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Semester 1 > Acute Confusional State > Flashcards

Acute Confusional State Flashcards

1
Q

Process of the formation of fibril

A

Collagen:

  • translation glycosylation
  • procollagen transported to Golgi
  • excreted by exocytosis
  • trimmed to tropocollagen
  • cross-linked to form fibril
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2
Q

Where is elastin made and why does it recoil?

A

Made in fibroblasts as well as smooth muscle cells and chondroblasts

Hydrophobic effect is main driving force for recoil

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3
Q

What is GAG?

A

Glycosamino glycans

  • long chain of repeating disaccharide units
  • highly charged negative and highly hydrated
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4
Q

What adheres actin filaments to the membrane?

A

Plaque

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5
Q

Which cadherins provide cell adhesion in different tissues?

A

E Calderon - Epithelia
N cadherin - neurones and heart muscle
P cadherin - plasma and epidermis
VE cadherin - endothelial cells

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6
Q

What are focal adhesions?

A

Link the ECM through transmembrane proteins (integrins) with cytoskeleton (actin filaments)
Also act as signalling platforms
Link to fibronectin

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7
Q

What are hemidesmosomes?

A

Link the ECM through integrins with cytoskeleton (intermediate filaments)
More stable e.g linking epithelial cells to basement membrane

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8
Q

What are integrins?

A

Large family of proteins that bridges between cytosol and ECM

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9
Q

Stages of ECM in cancer

A
  1. Cell adhesion in cancer stages
    - tumour cells accumulate
    - cells haven’t breached the basement membrane
    - carcinoma in situ
    - cells undergo epithelial to mesenchymal transition
  2. Microinvasion
    - cells convert to mesenchymal cells and expression of cadherins reduced
    - microinvasion starts aided by actin based protrusions called invadapodia
    - secretion of metalloproteases
    - basement membrane breached
    - invading Tumour leading cells express integrins promoting interaction with ECM and non epithelial cells during movement
  3. Progression to metastasis
    - increased motility of tumour cells and decreases e cadherin
    - angiogenesis factors (promote vascularisation)
    - entry into and through lymphatic and blood vessels
    - dissemination - metastasis
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10
Q

Complement cascade

A

Diagram

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11
Q

Which are APC?

A

Macrophages, monocytes and dentritic cells

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12
Q

Action of antibodies

A

IgG1, IgG3 and IgM: activate complement by classical pathway

IgG1 and IgG3: cross the placenta

IgE coats granulocytes (mast cells, eosinophils and basophils)

IgA: secreted across gut mucosal membranes to protect the GI tract

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13
Q

Treatment for delirium

A
  • identify and treat underlying cause
  • Reduce or remove culprit medications
  • Maintain hydration and nutrition
  • Reorientation strategies
  • Maintain mobility
  • Normalise sleep wake cycle

Haloperidol and benodiazepines

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14
Q

Function of myofibroblasts

A

during injury, fibroblasts differentiate into myofibroblasts and they:

  • proliferate
  • secret collagen
  • consolidate damaged area
  • contract to reduce size of damaged area
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15
Q

Functions of tight junctions

A
  • define polarity
  • control passage of substances between cells
  • can link to actin cytoskeleton
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16
Q

What are desmosomes?

A

link between strong intermediate filaments in adjacent cells

17
Q

What are the features of the innate immunity?

A
  • uses constitutent physical barriers
  • recognition is through non-antigen specific activation receptors on cells
  • complement system
18
Q

Functions of the complement cascade proteins

A
  • induce inflammation
  • opsonise pathogens
  • lyse bacteria
  • mediate immune complex clearance
19
Q

Complement cascade activation

A

Classical pathway:

  • antigen:antibody complexes
  • C1q, C1r, C1s, C4, C2

MB-Lectin pathway:

  • MB-lectin binds to mannose on pathogen surfaces
  • MBL, MASP-1, MASP-2, C4, C2

Alternative pathway:

  • pathogen surfaces
  • C3, B, D

All pathways make C3 convertase

20
Q

What does C3 convertase do?

A

C3a, C5a
- inflammatory mediators

C3b:
- opsonisation of pathogens

C5b, C6, C7, C8, C9:
- membrane attack complex, lysis of certain pathogens and cells

21
Q

what are the innate immune cells?

A
  • neutrophils
  • macrophages
  • innate lymphoid cells (ILC1, ILC2, ILC3 and natural killer cells)
  • dentritic cells
22
Q

What is the antigen binding site for B cell receptors?

A

Vh + Vl = antigen binding site

23
Q

What is the process of B lymphocyte development?

A

stem cell –> lymphoid progenitory –> pre-b cell –> early pre-b cell –> late pre-b cell –> immature b cell –> mature b-cell –> (plasma cell) + (memory b-cell)

draw diagram

24
Q

T lymphocyte development process

A

stem cell (bone marrow) –>

thymocyte –> mature t-lymphocyte (thymus) –>

(b cell help) + (cytolysis) + (activation of inflammation) (periphery

25
MHC class I and MHC class II recognition
MHC class I: - recognised by cytotoxic T cells CD8+ - infected host cells MHC class II: - recognised by T helper CD4+ - don't kill but drive immune responses
26
which tissues/cells express MHC molecules?
MHC class I: - macrophages/dentritic cells - B cells - T cells - Neutrophils - All cells that are at risk of viral infection MHC class II: - macrophages/dentritic cells - B cells
27
The different types of immune responses
Type 1: - ILC 1 and NK cells - Cytotoxic T cells and helper T cells Type 2: - ILC 2 - t helper cells - expulsion of extracellular parasites Type 3: - ILC 3 - t helper cells - immunity to extracellular bacteria and fungi
28
What are the four criteria for valid consent?
1. patient must have capacity 2. patient must give consent voluntarily 3. patient must be informed 4. consent must be continuing
29
What are the types of consent?
1. implied 2. express 3. oral 4. written
30
Why might someone lack capacity?
Impairment of, disturbance in the functioning of, the mind or the brain: – Can be permanent – Can be temporary
31
What is the criteria for capacity?
1. Understand the information 2. Retain the information 3. Use or weigh the information 4. Communicate their decision 5. Hold decision consistently
32
What defines incapacity?
Incapacity is when a person is incapable of: 1. Acting or 2. Making decisions or 3. Communicating decisions or 4. Understanding decisions or 5. Retaining the memory of decisions
33
What is hyperactive delirium?
- Hyperactive delirium causes the person to experience agitation, restlessness, aggression, loss of concentration, confusion - May have hallucinations/delusions - Can be difficult for carers to manage
34
What is hypoactive delirium?
- Hypoactive delirium causes a slowing down, sleepiness/lethargy, reduction of consciousness and reduced speech or interaction - Easily missed – depression or fatigue - Poor oral intake -> dehydration - Higher mortality/poor prognosis
35
Who develops delirium?
- Anyone with a severe enough insult - Very common in ITU - Vulnerable and frail people develop delirium with a much smaller insult - Common in people with dementia
36
What are the risk factors for delirium?
- Age > 65 - Background cognitive impairment or dementia - Surgery esp Hip fracture - Comorbidities - Polypharmacy - Sensory impairment - Functional impairment - Sleep disturbance - Hospital admission
37
Identifying delirium?
Use a screening tool SQiD: – Do you think your relative has been more confused recently? - Sensitivity 80%, specificity 71% CAM – confusion assessment method. - Sensitivity 94%, specificity 89% - 4AT – recommended by Scottish Delirium Association and used across Tayside and Fife. - Sensitivity 87%, specificity 70%
38
Assessment for delirium
- Full history – obtain collateral history - Key factors are acute onset, fluctuation, decreased attention - Review medication - Vital signs (EWS) - Physical and neurological examination for signs infection, dehydration, neurological changes - Consider capacity
39
What are the trigger medications for delirium?
 Opiates (morphine, codeine, tramadol) Anticholinergics eg for bladder symptoms, painkillers  Benzodiazepines eg diazepam, nitrazepam  Drugs used in Parkinson’s  Antipsychotics  Antiepileptics  Antihistamines  Antihypertensives (if BP too low or low Na)

Semester 1 (13 decks)

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