Microbiology and Pathology (before Xmas) Flashcards
1
Q
How do you identify between gram positive and gram negative bacteria?
A
Carry out gram staining and:
Gram positive= purple
Gram negative= pink
2
Q
What is the significance of the catalase test to gram positive bacteria?
A
positive test = staphylococci
negative test= streptococci
3
Q
What occurs when a haemolysis test is done to streptococci
A
Beta or alpha
Beta = Clear
Alpha = green
Beta haemolytic strip becomes Lancfield Group (A(pyogenes), B, C, D, G)
Alpha Haemolytic Strip (complete optochin test)
4
Q
How do you distinguish Staphylococci bacteria?
A
Coagulase Test
positive= staph. aureus (GOLD on blood agar) negative= staph. epidermidis
5
Q
What is Lancefield Grouping?
A
beta haemolytic streptococci differentiation
6
Q
What organism in lancefield group A is resistant to optochin?
A
strep. pyogenes
7
Q
How do we differentiate different gram negative bacterias?
A
MacConkey
1) They may be lactose fermenters or
2) Non lactose fermenters
carry out oxidase test also on non-lactose fermenters
8
Q
Name examples of lactose fermenter gram negative bacteria
A
e. coli
klebsiella
9
Q
Name some examples of non lactose fermenter gram negative bacteria
A
shigella
salmonella
pseudomonas
10
Q
Why do gram positive bacteria stain purple
A
Due to a thick layer of peptidoglycan in cell wall
11
Q
Name the two big groups of gram + bacteria
A
Streptococci
Staphylococci
12
Q
What is the physical appearance difference between staph and strep
A
strep= chains staph= clusters
13
Q
What is inflammation?
A
Local physiological response to tissue injury
14
Q
Why does inflammation occur?
A
To bring all the cells require for healing to the damaged area
15
Q
Benefits of inflammation?
A
destruction of invading microbes
infection and injury
16
Q
Harmful effects of inflammation?
A
- digestion of normal tissue
- swelling
- inappropriate response
- autoimmunity and over-reaction
17
Q
ACUTE vs CHRONIC inflammation?
A
sudden vs slow onset
short vs long duration
usually resolves vs may never resolves
hypersensitivity vs autoimmunity
tissue necrosis and infections vs transplant rejection and persistant acute
18
Q
5 cardinal signs of ACUTE inflammation>
A
1) swelling- oedema
2) redness - dilation of BV’s
3) Heat- hyperaemia (more blood flow)
4) pain- stretch of tissue
5) loss of function
19
Q
What cells are involved in acute inflammation?
A
- neutrophils- phagocytosis
- Macrophages- secrete chemical mediators for chemotaxis
20
Q
What do chemical mediators do?
A
spread the inflammation response
21
Q
Where does histamine get released from?
A
mast cells
22
Q
What is the function of thrombin?
A
increase vessel permeability through platelets
23
Q
What does histamine and thrombin cause?
A
Neutrophil adhesion to endothelial surface
24
Q
What are the 3 main stages of Acute Inflammation?
A
1) changes in vessel calibre- (vasodilation so l=blood to the area)
2) Fluid exudate (vasodilation and chemical mediators means permeability increases, this allows proteins to leave= decreased oncotic pressure)
3) Cellular Exudate (accumulation of neutrophils into Extracellular space)
25
What is Chemotaxis?
Attraction of cells to a site through release of chemicals. e.g. neutrophils attracted to mediators released
26
What are the 3 outcomes of acute inflammation?
- resolution (complete restoration)
- suppuration (pus formation, granulation tissue and scarring)
- organisation (tissue replaced with granulation tissue as part of healing process)
27
What are the 3 primary influences predispose to thrombus formation? (Virchow's Triad)?
- Stasis of Blood flow (atherosclerosis, aneurysm, AF)
- Endothelial Injury (MI, atherosclerosis, smoking)
- Hypercoagulability (genetic and acquired)
28
What are neutrophil polymorphs?
- short lived cells first on the scene of inflammation
- cytoplasmic granules with enzymes that kill bacteria
- release chemicals that attract other cells such as macrophages
29
What are macrophages
- long lived
- present antigens to lymphocytes
- ingest and carry debris
30
What are lymphocytes?
- long lived
- produce chemicals to attract other cells
- can produce memory cells
31
wHAT ARE ENDOTHELIAL CELLS?
Cells that line capillary blood vessels in areas of inflammation
- Sticky= inflammation cells adhere
- Porous= allows inflammatory cells to pass into tissues
- Grow into damaged areas to form new capillary vessels
32
What are fibroblasts?
Long lived cells that form collagen in areas of chronic inflammation
33
What is the difference between repair and resolution?
repair is when tissue is unable to regenerate and is replaced with fibrous tissue. Initiating factor still present
34
Which cells in the body cant regenerate?
Myocardial cells
| neurones
35
What is Thrombosis?
Solid mass of blood constituents formed within intact vascular system during life
36
what is an Embolus?
Mass of material in vascular system able to become lodged within a vessel ands block it
37
What is Ischaemia?
Reduction in blood flow
38
What is infarction?
Reduced bllod flow with subsequent death of cells
39
What is in a Plaque?
- fibrous tissue
- lipids (cholesterol)
- lymphocytes
40
Types of Skin wounds?
- ABRASION
HEALING BY 1ST INTENSION
- healing by 2nd intension
41
What is apoptosis?
programmed cell death
42
What is necrosis?
TRAUMATIC CELL DEATH
43
Definition of acquired?
caused by non genetic environmental factors
44
What is the definition of congenital?
present at birth
45
What is Metaplasia?
change in differentiation of a cell. 1 fully differentiated cell changes into another
46
What is Dysplasia?
Morphological changes seen in cells progressing to cancer
47
Name some evidence of Ageing?
- dermal elastosis
- osteoporosis
- cataracts
- sarcopenia
- dementia
- deafness
48
If there is basal cell carcinoma of the skin, which cells does it invade?
only invades locally
49
How do carcinomas spread?
to the lymph nodes that drain the site of carcinoma and can spread from blood to bone
50
What is Adjuvant Therapy?
extra treatment after surgical excision
51
Which tumours commonly metastasise to the liver?
Colon
Stomach
Pancreas
Carcinoid tumour of intestine
52
which tumours commonly metastasise to bone?
```
Prostate
breast
thyroid
lung
Kidney
```
53
What is carcinogenesis?
malignant neoplasms
54
What is oncogenesis?
both benign and malignant
55
What is cancer causing?
Carcinogens
56
What is tumour causing?
Oncogens
57
What is a tumour?
abnormal swelling
58
List examples of chemical carcinogens?
- aromatic amines
- nitrosamines
- alkylating agents
- polycyclic aromatic carbons
59
Name the classes of carcinogens?
- Viral
- Ionising/ non radiation
- hormones
- parasites
60
What are host factors?
premalignant conditions
61
What is a neoplasm?
a new growth. A lesion that persists after initiating stimulus is removed
62
What are benign neoplasms?
- non-invasive
- slow growth
- low mitotic activity
- no necrosis/ ulceration
63
What are malignant neoplasms?
- invasive and rapid growth
- irregular shape with metastases
- necrosis and ulceration can be found
64
How are malignant neoplasms caused?
they outgrow their blood supply
65
Name some types of neoplasm?
- lipoma = adipocytes
- chondroma = cartilage
- osteoma = bone
- angioma = vascular
- Rhabdomyoma = striated muscle
- Leiomyoma= smooth muscle
66
What is a Carcinoma
Malignant epithelial neoplasm
67
What is a sarcoma?
Malignant connective tissue neoplasms
68
What do we call cells of unknown origin?
Anaplastic
69
What is melanoma
Malignant neoplasm of melanocytes
70
What is lymphoma
malignant neoplasm off lymphoid cells
71
Describe the pathology of Metastases?
Invasion –erosion of tissue boundaries by enzymes secreted by
- Intravasion- gain access to metastatic routes e.g. blood/lymph
- Evasion of host defence
- Adherence- to endothelium
- Extravasation- colonisation of new site
- Angiogenesis- develops its own bloody supply
wow.
72
What is an adenoma?
benign secretory epithelial neoplasm
73
What is a papilloma?
benign non secretory epithelial neoplasm
74
What are the 3 types of Complement Activation?
Classical pathway= Antibody-antigen immune complexes
Alternate pathway= foreign surface antigens
Lectin pathway= mannose binding lectin- mannose residues on pathogen surface
75
What is the mechanism of action of complement factors?
1) Lyse microbes directly (membrane attach complex MAC)
2) Increase chemotaxis (C3a and C5a), and inflammatory response
3) Opsonisation- increase phagocytosis (C3b)
76
Differences between innate and adaptive immunity.
```
Present at birth vs develops over time
non specific vs specific
no memory vs memory
barriers (skin) vs lymphoid organs (nodes, thymus)
Phagocytes vs Lymphocytes
Natural Killer cells vs
Basophils and eosinophils vs
complement proteins vs antibodies
PAMPS vs Epitopes
Limited receptors vs receptor diversity requires somatic mutation
```
77
What is the function of Pattern recognition receptors?
Distinguishing foreign bodies by pattern recognition, recognising PAMPs and DAMPs, to then trigger innate response and an inflammatory response
78
What are PAMPs and DAMPs?
- Pattern associated molecular patterns
| - Damage associated molecular patterns
79
Name some types of PRR's?
- Nod like receptors (NLR's)
- Toll like receptors (TLR's- main is TLR4)
- Secreted and circulating mannose binding lectins and collectins
80
What happens when the innate response is triggered?
- opsonise pathogen
- activate complements (mannose binding lectin)
- activate inflammatory mediators
- secrete interferons and pro- inflammatory cytokines
- induce apoptosis of infected cells
81
Signs of chronic inflammation?
- less swelling and exudate
- inflammation and repair occurring at same time
- fibrosis (scar formation)
82
Causes of chronic inflammation?
- agent resistant to phagocytes
- agent indigestible
- autoimmune disease
- Crohns/ UC
- Transplant rejection
83
Cells involved in chronic inflammation?
- B-lymph (differentiate into plasma cells)
- T-lymph (cell- mediated immunity)
- Plasma (antibody production)
- M1 Macrophages (encourage inflammation)
- M2 Macrophages (decrease inflammation and encourage repair)
84
Fucntion of Macrophages?
To eat up debris and display antigen on surface
85
What is a granuloma?
Aggregate of Epitheloid Histocytes
86
What do epithelioid Histocytes secrete?
- ACE (which is a blood marker if someone has systematic granulomatosis disease)
87
Function of Lymph Nodes?
- house T cells, B (plasma) and phagocytes
88
What are the two parts of the spleen
- red pulp (old blood cells are destroyed)
| - white pulp= filters blood, antibodies made by B cells, antibody coated bacteria are filtered out
89
function of the thymus
involved in the development of T cells and destroys t cells that react to self-antigens
90
What does aspirin do?
irreversible COX 1>2 inhibition
91
What does an NSAID do
non-selective competitive reversible COX inhibition
92
Overdose management of opiate/ opioid
Naloxone
93
overdose management of aspirin
Haemodialysis
94
Process of Phagocytosis
1) Chemotaxis and adherence of microbe to phagocyte
2) Ingestion of microbe by phagocyte
3) formation of phagosome
4) Fusion of phagosome and lysosome= phagolysosome
5) Digestion of ingested microbe by enzymes
6) Formation of residual body containing indigestible material
7) Discharge of waste material
95
Function of Natural Killer T cells
Kill own cells by apoptosis if infected with virus/ become cancerous
96
function of mast cells
release: histamine, heparin, chemokines and cytokines
97
function of basophils
hypersensitivity reactions and parasitic infections/ release histamine
98
function of eosinophils
Raised in allergy and parasitic infections
99
Humoral Adaptive Immunity response control freely circulating pathogens, describe the process
1) A B cell binds to its specific antigen
2) B cell differentiates into plasma cell
3) plasma cell proliferates and produce antibodies against the pathogens
100
Cell- mediated Adaptive Immunity controls intracellular pathogens, describe the process
1) T cell binds to antigen and this activates its cytokine receptors
2) Helper T cell produces cytokines that cause differentiation into a cytotoxic T cell. These cytokines also influence formation of B cells, macrophages and plasma cells
3) Infected cell is lysed by cytotoxic T cell
101
definition of an antigen
a toxin or other foreign substance which induces an immune response in the body
102
Name 3 antigen- presenting cells
macrophages, dendritic cells, B cells
103
What are major histocompatibility complexes
Proteins that mark a cell as SELF (show antigen)
```
class 1= all cells
class 2= antigen- presenting cells
```
104
What do B cells do?
proliferate into plasma cells/ memory B cells and recognise soluble antigens in the blood
105
What is a FAB
region on antibody that recognises antigen
106
Function of Helper T cells
- stimulate proliferation of other T cells
| - stimulate B cells to produce antibodies
107
WHat is an Epitope?
Part of the antigen that binds to an antibodies FAB region
108
How do antibodies protect against infection?
- Neutralisation (specific binding neutralise toxins and form complexes)
- Opsonisation ( Enhance innate mechanisms; activate classical complement pathway, release of inflammatory mediators by mast cells, enhancing phagocytosis)
109
Immunoglobulin classes and function?
IgM- 1st response to antigen, cant cross placenta
IgG- most common, crosses placenta (passive immunity)
IgA- Secreted from mucous membranes
IgD- B cell activation; cant cross placenta
IgE- histamine reactions and allergies
110
What is Pharmacodynamics?
How the drug affects the body
111
What is Pharmacokinetics?
How the body affects the drug
- absorption
- distribution
- metabolism
- excretion
112
What is Absorption
process of transfer from where the drug was administered to the circulation
113
What is Distribution
Drug reversibly leaves blood stream and enters extracellular fluid and tissues
114
What is Metabolism?
Transformation of drug molecule into different molecule
115
What is Ecretion?
Molecule expelled in liquid, solid or gaseous waste
116
Whats Bioavailability?
Fraction of administered drug that reaches the systematic circulation unaltered
117
What is Efficacy?
How well a ligand activates a receptor
118
WHat is Potency?
The binding affinity
119
What is the difference between parasympathetic receptors and sympathetic receptors on a target organ
?
```
Para= muscarinic
Symp= NAd receptor (alpha or beta)
```
120
What is a Thrombus?
Solid mass of blood constituents
121
What is a Physiological reason for a thrombus?
haemostasis/ prevent bleeding
| imbalance in blood coagulation system
122
What is a Pathological reason for a Thrombus?
imbalance in blood coagulation system
123
Features of Arterial Thrombosis?
- superimposed on atheroma
- high pressure
- mainly platelets (white)
- cause MI/Stroke
124
Features of Venous Thrombosis?
- due to stasis
- low pressure- mainly coagulation factors&RBC (red)
- cause DVT/PE
125
Tretament of Thrombosis?
```
Antiplatelet= clopidogrel/ aspirin
Anticoagulants= warfarin, heparin, NOACs
```
126
Name the process of Atherosclerosis
1) Endothelial cells damaged by cholesterol
2) High levels of LDL accumulate on arterial wall
3) Macrophages attract to site- take up lipid to form foam cells
4) formation of fatty streak
5) Cytokines and growth factors released from macrophage
6) Smooth muscle proliferation around lipid core and formation of a fibrous cap
127
What is an EMbolism?
Mass of material in vascular system able to get stuck
128
What is Infarction?
issue death due to lack of blood supply
129
Name a few inducers and inhibitors of Cytochrome P450
inducers: Antiepileptics, smokers, chronic alcohol intake
inhibitors- erythromycin, allopurinol, anti-fungal, SSRI, acute alcohol
130
Name some Enteral routes of Administration
- enteric coated (oral)- intestinal absorption
- extended release
- sublingual/ buccal
131
Name some Parenteral routes of administration
- intravenous
- intramuscular
- subcutaneous
132
Name mechanisms of Absorption
- diffusion
- active transport
- endocytosis
133
Name some variables of Absorption
- pH
- vascularity
- surface area
- contact time
134
how do you work out bioavailability of a drug?
AUC oral/ AUC injected x 100 (e.g IV is 100%)
135
NAme some factors of bioavailability
```
first pass hepatic metabolism (liver transforming drug)
solubility
chemical instability (GI breakdown by enzymes)
```
136
Factors of Distribution
- blood flow
- capillary permeability
- plasma binding protein
137
Difference between phase 1 and phase 2 metabolism
1= catalysed by cytochrome P450, polarise lipophilic drug (functionalisation by adding chemically reactive group permitting conjugation) (oxidation, reduction, hydrolysis)
2= conjugation by glucuronic acid e.g
to then be excreted by renal/biliary system (add exogenous compound increasing polarity)
138
What is a first order and zero order rate?
```
1st= catalysed by enzymes, rate of metabolism directly proportional to drug conc
zero= enzyme saturated by high drug dose, rate of metabolism is constant
```
139
How does elimination occur
- excretion by urine, must be sufficiently polar (role of phase 2 and conjugation)
140
What is drug signal transduction?
- binding of drug to EC/IC receptor e.g ligang gated ion channels/ G- protein coupled receptor
- leads to amplification or down- regulation of signals
141
What does allosteric mean?
binds to other site of the cell irreversibly
142
How do opioids work?
Inhibitng descending pain signals, all durgs are μ receptor agonists
143
What is naloxone?
opioids antagonist used in overdose or respiratory depression
144
side effects of opioids?
- respiratory depression
- sedation
- nausea/ vomit
- constipation
145
effect of Muscarinic receptor M1?
mainly brain
146
effect of Muscarinic receptor M2?
mainly slowing of the heart
147
effect of Muscarinic receptor M3
glandular and smooth muscle
bronchoconstriction
sweating
salivary gland secretion
148
effect of Muscarinic receptor M4 and M5?
CNS
149
What is Salbutamol
beta 2 adrenoreceptor agonist (SABA)
150
what is the effect when NAd binds to an alpha 1 receptor?
- vasoconstriction
- mydriasis (pupil dilate)
- contraction of bladder neck (urinary retention)
- increased peripheral resistance
151
what is the effect when NAd binds to an alpha 2 receptor?
- inhibits release of NAd and ACh
| - reduces insulin produced from the pancreas
152
what is the effect when NAd binds to a beta 1 receptor?
- positive chronotropic effect on the heart
- increased renin from the kidney (increased BP)
- increased lipolysis
153
what is the effect when NAd binds to a beta 2 receptor?
- bronchodilation
- vasodilation
- decreased GI motility
- decreased peripheral resistance
154
what is the effect when NAd binds to a beta 3 receptor?
- increased lipolysis
| - relaxation of the bladder
155
beta blocker side effects?
- wheeze
- tired
- bradycardia
- hypoglycaemia
156
what is a COX enzyme?
an enzyme that allows production of thromboxane and prostaglandins
157
how does aspirin work?
aspirin inhibits COX1 and COX2 enzymes which stops the production of thromboxane's and prostaglandins
158
What do thromboxane's do?
cause vasoconstriction and platelet aggregation therefore aspirin stops this occurring
159
what can prostaglandins do?
cause inflammation/ anaphylactic reaction and pain! therefore aspirin stops this occurring?
160
which enzyme catalyses thromboxane production?
COX1
161
which enzyme catalyses prostaglandin production?
COX2
162
Describe the breakdown of paracetamol in the body
Paracetamol is converted into a reactive intermediate by CYP450
it then becomes a cellular macromolecule or stable metabolite
It then undergoes cellular necrosis if it become a cellular macromolecule
163
What is bradykinin?
a potent vasodilator
164
Alpha 1 agonists?
decongestants (phenylephrine)
165
alpha 1 antagonists?
Tamsulosin
166
beta 1 agonists?
Inotropes (epinephrine and dopamine)
167
BETA 1 ANTAGONISTS?
selective/ non selective beta blockers
168
beta 2 agonists?
SABA/LABA
169
beta 2 antagonists?
non selective beta blockers
170
histamine antagonist?
cetirizine
| loratidine
171
What are the factors of dose- response relationship?
- drug conc (dose of drug + pharmacokinetic profile)
| - receptor availability (maximal effect once receptors and saturated irrelevant of increased dose)
172
parasympathetic pathway?
acetylcholine -- nicotinic receptor -- acetylcholine -- muscarinic receptor
173
sympathetic pathway?
acetylcholine -- nicotinic receptor -- norepinephrine -- adrenergic receptor
174
What are type 1 hypersensitivity reactions related to
Allergies (anaphylaxis and asthma)
| IgE, mast cells, histamine
175
What are type 2 hypersensitivity reactions related to
Cytotoxic cells, antibody dependant
Ab binds to Ag on target cell and kills it via complement
176
What are type 3 hypersensitivity reactions related to
Immune complex disease
Circulating Ab binds to Ag to form a complex. Circulating complex deposited in tissue = inflammation e.g reactive arthritis
177
What are type 4 hypersensitivity reactions related to
Delayed type hypersensitivity
Ag presenting cell presents Ag to T cell, T cell activated to Th1, forms memory Th1 cell. When Ag presented again, memory Th1 cell activates macrophages- inflammation
178
Definition of Allergy?
Abnormal response to harmless foreign material
179
Definition of Atopy?
tendency to develop allergies
180
What is Anaphylaxis?
Acute allergic reaction to an antigen to which the body has become hypersensitive.
181
Pathogenesis of Allergies?
IgE binds to FceRI on mast cell and basophil
(IgE has high affinity for FceRI 1:1),
this causes degranulation of the cells which releases histamine= bronchoconstriction and arteriolar dilation
182
What is FceRI found on?
- mast cells (tissues)
- Eosinophils and Basophils (circulating)
Involved in host defence against parasites
183
What are mast cells derived from and where are they found
myeloid stem cells and found in tissues
184
Effects of Histamine
bronchoconstriction and arteriolar dilation
185
Effects of LT
capillary contraction- increasing vascular permeability
186
Effects of PGD2
Smooth muscle contraction
187
Effects of Platelet Aggregation Factor (PAF)
Increasing vascular permeability and platelet aggregation
188
Describe what happens in anaphylaxis in terms of the CVS, Resp, Skin and GI systems
Mast cell/ Basophil activation - IgE activation- histamine elevation
```
CVS= vasodilation, increased vascular permeability and increased BP
Resp= Bronchial smooth muscle contraction, mucous
Skin= Rash/swelling
GI= pain/ vomiting
```
189
Treatment of Allergies?
1) Avoid allergens
2) Desensitisation to allergens- increase dose of Ag
3) Prevent IgE production- block Th2 cytokines (Lumiluximab)
4) Bind to and inactivate receptor of IgE (omalizumab)
5) Prevent mast cell activation- mast cell membrane stabiliser (prednisolone)
6) Inhibit mast cell products- PT/LT antagonist
190
Describe the Optochin test
Differentiate between Alpha haemolytic streps
resistant= s.viridans
(positive) sensitive= s.pneumoniae
191
What bacteria is it if there is a positive oxidase test (gram negative non lactose fermenter)
Positive oxidase test= pseudomonas oxidase
192
What antibiotic is given to treat MRSA
vancomycin
193
Causes of Chronic Inflammation?
Persistent acute
develops from acute
Primary Chronic Inflammation
194
Sarcoidosis blood marker?
ACE
195
Final differentiation between bacteria?
Serotyping (API strip)
196
Name the leukocytes?
Neutrophils, basophils, eosinophils
197
Efficacy and Affinity are receptor related, what do agonists and antagonists show?
```
Agonists = both
Antagonists = just affinity
```
198
What is Tolerance and Desensitisation?
Tolerance - reduction in drug effect over time (continuously repeated high conc)
Desensitisation - receptors become degraded / uncoupled
