MD3001 Week 5 Flashcards

1
Q

5 A’s to smoking cessation

A
  1. ask about tobacco use
  2. advice to quite
  3. assess willingness to quit
    (5 Rs)
  4. assist to quit
  5. arrange follow up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

5 R’s for patients who decline advice to quite smoking

A
  1. relevance
  2. risks
  3. rewards
  4. roadblocks
  5. repetition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

epidemiological approaches (4)

A
  1. descriptive study
  2. longitudinal study (understand history of condition)
  3. observational studies (identify cause)
  4. monitor or intervene (act/evaluate health promoting interventions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

salutogenic factor

A

factor linked to health

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Framingham Study Definition

A

Study looking at personal behaviour, lifestyle, genetics, etc. to see what is associated w/ health condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

marker of risk

A

associated w/ probability of disease but not causal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Epidemiological information that can be used for performance monitoring (4)

A
  1. quality outcomes framework
  2. smoking cessation services
  3. lifestyle surveys
  4. outcomes for individual clinicians
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

4 phases of cardiac rehab

A
  1. hospital stay
  2. recovery at home
  3. exercise
  4. gym
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

properties of heart related quality of life measurement scale (4)

A
  1. reliability
  2. validity
  3. responsiveness
  4. sensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

define sepsis

A

infection plus SIRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

define severe sepsis

A

sepsis plus organ dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

septic shock

A

severe sepsis plus hypotension despite fluid resuscitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

SIRS is presence of 2 or more of… (5)

A
  1. RR >20/m
  2. HR >90/m
  3. WBC >12x10^9 or <4
  4. > 38C or <36C
  5. PaCO2 < 4.3 kPa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CV features of SIRS (4)

A
  1. high CO
  2. peripheral vasodilation leading to decreased diastolic BP
  3. decreased after load, therefore stroke volume and BP maintained
  4. large difference b/w DBP and SBP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

factors affecting signs of sepsis (5)

A
  1. virulence of pathogen
  2. bioburden
  3. portal of entry
  4. host susceptibility
  5. temporal evolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3 inflammatory markers

A
  1. interleukins
  2. tumour necrosis factor alpha
  3. reactive oxygen species
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

effects of TNFa and IL1 on CVS (5)

A
  1. vasodilation caused by NO
  2. increased vascular permeability
  3. intravascular fluid loss
  4. myocardial depression (tissue hypoxia)
  5. circulatory shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how is sepsis treated? (4)

A
  1. antibiotics
  2. oxygen and positive inotrope (dobutamine) for contractility
  3. IV fluids for SV
  4. vasoconstrictor (NA) for TPR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

equation for net pressure

A

(hydrostatic P of blood - tissue) - (oncotic P of blood - tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

4 classes of shock

A
  1. cardiogenic
  2. hypovolaemic (blood loss)
  3. obstructive
  4. distributive (loss of blood vessel tone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

types of distributive shock (3)

A
  1. anaphylactic shock
  2. septic shock
  3. neurogenic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

4 stages of shock

A
  1. initial
  2. compensatory
  3. progressive
  4. irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

a cardiac glycoside

A

digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

FITT principle of exercise

A

Frequency
Intensity
Time
Type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
sign of good level of moderate exercise
slightly short of breath but able to chat
26
3 models of quality of life
1. international classification of functioning disability and health (WHO) 2. wilson and cleary model 3. ferrans et al revised wilson and clearly model
27
where to apply chest leads?
``` C1 - 4th R intercostal space C2 - 4th L intercostal space C3 - b/w C2 and C4 C4 - 5th L intercostal space C5 - b/w C4 and C5 C6 - L midaxillary at level of C4 ```
28
early after depolarization
abnormal AP in phase 2 (Ca2+ channels) or phase 3 (Na+ channels)
29
delayed after depolarization
high intracellular Ca2+, which can breach threshold to recruit Na+ channels and cause depo
30
cardiac rehabilitation
set of services that enables people w/ coronary heart disease to have best possible help to function in society
31
implications of misconception about life after MI
- slower recovery - reduced rate of work return - increased hospitalization - poor attendance to cardiac rehab - emotional distress
32
determinants of QOL (5)
1. physical functioning 2. psychological functioning 3. social functioning 4. occupational functioning 5. perception of health status
33
2 factors that lower stroke volume in sepsis
1. increase vascular permeability (low EDV) | 2. tissue hypoxia (low contractility)
34
Q wave
depo of inter ventricular septum from L to R
35
lung volume changes in obstructive lung disease
this type of lung disease increases residual volume due to lost elasticity
36
common restrictive lung disease
sarcoidosis is an example of this type of lung disease
37
define asthma
chronic inflammatory disorder of airways in susceptible individuals associated w/ an increase in airway response to variety of stimuli. Reversible.
38
changes in airway structure in asthma (8)
1. mucous plug 2. thickened BM 3. oedematous submucosa 4. smooth muscle hypertrophy and hyperplasia 5. desquamation of epithelium 6. cellular infiltration 7. hyperplasia of mucous gland 8. neovascularization
39
define COPD
preventable disease characterized by persistent airflow limitations usually progressive and associated w/ chronic inflammatory response in airways and lung to noxious substance
40
likely cause of early onset COPD w/ emphysema in lower lobe
a1 antitrypsin deficiency
41
a1 antitrypsin
enzyme produced in liver that counteracts proteinases
42
requirements to acquire domiciliary oxygen therapy
1. patient w/ a PO2 <7.3kPa 2. stopped smoking 3. must agree with it breathed for >15h/day
43
describe case control study
compare histories of diseased and non-diseased
44
advantages of case control study
- simultaneously look at multiple risk factors - good for studying rare conditions or diseases - useful as initial studies to establish association
45
describe cohort study
follow smokers and non smokers and follow for outcome
46
define crossover in EBM
each subject receives both intervention and control treatment separated by a washout period
47
advantages of RCT
- unbiased distribution of confounders - clearly identified pop - more likely to be blinded
48
problems associated w/ RCTs
- impossible w/ rare diseases where patients are limited - unnecessary when a treatment produces dramatic benefit - stopping trials early - expensive, lengthly
49
common features of inhaled allergens (4)
1. a protein which induce T cell response 2. low dose which favours IL4 producing CD4 3. small size so can diffuse 4. high soluble
50
example of an enzyme as allergen and how it works
Der p 1 in faces of house dust mite can cleave tight junctions b/w epithelial cells in airway. Taken up by dendritic cells, presented to T cells, which become Th2, and cause B cells to secrete IgE
51
how do inhaled allergens affect body?
they affect nasal epithelium, causing allergic rhinitis (ie. hay fever)
52
how do allergens further down airway affect body?
cause allergic asthma
53
chronic asthma
driven originally by specific allergen, but may result in hyperactive airways to other irritants
54
2 main symptoms of ingested allergens
1. activation of GI mast cells results in transepithelial fluid loss and smooth muscle contraction (diarrhea/vomiting) 2. if enters bloodstream, urticaria (hives)
55
explain desensitization to treat allergic reaction
inject patient w/ escalating doses of allergen to shift Th2 to Th1 T cells so IgG is made instead of IgE
56
how do Helminths control allergy?
they induce a set of T cells (Tregs) that actively suppress Th2
57
what is the window for coronary flow?
aortic pressure > ventricular pressure
58
what enzyme do triazole drugs inhibit?
inhibit 14 a-demethylase
59
side effects of fluconazole (2)
1. hepatotoxicity | 2. elongated QT
60
mechanism of action of echinocandins
inhibit beta-1,3-d-glucan synthase
61
mechanism of action of tertian fine
inhibit ergosterol pathway and makes toxic products that kill fungus
62
first line treatment for invasive candidiasis
echinocandins are first line treatment for this fungal infection
63
treatment for vaginal candidiases
treated w/ micanazole or fluconazole
64
treatment for oropharyngeal candidiasis
nystatin mouthwash
65
treatment for aspergillosis
- voriconazole - amphotericin - caspofungin, itraconazole, posoconazole
66
treatment for cryptococcal meningitis
treated w/ amphotericin w/ flucytosine/fluconazole
67
define resistance
when previous susceptible organism no longer inhibited by a clinical safe level of antibiotic
68
what lung capacity is decreased in COPD but not asthma?
difference in FVC b/w COPD and asthma
69
minimum inhibitory concentration
lowest concentration of an antibiotic that completely inhibits growth of bacterium
70
what defines breakpoint against antibiotic resistance ? (3)
1. distribution of MICs of target bacteria 2. achievable therapeutic concentration 3. max achievable concentration
71
type of resistance that can build against ahminoglycosides
enzyme inactivation by addition causes resistance to this drug
72
what drugs can bacteria build efflux resistance against? (3)
1. tetracyclines 2. quinolone 3. macrocodes
73
mechanism of resistance for MRSA
gene Mec A in methicillin provides alternate pathway for peptidoglycan synthesis when penicillin binding protein is blocked
74
effect of point mutation in both gyrA and parC
this causes high level resistance against quinolone
75
transposons and integrons
small segments of DNA that encode their own transmission
76
3 effects of Na+ channel blockers on AP in dysrhythmia
1. reduces rate of phase 0 2. maintains depo, keeping channels in refractory state 3. increases threshold so harder to depolarize
77
disopyramide
class 1a Vaughan Williams drug that treats ventricular dysrhythmias, and prevents recurrent atrial fibrillation triggered by vagal over activity
78
lignocaine
class 1b Vaughan Williams drug that treats/prevents ventricular tachycardia and fibrillation during and immediately after MI
79
flecainide
class 1c Vaughan Williams drug suppresses ventricular ectopic beats and prevents paroxysmal atrial fib and recurrent tachycardias
80
example and mechanism of class 3 Vaughan Williams drug
amiodarone - prolongs AP and thus refractory period
81
what does amiodarone treat?
this drug treats Wolff-Parkinson-White syndrome and other supraventricular and ventricular tachyarrhythmias
82
what drug combines class 3 and 2 Vaughan Williams actions?
sotalol combines these Vaughan Williams classes
83
what does sotalol treat?
used in supra ventricular dysrhythmias and suppresses ventricular ectopic beats and short runs of ventricular tachycardias
84
affects of class 4 Vaughan Williams drugs
1. shorten plateau of AP | 2. reduces contractility
85
what dysrhythmias do Ca2+ antagonists treat?
prevent recurrence of supra ventricular tachycardias