Introduction to Clinical Sciences (ICS) Flashcards

Question

What are the main features of an arterial thrombus?

Answer 1

- Commonly caused by atheroma (fatty streaks) - Formed under high pressure - Mainly comprised of platelets - Can lead to myocardial infarction/ stroke

Answer 2

Anti-platelets e.g. aspirin or clopidogrel

Answer 3

- Commonly caused by stasis - Low pressure - Mainly comprised of RBCs - Can lead to DVT/PE

Answer 4

The initial management for a suspected or confirmed DVT or PE for most patients is treatment dose apixaban or rivaroxaban (NICE 2020). Long term anticoagulation in VTE is a DOAC, warfarin, or LMWH for at least 3 months 3 - 6 months in active cancer

Answer 5

1. An embolus enters the venous system often from a deep vein thrombosis 2. It travels to the vena cava > right side of the heart 3. It lodges somewhere in the pulmonary circulation. 4. Loss of blood flow to lung tissue (infarction) and right ventricular strain, as RV pumps against the increased pulmonary resistance.

Answer 6

- May go unnoticed and be resolved - May become organised and cause damage aka "idiopathic pulmonary hypertension"

Answer 7

- Can result in acute respiratory or cardiac problems - Resolves slowly with or without treatment - Can cause chest pain and shortness of breath as an area of the lung cannot be supplied by occluded vessel

Answer 8

- Results in sudden death - Usually long thrombi from leg veins - Impacted (stuck) across the bifurcation of one of the major pulmonary artery

Answer 9

Because if an embolus enters the arterial system, it can travel anywhere downstream of its entry point in the systemic arterial circulatory system

Answer 10

1. Thrombi overlying a myocardial infarct in the heart's left ventricle 2. Cholesterol crystals from an atheromatous plaque 3. Atrial fibrillation

Answer 11

Blood vessels in the lungs split down to capillary size, so are too small for any venous emboli to pass through

Answer 12

Anywhere in the systemic circulation downstream of the thrombus' entry point

Answer 13

Any lower limb and renal arteries

Answer 14

Ischaemia is the reduction in blood flow to a tissue or part of the body caused by constriction or blockage of the blood vessel supplying it

Answer 15

Infarction is the necrosis of part of a whole organ that occurs when the artery supplying it becomes obstructed

Answer 16

- Effects can be reversible - Duration of an ischaemic attack is brief - Cardiomyocytes and cerebral neurons are most vulnerable due to high metabolic demands

Answer 17

- Usually a macroscopic event - Most organs only have a single artery supplying them so susceptible to infarcts - Liver, brain and lungs have dual supply = less susceptible - Reperfusion injury = damage to tissue during re-oxygenation

Answer 18

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

Answer 19

Hypercholesterolaemia (high cholesterol levels)

Answer 20

- Smoking - Hypertension - Diabetes - Male gender - Increasing age

Answer 21

1. Endothelial cell injury at site of plaque formation 2. Inflammatory cells and lipids accumulate in arterial walls 3. Macrophages are attracted to the site of damage and form foam cells by taking up lipids 4. Fatty streak formation (earliest stage of atherosclerotic plaque) 5. Platelet aggregation - plaque protrudes into lumen, disrupting laminar flow > platelets arrive at site 6. Growth factors e.g. platelet-derived growth factor (PDGF) secreted by platelets, injured endothelium, macrophages and smooth muscle cells stimulate proliferation of smooth muscle cells on arterial intima 7. Results in formation of fibrous cap which encloses the lipid-rich core

Answer 22

- A fully developed plaque is a lesion with a central lipid core with a fibrous cap covered by the arterial endothelium - Macrophages, T-lymphocytes and mast cells reside in the fibrous cap - The plaque is highly thrombogenic often bordered by foam cells

Answer 23

A process where a programmed sequence of intracellular events leads to the removal of a cell WITHOUT the release of products harmful to surrounding cells

Answer 24

Traumatic cell death which induces inflammation and repair Characterised by bioenergetic failure (failure to produce ATP) and loss of plasma membrane integrity

Answer 25

- Uses the pro- and anti-apoptotic members of the Bcl-2 family - Bcl-2 inhibits factors that induce apoptosis - Bax forms Bax-Bax dimers which leads to caspase activation > apoptosis Ratio of Bcl-2 to Bax determines the cell's susceptibility to apoptotic stimuli and will determine whether the cell survives or dies due to apoptosis

Answer 26

Growth factors or withdrawal of them and biochemical stressors (e.g. inflammation, hunger, injuries)

Answer 27

P53 protein, encoded by the p53 gene, can induce cell cycle arrest and initiate DNA damage repair

Answer 28

p53 can induce apoptosis of the cell via activation of pro-apoptotic members of the Bcl-2 family

Answer 29

- Ligand (e.g. TNF-alpha, Fas-L) binding at death receptors on the cell surface - Receptors include tumour necrosis factor receptor-1 (TNFR1), FAS and CD95 - Ligand-binding results in the clustering of receptor molecules on the cell surface and the initiation of signal transduction cascade - Caspases are activated, triggering apoptosis - The immune system uses this pathway to eliminate lymphocytes

Answer 30

Release of capases - enzymes that trigger apoptosis!

Answer 31

Increase in cell size without cell division (e.g. muscle hypertrophy in athletes)

Answer 32

Increase in cell number by mitosis (e.g. benign prostatic hyperplasia)

Answer 33

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

Answer 34

The change in a cell from one fully-differentiated cell type to a different fully-differentiated cell type (e.g. Barret's oesophagus)

Answer 35

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

Answer 36

Hyperplasia can only happen in cells that divide, nerve and myocardial cells cannot divide

Answer 37

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

Answer 38

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

Answer 39

Any abnormal swelling

Answer 40

1. Neoplasm 2. Inflammation 3. Hypertrophy 4. Hyperplasia

Answer 41

An environmental agent participating in the causation of cancerous tumours

Answer 42

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

Answer 43

Basal cell carcinoma (type of skin cancer)

Answer 44

- Behaviour (benign or metastatic) - Histogenesis (origin cells of tumour)

Answer 45

1. Does not invade basement membrane 2. Exophytic (grows outwards) 3. Low mitotic activity 4. Circumscribed 5. Necrosis and ulceration rare

Answer 46

- Invades basement membrane - Endophytic (grows inwards) - High mitotic activity - Poorly circumscribed - Necrosis and ulceration common

Answer 47

- Epithelial cells give rise to carcinomas - Connective tissues give rise to sarcomas - Lymphoid (always malignant) and haemopoietic organs give rise to lymphomas or leukaemias

Answer 48

Grade is based on the extent to which the tumour resembles its original histology Grade 1 – Well differentiated (most closely resembles parent tissue) Grade 2 – Moderately differentiated Grade 3 – Poorly differentiated

Answer 49

1. Detachment of tumour cells from their neighbours and embolism 2. Invasion of the surrounding connective tissue to reach conduits that allow metastasis to occur 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 (e.g. lungs) 6. Extravasation of the tumour cells from the vessel lumen into the surrounding tissue

Answer 50

- Haematogenous - Lymphatic - Transcolemic (across the peritoneal cavity) spread via the potential space between the parietal and visceral peritoneum.

Answer 51

Spread by blood stream to form secondary tumours in the organ perfused by the blood drained from the tumour

Answer 52

BLT + KP 1. Breast 2. Lung 3. Thyroid 4. Kidney 5. Prostate

Answer 53

The spread of metastatic tumours via lymphatic vessels, and might form a secondary tumour in a different organ or form secondary tumours in the regional lymph nodes

Answer 54

Spread through pleural, pericardial & peritoneal cavities - results in a neoplastic effusion (abnormal fluid accumulation)

Answer 55

A system doctors use to determine the extent of a tumour spread T - Tumour size N – Node (extent of lymph node involvement) M – Metastasis (extent of metastases)

Answer 56

Inflammation can destroy invading micro-organisms and can prevent the spread of infection.

Answer 57

Inflammation can produce disease and can lead to distorted tissues with permanently altered function.

Answer 58

Malignant epithelial neoplasm

Answer 59

Malignant connective tissue neoplasm

Answer 60

Benign tumour of adipocytes

Answer 61

Benign tumour of striated muscle

Answer 62

Benign tumour of smooth muscle cells

Answer 63

Benign tumour of cartilage

Answer 64

Benign tumour of bone

Answer 65

Benign vascular tumour

Answer 66

Benign tumour of nervous tissue

Answer 67

Malignant tumour of adipocytes

Answer 68

Malignant tumour of straited muscle

Answer 69

Malignant tumour of smooth muscle cells

Answer 70

Malignant tumour of cartilage

Answer 71

Malignant tumour of the bone

Answer 72

Malignant vascular tumour

Answer 73

Malignant neoplasm of melanocytes

Answer 74

Malignant neoplasm of lymphoid cells, all are malignant

Answer 75

Malignant tumour of mesothelial cells which line body cavities (pleura, peritoneum and pericardium) and outer surface of internal organs, secrete lubricating fluid - particularly in the lungs associated with asbestos exposure

Answer 76

1. Chemical (smoking, alcohol) 2. Viruses (Helicobacter pylori, human papillomavirus) 3. Ionising and non-ionising radiation (UV rays, X-rays) 4. Hormones, parasites and mycotoxins 5. Miscellaneous (e.g. asbestos)

Answer 77

Lung cancer - particularly NSCLC squamous cell carcinoma

Answer 78

Bladder cancer

Answer 79

Scrotal carcinoma

Answer 80

Burkitt's lymphoma (B-cells)

Answer 81

Cervical cancer

Answer 82

APC (adenomatous polyposis coli) gene - a tumour suppressor gene

Answer 83

FAP results in adenomas at an early age particularly in the large intestine - they undergo malignant change which almost inevitable progress to adenocarcinoma by age 35

Answer 84

Cervical, Breast and Colorectal cancer

Answer 85

Secondary prevention - method of early detection

Answer 86

Cervical swab done every 3 years from age 25 - 49, every 5 years from 50 - 64

Answer 87

Mammogram every 3 years from age 50 - 71

Answer 88

Faecal immunochemical test (FIT) from age 60 - 74. This is a home test kit sent to a lab

Answer 89

Non-specific immunity you were born with e.g. mucus, inflammation

Answer 90

1. Non-specific + instinctive 2. Response is not improved by repeat infection 3. Rapid response (hours) 4. Depend on phagocytes & natural killer (NK) cells 5. Limited receptors e.g. Toll-like receptors (TLR) recognising pathogen-associated molecular patterns (PAMPs)

Answer 91

- Neutrophils (most abundant WBC, extravasates to affected tissue) - Macrophages (detection, phagocytosis and destruction of bacteria etc. Also present antigens to T cells and initiate inflammation by releasing cytokines - Basophils (circulating form of mast cells, release histamine) - Eosinophils (IgE receptors, combats parasites) - Mast cells ( resident cell of connective tissue containing histamine granules) - Dendritic cells (APC) - Natural Killer cells (NK)

Answer 92

Acute inflammation

Answer 93

Neutrophils

Answer 94

Phagocytosis, antigen presenting & chemokine (IL-8 recruit neutrophils) and cytokine secretion Macrophages are formed when monocytes migrate from blood to tissue Alveolar macrophage - Lung alveoli Kupffer cells - Liver Microglia - Central nervous system

Answer 95

They are circulating forms of mast cells and release histamine - involved in analyphaxis E.g. Allergic reactions, eczema, hay fever

Answer 96

Parasitic infection IgE receptors Neutralise histamine therefore inhibits mast cells

Answer 97

- Anaphylaxis and asthma- IgE binds to allergen, which then binds to mast cells - These mast cells would already be sensitized to that particular allergen and already have specific IgE bound to their surface - Second exposure = IgE crosslinks >causing the mast cells to release histamines, causing Sthe response e.g. bronchoconstriction

Answer 98

Release lytic granules that kill virus infected cells - Provide non-specific immunity against cells displaying foreign proteins such as cancer cells and virally- infected cells. - < 5% of circulating leukocytes. - NK cells can detect abnormal cells and release perforins - cytolytic proteins which create channels which allow extracellular fluid into the cells, causing them to lyse.

Answer 99

These cells process and present antigens from pathogens for recognition by e.g. CD4 cells which then differentiate into T-helper cells Main APCs are dendritic cells, but macrophages and B cells are APCs Once T cells are exposed to an antigen, they go from naive to primed.

Answer 100

A complex series of interacting plasma proteins (C1 - C9) which work alongside the innate and adaptive immunity system to help destroy pathogens. Complement system triggered by: - Lectin pathway, alternative pathway - pathogens - Classical pathway - initiated by antibody-antigen complexes Complement system results in activation of oposinins, perpetuates inflammation and destroys pathogens.

Answer 101

To remove or destroy antigen, either by direct lysis or by opsonisation (process where an antigen on a pathogen becomes coated with substances (i.e. complement) that make it more easily engulfed by neutrophils and macrophages.

Answer 102

- Lyse microbes directly through Membrane Attack Complexes (MACs). - Increase chemotaxis (C3a & C5a) - attracts neutrophils to site of infection/injury - Enhance inflammation - Induce opsonisation (C3b)

Answer 103

When a group of complement proteins create a channel in pathogen's cell membrane which causes an influx of fluids that results in lysis and thus the destruction of the pathogen

Answer 104

Receptors found on macrophages, dendritic cells & neutrophils, they recognise and bind to pathogen-associated molecular patterns PAMPs (e.g. lipopolysaccharide, viral and bacterial nucleic acids and a protein in bacterial flagella

Answer 105

TLR-2 - gram +ve bacteria & TB TLR-4 - lipopolysaccharides on gram -ve bacteria (important!) TLR-5 - flagella TLR-7 - single strand RNA TLR-9 - non-methylated DNA

Answer 106

1. TLR-4 on macrophages is activated by lipopolysaccharides on gram -ve bacteria (endotoxin) 2. Lectins in bloodstream bind pathogen - triggering immune response 3. Complement system activated 4. Macrophages phagocytose the bacteria and release cytokine: - TNF-alpha (All of below) - IL1 (fever) - IL6 (acute phase proteins, opsonins, from the liver) - IL-8 (recruit neutrophils) - IL2 and 12 (activates NK cells))

Answer 107

Acquired defence system to destroy/prevent growth of pathogens

Answer 108

- Specific - Slower primary immune response to a pathogen not previously encountered (days - weeks) - Response to specific antigens - Memory to specific antigens (immunological memory) - faster secondary immune response - Cell-mediated - T-lymphocytes for intracellular microbes - Antibodies - B-lymphocytes for extracellular microbes

Answer 109

Proteins found on cell surfaces that present antigenic peptides to T-cells. T-cells only recognise antigen that have formed a complex with that individual's MHC - MHC class I molecules are found on all nucleated cells (not just professional APCs) and typically present intracellular antigens such as viruses. - MHC class II molecules are only found on APCs and typically present extracellular antigens such as bacteria.

Answer 110

Cytotoxic T cells (expresses CD8)

Answer 111

On the surface of virtually all (nucleated) cells in the body except erythrocytes (non-nucleated)

Answer 112

When cytotoxic T cells (CD8) detects a foreign antigen associated with the MHC I, they will release perforin to kill the cell containing the intracellular pathogen

Answer 113

Helper T cells (CD4)

Answer 114

Mainly on the surface of macrophages, B cells and dendritic cells (i.e. antigen presenting cells)

Answer 115

When helper T cells (CD4) detect foreign antigens on the MHCII, they activate B cells to make antibodies to that specific extracellular pathogen

Answer 116

- T helper cells (T helper cell 1 and 2) - Cytotoxic T cells

Answer 117

They mediate processes associated with cytotoxicity and local inflammatory reactions: 1. Activate macrophages which triggers inflammation 2. They help cytotoxic T-cells develop into effector cells to kill virally-infected target cells 3. Induce B cells to make IgG antibodies

Answer 118

IL-2 (interleukin 2), IL12, gamma-interferon (IFN-gamma) and TNF-beta (tumour necrosis factor)

Answer 119

1. Activate eosinophils and mast cells 2. Important in helminth infections and allergies 3. Induce B cells to make IgE which promotes the release of inflammatory mediators e.g. histamine from mast cells. Therefore T-helper cells 2 are involved in protecting the body against free-living, EXTRACELLULAR, microorganisms

Answer 120

B-cell proliferation (clonal expansion)

Answer 121

B-cell differentiation into plasma cells, class switching to secreting all immunoglobulins

Answer 122

IL-4, -5, -6, -10, -13

Answer 123

- Naive CD8 T cells are activated by antigens presented via MHC class I molecules, usually derived from intracellular microorganisms, on the surface of infected cells

Answer 124

- Effector CD8 T cells release pro-inflammatory and macrophage-activating cytokines - Effector CD8 T cells also release perforins and granulysin to kill infected cells by forming pores in the cell members - Effector CD8 T cells can also induce apoptosis by acting on the FAS molecule of the target cell

Answer 125

- Effector CD8 T cells release pro-inflammatory and macrophage-activating cytokines - Effector CD8 T cells also release perforins and granulysin to kill infected cells by forming pores in the cell members - Effector CD8 T cells can also induce apoptosis by acting on the FAS receptor of the target cell

Answer 126

Plasma cells

Answer 127

1. Naive B cells present pathogen antigens on their cell surface via MHC class II. (naive B cells can only secrete IgM and IgD. 2. The B cells then present the antigen to a T-helper 2 cell (CD4) - which has been activated by being presented with the same antigen by a different APC 3. The T-helper cell binds to the MHC class II via its T-cell receptor (TCR) 4. T-cell then stimulates the B cells to divide (clonal expansion) and allow B cell class switching (can produce IgMAGED) - occurs in lymph nodes 5. The B cells differentiate into short-lived plasma cells (which produce antibodies to that same antigen) and memory cells (which will recognise the same antigen to illicit a faster immune response in the future)

Answer 128

Thymus T lymphocytes originate from haematopoietic stem cells within the bone marrow. Some of these multipotent cells subsequently become lymphoid progenitor cells that leave the bone marrow and travel to the thymus via the blood. Selection process in the thymus

Answer 129

The process by which T-cells in the thymus are selected (I.e. which T-cells are "good") - Positive selection - T cells that recognise the thymus MHC I and II as "self" - markers that tell the immune system that a particular cell is part of the host = selected for - Negative selection - T cells mount a response to the thymus MHC I and II = selected against

Answer 130

B-cell differentiation into plasma cells > release immunoglobulins

Answer 131

Bone marrow - selection process occurs - Positive selection - B cells with functional receptors are allowed to develop further. B cell receptor successfully binds its ligand, which induces survival signals. - Negative selection happens when B cells respond to self-antigens in the bone marrow and undergo apoptosis. - Promotes central tolerance ( eliminating any developing T or B lymphocytes that are autoreactive) and minimises the risk of autoimmune reactions when the B cells eventually mature and move to the peripheral circulation.

Answer 132

GAMED -IgG -IgA -IgM -IgE -IgD

Answer 133

- Most abundant Ig in blood - Important in secondary immune response (act as markers of immunological memory) - IgG 1, 2, 3, 4 subtypes

Answer 134

- Most abundant Ig in body - Found on mucosal linings (GI and urinary tract) and secretions (breast milk, sweat, tears) - Forms dimers

Answer 135

- First Ig released in adaptive response - less specific than IgG - Forms pentamers

Answer 136

- IgE activates mast cells and basophils - Important n allergy and helminth infection - Least abundant in blood

Answer 137

Not that important; the function is debated in the literature

Answer 138

1. Type I - anaphylaxis 2. Type II - cell bound 3. Type III - antibody-antigen immune complex 4. Type IV - delayed hypersensitivity

Answer 139

IgG/M bind to antigenon host cells and activates the complement system - chemotactic and attracts neutrophils Neutrophils release peroxidase enzymes that damage host cells by producing reactive oxygen species. COmplement system molecules (C5b - C9) can form membrane attack complexes that create pores in the cell and destroy it MAC at the site of the antigen-antibody complex Examples include Goodpasture's syndrome or penicillin reaction

Answer 140

Type I (anaphylaxis) - IgE mediated. IgE binds to mast cells/basophils > histamine release > vasodilation, bronchoconstriction, facial flush, pruritus, tongue and face swelling

Answer 141

Antibody-antigen complex mediated In type III hypersensitivity reactions, antibodies bind to free soluble antigens in the blood (not cell-bound like type II) B cells produce antibodies (immunoglobulin) - IgM initially IgM on B cell surface cross-linked by DNA autoantigen binding B-cell presents antigen to T-helper cells, which activates the B cell and induces class switching - can make IgG now Antibody (IgG)-antigen complex activates the complement system - recruit neutrophils which try to phagocytose the antibody-antigen complex and release ROS toxic to cells - vasculitis mostly commonly in kidneys and joints Examples include systemic lupus erythematosus.

Answer 142

- Anaphylaxis - Atopy (e.g. asthma, eczema and hayfever)

Answer 143

- Autoimmune haemolytic anaemia - Goodpasture's syndrome (autoimmune disease where antibodies attack the host's lungs and kidneys) - Pernicious anaemia - Rheumatic fever

Answer 144

- Systemic lupus erythematosus (SLE)

Answer 145

- Graft vs host disease - Tuberculosis - Multiple sclerosis - Guillain Barre syndrome

Answer 146

IgG/M bind to antigen and activates MAC at the site of the antigen-antibody complex

Answer 147

T cell-mediated - T helper cell 1 and cytotoxic T cells are activated by APCs presenting antigen on their MHC class leading to an immune response

Answer 148

How a drug affects the body i.e. what does the drug do once it’s in the body?

Answer 149

What does the body do to the drug i.e. what does it do once the drug is in it? ADME 1. Absorption/adminstration 2. Distribution 3. Metabolism 4. Excretion

Answer 150

Look in your notes

Answer 151

The maximum effect a drug can have in the body (i.e. the degree to how well the works on a specific receptor)

Answer 152

How much of a drug is needed to elicit a response in the body (measures of how well a drug works)

Answer 153

A compound that binds to a receptor and activates it Full affinity (how well it binds) Full efficacy (how well the receptor is activated)

Answer 154

A compound that reduces the effect of an agonist Full affinity (how well it binds) Zero efficacy (how well the receptor is activated)

Answer 155

- Competitive inhibitors - Non-competitive inhibitors

Answer 156

An antagonist that blocks other molecules from binding to the receptor by binding to a different part of the receptor other than the active site. This causes the active site to change shape

Answer 157

Transportation of the unmetabolized drug from the site of administration to the body circulation system Routes of administration include oral, intravenous or inhalation etc. Route of administration affects bioavailability

Answer 158

Protein binding: protein binding lowers the free concentration of a drug. Ideally, the induction drug should have low protein binding to enable a high initial plasma concentration.

Answer 159

The drug should have a high lipid solubility in order for it to readily cross the blood-brain barrier and reach its site of action - BBB favours small lipid-soluble molecules.

Answer 160

How fast and to what extent the drug reaches systemic circulation First-pass metabolism via the liver reduces the bioavailability of an orally administered drug IV = 100% IM: 100% Other routes of administration are compared to IV

Answer 161

Due to first-pass metabolism, the oral dose of morphine needs to be twice that of intravenous morphine to have the same effect e.g. IV dose is 5mg and the oral dose is 10mg.

Answer 162

- Morphine is metabolised in the liver to morphine-6-glucuronide - More potent than morphine. - Excreted by the kidneys so if a patient has renal failure, it will not be as readily excreted - The dose and frequency of administration will need to be reduced to accommodate patient

Answer 163

How the drug is distributed in the plasma according to its chemical properties (e.g. hydrophobicity) and size

Answer 164

Breakdown of an orally administered drug that occurs in the intestine or liver before it reaches the systemic circulation and results in a reduction in the concentration of the drug

Answer 165

How the body gets rid of the drug - urine or faeces

Answer 166

- Oral. - IV. - Subcutaneous. - Intramuscular. - Topical. - Rectal. - Intrathecal (spinal) - Sublingual/buccal. - Inhalation.

Answer 167

Acetylcholine

Answer 168

Preganglionic neurotransmitter: acetylcholine Postganglionic neurotransmitter: noradrenaline

Answer 169

1. Nicotinic (nAChR) - ion channel receptors 2. Muscarinic (mAChR) - G-protein coupled receptor

Answer 170

Muscarinic ACh receptors - the most common mAChR being M1, M2, M3 Found in heart, brain and smooth muscle cells

Answer 171

Nicotinic ACh receptors (nAChR) and they mediate the response of the somatic system at the NMJ

Answer 172

Synthesis - choline acetyltransferase enzyme synthesises ACh from acetyl CoA and choline (substrate) in the neurone Vesicle storage - ACh is then packaged into a vesicle ready to be released when the neurone is stimulated Release - ACh is released when the neurone receives a stimulus Breakdown - after ACh has been used it is broken down in the synaptic cleft by acetylcholinesterase AChE into choline and acetate Reuptake - Choline is taken up into the neurone where it can be used to make more ACh

Answer 173

Acetylcholine

Answer 174

Noradrenaline

Answer 175

Rest & digest! * Constricts pupils * Stimulates tears * Stimulates salivation * Lowers heart rate * Reduces respiration * Constricts blood vessels * Stimulates digestion * Contracts bladder

Answer 176

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

Answer 177

Ion channel receptor

Answer 178

G-protein coupled receptor

Answer 179

M1 - brain M2 - heart M3 - lungs (smooth muscle cells)

Answer 180

Cholinergic crisis :( - overstimulation at NMJ due to excess of ACh or drugs that mimics its actions SLUDGE syndrome Salivation Lacrimation (tears) Urination Defecation Gastrointestinal distress Emesis (vomiting) Nerve agents such as sarin, VX, novichok agents can cause SLUDGE syndrome

Answer 181

- Noradrenaline (NAd) is a neurotransmitter - Adrenaline (Ad) is a hormone

Answer 182

Tyrosine > L-DOPA > dopamine > noradrenaline > adrenaline

Answer 183

Alpha: - Alpha-1 - Alpha-2 Beta: - Beta-1 - Beta-2 - Beta-3

Answer 184

O - blood vessels N - neck of bladder E - eye Effects - Vasoconstriction - Pupil dilation - Bladder contraction

Answer 185

Presynaptic nerve terminals - inhibitory receptors responding to adrenaline and noradrenaline Effect is the presynaptic inhibition of noradrenaline (e.g. blood sugars low = alpha-2 in pancreas stimulated to reduced noradrenaline release = less insulin release from pancreas) TWO = Terminals Weaning Off

Answer 186

Heart, kidneys - response to noradrenaline Effects: - Increased force of heart contraction (positive inotropic effect) - Increased heart rate - Increased electrical conduction in heart - Increased renin release from kidneys - Increased BP

Answer 187

Lungs, blood vessels, GI tract - response to noradrenaline and adrenaline Effect is smooth muscle relaxation leading to bronchodilation, vasodilation, reduced GI motility

Answer 188

Adipose tissue, bladder Effect is increased lipolysis and relaxation of bladder

Answer 189

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug. It has to be noxious and unintended

Answer 190

ABCDE Type A - Augmented Type B - Bizarre Type C - Chronic Type D - Delayed Type E - End of use

Answer 191

- Most common - An extension of the clinical effect - Predictable - Dose related - Self-limiting

Answer 192

- Diuretic causing dehydration - Anticoagulant causing bleeding - Drug for hypertension causing hypotension

Answer 193

- Unexpected - Unrelated to dosage and not expected from known pharmacological action - Unpredictable - Mostly immunological mechanisms - Hypersensitivity

Answer 194

- Heparin causing hair loss - Penicillin causing allergic reaction?

Answer 195

- Occurs after long term therapy - May not be immediately obvious with new medicines

Answer 196

Steroids can cause hyperglycemia which may result in diabetes

Answer 197

Also occurs after a long period of time after treatment - many years Common to see patients developing an ADR 20-30 years after treatment

Answer 198

- Relatively long term use (days/weeks) - Withdrawal reactions - Serious complication of stopping related to clinical effect

Answer 199

Opioids - stopping abruptly causes withdrawal syndrome

Answer 200

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

Answer 201

The system for recording adverse incidents with medicines and medical devices in the UK Patients can report through the yellow card website, app or phone

Answer 202

All serious suspected ADRs for established medicines and vaccines need to be reported, even if the effect is well recognised: - Fatal - Life-threatening - Disabling - Results in prolonged hospitalisation Particularly suspected ADRs: - in children - in patients that are over 65 - to biological medicines and vaccines - associated with delayed drug effects and interactions - to complementary remedies such as homeopathic and herbal products

Answer 203

Naturally occurring opioids - from the opium poppy Morphine Codeine (weak) Simple chemical modifications (1900s) Diamorphine (heroin) Oxycodone Dihydrocodeine Synthetic Opioids (1950s on) Fentanyl (very potent) Synthetic Partial Agonists Buprenorphine

Answer 204

Naloxone - opioid receptor antagonist

Answer 205

- Oral - Parenteral (into the body but outside GI tract) - IV, subcutaneous & intramuscular - Patient Controlled Analgesia (clicker) - Epidural / CSF - Trans-dermal patches for lipid soluble drugs (e.g. fentanyl)

Answer 206

Because 50% of oral morphine is metabolised by first pass metabolism in the liver! 10mg oral morphine = 5mg parenteral morphine (IV, subcutaneous, intramuscular)

Answer 207

- Opioids use the body's natural pain modulation pathways - endorphins (endogenous morphine) and enkephalins - They bind to opioid receptors, G-protein coupled receptors that act via secondary messengers. - They inhibit the transmission of pain signals from spinal cord to the brain and change pain perception to cause euphoria

Answer 208

- Opioids use the body's natural pain modulation pathways - endorphins (endogenous morphine) and enkephalins - They bind to opioid receptors, G-protein coupled receptors that act via secondary messengers. - They inhibit the release of pain transmitters at spinal cord and midbrain and change pain perception to cause euphoria

Answer 209

The following dose of each drug is needed to elicit the same effect: 5mg heroin (most potent) = 10mg morphine = 100mg pethidine (least potent)

Answer 210

Side effect is an unintended effect of a drug related to its pharmacological properties and can include unexpected benefits of treatment

Answer 211

- Bradykinin accumulation in lungs cause dry cough - switch to angiotensin receptor blockers - Dilates afferent arterioles in the glomerulus - leading to worsened kidney function > AKI -

Answer 212

ACE inhibitors used to treat heart failure and high blood pressure and are often prescribed to people following a heart attack They block the action of ACE to prevent the conversion of angiotensin I to angiotensin II. Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion - so blocking its action > reduced peripheral vascular resistance > lowers blood pressure

Answer 213

ACE inhibitors used to treat heart failure and high blood pressure and are often prescribed to people following a heart attack They block the action of ACE to prevent the conversion of angiotensin I to angiotensin II. Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion - so blocking its action > reduced peripheral vascular resistance > lowers blood pressure

Answer 214

- NSAIDs are cyclooxygenase (COX) inhibitors which then prevents production of prostaglandins. - Mucus secretion is stimulated by prostaglandins - COX-1 needed for prostaglandin synthesis - COX-2 inhibition is useful, COX-1 inhibition causes the adverse effects such as reducing the mucosal defence in stomach

Answer 215

As NSAIDs reduce the mucosal defence, it can cause GI upset, GI bleeding, renal impairment and peptic ulcers

Answer 216

- Inhibit Na+/K+/Cl- cotransporter in ascending loop of Henle - Usually all 3 are absorbed in the kidneys and water follows - Blocked= less water reabsorbed E.g. Furosemide, bumetanide

Answer 217

Dizziness; electrolyte imbalance (hyponatraemia, hypochloraemia, hypokalaemia), fatigue; hypotension

Answer 218

Thiazides inhibit Na+/Cl- co-transporters in the distal convoluted tubule of the nephron > prevents reabsorption Na+ and water > lower extracellular fluid volume > lower blood pressure E.g. Bendroflumethiazide

Answer 219

- Hyponatraemia - Hypokalaemia - Cardiac arrhythmias - Impotence in men

Answer 220

Potassium-sparing diuretics (e.g. spironolactalone) are weak alone but often used in combination with another diuretic. Used to treat hypokalaemia caused or loop or thiazide diuretics Spironolactone is an antagonist of aldosterone and prevents the reabsorption of sodium (and therefore water) by binding to and blocking aldosterone-dependent epithelial sodium channels (ENaC) at the distal convoluted tubule > sodium and water excretion > potassium retention

Answer 221

- GI upset - Dizziness, hypotension, hyperkalemia (discontinue)

Answer 222

First line for ischaemic heart disease, chronic heart failure, atrial fibrillation, supraventricular tachycardia (SVT) Hypertension - when other treatments are insufficient

Answer 223

Beta-blockers are antagonista of and act on beta-1 adrenergic receptors in the heart and reduce force of contraction, heart rate and speed of conduction in the heart

Answer 224

1. Prevention and treatment of peptic ulcer disease 2. Symptom relief of GORD 3. Helicobacter pylori infection in combo with amoxicillin and clarithromycin

Answer 225

PPIs reduce gastric acid secretion by irreversibly inhibiting H+/K+-ATPase in gastric parietal cells

Answer 226

- Prolonged use in the elderly can increased risk of fractures - GI disturbances - Headaches - Reduced host deference against infection e.g. Clostridium difficile

Answer 227

E.g. morphine (naturally-occurring) and oxycodone (synthetic) Opioids activate the opioid μ (mu) receptors in the CNS, which result in reduced neuronal excitability and pain transmission. They also act on the medulla to decrease respiratory drive and thus calms the "fight and flight" response

Answer 228

- Respiratory depression > reverse with naloxone - Nausea and vomiting - Constipation - Itching - Tolerance - Dependence - Withdrawal reaction

Answer 229

“Come In And Stain” Crystal violet dye (purple) Iodine - binds to crystal violet and fixes it to cell wall 95% Ethyl Alcohol - decolouriser Safranin - counterstain (pink) Gram +ve bacteria retain crystal violet = purple Gram -ve bacteria decolourise and are stained with safranin = pink

Answer 230

Gram-positive bacteria = multi-layered peptidoglycan wall Gram positive: purple

Answer 231

Gram-negative bacteria = single layer of lipopolysaccharide membrane Gram Negative: piNk

Answer 232

Streptococcus

Answer 233

Fastidious Neisseria (e.g. Neisseria gonorrhoeae)

Answer 234

Salmonella and Shigella If present, they both turn red on the medium, but Salmonella will show up as black dots

Answer 235

- MacConkey agar contain red dyes and lactose. - Only gram-negative bacilli can grow on MacConkey agar - Used to differentiate: lactose-fermenting - turns pink/red e.g. e.coli non-lactose-fermenting - turns white/transparent e.g. salmonella

Answer 236

Add hydrogen peroxide 3% (H2O2) to a small sample of pure colony

Answer 237

Staphylococcus = catalase +ve If bubbles are produced = catalase +ve bacteria present as catalase catalyses the following reaction: 2H2O2 => 2H2O + O2 (gas bubbles)

Answer 238

Streptococcus = catalase -ve

Answer 239

Apply rabbit plasma to a small sample of pure colony. Observe for fibrin clot clumps - coagulase is an enzyme that clots blood plasma

Answer 240

Staphylococcus aureus - coagulase +ve Coagulase Negative Staphylococcus (CONS) - coagulase -ve

Answer 241

S. epidermis S. saprophyticus

Answer 242

Detects the presence of alpha or beta-haemolysin in the bacteria being tested. Haemolysin is an enzyme that breaks down red blood cells Used for classifying different types of streptococci

Answer 243

Bacteria are cultured on blood agar Alpha-haemolytic - greenish/brown discolouration surrounding colonies indicates partial breakdown of RBCs Beta-haemolytic - clear zone surrounding colonies indicating complete lysis of RBCs Gamma haemolysis - no haemolysis

Answer 244

Optochin test

Answer 245

Lancefield test - differentiate beta haemolytic bacteria by detecting surface antigens, each antigen is given a letter: - A, C, G - tonsillitis & skin infection - B - neonatal sepsis & meningitis

Answer 246

Strep pneumoniae & strep viridans

Answer 247

Strep pyogenes (tonsillitis and skin infections) & strep agalactiae (neonatal sepsis and meningitis)

Answer 248

Streptococcus pneumoniae and other alpha-haemolytic streps S. pneumoniae- susceptible to optochin All other alpha-haemolytic streps - resistant to optochin

Answer 249

Gram stain can differentiate MOST bacteria - But mycobacteria e.g. TB are acid-fast bacilli that DO NOT take up the gram stain - Instead they take up a stain called Ziehl-Neelsen

Answer 250

-Mycobacterium is an acid-fast bacilli (resistant to decolourisation) and show as red

Answer 251

-E.coli is an non acid-fast bacilli and show as blue

Answer 252

- Optochin is a chemical - Filter paper disc containing optochin is placed in the petri dish - If the bacteria is susceptible (S. pneumoniae) = clear ring around the optochin as the bacteria could not grow - If the bacteria is resistant (all other alpha-haemolytic streps) = bacteria surrounds the optochin disc

Answer 253

- Optochin is a chemical - Filter paper disc containing optochin is placed in the petri dish - If the bacteria is susceptible (S. pneumoniae) = clear ring around the optochin as the bacteria could not grow - If the bacteria is resistant (all other alpha-haemolytic streps) = bacteria surrounds the optochin disc

Answer 254

Cell wall = extra layer outside cell membrane on bacteria to protect the cell from osmotic lysis Gram +ve have many layers of peptidoglycan forming cell wall Gram +ve = thicker cell wall Gram-negative bacteria cell wall have 2 layers: - inner peptidoglycans (thinner) - Outer phospholipid bilayer containing lipopolysaccharide (endotoxin that immune system react to) Gram -ve = thinner cell wall Gram +ve do not have LPS

Answer 255

Inner membrane (cell membrane) > inter-membrane space (cell wall made of peptidoglycan) > outer membrane

Answer 256

Inner membrane (cell membrane) > cell wall composed of many layers of peptidoglycans

Answer 257

- Streptococci (chains) - Staphylococci (clusters)

Answer 258

Escherichia coli - commensal Shigella Salmonella

Answer 259

"The Queens Guidance Counsellor Said Antibiotics Can Protect Many (if not) Most Royal Members" Tetracycline Quinolone/Fluoroquinolone Glycopeptide Cephalosporin (beta-lactam) Sulfonamides Aminoglycoside Carbapenem (beta-lactam) Penicillin (beta-lactam) Macrolides Monobactam (beta-lactam) Rifampicin Metronidazole

Answer 260

"The Queens Guidance Counsellor Said Antibiotics Can Protect Many (if not) Most Royal Members" Tetracycline - tetracycline/doxycycline Quinolone/Fluoroquinolone - ciprofloxacin Glycopeptide - vancomycin Cephalosporin - cefotaxime Sulfonamides - sulfamethoxazole Aminoglycoside - gentamicin Carbapenem - meropenem Penicillin - amoxicillin *Macrolides - clarithromycin Monobactam - aztreonam Rifampicin - rifampcin Metronidazole - metronidazole

Answer 261

Mechanism: inhibition of the 30s ribosomal subunit - preventing translation Both gram +ve and -ve - broad spectrum, examples: - Staph aureus (+ve) - Strep pyogenes (+ve) - Strep viridians (+ve)

Answer 262

Mechanism- inhibition of DNA synthesis (topoisomerase II and IV) in bacteria Both Gram + and - - Strep viridians (+ve) - strep pyogenes. (+ve) - Pseudomonas auerginosa (-ve)

Answer 263

Mechanism: inhibits synthesis of bacterial cell wall does not affect mammalian cells as no cell wall Gram positive (Strep, staph) Severe staph. infections e.g. MRSA/ C. Difficile

Answer 264

Part of the beta-lactam class of antibiotics, interferes with cell wall assembly consisting of peptidoglycans by inhibiting transpeptidase enzyme > weakens cell wall > lysis of the bacteria Both Gram + and - Hypersensitivity reactions - Staph. Aureus, - Streptococci - Nisseriae - Haemophilus influenza - Coliforms.

Answer 265

Both Used for pneumocystis pneumonia treatment and prophylaxis

Answer 266

Mechanism: inhibits protein synthesis by 30s ribosomal subunit inhibition Staph aureus - severe sepsis

Answer 267

Beta-lactam - interferes with cell wall assembly consisting of peptidoglycans by inhibiting transpeptidase enzyme > weakens cell wall > lysis of the bacteria. Both Gram + and - Broad spectrum Severe infection Sepsis Peritonitis

Answer 268

Beta-lactam inhibits cell wall synthesis > weakens cell wall > lysis of the target bacteria Penicillin G - gram positive Ampicillin - both Methicillin - both Narrow spectrum: benzylpenicillin; active against streptococci Moderate spectrum: amoxicillin; active against a range of Gram-positive and Gram negative bacteria -Penicillins resistant to staphylococcal b-lactamase = flucloxacillin

Answer 269

MOA: Inhibition of 50S ribosome subunit leading to inhibition of protein systhesis Gram positive Used in streptococcal and staphylococcal soft tissue infections; respiratory infections including those caused by Mycoplasma pneumoniae, Legionella

Answer 270

MOA : inhibition of cell wall synthesis Gram negative Not on guide so dont need to know

Answer 271

Trimethoprim: - Used for UTIs - Inhibition of folic acid synthesis and causes folate deficiency. - Do not use in pregnancy

Answer 272

MOA: binds to and inhibits bacterial RNA polymerase Both Gram+ and - Used in combination with isoniazid, pyrazinamide and ethambutol in treatment of TB

Answer 273

MOA: causes DNA strand breaks and dysregulates DNA synthesis Both Gram+ and - Used to treat anaerobic infections and dental infections

Answer 274

Glycopeptide Cephalosporin Carbapenem Penicillin Monobactam

Answer 275

Tetracycline Aminoglycoside

Answer 276

Macrolides

Answer 277

Quinolone/Fluoroquinolone

Answer 278

Sulfonamides

Answer 279

Rifampicin

Answer 280

Metronidazole

Answer 281

Penicillin Cephalosporins Carbapenems

Answer 282

Use: gram-positive and negative infections, hospital-acquired pneumonia MOA: cefuroxime is a cephalosporin, which are antibacterials that attach to penicillin binding proteins to interrupt cell wall biosynthesis, leading to bacterial cell lysis and death. Side effects: Abdominal pain; diarrhoea; dizziness

Answer 283

1) infection due to beta-lactamase-secreting bacteria 2) Co-amoxiclav is a penicillin. They are bactericidal and act by interfering with bacterial cell wall synthesis 3) Diarrhoea; hypersensitivity; nausea

Answer 284

1) Infection (e.g. impetigo, cellulitis) 2) Macrolide - inhibtes synthesis of the bacterial 50s ribosomal subunit - preventing translation 3) Appetite decreased; diarrhoea; dizziness

Answer 285

1) Endocarditis and tuberculosis alongside other drugs 2) Inhibits bacterial DNA-dependent RNA polymerase 3) Nausea; thrombocytopenia; vomiting

Answer 286

Transpeptidases (specifically penicillin binding protein) help crosslink the peptidoglycans on bacterial cell wall Beta-lactam antibiotics work by binding and disrupting these transpeptidases - thus breaking the cell wall However, some bacteria have developed antibiotics resistance by mutations in their transpeptidase gene, the resulting shape change means the transpeptidase no longer bind to the antibiotics molecules

Answer 287

- Some gram-negative bacteria can produce beta-lactamase - an enzyme which hydrolyses beta-lactam antibiotic molecules. - They can share the gene that encode for beta-lactamase with other bacterial cells, thus spreading antibiotic resistance

Answer 288

resistance gene mecA

Answer 289

Penicillin-binding protein 2a (PBP2a) - which builds bacterial cell wall by crosslinking amino acids on the peptidoglycans

Answer 290

PBP2a does not bind penicillin, therefore confers resistance to all beta-lactam antibiotics and methicillin

Answer 291

Remember KEEPS! Klebsiella E.coli (80 - 90% cases) Enterococcus Proteus mirabilis Staph saprophyticus (common in young women)

Answer 292

Symptoms Dysuria (painful urination) Urgency Increased frequency Cloudy/foul-smelling urine SIgns Haematuria (blood in urine - micro/macro) Suprapubic tenderness

Answer 293

Fever Confusion Loin tenderness History of lower UTI symptoms

Answer 294

1st line: Urine dipstick: nitrite and leukocyte positive Midstream urine and culture if dipstick positve: gold standard for Dx of the causative agent, urinalysis - white cells and microscopic haematuria

Answer 295

5 - 10 days

Answer 296

Oral Nitrofurantoin or Trimethoprim

Answer 297

First-line = nitrofurantoin DO NOT use trimethoprim as it inhibits folate synthesis and can harm the foetus

Answer 298

Nitrofurantoin is linked with haemolytic anaemia in the newborn Give amoxicillin instead if not allergic

Answer 299

an infectious, obligate intracellular pathogen comprising of genetic material (DNA/RNA) surrounded by a protein coat and/or membrane

Answer 300

Organism that causes or is capable of causing disease

Answer 301

Organism which colonises the host but causes no disease in normal circumstances

Answer 302

Microbe that only causes disease if host defences are compromised

Answer 303

The degree to which a given organism is pathogenic.

Answer 304

When a pathogen is carried harmlessly at a tissue site where it causes no disease

Answer 305

Bacteria: has cell wall, DNA, RNA and organelles. Considered living and NOT dependent on host Virus: no cell wall, no organelles, contain only DNA or RNA. Not living and dependent on host

Answer 306

1. Attachment 2. Cell entry 3. Genome interaction 4. Genome replication 5. Assembly 6. Exit

Answer 307

Virus binds to host cell receptors e.g. gp120 on HIV binding to CD4 on T cells

Answer 308

Viral "core" containing nucleic acids, enzymes for replication and negotiation of host cell defences are released into the host cell cytoplasm Outer protein coat not released

Answer 309

Virus uses cell materials including enzymes, amino acids, nucleotides for their own replication and to evade host cell defences. Some viruses like HIV produce proviral DNA that integrates itself into the host genome

Answer 310

Once the viral nucleic acids are in the host cell, transcription or translation of the viral genome is initiated. This process results in synthesis of viral nucleic acids, proteins and genome.

Answer 311

This is where the virus puts itself together and encapsulate their genome into a shell called a capsid Can occur in: - nucleus e.g. herpesvirus - cytoplasm e.g. polio virus - cell membrane e.g. influenza virus

Answer 312

This is where the progeny leave the host cell, few enter but millions exit because of replication :( Different viruses leave in different ways: - By bursting open (lysis) of cell e.g. rhinovirus - By ‘leaking’ (exocytosis) from the cell over time e.g. HIV & influenza

Answer 313

Neisseria meningitidis (meningococcus) Streptococcus pneumoniae (pneumococcus)

Answer 314

Lancerfield group B strep (GBS) = strep agalactiae - usually lives harmlessly in mother's vagina

Answer 315

Herpes simplex virus 1/2 (HSV 1/2) Enterovirus Varicella zoster virus (VZV)

Answer 316

Herpes simplex virus - HSV 1 95% cases Children: Herpes simple type-1 (HSV-1) from cold sores Neonates: Herpes simple type-2 (HSV-1) from genital herpes contracted during birth

Answer 317

- Staphylococcus aureus - Group A streptococcus (mainly strep pyogenes)

Answer 318

Flucloxacillin - oral or IV

Answer 319

Clarithromycin

Answer 320

Microscopic unicellular eukaryotes, can be free-living or parasitic

Answer 321

Malaria is an infectious disease caused by members of the Plasmodium family of protozoan parasites.

Answer 322

- P. falciparum (most common and dangerous - 75% cases in UK) - P. ovale - P. vivax - P. malariae

Answer 323

The bite of the female Anopheles mosquitoes Infection is acquired when feeding on an infected human

Answer 324

Differs between species but generally: Sporozoites > Merozoites > Trophozoites > Schizonts > Merozoites

Answer 325

A female anopheles mosquito sucks up infected blood, the malaria in the blood reproduce in the mosquito gut producing thousands of sporozoites Mosquito bites another human > sporozoites injected > sporozoites travel to liver of newly infected person

Answer 326

P.vivax P.ovale

Answer 327

They mature into merozoites which enter blood and infect RBCs > reproduce over 48 hours > RBCs rupture > release more merozoites into blood > haemolytic anaemia People infected with malaria therefore have high fever spikes every 48 hours

Answer 328

Eukaryotic organism with cell wall made of chitin and glucan Clinically usually opportunistic

Answer 329

Candida albicans Aspergillus fumigatus

Answer 330

Thrush - vaginal and oral Sepsis (candidiasis) Line/catheter infections Can kill rapidly if untreated

Answer 331

Lung infections, allergic disease. Usually affect those with weakened immune system or underlying lung conditions Poor prognosis but kills slowly

Answer 332

Generally difficult to treat as fungi are eukaryotic like human cells. Usually antifungal drugs that target fungal cell wall/plasma membrane E.g. azole group (e.g. Fluconazole, Clotrimazole & ketoconazole)

Answer 333

Within the first 72 hours of life - Physical examination - Heel prick test - newborn screening The purpose: - Screen for congenital abnormalities that will benefit from early intervention - To make referrals for further tests or treatment as appropriate - To provide reassurance to the parents

Answer 334

The HCP checks the baby's eyes, heart, hips and testicles (in boys) to detect any problems A newborn hearing screen is conducted as well.

Answer 335

Carried out when the baby is 5 days old, and screens for: - Sickle cell anaemia - Cystic fibrosis - Congenital hypothyroidism - Inherited metabolic disease (e.g. phenylketonuria) - Severe combined immunodeficiency (SCID) (in some areas of England)

Answer 336

When the baby is 6 - 8 weeks of age

Answer 337

The GP will ask mum questions to assess her and the baby's health - physical symptoms, psychological problems, social problems, sex & contraception

Answer 338

6-in-1vaccination against: - Diphtheria - Hepatitis B - Hib (Haemophilus influenzae type b) - Polio - Tetanus - Whooping cough (pertussis)

Answer 339

Oral, rectal (PR) and IV

Answer 340

Serology testing (detects antibodies against virus) - ELISA (enzyme-linked immunosorbent assay), immunofluorescence, complement fixation Viral detection - EM, PCR (quick, easy and cheap when you suspect a particular virus) Diagnostic swabs - green swabs for viral infections and black charcoal swabs for bacterial infection - differentiate between the different sources of infection

Answer 341

Infectious mononucleosis (glandular fever)

Answer 342

Streptococcal pharyngitis caused by S.pyogenes - EBV pharyngitis is usually clinically indistinguishable from strep. pharyngitis

Answer 343

Streptococcal pharyngitis - EBV pharyngitis is usually clinically indistinguishable from strep. pharyngitis Exclude S.pyogenes infection using black charcoal swabs

Answer 344

Primary investigations: - FBC: may show more than 20% atypical/reactive lymphocytes or a lymphocytosis - available in hours - Monospot test (heterophile antibodies): tested in the 2nd week of symptoms to confirm the diagnosis

Answer 345

Symptoms: - Tonsillitis - Cough - Fever Signs: - Splenomegaly

Answer 346

Conservative. However, hospital admission if the patient has stridor (high-pitched sound on auscultation indicating airway obstruction), dehydration or difficulty swallowing fluids, or a complication such as a splenic rupture. 1st line: conservative measures: oral fluids and paracetamol/ibuprofen for pain and fever relief Avoid heavy lifting: for the first month of the illness to reduce the risk of splenic rupture.

Answer 347

CMV colitis/gastroenteritis - inflammation of GI tract due to CMV infection. Characteristic "owl-eye" inclusion bodies under the microscopy

Answer 348

- As usually asymptomatic, if CMV infects healthy patients, it is an AIDS defining illness

Answer 349

Mild, self-limiting illness is usually managed conservatively. Intravenous ganciclovir (Antiviral) is the first-line antiviral treatment of severe CMV disease, including severe colitis and pneumonitis

Answer 350

- It is a glycosaminoglycan - Binds to antithrombin and increases its activity (antithrombin inactivates several factors of the coagulation cascade - factor IIa (thrombin) and factor Xa) - Monitor with activated partial thromboplastin time (APTT), aim ratio 1.2-2.8 - Given by continuous infusion

Answer 351

- Smaller molecule compared to heparin, less variation in dose, and renally excreted - Affects instinct pathway, activates antithrombin - inactivates factor Xa and IIa (thrombin) - Once daily, weight-adjusted dose given subcutaneously - Used for treatment and prophylaxis, preferred over heparin as reduced risk of heparin-induced thrombocytopenia) and generally more convenient to use

Answer 352

- Warfarin affects the extrinsic pathway, and it is a vitamin K antagonist. Therefore it inhibits vitamin K-dependent clotting factor synthesis - factors X, IX, VII and II (1972) - Difficult to use, need to monitor - Measure INR (international normalised ratio, derived from prothrombin time (PT)) - Target range: 2-3, higher range: 3-4.5

Answer 353

- Directly-acting Oral Anticoagulants - Affects intrinsic pathway, direct inhibitor of activated factor X (factor Xa) - No blood tests or monitoring - Side effects: anaemia; asthenia (weakness); constipation; diarrhoea - teratogenic

Answer 354

1) Inotropic support in infarction, cardiac surgery, cardiomyopathies 2) Dobutamine is a cardiac stimulant which acts on beta1 receptors in cardiac muscle and increases contractility. 3) Arrhythmias; bronchospasm; chest pain

Answer 355

Controlled and safe exposure to part of a pathogen that is immunogenic and will induce immunological memory with little to no harm to the host. A lot of vaccines have an initial “prime” dose followed by a “boost dose”. An ideal vaccine will induce both T and B memory cells.

Answer 356

An adjuvant is a substance added to a vaccination to stimulate an immune response. They convince your immune system that you’re infected.

Answer 357

TLR4 agonist (mimics lipopolysaccharide)

Answer 358

- Live/attenuated vaccines contains the live pathogen with reduced virulence - Very effective, prolonged and comprehensive. - Immunological memory produced. - Often only 1 vaccine is needed.

Answer 359

- Immunocompromised patients may become ill. - Vaccines often need to be refrigerated which can be a problem in remote areas.

Answer 360

Vaccines consisting of the pathogens that have been grown in culture and then killed to destroy disease-producing capacity - No risk of infection - Storage method is less critical

Answer 361

- Inactivated vaccines tend to only activate the humoral response; there is a lack of T cell involvement. - Boosters are needed and so patient compliance may be poor.

Answer 362

Toxoids (inactivated toxins), proteins, chemicals (aluminium salts) etc.

Answer 363

1) Safe. 2) Induces a suitable immune response. 3) Shouldn’t require repeated boosters. 4) Generates immunological memory (T and B cell response) 5) Stable and easy to transport.

Answer 364

Aspirin works by IRREVERSIBLY inhibiting Cox and prevents the breakdown of arachidonic acid into prostaglandin H2. It is non-selective for Cox-1 and Cox-2. Used in secondary prevention of CVD (75mg) Management of unstable angina, non-STEMI, STEMI, acute ischaemic stroke (300mg) Secondary prevention of ischaemic stroke (not associated with AF) (75mg) Side effects: general: asthma attack, bronchospasm Specific: oral use = dyspepsia, haemorrhage