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ICS Flashcards

1
Q

ACUTE INFLAMMATION

A

Acute inflammation is the initial and often transient series of tissue reactions to
injury - may last from a few hours to a few days

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2
Q

Causes of acute inflammation:

6

A
  • Microbial infections e.g pyogenic (pus causing) bacteria, viruses
  • Hypersensitivity reactions e.g parasites, tubercle bacilli
  • Physical agents e.g trauma, ionising radiation, heat, cold (frost-bite)
  • Chemicals e.g corrosives, acids, alkalis, reducing agents
  • Bacterial toxins
  • Tissue necrosis e.g ischaemic infarction
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3
Q

Essential macroscopic appearances of acute inflammation:

5

A
  • Redness - rubor
  • Heat - calor
  • Swelling - tumor
  • Pain - dolor
  • Loss of function is also characteristic
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4
Q

Acute inflammatory response process:

3

A
  1. Changes in vessel calibre (gets wider) and consequently increased vessel flow
  2. Increased vascular permeability and formation of the fluid exudate
  3. Formation of the cellular exudate - emigration of the neutrophil polymorphs into the extravascular space
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5
Q

THE diagnostic histological feature of acute inflammation is …

A

… the accumulation of neutrophil polymorphs within the extracellular space

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6
Q

Stages in neutrophil polymorph emigration

A
  1. Margination of neutrophils
  2. Adhesion of neutrophils
  3. Neutrophil emigration
  4. Diapedesis
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7
Q

Endogenous chemical mediators of acute inflammation cause:

5

A

• Vasodilation
• Emigration of neutrophils
• Chemotaxis (the attraction of neutrophil polymorphs towards certain
chemicals e.g at the site of inflammation)
• Increased vascular permeability
• Itching & pain

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8
Q

CHRONIC INFLAMMATION

A

• The subsequent and often prolonged tissue reactions to injury following the initial
response
• Can be defined as an inflammatory process in which lymphocytes, plasma cells and macrophages predominate

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9
Q

Characteristic microscopic features of chronic inflammation:

3

A
  • The cellular infiltrate consists characteristically of lymphocytes, plasma cells &
    macrophages
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10
Q

A granuloma is …

A

… an aggregate of epithelioid histiocytes

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11
Q

ORGANISATION IS …

The repair of specialised tissue by …

A

… the formation of a fibrous scar

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12
Q

Cells that regenerate:

6

A
  • Hepatocytes
  • Pneumocytes
  • All blood cells
  • Gut epithelium
  • Skin epithelium
  • Osteocytes
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13
Q

Cells that do not regenerate:

2

A
  • Myocardial cells

- Neurones

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14
Q

THROMBOSIS

why is it different from a clot?

A
  • The solidification of blood contents that forms within the vascular system
    during life

Blood coagulated outside of the vascular system or after death

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15
Q

Aspirin can … ?

Warfarin … ?

A 
INHIBIT PLATELET AGGREGATION thus a low dose can help prevent thrombosis. 
In severe cases, warfarin can be used (inhibits
vitamin K (clotting factor) - thereby preventing clotting)
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16
Q

EMBOLISM

A

An embolus is a mass of material in the vascular system able to lodge in a
vessel and block its lumen

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17
Q

ISCHAEMIA

A

A reduction in blood flow to a tissue or part of the body caused by constriction
or blockage of the blood vessels supplying it

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18
Q

INFARCTION

A 
The death (necrosis) of part or the whole of an organ that occurs when the
artery supplying it becomes obstructed
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19
Q

GANGRENE

A

When whole areas of a limb or a region of the gut have their arterial
supply cut off and large areas of mixed tissue die in bulk

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20
Q

ATHEROSCLEROSIS

A

Disease characterised by the formation of atherosclerotic plaques in the intima of
large (aorta) and medium-sized arteries, such as the coronary arteries

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21
Q

Atherosclerosis can cause …

6

A
  • Cerebral infarction
  • Carotid atheroma - emboli causing transient
    ischaemic attacks or cerebral infarcts
  • Myocardial infarction
  • Aortic aneurysm - rupture causes certain
    death
  • Peripheral vascular disease
  • Gangrene
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22
Q

Risk factors for Atherosclerosis risk factors …

6

A 
- Hypercholesterolaemia:
• Essentially high cholesterol levels
• MOST IMPORTANT RISK FACTOR
• It can cause plaque formation and growth in the absence of other known
risk factors
• Lipids directly damage endothelial cells
- Smoking:
• Increases blood pressure
• Damages endothelial cells
- Hypertension
- Diabetes
- Male gender
- Increasing age
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23
Q

Preventive and therapeutic measures to atherosclerosis:

5

A
  • Smoking cessation
  • Control of blood pressure
  • Weigh reduction
  • Low dose aspirin - inhibits the aggregation of platelets, advised for people
    with clinical evidence of atheromatous disease
  • Statins - cholesterol reducing drug
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24
Q

ANEURYSMS

A

A localised permanent dilation of part of the vascular tree

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25
Q

APOPTOSIS

A

A physiological cellular process in which a defined and programmed
sequence of intracellular events leads to the removal of a cell WITHOUT the
release of products harmful to surrounding cells

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26
Q

Inhibitors of apoptosis

4

A
  • Growth factors
  • Extracellular cell matrix
  • Sex steroids
  • Some viral proteins
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27
Q

Inducers of apoptosis

8

A
  • Growth factor withdrawal
  • Loss of matrix attachment
  • Glucocorticoids
  • Some viruses
  • Free radicals
  • Ionising radiation
  • DNA damage
  • Ligand-binding at ‘death receptors’
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28
Q

Apoptosis intrinsic pathway …

2

A

Uses the pro- and anti-apoptotic members of the Bcl-2 family:
• Bcl-2 can inhibit many factors that induce apoptosis
• Bax forms Bax-Bax dimers which enhance apoptotic stimuli

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29
Q

CONGENITAL DISEASE

A

• Simply a disease that is present at birth

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30
Q

INHERITED

A

Disease caused by an inherited genetic abnormality
IS GENETIC
doesn’t need to be present at birth

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31
Q

SPONTANEOUS

A

Disease caused by a spontaneous mutation

IS GENETIC

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32
Q

ENVIRONMENTAL

A

Acquired by environmental factors

NON-GENETIC

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33
Q

ACQUIRED DISEASE

A

• Disease caused by non-genetic environmental factors

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34
Q

HYPERTROPHY

A

• Increase in cell size without cell division (SAME NUMBER)

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35
Q

HYPERPLASIA

A

Increase in cell number by mitosis

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36
Q

ATROPHY

A

The decrease in size of an organ or cell by reduction in cell size and/or
reduction in cell numbers, often by a mechanism involving apoptosis

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37
Q

NECROSIS

A

Traumatic cell death which induces inflammation and repair

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38
Q

METAPLASIA

A

The change in differentiation of a cell from one fully-differentiated cell type to
a different fully-differentiated cell type

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39
Q

DYSPLASIA

A

Imprecise term for the morphological changes seen in cells in the progression
to becoming cancer

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40
Q

CARCINOGENESIS

A

The transformation of normal cells to neoplastic cells through permanent
genetic alterations or mutations

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41
Q

NEOPLASIA IS …

4

A

-Autonomous
• Abnormal
• Persistent
• New growth

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42
Q

NEOPLASM

A

A lesion resulting from the autonomous or relatively autonomous abnormal
growth of cells which persists after the initiating stimulus has been removed - a
new growth

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43
Q

TUMOURS

A

Any abnormal swelling

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44
Q

Tumours include:

4

A
  • Neoplasm
  • Inflammation
  • Hypertrophy
  • Hyperplasia
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45
Q

Tumours can cause morbidity and mortality due to:

5

A
  • Pressure on adjacent structures (e.g. benign meningeal tumour causing epilepsy)
  • Obstruction to the flow of fluid (e.g. benign epithelial tumour blocking duct)
  • Production of a hormone (e.g. benign thyroid tumour causing thyrotoxicosis (excessive thyroid hormone)
  • Transformation into a malignant neoplasm
  • Anxiety & stress since patient thinks the lesions may be something more sinister
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46
Q

Malignant neoplasms can cause morbidity and mortality due to:

(7)

A

• Pressure on and destruction of adjacent tissue
• Formation of secondary tumours (metastases)
• Blood loss from ulcerated surfaces
• Obstruction of flow (e.g. malignant tumour of the colon causing intestinal obstruction)
• Hormone production
• Paraneoplastic effects resulting in weight loss and debility
• Anxiety & pain - many cancer cause no pain until quite late
into the disease

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47
Q

HISTEOGENESIS

A

the specific cell or origin of a tumour

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48
Q

Histogenic classification major
categories of origin:

(3)

A

• Epithelial cells (forming carcinomas)
• Connective tissues (forming sarcomas)
• Lymphoid (ONLY GIVE RISE TO MALIGNANT NEOPLASMS) and/or
haemopoietic organs (forming lymphomas or leukaemias)

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49
Q

MALIGNANT TUMOUR GRADING

A
  • Well differentiated - Grade 1
  • Moderately differentiated - Grade 2
  • Poorly differentiated - Grade 3
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50
Q

Nomenclature of Neoplasia of Connective tissue and other mesenchymal
tumours:

BENIGN (7)

A

named according to cell of origin and behavioural
classification
B- named after cell or tissue of origin suffixed by -oma:
- Lipoma: benign tumour of adipocytes
- Rhabdomyoma: benign tumour of striated muscle
- Leiomyoma: benign tumour of smooth muscle cells
- Chondroma: benign tumour of cartilage
- Osteoma: benign tumour of bone
- Angioma: benign vascular tumour
- Neuroma: benign tumour of the nerve

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51
Q

Nomenclature of Neoplasia of Connective tissue and other mesenchymal
tumours:

MALIGNANT (7)

A

M- always designated sarcoma, prefixed by the name that describes the cell or tissue of origin:

  • Liposarcoma: malignant tumour of adipocytes
  • Rhabdomyosarcoma: malignant tumour of striated muscle
  • Leiomyosarcoma: malignant tumour of smooth muscle cells
  • Chondrosarcoma: malignant tumour of cartilage
  • Osteosarcoma: malignant tumour of bone
  • Angiosarcoma: malignant vascular tumour
  • Neurosarcoma: malignant tumour of the nerve
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52
Q

Exceptions to the rules of nomenclature:

  • OMAS (3)
  • MALIGNANT TUMOURS (3)
  • NAMED (4)
  • RANDOM (2)
A

• Not all -omas are neoplasms:
- Granuloma - chronic inflammation
- Mycetoma - fungus in body
- Tuberculoma - mass of TB
• Not all malignant tumours are carcinoma or sarcoma:
- Melanoma - malignant neoplasm of melanocytes
- Mesothelioma - malignant tumour of mesothelial cells (line body
cavities and outer surface of internal organs, secrete lubricating
fluid)
- Lymphoma - malignant neoplasm of lymphoid cells, all are
malignant
• Tumours named after the person who first discovered/described them:
- Burkitt’s lymphoma - B-cell lymphoma caused by Epstein Barr virus
- Ewing’s sarcoma - malignant tumour of bone
- Hodgkin’s lymphoma - malignant lymphoma characterised by the
presence of Reed-Sternberg cells
- Kaposi’s sarcoma - malignant neoplasm derived from vascular
endothelium, commonly associated with AIDs
• Teratoma - neoplasm of germ cell origin that forms cells representing all
three germ cell layers of the embryo; ectoderm, mesoderm & endoderm
• Carcinosarcomas - mixed malignant tumours showing characteristics of
epithelium & connective tissue

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53
Q

CARCINOGEN

A

An environmental agent participating in the causation of tumours

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54
Q

Classes of carcinogen

5

A
  • Chemical
  • Viruses
  • Ionising & non-ionising radiation
  • Hormones, parasites & mycotoxins
  • Miscellaneous
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55
Q

Host factors that influence carcinogenesis:

5

A

Race

  • Diet
  • Constitutional factors - age, gender etc.
  • Premalignant lesions
  • Transplacental exposure
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56
Q

ONCOGENES

A

These are genes driving the neoplastic behaviour of cells

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57
Q

Three major families OF Proteinases and inhibitors OF INVASION:

A
  • Interstitial collagenases; degrade types I,II & III collagen
  • Gelatinases; degrade type IV collagen and gelatin
  • Stromelysins; degrade type IV collagen and proteoglycans
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58
Q

Most important sole criterion for malignancy IS

A

INVASION

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59
Q

METASTASIS

A

The process whereby malignant tumours spread from their site of origin
(the primary tumour) to form other tumours (secondary tumours) at distant
sites

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60
Q

Metastasis sequence

6

A
  1. Detachment of tumour cells from their neighbours
  2. Invasion of the surrounding connective tissue to reach
    conduits of metastasis i.e. blood & lymphatic vessels
  3. Intravasation into the lumen of vessels
  4. Evasion of host defence mechanisms, such as natural killer
    cells in the blood
  5. Adherence to endothelium at a remote location
  6. Extravasation of the cells from the vessel lumen into the
    surrounding tissue
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61
Q

Bone is a site favoured by haematogenous metastases

from five carcinomas:

A
  • Lung
  • Breast
  • Kidney
  • Thyroid
  • Prostate
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62
Q

TUMOUR GRADE

A

This is an assessment of its degree of malignancy or aggressiveness (can be
inferred from its histology)

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63
Q

TUMOUR STAGE

A

This is the extent of a tumours spread

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64
Q

TUMOUR STAGE - how to classify

A

TNM system:
• T
- Refers to the primary tumour and is suffixed by a number that
denotes tumour size
- The number varies according to the organ harbouring the tumour
• N
- Refers to lymph node status and is suffixed by a number that
denotes the number of lymph nodes or groups of lymph nodes
containing metastases
• M
- Refers to the anatomical extent of distant metastases

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65
Q

UK screening programs

A
  • Cervical cancer
  • Breast cancer
  • Colorectal cancer
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66
Q

Biases in screening programs

A
  • Lead time bias:
    • Earlier detection does not affect the inevitable fatal outcome, but
    prolongs the apparent survival time
  • Length bias:
    • Preferential detection of slow growing tumours with intrinsically better
    prognosis
  • Overdiagnosis bias:
    • Diagnosis of lesions that, although histologically malignant, are
    clinically relatively harmless
  • Selection bias:
    • Volunteers for screening are more at risk of good-prognosis tumours
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67
Q

COMPLEMENT

A

• A complex series of interacting plasma proteins which form a major
effector system for antibody-mediated immune reactions

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68
Q

The major purpose of the complement pathway is

A

to remove or destroy

antigen, either by direct lysis or by opsonisation

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69
Q

When activated by coming into contact with pathogen complement can:

(4)

A
  • Lyse microbes directly (Membrane Attack Complex - when a group
    of complement proteins make a hole in a pathogen which causes
    an inrushing of fluids that results in lysis and thus the destruction
    of the pathogen)
  • Increase chemotaxis (C3a & C5a)
  • Enhance inflammation
  • Induce opsonisation (C3b) - process by which an antigen becomes
    coated with substances (i.e. complement) that make it more easily
    engulfed by phagocytic cells since macrophages have special
    receptors for specific complement proteins
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70
Q

ANTIBODIES AKA IMMUNOGLOBULINS

A

A protein produced in response to an antigen. It can only bind with the
antigen that induced its formation i.e. specificity

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71
Q

ANTIGEN

A

A molecule that reacts with preformed antibody and specific

receptors on T and B cells

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72
Q

EPITOPE

A

The part of the antigen that binds to the antibody/receptor binding
site

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73
Q

AFFINITY

A

A measure of binding strength between an epitope and an

antibody binding site - the higher the affinity the better

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74
Q

CYTOKINES

A

Soluble proteins secreted by lymphocytes or macrophages/monocytes
that act as stimulatory or inhibitory signals between cells

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75
Q

Adaptive immunity hallmarks:

7

A

** Cell mediated - T cells for intracellular microbes
** Antibodies - B cells for extracellular microbes
SPECIFIC
• Response specific to antigen
• Memory to specific antigen
• Quicker response
• Requires lymphocytes

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76
Q

Major Histocompatibility Complex (MHC):

cell surface glycoproteins of two basic types:

A
  • MHC I:
    • Intracellular i.e virus
    • Found on the surface of virtually all cells of the body
    except erythrocytes
    • Cytotoxic T cells (CD8) require an antigen to be
    associated with class I MHC proteins before they kill
    the cell containing the intracellular pathogen
  • MHC II:
    • Extracellular i.e. phagocytosis
    • Found mainly on the surface of macrophages, B
    cells & dendritic cells (i.e antigen presenting cells)
    • Helper T cells (CD4) require class II MHC proteins
    before they help B cells to make antibodies to the
    extracellular pathogen
77
Q

ALLERGY

A

Abnormal response to harmless foreign material

78
Q

ATOPY

A

Inherited tendency for overproduction of IgE antibodies to common
environmental antigens

79
Q

HYPERSENSISTIVITY REACTIONS:

GELL & COOMBS CLASSIFICATION:

A
  • Type 1. IgE - ALLERGIC,ACUTE
    • acute anaphylaxis, hay fever
    • IMMEDIATE & ACUTE
  • Type 2. IgG bound to cell surface antigens/ IgM
    • transfusion reactions, autoimmune disease
    • FAIRLY QUICK
  • Type 3. Immune complexes, activation of complement/IgG
    • SLE, Post-streptococcal GN
  • Type 4. T Cell Mediated Delayed Type Hypersensitivity (DTH)
    • TB & Contact dermatitis
80
Q

The ultimate goal of tumour immunology is …

A

… to induce clinical effective anti-
tumour immune responses that would discriminate between tumour cells
and normal cells in cancer patients

81
Q

Natural passive immunity provides protection against:

6

A
  • Diptheria
  • Tetanus
  • Streptococcus
  • Rubella
  • Mumps
  • Polio virus
82
Q

Aims of a “perfect” vaccine:

5

A

• To achieve long term protection (ideally from a small number of
immunisations)
• To stimulate both B cells and T cells
• To induce MEMORY B cells and T cells
• To stimulate protective high affinity IgG production (IgA too if possible
(can migrate through mucosal barriers useful some pathogens infect
primarily through mucous membranes))
• The importance the memory B cell response depends on the nature of
the pathogen

83
Q

ADJUVANTS

A

Any substance that is added to a vaccine to stimulate the immune system

84
Q

IMMUNODEFICIENCY

A

• Deficiency in the immune response, can either be acquired (HIV) or inherited
(defects in T cell function)

85
Q

PHARMACOLOGY

A

the study of the effects of drugs

86
Q

PHARMOKINETICS

A

how the body affects the drug; Absorption, Distribution,

Metabolism and Excretion (ADME)

87
Q

PHARMOCODYNAMICS

A

how the drug affects the body - D in dynamic = drug!!

88
Q

POTENCY

A

measure of how well a drug works

89
Q

AGONIST

A

a compound that binds to a receptor and activates it

90
Q

INTRINSIC ACTIVITY

A

Emax of partial agonist ÷ Emax of full agonist

91
Q

ANTAGONIST

A

a compound that reduces the effect of an agonist

92
Q

AFFINITY

A

describes how well a ligand BINDS to the receptor

93
Q

EFFICACY

A

describes how well a ligand ACTIVATES the receptor

94
Q

Three phases of plasma level

A
  • Uptake into the plasma
  • Distribution from the plasma
  • Elimination from the plasma
95
Q

Order of reactions for a dissolved drug (in the plasma)

A
  • First order = rate is directly proportional to the concentration of
    drug (rate ∝ [drug])
  • Second order = rate is directly proportional to the square of the
    concentration of the drug (rate ∝ [drug]2)

171

KP

All information is taken from lectures and textbooks, there may be mistakes!!
- Third order = rate is directly proportional to the cube of the
concentration of the drug (rate ∝ [drug]3)
- Zero order = rate is unrelated to the concentration of the drug
(rate ∝ [drug]0)

96
Q

Basic components: compartments

A

Plasma (5 litres), Interstitial (15 litres) & Intracellular (45 litres)

97
Q

Non ionic diffusion

When pH is INCREASED:

A
  • Weak acid - MORE IONISED

- Weak base - LESS IONISED

98
Q

Non ionic diffusion

When pH is DECREASED:

A
  • Weak acid - LESS IONISED

- Weak base - MORE IONISED

99
Q

BIOAVAILABILITY

A

amount of drug taken up as a proportion of the amount administered

100
Q

Uptake of aspirin:

A

Gastric pH affects the amount of aspirin uptake

101
Q

A raised GASTRIC pH results in …

A

… The reduced uptake of aspirin from the

stomach and thus a reduction in bioavailability

102
Q
  • Proteins/large molecules are only active
  • Water soluble molecules are active in
  • Lipid soluble molecules are only active
  • A drug is distributed in the plasma according to
  • Dissolved gases & small ionic molecules are found in
  • Lipophilic drugs tend to adhere to
A

-in the plasma compartment (5L)
-plasma and interstitial compartment
(5L + 15L)
-in the intracellular fluid (45L)
-its chemical properties and
molecular size
-the aqueous phase
-hydrophobic areas of plasma proteins

103
Q

Volume of distribution =

A

Total amount of drug in body ➗ Concentration of drug in plasma

104
Q

VOLUME OF DISTRIBUTION (VD)

A

the volume (litres) that the drug would occupy if it was distributed through all the compartments as if they were all plasma

105
Q

DRUGS found in each compartment:

A

–Interstitial:
- Aspirin/ other NSAIDs
• Antibiotics
• Muscle relaxants
– Intracellular:
• Steroids
• Local anaesthetics
• Opioids
• An CNS drugs
- Paracetamol
-Amiodarone (has a volume of distribution of 450L i.e. very
easily taken up by tissue)

106
Q

The elimination of a drug is

A

from the plasma compartment

107
Q

CLEARANCE

A

-The volume of plasma that can be completely cleared of drug per unit
time (mls minute-1 (ml/min))
-The rate at which plasma drug is eliminated per unit plasma
concentration (mls minute-1 (ml/min))
**= Rate of appearance in urine ➗ Plasma concentration

108
Q

HOW UNITS ARE DERIVED

A

The rate at which plasma drug is eliminated = mg per minute
• Per unit plasma concentration = mg per ml
• Total = mg per minute ➗ mg per ml
• Cancel out the “mg”
• Results in = mls minute-1 (ml/min)
***** Thus the units of clearance are mls minute-1 (ml/min)

109
Q

Adult renal clearance values:

A
  • Renal blood flow is 18% of cardiac output = 1L/min
  • Renal plasma flow is 60% of blood flow = 600mls/min
  • Glomerular filtration is 12% of renal blood flow = 130mls/min
110
Q

Hepatic blood flow is

A

24% of cardiac output (3/4 from portal vein and 1/4 from hepatic artery)

111
Q

Hepatic extraction ratio (HER):

A

The proportion of drug removed by one passage through the liver

112
Q

There is minimal effect on drug metabolism until at least

A

70% of functioning liver is lost

113
Q

Drugs with active metabolites:

A
  • Prednisone
  • Isosorbide dinitrate
  • Codeine
  • Diamorphine
  • L-dopa
  • Cortisone
  • Morphine
114
Q

Steady state means that infusion dosage =

A

rate of elimination from plasma

115
Q

Peripheral nervous system (PNS):

A
  • Somatic (NMJ) = voluntary = Acetyl choline (ACh)

* Autonomic = involuntary = ACh & Noradrenaline (NAd)

116
Q

Autonomic nervous system:

A
  • Parasympathetic - ACh

* Sympathetic - NAd

117
Q

Nicotinic ACh receptors (nAChR) are found …

A

… in the neuromuscular junction (NMJ)

118
Q

Adverse effects of muscarinic agonists:

7

A
  • Diarrhoea
  • Urination
  • Miosis (excessive pupil constriction)
  • Bradycardia
  • Emesis (vomiting)
  • Lacrimation (tears)
  • Salivation/sweating
  • Remember by DUMBELS!
119
Q

Parasympathetic nervous system:

10

A
  • Acetyl choline
  • Rest & digest
  • Constricts pupils
  • Stimulates tears
  • Stimulates salivation
  • Lowers heart rate
  • Reduces respiration
  • Constricts blood vessels
  • Stimulates digestion
  • Contracts bladder
120
Q

Sympathetic nervous system:

12

A
  • Noradrenaline
  • Fight or flight
  • Dilates pupil
  • Inhibits tears
  • Inhibits salivation
  • Activates sweat glands
  • Increases heart rate
  • Increases respiration
  • Inhibits digestion
  • Release of adrenaline
  • Relaxes bladder
  • Ejaculation in males
121
Q

TYROSINE >

A

DOPA > dopamine > noradrenaline > adrenaline

122
Q

Effects of alpha-adrenoceptors:
• Alpha-1:
• Alpha-2:

A 
• Alpha-1:
- Vasoconstriction
- Pupil dilation
- Bladder contraction
• Alpha-2:
- Presynaptic inhibition of noradrenaline (negative feedback) i.e. when blood sugar is low then alpha-2 in pancreas will be stimulated to reduce noradrenaline release thereby reducing insulin levels being released from the pancreas
123
Q

Effects of beta-adrenoceptors:
• Beta-1:
• Beta-2:
• Beta-3:

A 
• Beta-1:
- Increased force of heart contraction (positive inotropic effect)
- Increased heart rate
- Increased electrical conduction in heart
- Increased renin release from kidney
- Increased blood pressure
• Beta-2:
- Bronchodilation
- Vasodilation
- Reduced GI motility
• Beta-3:
- Increased lipolysis
- Relaxation of bladder
124
Q

Adrenergic agonists:
• Adrenaline (non-selective agonist):
Targets:

A
  • Blood vessels (Alpha-1)
  • Heart (Beta-1)
  • Bronchial smooth muscle (Beta-2)
125
Q

Adrenergic agonists:
• Adrenaline (non-selective agonist):
Effects:

A
  • Vasoconstriction (Alpha-1)
  • Positive inotropic effect (Beta-1)
  • Bronchodilation (Beta-2)
126
Q

Do NOT use Beta-blockers

A

in ASTHMATICS since most will already be on Beta-2 agonists

127
Q 
-Alpha-1 = 
• Alpha-2 = 
• Beta-1 = 
• Beta-2 = 
• Beta-3 =
A

-Alpha-1 = Vasoconstriction & Bladder contraction
• Alpha-2 = Presynaptic inhibition
• Beta-1 = Increased cardiac effects
• Beta-2 = Bronchodilation
• Beta-3 = Bladder relaxation & Increased lipolysis

128
Q

The chirality of a molecule influences biological activity; D (S form) or L (R form):
- Biological systems use

A

L-amino acids (R form)

129
Q

Pain:

A
  • Unpleasant sensory and emotional experience associated with actual or potential tissue damage
130
Q

Pain Positive role:

A
  • Warning of tissue damage
  • Immobilisation for healing
  • Protection of the species: establishment of memory
131
Q

Pain Physiological effects:

A
  • Increased heart rate
  • Increased blood pressure
  • Increased respiratory rate
132
Q

CHRONIC PAIN

A

Ongoing persistent pain greater than 3-6 months

133
Q

ADVERSE DRUG REACTIONS

A

A response to a drug which is noxious and unintended

134
Q

Types of adverse drug reactions (ADR’s) - ABCDE (Rawlins-Thompson)

A
  • A - Augmented
  • B - Bizarre
  • C - Chronic
  • D - Delayed
  • E - End of Use
135
Q

Drug history is important:
• To identify which type of ADR it is, ask yourself:

(5)

A
  • Is there a history of allergy? - Type B (Bizarre)
  • Is it predictable from the mechanism of action? Does it seem
    dose-related? - Type A (Augmented)
  • Has the patient been using the medication for a long time? - Type
    C (Chronic)
  • Is the patient withdrawing from a medicine? - Type E (End of
    Use)
  • Has the patient uses a drug in the past that could be causing a
    problem now? - Type D (Delayed)
136
Q

Hypersensitivity:

TYPE EXPL

A

• Type 1: IgE-mediated drug hypersensitivity - ANAPHYLAXIS
• Type 2: IgG-mediated cytotoxicity - some drugs can cause renal failure
through this type
• Type 3: Immune-complex deposition - reacts with antibiotics
• Type 4: T-cell mediated - usually substance containing metals

137
Q

Mast cell degranulation:
• Cross linking of IgE receptors releasing:

(3)

A
  • Histamine
  • Thromboxanes, prostaglandins
  • Tumour Necrosis Factor (TNF)
138
Q

Main features of anaphylaxis:

6

A 
• Exposure to drug, immediate rapid
onset
• Rash withe characteristic blotches
• Swelling of lips, face, oedema, central
cyanosis (go blue/purple)
• Wheeze
• Hypotension (Anaphylactic shock)
• Cardiac arrest
139
Q

Alternative presentation of anaphylaxis:

2

A
  • Cardiorespiratory arrest

* NO SKIN CHANGES!

140
Q

Management of Anaphylaxis:

3

A

• Commence basic life support ; A (airway), B (breathing), C (circulation)
• Specific treatment:
- STOP DRUG if infusion
- Adrenaline 1mg (10mls of 1:10,000 (IV)) 1ml IV increments -
note: if cardiac arrest then may need to give cardiac massage in
order to get drugs circulating
- IV Anti histamine (Chlorphenamine 10mg)
- IV Hydrocortisone (100 to 200mg) - note: unlikely to cause harm
in excess so can’t really give too much
• Effect of adrenaline:
- Vasoconstriction, bronchodilation & increased cardiac output

141
Q

If ADR is suspected:

Identify markers:

A

• Type A : Serum concentration - plasma monitoring
• Type B:
- Tryptase - released from only mast cells - BEST TEST TO CONFIRM ALLERGY BASED ADR
- Urine Methylhistamine - breakdown product of histamine

142
Q

Drug interactions
Risk factors - Patient:

(5)

A
  • Polypharmacy - on many different drugs
  • Old age
  • Genetics - e.g. slow/fast metabolism
  • Hepatic disease
  • Renal disease
143
Q

Drug interactions
Risk factors - Drug:

(3)

A
  • NARROW therapeutic index
  • Steep dose/response curve
  • Saturable metabolism - e.g. paracetamol and
    alcohol are metabolised at a SET RATE
144
Q

Renal excretion

Weak acids are … eg.

A 
cleared faster if urine alkali.
• Aspirin - try to alkalinise urine to help increase excretion
with aspirin overdose
• Ibuprofen
• Paracetamol
• Warfarin
145
Q

Renal excretion

Weak bases are … eg.

A 
cleared faster if urine acidic
• Amphetamine
• Atropine
• Propranolol
• Salbutamol
146
Q

Whats required for a prescription:

8

A
  • Patient name
  • Dose
  • Route
  • Frequency
  • Duration
  • Total number of tablets
  • Drug name
  • Date & Signature
147
Q

Drugs discontinued before surgery:

A

Nil by mouth policy for fluids is 2 hours - due to fear of aspiration under anaesthesia

148
Q

Opioid induced respiratory depression:

Opioid antagonists:

A

• Naloxone - give to reverse overdose - IV is fastest route - 400 micrograms per ml

149
Q

10mg of morphine orally is equivalent to

A 
5mg parenterally (sub-cutaneous,
intramuscular & IV)
150
Q

Pathogen:

  • Commensal:
  • Opportunist pathogen:
  • Virulence/Pathogenicity:
  • Asymptomatic carriage:
A

– Organism that causes or is capable of causing disease

  • Organism which colonises the host but causes no disease in normal circumstances
  • Microbe that only causes disease if host defences are compromised
  • The degree to which a given organism is pathogenic/ any strategy to achieve this
  • When a pathogen is carried harmlessly at a tissue site where it causes no disease
151
Q
  • Gram positive:

* Gram negative:

A
  • Gram positive: Purple
  • Gram negative: Pink
  • Can remember since pink has an n and so does negative
152
Q
  • Acid-fast bacilli:

- Non acid-fast bacilli:

A
  • Acid-fast bacilli: Red e.g. Mycobacterium

- Non acid-fast bacilli: Blue e.g. E.coli

153
Q

Catalase test:
• Staphylococci are …
• Streptococci are …
• Many GRAM NEGATIVE bacteria e.g. E.coli and fungi (aspergillus spp.) are catalase …

A
  • catalase POSITIVE
  • catalase NEGATIVE
  • POSITIVE
154
Q

Coagulase test:
Staphylococcus. aureus is coagulase …
Other staphylococci are coagulase …

A
  • POSITIVE - clumping

- NEGATIVE - no clumping

155
Q

Alpha haemolysis:

Beta haemolysis:

A
  • green or brown - strep pneumoniae & strep viridans

- clear/colourless - strep pyogenes & staph aureus

156
Q

Optochin test

  • SENSITIVE:
  • RESISTANT:
A
  • Streptococci pneumoniae - clear zone of no growth around disc
  • Viridans streptococci and other alpha haemolytic streptococci - there will be growth around the disc
157
Q

Oxidase test

A
  • Oxidase positive: Blue - bacteria is AEROBIC e.g. V. cholerae
  • Oxidase negative: No colour change - bacteria may be aerobic or anaerobic
158
Q

Monkey agar

A

• Gram-negative bacilli ONLY
• Will turn PINK/RED if lactose-fermenting bacteria e.g. E.coli
• Will turn WHITE/TRANSPARENT if non-lactose fermenting e.g.
Salmonella

159
Q

XLD AGAR:

A
  • Used to differentiate SALMONELLA and SHIGELLA mainly
  • Salmonella: Red/pink colonies some with black spots
  • Shigella: Red/pink colonies
160
Q

Streptococci can be classified in three ways

A
  • Haemolysis
  • Lancefield typing
  • Biochemical properties
161
Q

Streptococci can be differentiated using haemolysis:

A
  • Alpha haemolysis - greenish/brownish e.g Strep. intermedius
  • Beta haemolysis - clear/colourless e.g. Strep. pyogenes
  • Gamma haemolysis - no lysis e.g. Strep. mutans
162
Q

Streptococci can be differentiated using lancefield typing:

Why?
• Important groupings:

A

• A method of grouping CATALASE NEGATIVE & COAGULASE NEGATIVE bacteria based on the bacterial carbohydrate cell surface antigens

  • Group A - Strep. pyogenes; an important pathogen
  • Group B - Strep. agalactiae; neonatal infections
163
Q

GRAM-NEGATIVE BACTERIA:
Lipopolysaccharide (LPS) is an endotoxin and forms the outer leaflet of the outer
membrane of gram-negative bacteria and comprises:

LPS on on gram-negative bacteria is the main ….

A
  • Lipid A - the toxic portion of LPS that is anchored in the outer leaflet of the
    outer membrane
  • Core (R) antigen - short chain of sugars, some are unique to LPS
  • Somatic (O) antigen - a highly antigenic repeating chain of oligosaccharides
    difference between gram-negative and gram-positive bacteria.
164
Q

MYCOBACTERIA…
Koch postulates:

(4)

A
  • Bacteria should be found in all people with disease
  • Bacteria should be isolated from the infected lesions in people with the disease
  • A pure culture inoculated into a susceptible person should produce symptoms of the disease
  • The same bacteria should be isolated from the intentionally infected individual
165
Q

Principles of mycobacteria treatment:

4

A
  • Slowly replicating bacteria so need prolonged treatment - 6 months of
    antimicrobials
  • There are different populations of mycobacteria in particular locations
    intracellularly and extracellularly or in environments of differing pH
  • Resistance may emerge on treatment so use multi-drug combinations to
    ensure target all populations and mutants
  • Compliance is essential; directly observed treatment used for many patient
    groups to ensure success
166
Q

The highly immunogenic nature of mycobacterial lipids stimulate T-cell
responses 3-9 weeks after exposure to M.tuberculosis:

+ve & -ve effects

A

• Positive effects; macrophage killing of mycobacteria, containment of
infection, formation of a tissue granuloma
• Negative effects: hypersensitivity reactions (type 4) with skin
lesions, eye lesions and swelling of joints

167
Q

PRE-PATENT PERIOD

A

the interval between infection and the

appearance of eggs in the stool

168
Q

Presentation of toxoplasmosis:

A
  • Recent HIV positive diagnosis: CD4 count: 70 (below
    450= low & below 100= high risk of AIDs)
  • 2-week history of progressive left sided weakness
  • Headaches & visual disturbances
  • Commonly presents when people are
    immunosuppressed e.g. HIV/AIDs or cancer on chemotherapy
169
Q

4 species of malaria cause human disease:

3

A
  • P. falciparum (most common)
  • P. ovale
  • P. vivax
  • P. malariae
170
Q

Malaria is transmitted by …

A

… the bite of the FEMALE ANOPHELES MOSQUITO

171
Q

The malaria vector is …

A
  • Female Anopheles mosquito - mainly bites at night
  • Worldwide distribution
  • Infection is acquired during feeding from infected human
172
Q

Malaria Parasitology:

5

A

-Can remember by OVO - Ovale Vivax Overstay
-Each cycle of this process, which is called erythrocytic schizogony, takes about 48 hours in P. falciparum, P. vivax & P.ovale disease
• Whereas in P. malariae it takes 72 hours
• Summary of stages of parasite:
- Sporozoites > Merozoites > Trophozoites > Schizonts >
Merozoites

173
Q

Anaemia due to anaemia is due to:

4

A
  • Haemolysis of infected red cells
  • Haemolysis of non-infected red cells (Blackwater fever - when
    malaria is left to go untreated results in dark coloured urine)
  • Splenomegaly
  • Folate depletion
174
Q

Clinical features of malaria

7

A 
• FEVER is common (BUT NOT ALWAYS PRESENT)
• Other common features:
- Chills & sweats
- Headache
- Myalgia
- Fatigue
- Nausea & vomiting
- Diarrhoea
175
Q

Stages of virus replication:

6

A
  1. Attachment:
    - Viral and cell receptors e.g. HIV (gp120 on HIV and CD4 on T cell)
  2. Cell entry:
    - Only the viral ‘core’ which carries the nucleic acid and some associated proteins acting as enzymes for replication and negation of intracellular host defence factors are freed into the host cell cytoplasm
    - Outer protein coat does not enter
  3. Interaction with host cells:
    - Virus uses cell materials (enzymes, amino acids, nucleotides) for their own replication
    - Also needs to subvert host cell defences
  4. Replication:
    - Production of progeny viral nucleic acid and viral proteins in nucleus, cytoplasm or both
  5. Assembly:
    - Can occur in nucleus e.g. herpesvirus
    - Can occur in cytoplasm e.g. polio virus
    - Can occur in cell membrane e.g. influenza virus
  6. Release:
    - By bursting open (lysis) of cell e.g. rhinovirus
    - By ‘leaking’ (exocytosis) from the cell overtime e.g. HIV & influenza virus (2-3 days from upper respiratory tract)
    - Only a few virus particles will enter the host but millions will exit due to replication
176
Q

The SINGLE MOST EFFECTIVE METHOD OF PREVENTING CROSS

INFECTION is …

A

• Hand hygiene:

177
Q

Antibiotics can also be called

A

Antimicrobial

178
Q

Clostridium difficile antibiotics:

A 
- In general ANY antibiotic that begins with the letter C can result in
clostridium difficile:
• Ciprofloxacin
• Clindamycin
• Cephalosporins
• Co-amoxiclav (augmentin)
• Carbapanems e.g. meropenem

• Note: Flucloxacillin is used to treat Staphylococcus Aureus

179
Q

Pathogens are …

A

… micro-organisms capable of causing disease

180
Q 
Bacteria 
Low number or virulence -
High number or virulence -
Extracellular bacteria - 
Intracellular bacteria -
A

The number of organisms and virulence as well as location determine the defence mechanism employed:
• Low number or virulence - phagocytes active
• High number or virulence - immune response
• Extracellular bacteria - antibody response
• Intracellular bacteria - cellular response

181
Q
  • Schistosomiasis:

process

A

Snail > larvae > human > liver > intestinal mesentery (bladder veins) > male + female (adult worms) > eggs > faeces/urine > snails

182
Q

Worm evasion

A

Glycolipid/glycoprotein coat is host derived so not perceived as foreign to the immune system - utilises host self antigens

183
Q
  • HIV, bird flu or variant Creutzfeldt-Jakob (vCJD) disease (mad cow disease) are or are not notifiable
A

NOT NOTIFIABLE

184
Q

Notifiable diseases

A

Acute encephalitis, acute infectious hepatitis, acute menigitus, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, diptheria, enteric fever (typhoid or paratyphoid), food poisonising, haemolytic uraemic syndrome, infectious bloody diarrhoea, invasice group A Strp disease, Legionnaire disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, SARS, scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever, whooping cough.

185
Q

Meningococcal infection is a … disease. Its seen as GRAM … under microscope

A

vaccine preventable

NEGATIVE PURPLE DIPLOCOCCI

186
Q

Meningococcal infection
Complications:

(9)

A
  • Brain abscess
  • Brain damage
  • Seizure disorders
  • Hearing impairment
  • Focal neurological disorders
  • Organ failure
  • Gangrene
  • Auto-amputation due to arterial occlusions
  • Death
187
Q

MICROBIOLOGY CHEATS:
• Gram-positive bacteria:
- If gram positive then use PENICILLIN TYPE ANTIBIOTICS

A

Sexy - Streptococcus spp.

  • Students - Staphylococcus spp.
  • Can - Corynebacterium spp.
  • Look - Listeria spp.
  • Bad - Bacillus spp.
  • Come morning - Clostridium spp.
188
Q

MICROBIOLOGY CHEATS:

• Gram-negative bacteria:

A
  • Huge - Helicobacter
  • Vaginas - Vibrio cholera
  • Can - Coliforms
  • Never - Neisseria
  • Provide - Parvobacteria
  • Pleasure - Pseudomonas
189
Q

MICROBIOLOGY CHEATS:

DNA viruses:

A
  • H - Herpes viridae
  • A - Adenovirus
  • P - Parvovridae
  • P - Papopviridae
  • H - Hepaviridae
  • Mneumonic - HAPPH

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