of MHC1 on cells, makes membrane porus);
Interferons (released later e.g. CRP, IL6);
Antibodies (B cells produce specific antibodies, work in numerous ways)

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6
Q

3 actions of interferons

A

signal neighboring cells to put up barriers; signal infected cells to die; recruitment of white blood cells to stimulate long lasting immunity

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7
Q

what should be considered along side CURB65 criteria when deciding whether to admit

A

O2 stats/score; CURB65 alone does not take into all factors

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8
Q

which type pf H.influenzae is fata

A

HI B is fatal -> ear infections + meningitis can be seen in children

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9
Q

what lobes does TB usually affect

A

upper lobes (due to V/Q ratio)

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10
Q

tetracyclines MOA

A

protein synthesis inhibitors - inhibit the initiation of translation in variety of ways by binding to the 30S ribosomal subunit

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11
Q

penicillin MOA (similar for other β-lactams e.g. amoxacillin, cephalosporin etc.)

A

specifically inhibiting the transpeptidase that catalyzes the final step in cell wall biosynthesis, the cross-linking of peptidoglycan (i.e. cell wall synthesis inhibition)

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12
Q

antimycobacterials (Rifampicin) MOA

A

inhibition of the cell wall synthesis and RNA polymerase blockade

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13
Q

quinolones (ciprofloxican) MOA

A

interfere with DNA replication by preventing bacterial DNA from unwinding and duplicating

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14
Q

what is a B-lactam and give some examples

A

antibiotics are antibiotics that contain a beta-lactam ring in their chemical structure - e.g. penicillin, amoxacillin, Oxacillin, cephalosporin

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15
Q

trimethoprim MOA

A

blocking the reduction of dihydrofolate to tetrahydrofolate, the active form of folic acid, by susceptible organisms - works best on gram +ve cocci

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16
Q

Macroldies (erythromyocin, clarythromyocin etc.) MOA

A

binds to the bacterial 50S ribosomal subunit causing the cessation of bacterial protein synthesis

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17
Q

what non-tuberculosis mycobacterium is essential to look out for in CF pts

A

Mycobacteroides abscessus
Bacteria

18
Q

what treatment cannot be given is M.abscessus is grown from the pt

A

lung transplant

19
Q

what can pts w an absent spleen not produce

A

loss of ability to filter out infected red blood cells;
reduced number of white blood cells as the spleen is also responsible for controlling the levels of blood cells

20
Q

asplenic pt vaccines (4)

A

Pneumococcal infections, such as pneumonia with a booster every 5 years;
Flu vaccine annually;
MenACWY;
MenB;

21
Q

asplenic pts antibiotics recommendation

A

recommended to take prophylactic antibiotics for the rest of the life to prevent bacterial infections

22
Q

what RTIs are HIV more likely to develop

A

sinusitis, bronchitis, bronchiectasis and pneumonia

23
Q

how does cough arise

A

postnasal mucous drip, also known as upper airway cough syndrome (UACS), other contributing factors may include bronchial hyperresponsiveness

24
Q

causes of chronic cough (8)

A

astroesophageal reflux disease (GERD); ACE Inhibitor use; asthma; bronchiectasis; COPD; chronic lung infection (e.g. tuberculosis); lung cancer and chronic micro aspiration

25
Q

how thick is the mucous blanket covering the RT

A

5 μm

26
Q

how is resistance reduced in cilia

A

Sublayer of water below mucus

27
Q

what does lactoferrin do?

A

binds to iron, limiting the growth of certain pathogenic bacteria that require it to create transport proteins; promotes the growth of beneficial low-iron requiring bacteria

28
Q

what are the 4 stages to macrophage defense in the alveoli

A
  1. recognition - surface receptors or from complement cascade (C3b);
  2. migration - neutrophils move from capillaries to alveolar space;
  3. ingestion - Microbes englufed but not fully killed until certain signals are received (activation signals from NKCs releasing GMCSF or inteferons);
  4. secretion of mediators - defensins (non-oxidative mech that kills many gram +/-ve species, fungi and certain viruses), surfactant proteins (type II Alveolar cells secrete surfactant proteins A and D to enhance phagocytosis)
29
Q

what is the main way in which neutrophils kills pathogens

A

Oxidation - Neutrophils phagocytose bacteria and kill them with reactive oxygen
metabolites like H2O2

30
Q

what is the effect of the enzyme elastase on the muco-cilia (secreted during an infection)

A

which causes excessive mucus, epithelial cell
damage and significant slowing of beat frequency in cilia

31
Q

what is the purpose of coughing

A

to clear material such as
sputum from the airways; It also helps protect the lungs against aspiration

32
Q

7 causes of cough

A

COUGHIN’
C - COPD
O - oedema
U - upper airways coughing syndrome
G - gastro-oesophageal reflux disease
H - hypertension medications (ACEi etc.)
I - infection
N - non-asthmatic eosinophilic bronchitis

33
Q

sensory components of cough

A

C fibres (affected by factors like bradykinin, histamines, prosoglandins etc.);
RAR (rapidly adapting airway mechanoreceptors) and SAR - mechanically driven due to bronchoconstriction, #oedema, high mucous levels etc.;
vagus nerve relays signals to brain

34
Q

“computing” component of cough

A

tractus solitarus (has nay afferent imputs incl ear, heart etc.); signal sent to pons -> cough signal recieved

35
Q

motor components of cough

A

Inspiratory centre: goes to muscle, pull diagram down, larynx closes -> pressure increase in lungs above 300 mmHg -> Expiratory phase: larynx open, and we cough as pressure changes

36
Q

4 phases of coughing

A

irritation, inspiraiton, compression, expulsion

37
Q

rifapentine side effects (7)

A

Black, tarry stools
coughing up blood
skin rash
sore throat
trouble breathing with exertion
ulcers, sores, or white spots in the mouth
unusual tiredness or weakness

38
Q

Rifampicin side effects

A

thrombocytopaenia; nausea; psychosis

39
Q

Isoniazid side effects

A

hepatic disorder; Severe cutaneous adverse reactions (SCARs)

40
Q

Ethambutol hydrochloride side effects

A

Hyperuricaemia; nerve disorders; visual impairment

41
Q

Pyrazinamide side effects (7)

A

Appetite decreased; arthralgia; dysuria; hepatic disorders; peptic ulcer aggravated; photosensitivity; skin reactions etc.