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Year 3 Sem 1 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

primary prevention of MH?

A

hierarchy of needs
connectedness/ family
education/ emotional intelligence
financial stability

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2
Q

secondary prevention of MH?

A

screening

high sensitivity, low specificity

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3
Q

how to dx a MHD?

A 
HPC
MSE
psychological interview
DSM-5 criteria 
look for physiological cause to exclude this
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4
Q

difference between MSE and MMSE?

A

MMSE: tries to look for organic or physiological cause of symptoms; screening measure of cognition but not sensitive enough in detecting mild cognitive impairment

MSE: augments other assessment components (HPC) and gives more info as to what needs to be further assessed - highly specific for mild cognitive impairment

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5
Q

what are the components of MSE?

A 
general appearance
psychomotor behaviour 
mood and affect 
speech 
cognition 
thought pattern
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6
Q

what is the screening for depression?

A

2 Qs
1- in the past month or 2 weeks have been bothered by feeling down, depressed or hopeless?
2- during the past month or 2 weeks have you been bothered by little interest in doing things?

or K-10 - 10 questions for psychological distress (not specific for depression)

or DASS-21 - measures distress along depression, anxiety or stress

or Edinburgh postnatal depression scale (EPDS)

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7
Q

scoring for K10?

A 
<20 = well
20-24= mild mental disorder
25-29= moderate mental disorder (refer to specialist)
>30= severe mental disorder (refer to specialist)
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8
Q

screening for anxiety?

A

K10 or DASS21

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9
Q

screening for psychosis?

A

PRIME

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10
Q

warning signs of psychosis?

A 
inability to concentrate and make decisions 
excessive feelings of guilt
fatigue/ sleep disturbances
noticeable changes in behaviour 
risk taking 
alcohol and drug use
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11
Q

what affects MH in kids/ infants? what can be done?

A

attachment

home visiting programs
parenting education

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12
Q

headspace services?

A

ages 12-25
MH care; general health care; vocational support; social recovery groups; outreach to schools; early interventions services; E-headspace; alcohol; drug counselling

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13
Q

HEAADSS assessment?

A 
home
education/ employment 
activities
appetite/eating
drug/ alcohol
suicide/ self harm 
sexuality/ relationships
sleep
psychosis
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14
Q

CARE in suicide risk?

A

Communicate
Ask Questions
Rate Risk - actual level of risk can be assessed by focusing on (intent, suicide plan, method; access to means; previous attempts; alcohol/ drugs; social supports)
Engage Help - acknowledge your limitations and tell them to seek professional help; be firms of your attention to help them if they don’t; make safety plan together; contact appropriate MH services; make appt for them and ensure that they have transportation; follow up and make sure they went to apt; consider your own needs

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15
Q

how do glucocorticoids affect macrophages/ monocyteS?

A

inhibit COX2 and PLA2

blocks production and release of IL1, IL6, TNF-alpha

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16
Q

how do glucocorticoids affect basophils?

A

inhibit IgE dependant release

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17
Q

how do glucocorticoids affect fibroblasts?

A

inhibit COX2 and PLA2

suppress GF for DNA synthesis and fibroblast proliferation

18
Q

MOA for corticosteroids?

A

bind intracellular GC receptor and initiates complex transcriptional regulation of genes involved in metabolic and inflammatory responses
receptor activation stimulates faster signal transduction in cytosol - phosphorylation of annexin1 (lipocortin) which inhibits leukocyte trafficking

19
Q

difference between natural and synthetic corticosteroids?

A

hydrocortisone and prednislone
synthetic agents have increased potency; better separation of GC from mineralocorticoid action and different formulations

20
Q

some corticosteroid action on inflammatory cells and mediators?

A

decreased transcription of genes for cell adhesion factors and cytokines leading to decreased activation of neutrophils, macs, mast cells = decreased release of neutrophils from BV

decreased activation of Th cells and decreased T cell proliferation and switch from Th1 to Th2 immune response

decreased fibroblast function, production of collagen, and glycosaminoglycans = decreased healing and repair

decreased activity of osteoblasts
decreased complement in plasma

decreased COX2 production = decreased inflammatory prostanoid production

decreased gene transcription = decreased generation of cytokines, TNF-a, cell adhesion factors and GM-CSF

decreased NO, histamine released from basophils and mast cells

decreased IgE production

increased synthesis of anti-inflammatory factors

21
Q

adverse effects of corticosteroids?

A 
opportunistic infections 
osteoporosis 
hyperglycaemia 
muscle wasting/ weakness
growth retardation in children 
CNS effects - euphoria, depression
sudden withdrawal after prolonged therapy = acute adrenal insufficiency via suppression of the HPA axis
22
Q

how do NSAIDs lead to increased CV events?

A

inhibition of PGI2 and PGE2 in BV wall by COX2 without the associated inhibition of TxA2 leads to HTN and thrombosis

23
Q

characteristics of osteoarthritis?

A

progressive loss of articular cartilage and formation of thick subchondral bone/ new bone at joint margins

24
Q

rheumatoid arthristis?

A

autoimmune inflammatory disorder
swollen limited, painful joint movements
symmetrical hand involvement
inflammation and proliferation of synovium and erosion of cartilage and bone

Th cells and Ab enter circulation go to joints and increase cytokine release = swelling and damage to cartilage/ bone erosion

25
Q

what are DMARDS?

A

methotrexate and sulfasalazine

26
Q

what are bMARDS?

A

TNF antagonists and cytokine modulators

27
Q

what drug inhibits folic acid synthesis

A

5-aminosalicyclates - sulfasalazine

28
Q

what drug is a folic acid antagonist?

A

methotrexate

29
Q

precautions of TNF-alpha antagonists?

A

demyelininating disorders (MS), HF, serious infections

30
Q

MOA of rituximab?

A

anti-CD20 monoclonal Ab - binds to CD20 on malignant B cells

31
Q

MOA of abatacept?

A

co-stimulation modulator - binds CD80/CD86 on APC and prevents full activation of CD28 on T cells – decrease cytokine production and inflammation

32
Q

MOA of methotrexate?

A

inhibition of enzymes involved in purine metabolism (AICAR transformylase) = accumulation of adenosine which is usually anti-inflammatory

33
Q

MOA of methotrexate in RA?

A

inhibits breakdown of AICAR
AICAR normally inhibits enzymes that breakdown AMP and adenosine
so more adenosine goes into receptors and cells and produce anti-inflammatory effects

34
Q

gout?

A

painful intermittent attacks of acute arthritis produced by deposition of crystals of sodium urate in synovial tissues of joints

inflammatory response evoked

local accumulation of neutrophil granulocytes which engulf the crystals by phagocytosis

release of tissue damaging toxic O2 metabolites and cause lysis of the cells with release of proteolytic enzymes

35
Q

colchine?

A

used in gout when NSAIDs and corticosteroids fail
inhibit neutrophil migration to site of irate crystals; adhesion of leukocytes and phagocytosis
-inhibits release of chemotactic glycoprotein that is produced during phagocytosis of crate crystals

36
Q

MOA of integrin antagonist?

A

Ab against a4b7 integrin present on the surface of leukocytes and T cells
inhibits adhesion of T cels to MadCAM1 expressed in GIT

37
Q

MOA of leukotriene receptor antagonist?

A

blocks action of leukotriene D4 and secondary ligands LTC4 and LTE4 in lungs and bronchioles

leads to decreased bronchoconstriction and inflammation

38
Q

which peptides do MHC1 molecules present?

A

present peptides derived from cytosolic Ag

39
Q

which peptides do MHCII molecules present?

A

present peptides derived from EC/ intravesicular Ag

40
Q

which molecule binds to release CLIP in MHCII Ag processing pathway?

A

HLA-DM

41
Q

common side effects with cytokine modulators (rituximab and abatacept)?

A

infusion related reactions and infections

42
Q

Give a specific effect of TNF-alpha inhibitors on the inflammatory process

A

inhibition of: leukocyte migration and activation eg endothelial activation and adhesion, neutrophil & macrophage phagocytosis, neutrophil chemoattraction; viral replication; systemic effects eg acute phase response, fever etc, damage to healthy tissue

Year 3 Sem 1 (12 decks)

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