Week 12 Flashcards

1
Q

which patients are clinically determined higher risk for CVD?

A
diabetes >60y/o
diabetes with microalbulineamia 
ABTSI >74
CKD
previous dx of familial hypercholesteraemia 
serum cholesterol >7.5 
SBP >180 DBP> 110
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2
Q

what are the lifestyle modifications given to low risk CVD patients?

A

at least 30 min of moderate exercise most days
smoking cessation
reduce was it circumference to 94 for men and 80 cm for women
BMI less than 25kg/m2
<4g/day of salt
no more than 2 SD/day of alcohol

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3
Q

what is the aim for lipid therapy?

A
total cholesterol <4
HDL >1
LDL <2
TG <2
nonHLD chol <2.5
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4
Q

high risk: lipid lowering recipients?

A

CHD or peripheral vascular disease which has become symptomatic
DM
family hx of CHD which has become symptomatic by the age of 55 in 2+ 1st degree relatives OR by the age of 45 in 1+ 1st degree relatives

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5
Q

5 palliative care principles?

A
focus on QOL
whole person approach 
care encopasses dying per and those that matter to them 
patient autonomy and chouce
open and sensitive community
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6
Q

4 common medications used in palliative carE?

A

nausea
pain
agitation
resp secretions

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7
Q

some points about palliative care?

A

provide relief from pain
not to prolong life
provide support for the patient and the family
incorporate spiritual and psychological aspects into care
team approach to address the needs of the patient and family
enhance QOL
application early in the course of illness

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8
Q

ARP?

A

acute resuscitation plan
- queensland health document for hospital

provides consistent documentation of clinical recommendations to withhold/ withdraw life sustaining measures, CPR and assisted ventilation
not a legal document but aims to guide clinicians if patient were to lose mental capacity

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9
Q

AHD?

A

advanced health directive
- clunk legal document
document that states your wishes and directions regarding your future health care for various medical conditions

may wish to happy AHD when you are unable to decide for yourself or you may want to only apply it when you are terminally ill

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10
Q

enduring power of attorney?

A

for welfare and finances

act on someones behalf regarding legal and financial matters

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11
Q

state of choice document?

A

value based document that records a patients wishes/ choices for their health care into the future

not a legal document but promotes EOL care discussion

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12
Q

consent order of priority?

A

patient has mental capacity and directs care
valid AHD
guardian appointed by tribunal
attorney appointed under most enduring document
statuary health directive
adult guardian

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13
Q

informed consent?

A

competence and capacity
voluntariness
disclosure of info
understanding and accepting info

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14
Q

what patients need in palliative care?

A
mental capacity
advanced care planning
will
ARP
EPoA
AHD
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15
Q

6 steps in verification of death?

A
no breath sounds 2 min 
no breathing effort/ breath felt
no carotid pulse
ho heart sound 2 min
fixed dilated pupils
no respones to noxious stimuli 
re-check patient identification
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16
Q

FLIP?

A
identify the problem
analyze the problem
design solutions
plan your program 
evaluate
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17
Q

evaluation in flip?

A

SMART- specific, measurable, achievable, relevant, timely

outcome evaluation - did you achieve your goals
impact evaluation - did you active your objective
process evaluation - did your strategies work?

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18
Q

type of genetic mutation in PID?

A

recessive mutations of single genes

many are subclinical

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19
Q

what is the most common PID?

A

selective IgA deficiency

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20
Q

what is the most common clinical manifestation in IgA deficiency?

A

autoimmune diseases

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21
Q

examples of some encapsulated extracellular bacteria

A
these are the most virulent
Escherichia coli (in some strains)
Neisseria meningitidis.
Haemophilus influenzae.
streptococcus pneumonia
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22
Q

what kind of pathogen is mycobacterium TB?

A

intracellular

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23
Q

what immune deficiencies results in mycobacterium?

A

(IC bacteria)
T cell def
NKC def
IL12

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24
Q

what defencies result in infection with encapsulated EC bacteria?

A

B cell or complement def

25
Q

what deficiencies results in viruses (herpes, varicella, CMI)?

A

T cell def

IL12/ NKC defects

26
Q

deficiencies results in enterovirus?

A

B cell def

27
Q

deficiencies that result in fingal infections?

A

T cell def

or phagocyte defects

28
Q

defects resulting in parasitic infection?

A

B cell def

T cell def

29
Q

defects resulting in opportunistic infections?

A

T cell def

30
Q

what are some infections associated with low CD4 T cell count?

A

parasites
IC bacteria (mTB, salmonella)
fungi
viruses ( herpes simplex, cytomegalovirus, herpes zoster)

31
Q

what are some flags indicating immunodeficiency?

A

hx of repeated infections (unusual frequency of infections, recurrent chronic infections, infections affecting a particular body site, unable to respond to standard microbial therapy)

lymphanopenia or hypogammaglobulineamia 
inability to respond to vaccines 
low AB production 
disease affecting particular family 
opportunistic infections 
localized infection may become systemic
32
Q

what is brutons tyrosine kinase important for?

A

development and normal functioning of B cell
XLA - mutation in BTK enzyme = stops B cell maturation and no B cells leave BM = no circulating Ab of all classes
little IgM
almost exclusively occurs in men (1 Xchron)

33
Q

different classes of PID and examples?

A

T cell and combined immunodeficiencies (SCID, AIDS)

B cell immunodeficiencies (hyperIgM, XLA, selective IgA deficiency, hypogammaglobulineamis of infancy)

complement and phagoctytic cell defiencies
(chronic granulomatous disease, leukocyte adhesion deficiency, chediak hagashi syndrome (WBC dysfunction - decreased phagocytosis))

34
Q

different classes of B cell defs in PID?

A
defects in early B cell development (BTK def = XLA)
defects in class switching (defects in the signals that T cell gives B cell = hyperIgM)
common variable immunodeficiencies (defects in AB production)
35
Q

some features of selective IgA def?

A

due to a B cell defect
ind are normally asymptomatic but with mild GI/ resp infections/ allergic disorder; recurrent sinus infections and autoimmune diseases

T cell, phagocyte and complement systems are all normal

36
Q

what are some different forms on severe combined immunodeficiency?

A

defects in Ag receptor gene rearrangements (RAG recombinases)
defects in TCR signalling
defects in cytokine R on the surface of T cells (IL2)
defects in thymic development
deficiencies in MHC expression (def in TAP)

37
Q

hyper IgM syndrome?

A

defects in T cell dependant B cell activation via CD40 and CD40L = no cytokines released to undergo class switching

38
Q

deficiencies in what aspects of complement leave ind susceptible to neisseria?

A
MAC deficiency (C5-9)
C3 deficiency 
alternative pathway deficiency (C1-C4)
39
Q

defects in phagocyte cell number and function

A

defects in phagocyte production (no polymorphonuclear development)
defect in phagocyte adhesion - inability to leave blood and migrate though the tissues - leukocyte adhesion deficienes
defects in phagocyte killing - mutations that affect generation in ROS involved in killing = no killing = wall off organism = chronic granulomatous disease
defects in phagocyte activation = mutations in TLR

40
Q

10 warning signs of PID?

A

4+ new ear infections within 1 year
2+ serious sinus infections within 1 year
2+ months on AB with little effect
2+ pneumonias within 1 year
failure of infant to grow / gain weight
recurrent deep skin or organ abcesses
persists thrush in mouth or recurrent fungal infections of skin
need for IV AB to clear infection
2+ deep seated infections including septicaemia
family hx of PID

41
Q

tx options for PID?

A

isolation - inactivated vaccine
Ab prophylaxis
replacement therapy (IVIG)

42
Q

what are some things that secondary immune deficiencies are associated with?

A
malnutrition
excess exercise
CKD
drugs 
infections
zinc/vit defs
stress
old age
43
Q

some features of immunosenescence

A

relative decrease in circulating CD4, relative increase in circulating CD8
T cell function in vitro and DTH decreases

older ind have high serum Ab titre levels of IgA

44
Q

what are some components affect in the immune system in EC bacteria?

A

phagocytes
AB
complement

45
Q

A child presents with recurrent abscesses from Staphyloccocus aureus abscess. Which of the following is the most likely primary immune deficiency?

A

chronic granulomatous infection (neutrophil/ phagocyte defect)

46
Q

A disease causing recurrent pyogenic infections is caused by dysfunction of

A

Phagocytes are defective in chronic granulomatous disease. Myeloperoxidase may be deficient but the vast majority of patients with myeloperoxidase deficiency do not experience disease

47
Q

Its absence in normal newborns leads the increased risk of infection with gram negative enteric organism

A

IgM is too large to cross the placenta and protects against these organisms

48
Q

Its absence is one of the defects found in autosomally inherited Severe Combined Immune Deficiency

A

ADA (adenosine deaminase) deficiency causes severe dysfunction of B, T and NK cells. Unlike the most common defect in SCID, which is X-linked, ADA deficiency is autosomal

49
Q

which gender are PIDS more common?

A

boys

50
Q

llergic urticaria is best described as being a manifestation of:

A

IgE mediated disorder

51
Q

The tuberculin test is a delayed-type hypersensitivity reaction involving Th1 cells. What is the product injected subcutaneously to elicit this response?

A

small amounts of peptides and carbohydrates derived from M. tuberculosis

52
Q

what defect is associated with chronic granulomatous disease?

A

Neutrophils and macrophages require the enzyme NADPH oxidase to produce reactive oxygen species, for respiratory burst (ie. to destroy bacteria after phagocytosis). Defects in subunits of NADPH oxidase can cause CGD.

53
Q

effects of malnutrition?

A

The deficiency of nutrients has effects on:
• Low availability of complement components + impaired phagocyte function
• Decrease function of B cells + macrophages
• Protein malnutrition → atrophy of primary lymphoid organs and immune cells

54
Q

who is at high risk for CVD?

A
diabetes and >60 y/o
diabetes with microglobulineamia 
CKD
previous dx of familial hypercholesteremia 
SBP >180, DBP >110
serum cholesterol >7.5
ABTSI >74
55
Q

HTN preventative intervention?

A

measure BP on 2 different occsaions
offer lifestyle modifications
medications - BP 140/90 is those with CVD and 130/80 for those with diabetes

56
Q

who is clinically determined high risk for HTN?

A
diabetes and age >60
diabetes with microalbumineria 
moderate/ severe CKD
previous dx of FH
SBP>180; DBP>110
serum cholesterol >7.5
ABTSI >74
57
Q

who is at high risk for lipids/ cholesterol and need lipid lowering mechanisms?

A

coronary heart disease and peripheral vascular disease = symptomatic
DM
Fx of CHD - systematic before age of 55 in 2 relative or before the age of 45 in 1 relative

58
Q

when would you tx any level of hyperlipademia?

A

indigenous
>60
microalbuminuria

59
Q

tests to detect diabetes?

A

fasting blood glucose test
oral glucose tolerance test
AUSRISK