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MD3001 > MD3001 Week 5 > Flashcards

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
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2
Q

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

A
  1. relevance
  2. risks
  3. rewards
  4. roadblocks
  5. repetition
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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
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4
Q

salutogenic factor

A

factor linked to health

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5
Q

Framingham Study Definition

A

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

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6
Q

marker of risk

A

associated w/ probability of disease but not causal

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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
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8
Q

4 phases of cardiac rehab

A
  1. hospital stay
  2. recovery at home
  3. exercise
  4. gym
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9
Q

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

A
  1. reliability
  2. validity
  3. responsiveness
  4. sensitivity
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10
Q

define sepsis

A

infection plus SIRS

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11
Q

define severe sepsis

A

sepsis plus organ dysfunction

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12
Q

septic shock

A

severe sepsis plus hypotension despite fluid resuscitation

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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
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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
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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
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16
Q

3 inflammatory markers

A
  1. interleukins
  2. tumour necrosis factor alpha
  3. reactive oxygen species
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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
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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
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19
Q

equation for net pressure

A

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

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20
Q

4 classes of shock

A
  1. cardiogenic
  2. hypovolaemic (blood loss)
  3. obstructive
  4. distributive (loss of blood vessel tone)
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21
Q

types of distributive shock (3)

A
  1. anaphylactic shock
  2. septic shock
  3. neurogenic shock
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22
Q

4 stages of shock

A
  1. initial
  2. compensatory
  3. progressive
  4. irreversible
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23
Q

a cardiac glycoside

A

digoxin

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24
Q

FITT principle of exercise

A

Frequency
Intensity
Time
Type

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25
Q

sign of good level of moderate exercise

A

slightly short of breath but able to chat

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26
Q

3 models of quality of life

A
  1. international classification of functioning disability and health (WHO)
  2. wilson and cleary model
  3. ferrans et al revised wilson and clearly model
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27
Q

where to apply chest leads?

A 
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
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28
Q

early after depolarization

A

abnormal AP in phase 2 (Ca2+ channels) or phase 3 (Na+ channels)

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29
Q

delayed after depolarization

A

high intracellular Ca2+, which can breach threshold to recruit Na+ channels and cause depo

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30
Q

cardiac rehabilitation

A

set of services that enables people w/ coronary heart disease to have best possible help to function in society

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31
Q

implications of misconception about life after MI

A
  • slower recovery
  • reduced rate of work return
  • increased hospitalization
  • poor attendance to cardiac rehab
  • emotional distress
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32
Q

determinants of QOL (5)

A
  1. physical functioning
  2. psychological functioning
  3. social functioning
  4. occupational functioning
  5. perception of health status
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33
Q

2 factors that lower stroke volume in sepsis

A
  1. increase vascular permeability (low EDV)

2. tissue hypoxia (low contractility)

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34
Q

Q wave

A

depo of inter ventricular septum from L to R

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35
Q

lung volume changes in obstructive lung disease

A

this type of lung disease increases residual volume due to lost elasticity

36
Q

common restrictive lung disease

A

sarcoidosis is an example of this type of lung disease

37
Q

define asthma

A

chronic inflammatory disorder of airways in susceptible individuals associated w/ an increase in airway response to variety of stimuli. Reversible.

38
Q

changes in airway structure in asthma (8)

A
  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
Q

define COPD

A

preventable disease characterized by persistent airflow limitations usually progressive and associated w/ chronic inflammatory response in airways and lung to noxious substance

40
Q

likely cause of early onset COPD w/ emphysema in lower lobe

A

a1 antitrypsin deficiency

41
Q

a1 antitrypsin

A

enzyme produced in liver that counteracts proteinases

42
Q

requirements to acquire domiciliary oxygen therapy

A
  1. patient w/ a PO2 <7.3kPa
  2. stopped smoking
  3. must agree with it breathed for >15h/day
43
Q

describe case control study

A

compare histories of diseased and non-diseased

44
Q

advantages of case control study

A
  • simultaneously look at multiple risk factors
  • good for studying rare conditions or diseases
  • useful as initial studies to establish association
45
Q

describe cohort study

A

follow smokers and non smokers and follow for outcome

46
Q

define crossover in EBM

A

each subject receives both intervention and control treatment separated by a washout period

47
Q

advantages of RCT

A
  • unbiased distribution of confounders
  • clearly identified pop
  • more likely to be blinded
48
Q

problems associated w/ RCTs

A
  • impossible w/ rare diseases where patients are limited
  • unnecessary when a treatment produces dramatic benefit
  • stopping trials early
  • expensive, lengthly
49
Q

common features of inhaled allergens (4)

A
  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
Q

example of an enzyme as allergen and how it works

A

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
Q

how do inhaled allergens affect body?

A

they affect nasal epithelium, causing allergic rhinitis (ie. hay fever)

52
Q

how do allergens further down airway affect body?

A

cause allergic asthma

53
Q

chronic asthma

A

driven originally by specific allergen, but may result in hyperactive airways to other irritants

54
Q

2 main symptoms of ingested allergens

A
  1. activation of GI mast cells results in transepithelial fluid loss and smooth muscle contraction (diarrhea/vomiting)
  2. if enters bloodstream, urticaria (hives)
55
Q

explain desensitization to treat allergic reaction

A

inject patient w/ escalating doses of allergen to shift Th2 to Th1 T cells so IgG is made instead of IgE

56
Q

how do Helminths control allergy?

A

they induce a set of T cells (Tregs) that actively suppress Th2

57
Q

what is the window for coronary flow?

A

aortic pressure > ventricular pressure

58
Q

what enzyme do triazole drugs inhibit?

A

inhibit 14 a-demethylase

59
Q

side effects of fluconazole (2)

A
  1. hepatotoxicity

2. elongated QT

60
Q

mechanism of action of echinocandins

A

inhibit beta-1,3-d-glucan synthase

61
Q

mechanism of action of tertian fine

A

inhibit ergosterol pathway and makes toxic products that kill fungus

62
Q

first line treatment for invasive candidiasis

A

echinocandins are first line treatment for this fungal infection

63
Q

treatment for vaginal candidiases

A

treated w/ micanazole or fluconazole

64
Q

treatment for oropharyngeal candidiasis

A

nystatin mouthwash

65
Q

treatment for aspergillosis

A
  • voriconazole
  • amphotericin
  • caspofungin, itraconazole, posoconazole
66
Q

treatment for cryptococcal meningitis

A

treated w/ amphotericin w/ flucytosine/fluconazole

67
Q

define resistance

A

when previous susceptible organism no longer inhibited by a clinical safe level of antibiotic

68
Q

what lung capacity is decreased in COPD but not asthma?

A

difference in FVC b/w COPD and asthma

69
Q

minimum inhibitory concentration

A

lowest concentration of an antibiotic that completely inhibits growth of bacterium

70
Q

what defines breakpoint against antibiotic resistance ? (3)

A
  1. distribution of MICs of target bacteria
  2. achievable therapeutic concentration
  3. max achievable concentration
71
Q

type of resistance that can build against ahminoglycosides

A

enzyme inactivation by addition causes resistance to this drug

72
Q

what drugs can bacteria build efflux resistance against? (3)

A
  1. tetracyclines
  2. quinolone
  3. macrocodes
73
Q

mechanism of resistance for MRSA

A

gene Mec A in methicillin provides alternate pathway for peptidoglycan synthesis when penicillin binding protein is blocked

74
Q

effect of point mutation in both gyrA and parC

A

this causes high level resistance against quinolone

75
Q

transposons and integrons

A

small segments of DNA that encode their own transmission

76
Q

3 effects of Na+ channel blockers on AP in dysrhythmia

A
  1. reduces rate of phase 0
  2. maintains depo, keeping channels in refractory state
  3. increases threshold so harder to depolarize
77
Q

disopyramide

A

class 1a Vaughan Williams drug that treats ventricular dysrhythmias, and prevents recurrent atrial fibrillation triggered by vagal over activity

78
Q

lignocaine

A

class 1b Vaughan Williams drug that treats/prevents ventricular tachycardia and fibrillation during and immediately after MI

79
Q

flecainide

A

class 1c Vaughan Williams drug suppresses ventricular ectopic beats and prevents paroxysmal atrial fib and recurrent tachycardias

80
Q

example and mechanism of class 3 Vaughan Williams drug

A

amiodarone - prolongs AP and thus refractory period

81
Q

what does amiodarone treat?

A

this drug treats Wolff-Parkinson-White syndrome and other supraventricular and ventricular tachyarrhythmias

82
Q

what drug combines class 3 and 2 Vaughan Williams actions?

A

sotalol combines these Vaughan Williams classes

83
Q

what does sotalol treat?

A

used in supra ventricular dysrhythmias and suppresses ventricular ectopic beats and short runs of ventricular tachycardias

84
Q

affects of class 4 Vaughan Williams drugs

A
  1. shorten plateau of AP

2. reduces contractility

85
Q

what dysrhythmias do Ca2+ antagonists treat?

A

prevent recurrence of supra ventricular tachycardias

MD3001 (10 decks)

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