Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Threats and Defence > PBL1: A daughter's concern > Flashcards

PBL1: A daughter's concern Flashcards

1
Q

Define pyrexia:

A

complex physiologic response to disease mediated by pyrogenic cytokines, characterised by rise in core temp - temps above 38.3 degrees celsius

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

Define tonsillectomy:

A

surgical removal of the tonsils - tonsils contain WBCs and when they become infected they swell causing a sore throat

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

Define haemotoma:

A

collection of blood outside the blood vessel

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

Define MRSA:

A

Meticillin- resistant staphylococcus aureus - superbug
1 in 30 people live with it on their skin - can catch it from touching someone who has it, sharing towels, clothes and bed sheets
People in hospital are at higher risk due to it entering blood, wounds, feeding drips etc

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

Define C. difficile:

A

bacterial infection that causes severe bowel problems - watery diarrhoea, stomach cramps, nausea, signs of dehydration, pyrexia, weight loss and/ or appetite
It is a normal commensal bacteria and they don’t cause any harm but when someone takes antibiotics it can disrupt the balance of bacteria within the gut causing the c.dif to multiply
Outside the body they exist as spores which can survive for long periods (e.g. toilet seats)

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

What are the five shape classifications of bacteria?

A 
Spherical (cocci)
Rod (bacilli)
Spiral (spirilla)
Comma (vibrios)
Corkscrew (spirochetes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the characteristic properties of Gram +ve bacteria?

A

Thicker peptidoglycan cell wall
Stains violet with iodine dye (gram stain)
More susceptible to beta-lactam antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the characteristic properties of Gram -ve bacteria?

A

Appear red or pink when stained
Additional phospholipid membrane surrounding their thinner peptidoglycan cel wall
Periplasmic space - separates the peptidoglycan cell wall and the phospholipid cell membrane
Tend to be more dangerous as immune system finds them more difficult to detect
LPS/endotoxin within the outer membrane - heat stable toxin released upon cell disruption, can increase inflammation and lead to septic shock, severe diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are endotoxins?

A

Heat stable toxin associated with the outer membranes of gram -ve bacteria e.g. Neisseria
Only released when the cell is disrupted
Less potent and less specific compared to exotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are exotoxins?

A

Substances secreted by bacteria outside of the cell wall
Usually proteins and are recognised by antibodies
More likely to be released by gram +ve bacteria e.g. cholera toxin, bacillus anthracis
Tend to be heat labile

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

How does binary fission work?

A

Vertical transmission

1) origin of replication within the bacterial chromosome opens and DNA replication begins
2) Cell elongates and the origin moves towards cells ends as DNA is copied. Septum forms down the middle of the cell
3) Cell pinches into two creating 2 bacterial cells

Similar to mitosis however DNA replication occurs at same time as DNA separation - very rapid but high mutation rate - divide every 20 mins
Asexual reproduction

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

What is budding?

A

Asexual reproduction
New cells develop form an outgrowth/bud of the original cell - occurs in yeast cells
Bud only dissociated from parent cell and once mature it buds off - in doing so it leaves behind scar tissue

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

What are different ways genetic variation can occur in bacteria?

A

Transformation
Transduction
Conjugation
Transposable elements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is transformation?

A

Bacteria takes up a piece of DNA floating in its environment
Circular = plasmid - can be copied in bacterial cell and then passed onto daughter cell
If the gene is uptakes is a toxin, then it can incorporate it into its DNA (homologous recombination) making the bacteria pathogenic - process in which bacteria become resistant to antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is transduction?

A

DNA accidentally moved from one bacterium to another by a virus
- virus that infects bacteria - bacteriophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is conjugation?

A

DNA is transferred between bacterial cells through a tube = horizontal transmission

  • transfers of DNA (plasmid) via a pilus - this structure pulls the bacterial cells close together
  • donor cells have fertility factor which is a section of DNA that codes for the sex plus (Special site of DNA transfer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are transposable elements?

A

chunks of DNA that move from one place to another - move bacterial genes that give bacteria antibiotic resistance or make them pathogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the steps to allow bacteria to cause disease?

A

1) Attach to host
2) Invade the tissue
3) Acquire nutrients and grow
4) Avoid host immune system
5) Cause disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens during bacterial attachment?

A

Use appendages - pili and timbre to attach to host

Upon attachment they induce their own methods to ensure survival

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

How do bacteria evade the hosts immune system?

A 
inhibit opsonisation
Inhibit cytokine synthesis
inhibit opsonin binding
Producing binding proteins 
inhibit activation of complement system 
Block cell cycle progression 
Survival in phagocytes 
Inhibit antigen presentation 
Inhibit apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the direct and indirect methods of damage induced by bacteria?

A

DIRECT: produce toxins - membrane damage toxins, neurotoxins (botulinum)

INDIRECT: over activation of inflammation. Molecular mimicry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the difference between passive and active carriers?

A

Passive = transmits the pathogen mechanically e.g. doctor failing to wash his hands - they themselves may not be infections but they pass it onto another patient

Active = infected individual passes on the infection - they may or may not be showing symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What treatments tend to be used for c.diff?

A

Vancomycin or metronidazole

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

How could you catch c.diff indirectly?

A

via spores or fomites or via a passive carrier

Spore-forming bacteria - present in faeces - produced when the bacteria are stressed. They can tolerate extreme conditions - heat resistant, not easily killed by alcohol based sanitisers or routine cleaners

  • faecal-oral route
  • spores are acid resistant and therefore are not killed by stomach acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the main physical barriers?

A

Skin
GIT
Respiratory tract
Genito-urinary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the key drainage and irrigation methods of preventing infection?

A

Irrigation is key in preventing infection
e.g. constant urinary flow from kidneys - if it becomes blocked it can cause urine to build and induce an infection

Tears, saliva, urine, bile, pancreatic secretions, sebaceous secretions and mucus are all important for inhibiting infection - if they get blocked these nutrient rich sites are key for infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are examples of chemical barriers?

A

stomach acid - sterilises partially digested food before it enters the small intestine

Lydozyme within the tears is bactericidal
Bile acids also inhibit growth of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the differential count of neutrophils?

A

50-70%

Range: 1,800 - 7,300 per micro litre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What do neutrophils look like and what is their function?

A

Round with a lobular nucleus (2-5 lobes) with large pale inclusions in the cytoplasm

Functions:

  • phagocytosis - engulfs marked cells
  • Respiratory burst - production of ROS to kill bacteria
  • degranulation - lysosome fuses with engulfed pathogen
  • release chemical enzymes: prostaglandins (increase capillary permeability = inflammation) and leukotrienes (coordinate arrival of other phagocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the differential count of eosinophils?

A

2-4%

0-700 per micro litre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What do eosinophils look like and what is their function?

A

Round, bi-lobed nucleus with large granules in the cytoplasm that stain red

Function

  • Phagocytosis - engulf antibody labelled cells
  • release cytotoxic enzymes: NO
  • reduce inflammation caused by mast cells and neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the differential count of basophils?

A

<1%

0-150 per micro litre

33
Q

What do basophils look like and what is their function?

A

Round, nucleus is generally not visible and dense blue stained granules in the cytoplasm

Function:

  • enter damaged tissue and release granules into interstitial fluid - release histamine (dilation of blood vessels) and heparin (prevent blood clotting)
  • chemicals released attract more eosinophils and basophils
34
Q

What is the differential count of monocytes?

A

2-8%

200-950 per microlitre

35
Q

What do monocytes look like and what is their function?

A

Very large and kidney bean shaped
Abundant pale cytoplasm

Function:
Enter tissue they become macrophages
- phagocytosis
- release chemicals to attract neutrophils, monocytes and other phagocytes
- release chemicals to promote fibroblasts

36
Q

What do mast cells looks like and what is their function?

A

Small, mobile connective tissue cells
Cytoplasm contains granules of histamine and heparin
- release these granules following injury/ infection to stimulate inflammatory response
- coordinate inflammatory response

37
Q

What are DAMPs?

A

Damage associated molecular pattern molecules - released by cells to alert innate immune system

38
Q

What are PRRs?

A

Pattern recognition receptors

  • not present on all cells but tend to be mainly found on macrophages and dendritic cells
  • A major group are toll-like receptors
  • different ones recognise different PAMPs
  • Can be present on the cells surface or within cells
39
Q

What are PAMPs?

A

Pattern associated molecular patterns present on bacteria which act as an alert signal for the innate immune system

40
Q

What are dendritic cells an what do they do?

A

APC - specialised cells that take up and present antigens to T lymphocytes to induce an immune response
- they have PRRs on their cell surface to allow them to detect PAMPs
These are conventional DCs. the other type is plasmacytoid DCs, which secrete interferons

1) Process antigen and present them on their MHC class I and class II
2) Migrate to T cell rich areas of secondary lymphoid tissues and present these antigens to T lymphocytes
3) Transmit danger signals via toll-like receptors

41
Q

What are the four groups of pattern recognition receptors?

A
  • free receptors (in serum)
  • membrane bound phagocytic
  • membrane bound signalling
  • cytoplasmic signalling
42
Q

What is the basic process of how PRRs and PAMPs work?

A

The bacterial (PAMPs) is recognised by one or more the PRRs on a macrophage or DC and then it is endocytose as a phagosome, which then binds with a lysosome forming a phagolysosome. The lysosome is then able to release chemicals to degrade the bacteria

43
Q

What are the membrane bound signalling PRRs?

A

GPCRs - they don’t signal for phagocytosis they signal to increase ability of the cell to kill

  • Receptor activates and therefore interacts with G protein.
  • The G protein becomes activated the GTP binds
  • it allows for respiratory burst to occur
44
Q

What are the key mechanisms of action of these PRRs?

A

Signal for:

  • phagocytosis
  • increased ability to kill (respiratory burst)
  • inflammation
45
Q

What are the 3 roles of inflammation in fighting infection?

A

Signal for additional effector cells to come to the site of infection
Induce local blood clotting to act as a physical barrier
Promote tissue repair

46
Q

What are the cascades triggered by inflammation and what do they do?

A

Kinin system (bradykinin)

  • increases vascular -permeability
  • influx of proteins
  • pain and immobilisation at site of infection

Coagulation

  • prevent blood loss
  • encase microorganisms
47
Q

What are toll-like receptors important in initiating?

A

An allergic response

48
Q

What cells are toll-like receptors found on?

A 
monocytes
DCs
mast cells 
eosinophils 
basophils 
NK cells
49
Q

What are the 2 types of PRRs found in the cytoplasm?

A

Nod like receptors

  • NOD subfamily - LOF mutation can lead to Crohn’s disease
  • NLRP family

Binding of pathogen increases cytokine release

50
Q

What are the 3 major families of cytokines released by the innate immune response?

A

TNF family
IL-1 family
Type 1 interferon family

51
Q

What are some of the effects of the endogenous pyrogens: Il-1beta, IL-6 and TNF-alpha?

A

Liver - increase CRP, mannose binding lectin, which goes onto activate complement and opsonisation

Bone marrow endothelium - neutrophil mobilization for phagocytosis

Hypothalamus - increased body temp to decrease pathogen replication, increase antigen processing and increase specific immune response

Fat, muscle - protein and energy metabolism to increase body temp, to decrease pathogen replication, increase antigen processing and increase specific immune response

Dendritic cells - TNF stimulates migration to lymph nodes and maturation to initiate adaptive immune response

52
Q

What do the plasmocytoid DCs release and what do they do?

A

Release interferon alpha and interferon beta

Bring the T cells to the lymph nodes and T cell zone by expressing CXCR3

53
Q

What are the overall initial responses to a viral infection?

A

Production of IFN-alpha, beta, TNF-alpha and IL-12

Then NK cells mediate killing of infected cells

Then T cell mediated killing of infected cells

54
Q

What is the key function of TLRs?

A

They interact with may adaptor molecules to transduce a signal into the nucleus

55
Q

What is the key function of inflammasomes?

A

Secrete IL-1 and IL-8 upon activation

56
Q

What is the key function of CRP?

A

produced in the liver and is present in serum within hours following tissue damage/infection to promote phagocytosis

opsonises pathogens and activates classical component cascade by binding C1q - binds to phosphocholine portion of some bacterial/fungal cell walls = conc rapidly increases after about 24-48 hours

57
Q

What is the key function of mannose binding lectin?

A

Binds mannose sugar present in large amounts on bacterial and fungal surfaces and this leads to activation of complement system

58
Q

What is the key function of NFK-beta ?

A

Transcription factor that regulates inflammatory response - kept inactive by ikbeta but PRR activation degrades this molecule therefore allowing NFKbeta to move into the nucleus

59
Q

What is the key function of dectin-1 and mannose receptor?

A

Bind to bacterial and fungal cell walls activating phagocytosis and inflammation

60
Q

What are the three different pathways involved in complement activation?

A

Classical pathway
Lectin binding pathway
Alternative pathway

61
Q

What are the main four functions of complement activation?

A

OPSONISATION - surface c3b and insoluble c3b recognised by complement receptors on phagocytes to promote phagocytosis

CELL LYSIS - formation of MAC - swelling and cell destruction

MAST CELL DEGRANULATION - c3 hydrolysed to c3a and c3b. c3a acts on local mast cells to induce degranulation

NEUTROPHIL CHEMOATTRACTANT - c5a attracts neutrophils

62
Q

What are the purposes of an inflammatory reaction?

A

recruit phagocytic cells to clear up debris
repair tissue damage
Kill pathogen

63
Q

What is the role of mast cells in the inflammatory response?

A

Enhance it

Releasing granules of histamine and generating lipid mediators (leukotrienes and prostaglandins)

64
Q

What triggers the activation of mast cells?

A

Direct recognition of microorganisms
Receptors for inflammatory factors
Activated by complement - c3a and c5a
Antigen cross linking of IgE bound to mast cells

65
Q

What are the mediators of the acute response?

A

Histamine - increases blood flow and blood vessel permeability allowing entry of immune cells
Endothelial cell activation - attracts leukocytes and increases cytokine secretion
Increased mucosal secretions - runny nise and eyes

66
Q

What are the cardinal features of inflammation?

A 
Redness - caused by increased blood flow
Heat - caused by increased blood flow
Swelling - movements of fluid into tissue
Pain 
Loss of function
67
Q

Explain the immunology of pain?

A

Swelling squeezes nociceptors
Prostaglandins can activate nociceptors
NSAIDs inhibit production of prostaglandins to reduce pain therefore higher levels also reduce inflammation

68
Q

What are the differences between acute and chronic pain?

A

Acute

  • protective against damage / infected cells
  • infiltration of phagocytes to clear up damage

Chronic

  • infiltration of lymphocytes, macrophages, and plasma cells
  • can arise from acute but it is chronic in nature
  • not beneficial like acute - disease inducing due to persistent inflammatory stimulus
69
Q

Define haemostasis:

A

process of stopping bleeding following blood vessel injury. Normal response involves the interaction of activated plasma clotting factors and platelets at the injury site

70
Q

What are the three overlapping stages of the coagulation cascade?

A

Initiation
Amplification
Propagation

71
Q

What is the normal concentration of platelets?

A

150-450x10 (to power of 9)/L

  • 8-12 day lifespan
  • circulate in inactive form
72
Q

What is the structure of platelets like?

A

Phospholipid bilayer contains glycoprotein receptors - GPIb and GPIIb/IIIa

They can alter their shape due to the actin and myosin within them

Contain 3 storage granules:

  • alpha: clotting factors V, VIII, fibrinogen, vWF, platelet factor 4 (heparin antagonist), PDGF
  • dense: mediators of platelet activation - 5HT, ADP, catecholamines and calcium
  • Glycogen: energy source
73
Q

What happens during fibrinolysis and blood vessel repair?

A

Both processes occur simultaneously

Fibrinolysis: process of degrading fibrin clot using plasmin

  • within clot vicinity, thrombin releases tissue plasminogen activator (tPA) from intact endothelial cells
  • circulating precursor protein plasminogen is then converted into plasmin by tPA which initiates proteolytic dissolution of the clot
  • leads to release of fibrin degradation products which are cleared by the reticulo-endothelial system

Blood vessel repair
- endothelial cells and smooth muscle cells undergo cell division until blood vessel damage is closed

74
Q

What are the anticoagulant mechanisms?

A

1) Anti-thrombin - inactivates thrombin, factors IX, X and XI
2) Protein C system - free thrombin binds thrombomodulin which binds circulating protein C. Thrombin cleaves protein C converting it into active form. It then joins cofactors protein S and inactive factor V to degrade active factor V and VIII to suppress coagulation
3) Natural heparins - present on endothelial surface and bind to and enhance anti-thrombin activity. Also synthesis release of a platelet inhibitory prostaglandin = prostacyclin

75
Q

What is the prothrombin time test?

A

Test for haemostatic system - check bruising or bleeding or monitoring warfarin or iv heparin

Normal prothrombin time = 11-13.5 seconds or INR of 0.8 -1.1
Prolonged PT indicates factor VII deficiency:
- mild liver disease causing reduced synthesis
- mild vitamin K deficiency
- hereditary

76
Q

What is the activated partial thromboplastin time (APTT)?

A

another haemostatic system functioning test
- if prolonged, further tests are required and if it does return to normal then it indicate clotting factor deficiency (VIII, IX, X, XII)

77
Q

What vitamin deficiency can lead to bleeding and why?

A

Vitamin K

- prothrombin factor, factor VII, IX, X need fat soluble vitamin K to be produced

78
Q

What are some of the key points about DNAR forms?

A

Not a legally binding document
Only refers to CPR
Patients (terminally ill) must be fully informed to make a decisions
Issued when a healthcare team feel CPR is not likely to be successful
Has to be issued and signed by a doctor

79
Q

From the 2014 guidelines what are the 5 distinct area for reducing hospital associated infections?

A

1) hospital environmental hygiene
2) hand hygiene
3) use of personal protective equipment
4) safe use and disposal of sharps
5) principles of asepsis

Threats and Defence (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions