Brainscape's Knowledge GenomeTM

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


See full index

ALS > Block 9 > Flashcards

Block 9 Flashcards

1
Q

what is a risk factor?

A

confers an increased risk of developing disease

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

what is meant by predisposition?

A

increased susceptibility to develop disease – usually inherited

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

what is meant by pathogenesis?

A

the pathological mechanisms resulting in clinical disease

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

what is meant by aetiology?

A

the cause of the disease

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

what is meant by disease?

A

consequences of a failure of homeostasis, with potential to impair function

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

what is meant by disease mechanism?

A

the way homeostasis is disturbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does nitro blue tetrazolium dye measure?

A

muscle dehydrogenases

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

what is steatosis?

A
  • Fatty, oily, unhealthy liver
  • Accumulation of fat cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does staining do to cells? (2)

A
  • adds colour
  • reduces transparency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what do acidic dyes react with? (2)

A

cationic or basic components (proteins)

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

what do basic dyes react with? (2)

A

react with anionic or acidic components (nucleic acids, extracellular material)

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

what does the H&E stain stain for? (2)

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

what is Haematoxylin?

A

a basic dye that stains acidic structures

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

what colour does Haematoxylin stain?

A

purplish-blue

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

What is eosin?

A

an acidic dye that stains basic structures

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

what parts of a cell does Haematoxylin stain? (2)

A

nucleus and some parts of cytoplasm RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what colour does Eosin stain?

A

pink

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

what parts of the cell does eosin stain?

A

cytoplasm

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

what are the 4 key targets of cell damage?

A
  • Mitochondria
  • Plasma membrane
  • Ionic channels in cell membranes
  • Cytoskeleton
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the final clue to irreversible cell damage?

A

calcium overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the sublethal changes to a cell? (3)

A
  • pale cytoplasm
  • increased vacuolation (cells become lipid rich)
    = vacuolar degeneration
  • intracellular lipid accumulation (fatty change)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the sublethal changes? (2)

A
  1. Programmed cell death
  2. Autophagy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is Pyknosis?

A

nuclear condensation

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

what is karyolysis?

A

nucleus membrane is still intact, but breakdown of nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is Karyorrhexis?

A

nucelus membrane is broken down

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

what are the types of necrosis? (3)

A
  • coagulative necrosis
  • colliquative/liquéfaction necrosis
  • caveating necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is an example of coagulative necrosis?

A

ischemic kidney disease

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

what are the characteristics of coagulative necrosis? (3)

A
  • Tissue structure is maintained
  • Staining intensity is lost
  • Clear glomerus structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the characteristics of colliquative/liquifaction necrosis?

A

large amounts of fluid or disruptive tissue processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is an example of colliquative/liquifiaction necrosis?

A

cerebral infarct

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

what is an example of caveating necrosis?

A

Tb granuloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how can you classify congenital diseases? (2)

A
  • genetic
  • non-genetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how can you classify acquired diseases? (9)

A
  1. Infections
  2. Vascular
  3. Injury/repair
  4. Tumours
  5. Immunological
  6. Metabolic
  7. Degenerative
  8. Functional
  9. Iatrogenic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is ploidy?

A

number of chromosomes you have

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how can you classify chromosomal abnormalities? (4)

A
  1. ploidy
  2. structural defects
  3. DNA mutations
  4. Gene mutations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are some examples of chromosomal structural defects and how does this lead to abnormalities?

A
  • Deletions, inversions, translocations.
  • Chromosomes are mis formed
  • Lead to wrong genetic alignment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is meant by hyperplasia?

A

increased cell number

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

when does hyperplasia occur? (2)

A
  • puberty
  • adrenal cortical hyperplasia in Cushing’s syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is hypertrophy?

A

increase in cell size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is hypertrophy the underlying cause of?

A

prostatic hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is atrophy?

A

decrease in size and number of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what happens in atrophy?

A
  • muscle wasting
  • thyme atrophy after puberty
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is metaplasia?

A

The replacement of one differentiated cell type with another mature differentiated cell type that is not normally present in that tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

types of metaplasia? (2)

A
  1. squamous metaplasia
  2. intestinal metaplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what happens in squamous metaplasia?

A

Normal columnar epithelium changes to squamous epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what happens in intestinal metaplasia?

A

replacing squamous epithelium with columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what can metaplasia be a precursor of?

A

dysplasia which in turn progress into carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

how can we recognise metaplasia? (2)

A
  • screening
  • surveillance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is dysplasia?

A

An irreversible condition in which cells have abnormal cellular architecture, with nuclear atypia, nuclear hyperchromasia and loss of cell polarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is an example of dysplasia?

A

cervical intra-epithelial neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is neoplasia?

A

New, uncontrolled growth not under physiological control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is iatrogenic disease?

A

The result of treatment or intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what are the layers of skin? (3)

A
  • epidermis
  • dermis
  • hypodermis/subcutis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what epithelium makes up the epidermis?

A

Stratified squamous epithelium, cornified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what epithelial cells are most present in the epidermis?

A

keratinocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what type of epithelium is found in the dermis?

A
  • Dense irregular connective tissue supported by fibroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what else does the dermis contain?

A
  • Contains glands etc, sensory nerves, some immune cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

where in the dermis is it less dense and what does it contain?

A
  • Less dense in papillary region which contains small blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is contained in the subcutis layer (2)

A
  • Loose connective tissue with adipose cells
  • Larger blood vessels, nerves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

which is the less abundant skin type?

A

thick skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is the fifth layer contained in thick skin called?

A

stratum lucidum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

where can you find the stratum lucidum between?

A

between the stratum granulosum and stratum corneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what does thin skin contain? (2)

A
  • Contains hair and glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what are the layers of the epidermis? (5)

A
  • Cornified layer (Stratum corneum)
  • Granular layer (Stratum granulosum)
  • Spinous layer (Stratum spinosum)
  • Basal layer (Stratum basale)
  • Dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

which is the deepest layer of the epidermis?

A

basal layer (stratum basale)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what happens to the newly formed daughter cells in the basal layer? (2)

A

either become new stem cells remaining in the basal layer or differentiate to form the epidermal layer above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what does the spinous layer contain?

A
  • Prominent intracellular keratin filaments
  • desmosomes (cell junction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what types of cells can be found in the spinous layer? (2)

A
  • tonofibrils
  • desmosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what type of cells are found in the granular layer (Stratum granulosum)?

A
  • Keratohyalin granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what do Keratohyalin granules contain and what is their function?

A
  • contain proteins which bind to and aggregate keratin filaments)
  • lamellar bodies (contain lipid important for the hydrophobic barrier to water)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what are the most abundant cells found in skin?

A

Keratinocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what cells can be found the epidermis? (4)

A
  • keratinocytes
  • melanocytes
  • immune cells
  • merkel cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what do keratinocytes produce?

A

keratin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what do keratinocytes undergo?

A

a continuous process of production and shedding in equilibrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what processes occur in the stratum corneum? (2)

A
  • desquamation - shedding of dead corneocytes
  • cornification - formation of the cornfield envelopes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what processes occur in the stratum granulosum? (2)

A
  • lipid extrusion
  • expression of late differentiation markers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what processes occur in the stratum spinous?

A

reinforcement of the cytoskeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what processes occur in the stratum basale?

A

constant cell renewal by proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what are melanocytes responsible for? (2)

A
  • skin pigmentation
  • protection against UV damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what do melanocytes synthesise?

A

the pigment melanin, packed into melanosomes that are transferred into neighbouring keratinocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what are langerhan cells?

A

antigen presenting cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what are langerhan cells important for?

A

immune defence against surface pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

where do langerhan cells arise and migrate?

A
  • arise - bone marrow
  • migrate - via blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what are Merkel cells and where are they found?

A

Specialised cells found in the basal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what are merkel cells associated with?

A
  • with nerve fibres responsible for fine touch sensation
  • e.g. fingers, toes, lips, mouth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

which layer is mainly responsible for the barrier of skin?

A

cornfield layer (stratum corneum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is the epidermis rich in and what does this form?

A

Rich in lipids and insoluble proteins
- which form a hydrophobic layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what pathological changes can occur in the epidermis? (6)

A
  1. Imbalance between cell renewal and cell loss e.g. scaling
  2. Breaking of cell-cell junctions e.g. blisters
  3. Trauma and wound repair – basal layer needed for regeneration
  4. Failure of barrier functions – usually consequences of above
  5. Infection and inflammation – various external and systemic causes
  6. Development of tumours – keratinocytes or melanocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what is the epidermal?

A

dermal junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what are downward projections in the epidermal called?

A

rete ridges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what are upward projections in the epidermal called?

A

dermal papillae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Why are these projections more prominent in thick skin than thin skin? (2)

A
  1. They create more surface area for the attachment of the epidermis to the dermal layer.
    To facilitate good adhesive contact between the dermis and epidermis
  2. Epidermis has no blood vasculature, allow for blood vessels to nourish and support the epidermis of our skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what is the P layer?

A

papillary dermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what is the papillary dermis made up of? (2)

A

Relatively loose connective tissue made up of fine collagen fibres and elastin fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what does the papillary dermis contain? (3)

A
  • extensive capillary networks
  • lymphatics
  • nerve endings.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what is the R layer?

A

Reticular dermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what is the papillary dermis made up of ? (2)

A

Dense irregular connective tissue containing prominent thick bundles of collagen fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what doe the reticular dermis contain? (2)

A
  • fibroblasts
  • immune cells (including mast cells, macrophages, lymphocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what is the role of fibroblasts in the dermis?

A

produce collagen and elastin which provide strength and flexibility to the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what is the dermis the site of? (3)

A
  • nerves
  • glands
  • skin vasculature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what are the pathological changes within the dermis?

A
  • Trauma and wound repair - Collagen synthesis by fibroblasts, initial scar effect
  • inflammatory and immune responses - Can be due to infection (e.g. of skin appendages or following trauma) or other
    immune processes (e.g. hypersensitivity, autoimmune)
  • vascular involvement - Important in both wound healing and inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what is the hypodermic made up of and what is it seperated by?

A

mature adipose tissue which may be separated by fibrous septa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what is the hypodermis function? (3)

A
  • insulator
  • protector
  • an energy store
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what are examples of skin appendages? (2)

A
  1. Hair and nails
  2. Glands –
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what are the three types of glands?

A
  • sebaceous
  • eccrine sweat
  • apocrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

what is a nail plate described as?

A

hard keratinised plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what does the nail plate rest on?

A

stratified squamous epithelium structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

how many layers is the nail plate formed of?

A

four layers as in the epidermis where the nail plate is analogous to the cornified layer of thick skin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

where is continually renewed by cells in the nail plate?

A

Continually renewed by cells within the nail root which proliferate to form the nail matrix.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

what is a hair follicle and where is it formed from?

A

A tubular structure formed from the basal layer of the epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what is at the base of a hair follicle?

A

a bulbous expansion containing the hair papilla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

what do epithelial cells contribute to the hair follicle?

A
  • Epithelial cells within the papilla divide and develop into structured layers which give rise to the anatomy of the hair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what is the anatomy of a hair follicle? (3)

A
  • cuticle
  • cortex
  • medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

what is the cycle of growth of a hair follicle? (3)

A
  • growth - anagen
  • transition - catagen
  • resting - telogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

what do sebaceous glands secrete?

A

sebum a lipid containing substance coats hair to keep it soft, supple and waterproof

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

what structure do sebaceous glands have?

A

branched acinar structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

what is the role of the acini in sebaceous glands?

A

The acini filled with lipid filled vacuoles converge into a small duct which empty into a hair follicle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

what do acinar cells become in sebaceous glands?

A

become distended with increasing lipid contents and die releasing their contents in a process termed holocrine secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

what is the function of the eccrine sweat gland?

A

to secrete sweat directly onto skin surface by means of merocrine secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

what is the structure of eccrine sweat glands?

A

coiled tubular glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

what is evaporation essential for?

A

thermoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what is sweat comprised of? (5)

A
  • water
  • sodium
  • chloride ions
  • urea
  • low mol. metabolites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

where are eccrine sweat glands located?

A

deep reticular dermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

where is expression of apocrine gland found? (3)

A
  • axillae
  • mammary
  • groin regions.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

what does apocrine glands secrete and what does this contain?

A

Secrete viscous, cloudy secretion which may contain pheromones and cause body odour upon reaction with skin bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what is the structure of apocrine glands and when do they become functional?

A

coiled tubular glands which become functional during puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

where are the apocrine glands located?

A
  • deep reticular dermis
  • subcutis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what are some physiological functions of the skin? (5)

A
  • thermoregulation
  • sensation
  • vitamin D synthesis
  • immunological role
  • protection against UV radiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

how does the skin function for thermoregulation? (3)

A
  • Alterations in blood flow through the vessels in the papillary dermis control the skin surface temperature and hence heat loss
  • Sweating causes heat loss by evaporation
  • These processes are under autonomic control
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

how does the skin function for sensation?

A
  • Due to specialised nerve endings and corpuscles: mechanoreceptors (various types), thermoreceptors
    nociceptors (pain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

how does the skin carry out Vit D synthesis?

A
  • Carried out by keratinocytes in the presence of UV light
  • Further conversion to active hormone needed in liver and kidney
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

how does the skin function as a immunological role? (2)

A
  • Langerhans cells (APCs) and lymphocytes in epidermis
  • Macrophages, mast cells and lymphocytes in dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

how does the skin protect against UV radiation?

A

UV absorbing pigment is melanin, made by melanocytes within the epidermis and transferred to keratinocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

what are some pathologies of the skin? (6)

A
  1. Wound healing
    e.g. cuts, burns
  2. Infectious disease
    e.g. streptococcal, warts, herpes, fungal
  3. Inflammatory disease
    e.g. psoriasis, eczema
  4. Immune disorders
    e.g. allergy, lupus erythematosus
  5. Genetic disease
    e.g. keratinisation and blistering syndromes
  6. Cancers
    e.g. basal cell carcinoma, melanoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

what are the types of wound healing in skin? (2)

A
  1. Superficial wounds – epidermis can regenerate from basal layer
  2. Deeper wounds – extending into dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

what are the stages of wound healing? (5)

A
  • Haemostasis
  • Inflammation
  • Fibroplasia
  • Epithelialisation
  • Remodelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

what occurs in the haemostasis stage of wound healing?

A

formation of fibrin clot stopping blood loss and filling wound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

what occurs in the inflammation stage of wound healing?

A

removal of bacteria and damaged tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what occurs in the fibroplasia stage of wound healing?

A

involvement of fibroblasts in laying down new collagen, accompanied by angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what occurs in the epithelialisation stage of wound healing?

A

migration and mitosis of keratinocytes from wound edges and remains of hair follicles etc to form new basal layer, followed by regeneration of other epidermal layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what occurs in the remodelling stage of wound healing?

A

initial new tissue replaced through turnover to create stronger structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

what are the terms used to describe liquid filled lesions? (4)

A
  • blister
  • vesicle
  • bulla
  • pustule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what are liquid filled lesions?

A

Fluid filled cavities within layers of the epidermis or at epidermis-dermis junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

what can solid lesions be due to? (3)

A

Can be increase in epidermal thickness, or tumour, or localised oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

what are the terms used to describe solid lesions? (4)

A
  • papule
  • plaque
  • nodule
  • wheal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

what terms can be used to describe lesions of skin colour? (4)

A
  • macule
  • patch
  • naevis
  • erythema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

what can lessens of skin colour be due to?

A

Can be due to
- change in melanocyte number or activity
- other pigments
- increased blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

what is scaling?

A

shedding of cornified layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what is a callus?

A

hyperplasia of epidermis following pressure or friction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what is erosion?

A

loss of superficial epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

what Is an ulcer?

A

loss of epidermis and papillary layer of dermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what is bruising?

A

leakage of blood into dermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

what is meant by haemodynamic?

A

the flow of blood through the circulatory system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what does fluid homeostasis require? (3)

A
  • Vessel wall integrity
  • Osmolarity (solutes in plasma e.g. ions, proteins, urea, sugars)
  • Maintenance of intravascular pressure (blood volume, smooth muscle tone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what does changes in the fluid homeostasis factors lead to? (2)

A
  • Extravasation (movement of fluid/blood) across the vascular wall
  • Reduction of blood fluidity (blockage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

abnormalities in blood supply, fluid balance or vessel wall integrity can lead to? (8)

A
  • Edema
  • Vascular Congestion
  • Hemorrhage
  • Thrombosis
  • Atherosclerosis - Atherothrombosis
  • Embolism
  • Infarction
  • Shock
157
Q

what is fluid balance maintained by?

A
  • hydrostatic pressure (HP)
  • colloid osmotic pressure (COP)
158
Q

what is hydrostatic pressure exerted by?

A

fluid

159
Q

what is capillary end pressure equal to?

A

the capillary bed

160
Q

what does hydrostatic pressure increase in response to?

A

fluid retention

161
Q

what is edema?

A

increased fluid in interstitial tissue space

162
Q

what is colloid osmotic pressure also known as?

A

oncotic pressure

163
Q

what is the role of colloid osmotic pressure?

A

Drains water from semi-permeable membranes where non-soluble solute is greater

164
Q

what is colloid osmotic pressure determined by?

A

mainly protein concentration albumin

165
Q

what are the causes of extravasation of water from vasculature?

A
  1. Increase in vascular volume/pressure
  2. Decrease in plasma protein content
  3. Changes in endothelial cell function (vessel wall)
166
Q

what are examples of edema? (3)

A
  • Hydrothorax – edema in the thoracic cavity
  • Hydropericardium – edema in the pericardial cavity
  • Pulmonary edema, cerebral edema, etc.
167
Q

what is edema caused by? (5)

A
  1. increased hydrostatic pressure
  2. decreased colloid osmotic pressure
  3. lymphatic obstruction (Lymphedema/Elephantiasis)
  4. sodium retention
  5. inflammation
168
Q

what is inflammation?

A

initial immune response to tissue damage

169
Q

what is redness? (2)

A

Blood vessel dilation and increased blood flow into tissue

170
Q

features of swelling? (2)

A
  • Increased blood vessel permeability
  • Movement of fluid, proteins and leukocytes from the blood to site of tissue damage
171
Q

reduction in BV activates what system?

A

RAAS

172
Q

describe the process of odema? (2)

A
  • Increase sodium, water retention to increase BV
  • Increases HP, causing slow hush of fluid out causing oedema
173
Q

what is hyperaemia?

A

adaptive local increase in blood volume in tissues in response to change in environment

174
Q

what is congestion? (2)

A
  • passive process caused by impaired venous return from the affected area
  • Reduction in BF from a certain area
175
Q

what are hyperaemia and congestion characterised by? (2)

A
  • a local increase in tissue blood volume
  • focused on microcirculation – arterioles, capillaries, venules
176
Q

what is reactive hyperaemia?

A

local vasodilation in response to oxygen debt or accumulation of metabolic waste

177
Q

what is active hyperaemia?

A

increased blood flow/vasodilation in response to period of activation (increase in blood in skeletal muscle during exercise)

178
Q

why can tissue become “redder”?

A

engorgement with oxygenated blood

179
Q

what is congestion caused by?

A
  • Physical obstruction of veins
  • Failure of the heart to pump blood away from affected area
180
Q

what does congestion result in?

A

increased venous pressure

181
Q

what is local congestion?

A
  • blood vessel compression (isolated venous obstruction) e.g.:
  • tumour
  • venous thrombosis
182
Q

what is systemic congestion associated with?

A

often associated with heart failure and can lead to widespread edema

183
Q

what are the features of centrilobular hepatic congestion? (4)

A
  • Mottled “nutmeg” appearance
  • Dark spots represent dilated and congested hepatic venules
  • Increade in VP, prevents blood leaving capillaries
  • Dark spot represents dilated hepatic venules
184
Q

what are the features of chronic pulmonary congestion? (3)

A
  • Blood backup, increased pressure on alveolar capillaries
  • Erythrocytes leak out
  • Alveolar macrophages engulf the erythrocytes, and become engorged with brownish hemosiderin (“heart failure cells”)
185
Q

haemostasias is the complex interactions of what systems? (4)

A
  • Blood vessels
  • Blood platelets
  • Coagulation system (fibrin mesh)
  • Fibrinolytic system
186
Q

what is the purpose of the haemostatic strategy? (2)

A
  • Prevent bleeding
  • Stop bleeding while keeping the blood within a damaged vessel
187
Q

what are the three phases to the homeostatic process?

A
  1. Hemorrhage – the process of bleeding
  2. Thrombosis – the process of clotting
  3. Fibrinolysis – the process of clot dissolution
188
Q

what is a haemorrhage?

A

extravasation of blood (due to vessel rupture)

189
Q

what effect does a loss of 15% of BV have?

A

no effect

190
Q

what effect does a loss of above 15% of BV have?

A

hypovolemic shock

191
Q

recurrent blood loss causes…?

A

iron deficiency

192
Q

what are the causes of a haemorrhage? (3)

A
  • Trauma
  • Inflammation
  • Erosion by tumor
193
Q

what is thrombosis?

A

formation of a blood clot within the vessel – attached to the wall

194
Q

what are the types of haemorrhages? (3)

A
  • Petechiae
  • Purpura
  • Ecchymosis - Haematoma/bruises (trauma)
195
Q

what is petechiae?

A

Minute hemorrhage (1-2mm diameter) of skin and mucosa.

196
Q

what is the cause of petechiae? (3)

A
  • thrombocytopenia
  • clotting factor deficiency
  • or increased pressure in capillaries
197
Q

what is purpura?

A

Small hemorrhage (3-10mm diameter)

198
Q

what is the cause of purport? (2)

A
  • trauma
  • vasculitis
199
Q

what is ecchymosis?

A

Subcutaneous haematoma (>1cm)

200
Q

what is the cause of ecchymosis? (3)

A
  • Trauma
  • platelet
  • clotting factor deficiencies
201
Q

what is the colour change of ecchymosis and what is this due to?

A
  • red–blue green–yellow brown
  • due to metabolism of haemoglobin to bilirubin and hemosiderin
202
Q

what is thrombosis?

A

Blood clot formed within the blood vessel, and which remains attached to the vessel wall

203
Q

what is thrombosis a result of?

A

inappropriate activation of the hemostatic system

204
Q

what is thrombosis caused by? (3)

A
  1. Endothelial injury
  2. Abnormal blood flow
  3. Hypercoagulability (blood composition)
205
Q

what is an emboli?

A

Thrombi that detach from the vessel wall

206
Q

types of arterial thrombi? (2)

A
  • mural thrombi - does not occlude vessel = minor or transient clinical events
  • occlusive thrombi - occludes vessel = major adverse clinical events
  • both platelet driven
207
Q

what occurs in a venous thrombi? (3)

A
  • change in blood flow (stasis)
  • leads to hypercoagulation = fibrin-driven response
208
Q

what is a thrombus?

A

cellular mass formed within the blood vessel

209
Q

what is a thrombus composed of? (4)

A
  • platelets
  • red blood cells
  • neutrophils
  • lymphocytes
210
Q

what are the features of arterial thrombi? (3)

A
  • Formed under high shear flow
  • Platelet-rich
  • Around ruptured atherosclerotic plaques and/or damaged endothelium
211
Q

what are the features of venous thrombi? (2)

A
  • Formed under low shear flow (around the valves)
  • Fibrin and erythrocyte-rich
212
Q

what is atherosclerosis?

A

Chronic inflammatory disease, caused by the formation of “fibro-fatty” lesions in the arterial wall

213
Q

what are the features of atherosclerosis? (4)

A
  • Disease state of the arterial wall
  • Begins early in life and can eventually lead to obstructive arterial disease
  • Major cause of heart attack, ischaemic stroke
  • Can occur in all arteries (aorta, carotid, coronary, iliac, femoral arteries)
214
Q

what is atherogenesis?

A

Development of an atheroma (atheromatous plaque)

215
Q

what are the stages of atheroma? (3)

A
  1. Initiation – fatty streak
  2. Plaque progression – fibrous cap atheroma
  3. Plaque rupture – thrombogenic potential after rupture (atherothrombosis)
216
Q

what is the process of initiation - fatty streak? (5)

A
  • LDL gets trapped in the sub-endothelial spaces
  • Endothelial dysfunction
  • Lipid entry and modification (formation of lipid layer or fatty streak within the intima layer)
  • Leukocyte recruitment
  • Foam cell formation (monocytes/macrophages that have phagocytised lipids)
217
Q

what are foam cells made up of?

A
  • Lipid macrophages
218
Q

what are dead foam cells made up of?

A

Lipid-rich necrotic core

219
Q

what are dead foam cells encapsulated by?

A

a fibrous cap between the vessel lumen and the core of the plaque.

220
Q

what is a fatty streak?

A

the first sign of atherosclerosis visible to the naked eye

221
Q

what is plaque rupture?

A

*Thrombogenic potential after rupture (atherothrombosis)

222
Q

what can matured/ruptured plaque cause? (3)

A
  • Acute narrowing of the vessel lumen
  • Chronic occlusion (due to the growing plaque)
  • Embolism (of ruptured plaque)
223
Q

what are some clinical complications of atherosclerosis? (5)

A
  • Coronary artery disease - It can cause angina (chest pain), myocardial infarction (necrosis), heart failure
  • Carotid artery disease - It can cause a brain transient ischaemic attack, ischaemic stroke (necrosis)
  • Peripheral artery disease – typically in arms or legs
  • Chronic kidney disease
  • Aneurysm
224
Q

what is an embolism?

A

Solid, liquid or gaseous mass carried in the blood to a site distant from the point of origin

225
Q

all emboli are the result of a dislodged thrombus. This is called what?

A

Thromboembolism

226
Q

features of embolism? (2)

A
  • Lodge in smaller vessels resulting in occlusion and infarction
  • Clinical significance related to where they lodge rather than origin
227
Q

what is a pulmonary embolism?

A

Blockage of an artery in the lungs

228
Q

what % of pulmonary emboli originate in the deep veins of the leg?

A

90%

229
Q

what is ischaemia?

A

Inadequate blood supply to an organ or tissue

230
Q

what does ischaemia result in? (2)

A
  • insufficient supply of oxygen + nutrients
  • accumulation of metabolic waste
231
Q

what is hypoxia?

A

Inadequate oxygen supply to tissue (result of ischaemia)

232
Q

what is an infarct?

A

an area of ischaemic necrosis caused by occlusion of either the arterial supply or venous drainage in a tissue

233
Q

nearly 99% of all infarcts are a result from…?

A

thrombosis or embolism

234
Q

what are important clinical conditions attributed to infarction? (5)

A
  • Myocardial Infarction
  • Cerebral Infarction (ischaemic stroke)
  • Pulmonary Infarction
  • Intestinal Infarction
  • Ischaemic Necrosis of Extremities (Gangrene)
235
Q

what can be aneurysm be a result of? (2)

A
  • Hereditary condition or birth defect
  • Acquired disease: high BP, atherosclerosis, trauma
236
Q

what are the complications of aneurysms? (2)

A
  • Rupture –> life-threatening internal bleeding!
  • Clot formation (thrombosis) and embolization
237
Q

how can you classify aneurysms by morphology? (2)

A
  • Fusiform – bulge all sides of a blood vessel
  • Saccular – bulge on one side
238
Q

how can you classify aneurysms by type? (2)

A
  • True aneurysm: it involves all three layers of the wall of an artery (intima, media and adventitia)
  • False aneurysm (pseudoaneurysm): locally contained haematoma
239
Q

what are the features of false aneurysm? (2)

A
  • Does not contain any layer of the vessel wall.
  • Result of trauma that punctures the artery (needle, knife, bullets), percutaneous surgical procedures (coronary angiography, arterial grafting)
240
Q

how can you classify aneurysms by location? (5)

A
  1. Heart – coronary artery aneurysms, ventricular aneurysms, aneurysm of sinus of Valsalva, aneurysms following cardiac surgery, etc.
  2. Aorta –abdominal aortic aneurysms, thoracic aortic aneurysms
  3. Brain – intracranial (“berry”) aneurysms, Charcot–Bouchard aneurysms
  4. Legs – popliteal aneurysm (popliteal arteries behind the knee)
  5. Visceral aneurysms – in arteries that supply blood to the bowel or kidneys.
241
Q

what is the definition of shock?

A

clinical state characterised by systemic hypoperfusion (lack of blood flow) leading to reduced delivery of oxygen and nutrients

242
Q

what is shock caused by? (2)

A
  • reduced cardiac output
  • ineffective circulation
243
Q

what can shock lead to?

A

multi-organ dysfunction syndrome (MODS)

244
Q

what are the types of shock? (6)

A
  • cardiogenic
  • hypovolemic
  • obstructive
  • neurogenic
  • septic
    anaphylactic
245
Q

what is cardiogenic shock + cause?

A
  • Failure of the heart to pump sufficient blood.
  • myocardial damage
246
Q

what is hypovolemic shock?

A

Loss of blood or plasma, e.g. hemorrhage, severe burns

247
Q

what is obstructive shock?

A

Obstruction to blood flow in the heart or main pulmonary artery, as occurs in massive pulmonary embolism

248
Q

what is neurogenic shock?

A

severe damage to the central nervous system

249
Q

what is the primary cause of septic shock?

A

bacteraemia (bacteria in the bloodstream) due to infection

250
Q

what is sepsis?

A

uncontrolled systemic reaction to infection leading to life-threatening MODS

251
Q

what is the mortality rate for sepsis?

A

15-25%

252
Q

what is the mortality rate of septic shock?

A

40-55%

253
Q

what is the septic shock pathophysiology? (7)

A
  • Bacterial components
  • Systemic release of cytokines
  • Activation of complement system
  • Activation of endothelial cells leading to systemic vasodilation and hypotension
  • Vascular leakage and edema which reduces intravascular pressure
  • Dysregulation of immune and haemostatic systems
  • Abnormal blood gases, respiratory distress, MODS
254
Q

what is Escherichia coli O157:H7 the cause of?

A

food poisoning

255
Q

what is bacillus subtilis?

A

soil bacterium, not a pathogen

256
Q

what is bacillus anthracis?

A

causative agent of anthrax

257
Q

what does Neisseria meningitidis cause?

A

bacterial meningitis

258
Q

what does Neisseria gonorrhoeae cause?

A

gonorrhoeae

259
Q

what does H.pylori cause? (2)

A
  • peptic ulcers
  • chronic gastritis.
260
Q

what does L. monocytogenes cause?

A

listeriosis

261
Q

what can you identify and class bacteria by? (4)

A
  • Gram positive or negative; acid fast
  • Morphology
  • Nutritional and enzymatic properties
  • Protein and lipid profiling
262
Q

describe the staining process to distinguish gram +ve from gram -ve bacteria?

A
  1. Stain with crystal violet (CV); stain is retained upon washing with alcohol in Gr+ due to biochemistry of cell wall.
  2. If CV is washed out; the counterstain with fuchsin (pink): is Gr-
  3. Usage of Gram stain for diagnostics of bacterial disease is decreasing
263
Q

what is the gram -ve cell wall made up of? (3)

A
  • outer membrane
  • periplasm
  • lipo-polysaccharide
264
Q

what is the gram +ve cell wall made up of? (2)

A
  • Teichoic acid
  • Peptidoglycan
265
Q

give an example of acid fast bacteria

A

Mycobacterium Tuberculosis

266
Q

what is Klebsiella pneumonia?

A

Slimy, mucoid raised translucent growth which strings into long threads when drawn with a loop (due to capsule)

267
Q

what is the causative agent of Lyme disease?

A

Borrelia burgdoferi

268
Q

what is clostridium botulinum?

A

toxin is produced in the gut after ingesting bacterium (honey contaminated with spores)

269
Q

gram +ve species can form spores by being resistant to? (3)

A
  • Heat (100 ˚C)
  • Desiccation
  • Chemical resistant
270
Q

what does all bacterial growth require? (6)

A
  • Carbon
  • Nitrogen
  • Phosphate
  • Sulphate
  • Minerals
  • Trace elements (e.g. iron)
271
Q

what do bacterial genera and species vary in? (3)

A
  • Ability to use simple compounds to grow
  • O2 requirement/tolerance
  • Requirement specific nutrients
272
Q

what are the advantages of using a classification approach in NHS microbiology labs? (3)

A
  • Highly automated
  • accurate (not perfect)
  • fast.
273
Q

what is NHS microbiology labs NOT suitable for? (2)

A
  • very closely related strains/species
  • or rare pathogens (not in database)
274
Q

what is serotyping?

A

antibodies to detect composition of surface structures; useful to distinguish between strains of same species

275
Q

what is the process of serotyping? (3)

A
  1. Capsule, O-antigen and flagella are immunogenic.
  2. Specific antibodies will be raised against these structures.
  3. These specific antibodies are used to determine presence or absence of a structure with a specific antigenic property (related to composition and structure).
276
Q

what are the features of Escherichia coli K12? (2)

A
  • commensal
  • non-pathogenic
277
Q

what does the genome of bacteria consist of? (2)

A
  1. Chromosome (mostly circular, usually one)
  2. Plasmids (circular, not all strains have plasmids)
278
Q

what is genetic content of bacteria important for? (3)

A
  1. Diagnostics
  2. Identifying mechanism of antibiotic resistance
  3. Research: key to understanding virulence mechanisms, pathogen evolution etc.
279
Q

what are the methods for researching genetic content of bacteria?

A
  1. PCR (polymerase chain reaction)
  2. Whole genome sequencing
280
Q

how does PCR work for researching genetic content of bacteria?

A

Amplify (make copies of) specific sequence of your choice from the genome

281
Q

what are the uses for PCR in relation to bacterial genetic content? (3)

A
  • Probe for presence of (unculturable) pathogen’s DNA in samples
  • Probe for absence/presence of genes in an isolate (antibiotic resistance genes) one gets a PCR product or not
  • Sequence PCR product for 16srRNA: unique for each bacterial species
282
Q

what are the applications of whole genome sequencing? (3)

A
  • Epidemiology; to determine if one strain is cause of outbreak.
  • Predictive for AMR, Resistance e.g. under development: TB-profiler*
  • Strain evolution: genetic variations/ mutations
283
Q

what is the importance of genome diversity? (2)

A
  • Acquisition and spread of antibiotic resistance
  • Evolution of pathogens
284
Q

how does genome diversity arise? (3)

A
  1. Mutations
  2. Genetic exchange
  3. Survival of the fittest
285
Q

what is meant by transformation?

A

free DNA is taken up by the cell. Most relevant for plasmids.

286
Q

what is meant by transduction?

A

phage (=bacterial virus) mediate transfer of non-phage DNA between bacteria

287
Q

what is meant by conjugation?

A
  • bacteria having sex- a conjugative plasmid moves from one bacterium to another (“self-transmissable”) - only some plasmids are self-transmissable!
288
Q

what is meant by transposons?

A

jumping genes - mobile genetic units that integrate into the genome

289
Q

what is a fast growth rate of bacteria?

A

doubling time of 20 minutes
(Escherichia coli K12 in rich medium 37C in the lab)

290
Q

how many hours of unlimited growth can be done by a single bacterium?

A

8 hours

291
Q

what is Koch’s postulates?

A

proving that a specific microorganism causes a specific disease (1890)

292
Q

Whether infection occurs and disease develops depends on…? (3)

A
  1. Where bacterium is in/enters the host
  2. Bacterial species or strain
  3. The host
293
Q

What is the first encounter host defenses if physical barrier is breached?

A

Phagocytic and immediate host defenses – innate immune system
* Phagocytes – macrophage and Polymorphonuclear granulocytes
* Soluble factors –complement, lysozyme

294
Q

after the first encounter of a host defence?

A

Adaptive immune response- lymphocyte based

295
Q

what does LD50 mean?

A
  • LD50 = lethal dose 50: - dosage that causes 50% mortality in animal model
296
Q

what is the chain of infection? (5)

A
  1. infectious agent (pathogen)
  2. reservoir
  3. portal of exit
  4. mode of transmission
  5. portal of entry
297
Q

what is an overt or strict pathogen? (2)

A
  • Only associated with human disease (human reservoir) and are not members of a normal, healthy microbial flora
  • E.g. Neisseria gonorrhoeae
298
Q

what is an opportunistic pathogen? (3)

A
  • Members of a host’s normal flora that only can cause disease when introduced into unprotected sites or other changes
  • and of specific concern when normal host defense mechanisms have been compromised (sick, very young, elderly, AIDS, burn patients, …)
  • E.g. Pseudomonas aeruginosa; Clostridium difficile
299
Q

what is a facultative pathogen? (2)

A
  • Can grow and survive in non-host environment as well as in host.
  • E.g. Bacillus anthracis; skin, lung- rare, Salmonella typhimurium
300
Q

To establish an infection and cause disease bacteria must have strategies that facilitate…? (5)

A
  • Attachment and entry into body
  • Local or spread in the body*
  • Multiplication
  • Evasion of host defenses
  • Cause damage in host
301
Q

give an example of an extracellular pathogen

A

Streptococcus pneumoniae (pneumolysin)

302
Q

give an example of an intracellular pathogen

A
  • Salmonella (enterica) serovar
    -Typhimurium
  • Listeria monocytogenes
303
Q

give an example of a toxin producing pathogen?

A
  • Clostridium botulinum
  • Streptococcus pneumoniae (pneumolysin)
  • Vibrio cholera
  • Escherichia coli O157:H7
304
Q

where does Streptococcus pneumoniae colonise? (2)

A
  • nasopharynx w/o causing disease
  • but from there can invade and cause among others pneumoniae, septicemia, meningitis
305
Q

is Streptococcus pneumoniae gram + or -?

A

Gr+ cocci

306
Q

what are some Streptococcus pneumoniae virulence factors? (5)

A
  • Capsule - prevents phagocytosis.
  • Surface adhesins - attach to respiratory lining
  • Secretory IgA protease - cleaves IgA
  • Neuroaminidase - cleaves neuraminic acids from sugar residues on host cell surface
  • Pneumolysins - pore forming; tissue damage
307
Q

what is a capsule?

A

a role in preventing phagocytosis, protection against complement

308
Q

what is an endotoxin?

A

LPS of Gr- bacteria

309
Q

what are the features of endotoxins? (5)

A
  • Cell bound.
  • Heat stable.
  • General symptoms (fever, diarrhea, vomiting). W
  • weakly toxic.
  • [recognized by host TLR4 receptor]
310
Q

what are exotoxins? (3)

A

(Proteins released extracellularly)
* produced by certain Gr+ and Gr- species
* Generally, heat labile, specific targets, usually highly toxic.

311
Q

what are enterotoxins? (3)

A

subgroup of exotoxins that act on the small intestine
* (i.e. C. difficile toxin A, cholera toxin, E. coli toxins)
* Cause change in intestinal permeability leading to diarrhea.

312
Q

what is a toxoid?

A

inactivated toxin useful as a vaccine

313
Q

what is beta-haemolysin? (3)

A
  • Streptococcus pyogenes; Gr+
  • Results in complete breakdown of hemoglobin
  • Apparent from lysis zone around colonies grown on blood agar plates.
314
Q

what is botulinum toxin?

A

Clostridium botulinum: Gr+, anaerobic, spore former

315
Q

how does botulinum toxin work?

A

Neurotoxin (blocks acetylcholine release in synapse)

316
Q

what does botulinum toxin lead to? (2)

A
  • flaccid paralysis
  • respiratory arrest
317
Q

Without supportive care, what % mortality can botulinum toxin lead to?

A

70%

318
Q

what is the clinical use of clostridium botulinum? (4)

A
  • For relief of spasticity
  • Mainly local application,
  • Approved for chronic migraine, excessive sweating, overactive bladder a
  • Cosmetic surgery
319
Q

what is cholera toxin? (3)

A
  • Vibrio cholerae
  • Gram negative (endotoxin)
  • curved rod
320
Q

what is vibrio cholerae’s transmission?

A

water-oral

321
Q

where does cholera toxin colonise?

A

small intestine

322
Q

what does cholera toxin cause?

A

causes increased adenylate cyclase activity; cAMP levels up; changes sodium/chloride flux in-out of cell

323
Q

a symptom of cholera toxin?

A

Massive loss of fluid and electrolytes (diarrhea)

324
Q

what is Salmonella enterica serovar Typhimurium?

A

Gr- rod; food borne, gastroenteritis

325
Q

what is listeria monocytogenes? (2)

A
  • Gr+ rod
  • Listeriosis
326
Q

where do you find Listeria monocytogenes?

A

Food borne (soft cheeses, pate, raw vegetables [silage]…)

327
Q

what does Listeria monocytogenes cause? (2)

A
  • systemic infection initiated in the gastrointestinal tract
  • can lead to meningitis
328
Q

what is the risk population of Listeria monocytogenes?

A

Risk population mainly pregnant women (for fetus), immuno-compromised individuals, leukemia patients

329
Q

is Listeria monocytogenes extracellular or intracellular?

A

a facultative intracellular pathogen

330
Q

what are the strategies for immune evasion? (4)

A
  • Hide: enter cell and stay intracellular
  • Antigenic variation and Phase variation
  • Molecular mimicry
  • Modify or block host immune response
331
Q

what is antigenic variation and phase variation?

A

Bacteria change immunogenicity at high frequency thus avoiding an established immune response (mostly of surface structures)

332
Q

what is molecular mimicry?

A

Decorate the outside with molecules that have (partial) chemical identity with host molecules

333
Q

give an example of a bacteria and molecular mimicry? (2)

A

Haemophilus infuenzae – places host phosphorylcholine and sialic acid on surface
This can trigger immune response against autoantigens.

Group A beta-hemolytic Streptococci (= S. pyogenes) and human myocardium
* Leads to development of rheumatic heart disease
* Antibodies made against bacterium cross-react with meromyosin

334
Q

what are 3 ways to modify or block host immune response (virulence factors)?

A
  • Phagocytosis –capsule
  • Antibody – cleave IgA protease
  • Interfere with host’s cell signaling pathways – Type III secreted effectors, bacterial proteins injected into host cell
335
Q

give examples of different genome sizes of E.coli strains? (3)

A
  • E. coli K12 (commensal)
    genome size is 4.6Mb (4.6 million base pairs)
  • E. coli K1 (Neonatal meningitis) (5.1Mb)
    Urinary tract infection E. coli isolate (5.2Mb)
  • E. coli O157:H7
    (EHEC, food poisoning / hemolytic uremia) (5.4 Mb)
    = E. coli K12 -528 K12 genes +1387 O157 genes
    Source – food poisoning (veg, meat), petting farms
336
Q

what is an antimicrobial?

A

a natural or synthetic chemical that kills or inhibits the growth of microorganisms

337
Q

what is an antibacterial agent?

A

antimicrobials that target bacteria

338
Q

what are antibiotics?

A

traditionally, antibacterial compounds produced by microorganisms.

339
Q

what is a narrow spectrum antimicrobial?

A

an antimicrobial effective against a limited number of bacterial genera (for example either Gram+ or Gram-)

340
Q

what is a broad spectrum antimicrboial?

A

an antimicrobial effective against many bacterial genera

341
Q

what do anti-microbial explot=it?

A

Exploit differences between bacteria and the eukaryotic cell (selective toxicity

342
Q

how do antimicrobials exploit differences? (6)

A

– Identify drug targets
– Find/design drugs that interfere with the target
– Determine efficacy in vitro
– Determine efficacy and safety in (model) organisms
– Determine safety in clinical trials: side effects etc
– Market

343
Q

what does a bactericidal do?

A

kills

344
Q

what does a bacteriostatic do?

A

inhibits growth

345
Q

what are the positives of broad spectrum antibiotics? (3)

A
  • empirical usage
  • polymicrobial infection
  • companies prefer (££)
346
Q

what are the concerns of broad spectrum?

A

resistance

347
Q

what are some pharmacological considerations regarding broad spectrum antibiotics? (7)

A
  • Stability, retention and compartmentalization of drug in host (pharmacokinetics-PK)
  • Dosage and method of administering
  • Accumulation in various tissues and organs
  • Toxicity to host
  • Interference with other drugs
  • Microbiome effects?
  • in vitro Minimum Inhibitory Concentration (MIC)
348
Q

how do we classify antibacterial agents?

A
  1. Bactericidal or bacteriostatic
  2. Chemical structure
  3. Targets
349
Q

what is selective toxicity?

A

exploit (even minor) differences between the prokaryotic and eukaryotic cell.

350
Q

what do antibacterial agents target? (4)

A
  1. anti-metabolites
  2. protein synthesis
  3. nucleic acid synthesis
  4. cell wall synthesis
351
Q

give an example of a beta-lactam?

A

penicillin

352
Q

who discovered Penicillin and in what year?

A

discovered by Alexander Fleming in 1929

353
Q

give an example of a penicillin

A

Amoxycillin

354
Q

what is penicillin produced from?

A

fungus - penicillium notatum

355
Q

when did the use of penicillin start?

A

Use of penicillin did not begin until the 1940s when large scale production was figured out.

356
Q

give an example of a cephalosporin

A

cefradine

357
Q

what are glycopeptides active against? (2)

A
  • Active only against Gram-positive organisms
  • Due to size cannot cross the cell wall/membranes of Gram-negative cells.
358
Q

how do glycopeptides work?

A

physically block the target of enzymes preventing new linkages

359
Q

how are new linkages formed in bacteria? (3)

A
  1. Peptidoglycan layers are built as units in the cytoplasm
  2. Linked to a lipid, brought to the membrane for delivery
  3. All the units are cross linked, gives sturdy mesh of peptidoglycan layer
360
Q

how do beta-lactams work?

A

inhibit enzyme (PBPs penicillin binding proteins) required for transpeptidation

361
Q

how does fosfomycin work? (2)

A
  • Inhibits enzyme (MurA,enolpyruvate transferase)
  • broad spectrum
362
Q

what is fosfomycin used for? (3)

A
  • For treatment of acute cystitis (uncomplicated UTI)
  • E. coli
  • Enterobacter faecalis
363
Q

what subunits do both eukaryotes and bacteria have? (2)

A
  • Eukaryotes have 80s (40s + 60s subunits) ribosomes
  • Bacteria 70s (30s + 50s subunits) ribosomes
364
Q

give examples of 30s inhibitors? (2)

A
  • Aminoglycosides
  • Tetracyclines
365
Q

give examples of 50s inhibitors? (4)

A
  • Chloramphenicol
  • Erythromycin (macrolide)
  • Clindamycin (lincosamides)
  • Oxazolidinones
366
Q

give examples of 50s inhibitors? (2)

A
  • Puromycin
  • Mupirocin
367
Q

give an example of an EF-G elongation factor?

A

Fusidic acid

368
Q

are aminoglycosides bactericidal or bacteriostatic?

A

bactericidal

369
Q

are tetracyclines bactericidal or bacteriostatic?

A

bacteriostatic

370
Q

what class of drug is gentamycin?

A

ahminoglycosides

371
Q

what class of drug is oxytetracycline?

A

Tetracyclines

372
Q

which subunit do gentamicin and oxytetracycline block?

A

30S

373
Q

how do rifamycins work?

A

blocks mRNA synthesis

374
Q

how do sulphonamides work?

A

prevent synthesis

375
Q

are sulfonamides bactericidal or bacteriostatic?

A

bacteriostatic

376
Q

give an example of a sulphonamide?

A

sulfamethoxazole

377
Q

how does trimethoprim work? (2)

A
  • Structural analog of folic acid inhibits enzyme (DHR to THFA).
  • Higher affinity of TMP for the bacterial enzyme than for the human enzyme
378
Q

how do polymyxins work?

A

interfere with cytoplasmic membrane function

379
Q

give an example of a polymyxin?

A

colistin

380
Q

what are some examples of narrow-spectrum antibiotics? (3)

A
  • Older penicillin’s (penG)
  • Macrolides
  • Vancomycin.
381
Q

what are some examples of narrow-spectrum antibiotics? (4)

A
  • Aminoglycosides
  • 2nd and 3rd generation cephalosporins
  • Quinolones
  • Some synthetic penicillin’s
382
Q

give an example of a narrow spectrum penicillin?

A

benzylpenicillin

383
Q

give an example of a broad-spectrum penicillin?

A

amoxicillin

384
Q

what is antibiotic resistance?

A

Relates to sensitivity of a bacterial isolate to an antibiotic at a certain concentration

385
Q

how do you classify antibiotic resistance? (3)

A
  • Resistant
  • Intermediate
  • Sensitive
386
Q

what does classification of antibiotic resistance rely on? (2)

A
  • Based on MIC: Minimum Inhibitory Concentration
  • Relies on lab-based Susceptibility testing
387
Q

what is MIC: minimum inhibitory concentration?

A

Minimum concentration of the antibacterial agent (in a given culture medium) below which bacterial growth is not inhibited.

  • The value depends on bacterial species and the specific isolate, drug properties
  • Determined in NHS labs to assess whether specific antibiotics would be effective for treatment of a particular (patient derived) isolate
  • This is an in vitro value. PK properties no role.
388
Q

what are the three major mechanisms of MIC? (3)

A
  • modifying the antibiotic target
  • limiting access of the antibiotic
  • enzymatic inactivation of antibiotic
389
Q
A

ALS (10 decks)

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