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Phase 2a > Pharmacology and Microbiology > Flashcards

Pharmacology and Microbiology Flashcards

1
Q

Describe noradrenaline?

A

Noradrenaline: released from the sympathetic nerve fibre ends - beloved in the management of shock in the ICU

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2
Q

Describe adrenaline?

A

Adrenaline: released from the adrenal glands - fight or flight and management of anaphylaxis

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3
Q

What is dopamine?

A

Precursor of adrenaline and noradrenaline

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4
Q

Describe alpha 1 receptors?

A

Agonists: NAd > Ad

Mechanism: increases intracellular calcium, Gq signalling

Consequence: Contracts smooth muscle e.g. pupils, blood vessels

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5
Q

Describe alpha 2 receptors?

A

Agonists: NAd = Ad

Mechanisms: Gi signalling, inhibition of cAMP generation

Consequence: Mixed effects on smooth muscle

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6
Q

Describe beta 1 receptors?

A

Agonists: NAd = Ad

Mechanism: Gs, raises cAMP

Consequence: Chronotropic and inotropic effects on the heart

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7
Q

Describe beta 2 receptors?

A

Agonists: Ad&raquo_space; NAd

Mechanism: Gs, raises cAMP

Consequences: relaxes smooth muscle

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8
Q

Describe beta 3 receptors ?

A

Agonists: NAd > Ad

Mechanism: Gs, raises cAMP

Consequences: enhances lipolysis, relaxes bladder detrusor

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9
Q

Describe alpha blockers?

A

Opposite effect to agonists

  • Block alpha 1 to lower BP e.g. doxazosin
  • Tamsulosin blocks a specific subtype (alpha 1a) in the prostate, helps treat prostatic hypertrophy
  • No useful alpha 2 blocker
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10
Q

Describe beta blockers?

A

Propranolol: blocks beta 1 and beta 2. Will slow heart rate, reduce tremor, but may cause wheeze

Atenolol: beta 1 selective, main effects on heart.

Lower blood pressure (by reduction in cardiac output and gradual reduction in central sympathetic outflow activity), reduce cardiac work, treat arrhythmias

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11
Q

What are some uses of beta blockers?

A

Angina

MI prevention

High blood pressure Anxiety

Arrhythmias

Heart failure

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12
Q

Side effects of beta blockers?

A 
Tiredness 
Cold extremities 
Bronchoconstriction 
Bradycardia 
Hypoglycaemia 
Cardiac depression
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13
Q

What is ‘druggablilty’ ?

A

The ability of a protein target to bind to small molecules with a high affinity

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14
Q

Describe the difference between exogenous and endogenous ligands?

A

Exogenous - drugs

Endogenous - hormones, neurotranmitters

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15
Q

What are the different types of chemicals detected by receptors?

A 
1. Neurotransmitters
–	acetylcholine, serotonin  
2. Autacoids (local)
–	cytokines, histamine 
3. Hormones
–	testosterone, hydrocortisone
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16
Q

What are the different types of receptors?

A
  1. Ligand-gated ion channels
    - nicotinic ACh receptor
  2. G protein coupled receptors
    - beta-adrenoceptors
  3. Kinase-linked receptors
    - receptors for growth factors
  4. Cytosolic/nuclear receptors
    - steroid receptors
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17
Q

How are cholinergic receptors characterised?

A 
Receptor = nAChR
Agonist = nictotine 
Antagonist = curare 
Receptor = mAChR 
Agonist = muscarine 
Antagonist = atropine
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18
Q

How are H2 (histamine) receptors characterised?

A 
•	Histamine (agonist) 
–	contraction of ileum
–	acid secretion from parietal cells
•	Mepyramine (antagonist) 
–	reversed contraction of ileum
–	no effect on acid secretion
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19
Q

Define: affinity?

A

Affinity describes how well a ligand bids to the receptor and is property shown by BOTH agonists and antagonists

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20
Q

Define: efficacy?

A

Describes how well a ligand activates the receptor and is a property shown ONLY by agonists

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21
Q

Define: tolerance?

A

It is a reduction in the agonist effect over time due to continuous repeated high concentration

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22
Q

Define: desensitisation?

A

Happens when the proteins are uncoupled, internalised or degreated

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23
Q

Describe receptor reserve?

A

Where agonist needs to activate only a small fraction of the existing receptors to produce the maximal system response.

Holds for a full agonist in a given tissue
– reserve can be large or small; depends on tissue

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24
Q

Describe adverse drug reactions?

A

ADRs are 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, has to be noxious and unintended

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25
Q

What are the classifications of ADRs?

A
  1. Toxic effects (beyond therapeutic range) can occur if dose is too high or drug excretion is reduced
  2. Collateral effects (therapeutic range)
  3. Hypersceptibility effects (below the therapeutic range)
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26
Q

What is a side effect?

A

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

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27
Q

What are the different reaction time classifications within ADRs?

A
  1. Rapid reactions – red man syndrome due to histamine release with rapid administration of vancomycin
  2. First dose reactions - hypotension and ACE inhibitors
  3. Early reactions – nitrate induced headache
  4. Intermediate reactions – eg delayed immunological reactions such as Stevens-Johnson syndrome with carbamazepine
  5. Late reactions – adverse effects of corticosteroids, seizures on withdrawal of long term benzodiazepines
  6. Delayed reaction – Thalidomide and phocomelia
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28
Q

What are the Rawlins Thompson classifications of Adverse Drug reactions?

A

A to F!
• Type A (Augmented pharmacological)– predictable, dose dependent, common (morphine and constipation, hypotension and antihypertensive)
• Type B (Bizarre or idiosyncratic)– not predictable and not dose dependent (anaphylaxis and penicillin)
• Type C (Chronic) – osteoporosis and steroids
• Type D (Delayed) – malignancies after immunosuppression
• Type E (End of treatment) – occur after abrupt drug withdrawal eg opiate withdrawal syndrome
• Type F (Failure of therapy) – Failure of OCP in presence of enzyme inducer

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29
Q

What are some of the risk factors for ADRs?

A

Patient Risk

  • Gender (F>M)
  • Elderly
  • Neonates
  • Polypharmacy (21% 5 or more drugs)
  • Genetic predisposition
  • Hypersensitivity/allergies
  • Hepatic/renal impairment
  • Adherence problems

Drug Risk

  • Steep dose-response curve
  • Low therapeutic index
  • Commonly causes ADR’s
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30
Q

When should we expect an ADR?

A
  • Symptoms soon after a new drug is started
  • Symptoms after a dosage increase
  • Symptoms disappear when the drug is stopped
  • Symptoms reappear when the drug is restarted
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31
Q

Name some common drugs to have ADRs?

A
  • Antibiotics
  • Anti-neoplastics
  • Cardiovascular drugs
  • Hypoglycaemics
  • NSAIDS
  • CNS drugs
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32
Q

Name some common systems to be affected by ADRs

A
  • GI
  • Renal
  • Haemorrhagic
  • Metabolic
  • Endocrine
  • Dermatologic
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33
Q

Name some common ADRs?

A
  • Confusion
  • Nausea
  • Balance problems
  • Diarrhoea
  • Constipation
  • Hypotension
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34
Q

Describe what to report on a yellow card, who can report and info to include?

A

What: All suspected reactions for herbal medicines, or black triangle drugs

Who: doctors, dentists, any medical staff and patients

Info:

  • Suspected drugs
  • Suspectied reactions
  • Patient details
  • Reporter details
  • Additional useful information
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35
Q

Define: pathogen?

A

An organism that causes or is capable of causing disease

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36
Q

Define: commensal?

A

An organism which colonises the host but causes no disease in normal circumstances

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37
Q

Define: opportunist pathogen?

A

A microbe that only causes disease if the host defences are compromised

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38
Q

Define: virulences/pathogenicity?

A

The degree to which an organism is pathogenic

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39
Q

Define: asymptomatic carriage?

A

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

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40
Q

What are the three main shapes of bacteria?

A

Coccus (sphere)

Bacillus (rod)

Spriochaete

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41
Q

What colour do gram positive bacteria stain?

A

Purple

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42
Q

What colour to gram negative bacteria stain?

A

Red

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43
Q

What are the different formations of cocci?

A

Diplococcus (two attached cocci) = gram +ve

Chains of cocci = gram +ve

Cluster of cocc i= gram +ve

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44
Q

What are the different formations of bacilli?

A

Chain of rods = gram +ve

Curved rod = -ve

Spiral rod = -ve

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45
Q

Describe bacterial DNA?

A

Bacteria have a chromosome of circular double stranded DNA

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46
Q

What does Ziehl Neelsan stain for?

A

Acid-fast bacilli .

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47
Q

What is an endotoxin?

A

Endotoxin is a component of the outer membrane of the bacteria e.g. lipopolysaccharide in Gram negative bacteria

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48
Q

What is an exotoxin?

A

Secreted proteins of Gram positive and Gram negative bacteria

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49
Q

Where does obligate intracellular bacteria grow?

A

Has to be grown inside cells, examples include Rickettsia, Chlamydia and Coxiella

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50
Q

Example of bacteria growing as filaments?

A

Actinomyces, nocardia, streptomyces

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51
Q

Example of bacteria growing as spriochetes?

A

Leptospira, treponema and borrelia

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52
Q

How does gram stain work?

A
  1. Apply a primary stain such as crystal violet (purple) to heat fixed bacteria
  2. Add iodide which binds to crystal violet and helps fix it to the cell wall
  3. Decolorise with ethanol or acetone
  4. Counterstain with safranin (pink)
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53
Q

What happens in gram negative bacteria with gram stain?

A
  • the decoloriser interacts with the lipids and cells lose their outer lipopolysaccharide membrane
  • the crystal violet-iodide (CV-I) complexes, thus they appear pink with counterstain
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54
Q

What happens in gram positive bacteria with gram stain?

A
  • Positive bacteria the decoloriser dehydrates the cell wall
  • the CV-I get trapped in the multi-layered petidoglycan
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55
Q

Do mycobacteria stain with Gram stain?

A

NO

High lipid content with mycolic acids in cell wall makes Mycobacteria resistant to Gram stain - acid fast bacilli

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56
Q

Give some examples of mycobacteria of clinical importance?

A

M.tuberculosis - tuberculosis

M.leprae - leprosy

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57
Q

Describe the microbiology of tuberculosis ?

A
  • Aerobic (non spore forming bacillus)
  • Cell wall: high molecular weight, weakly gram positive, survive inside macrophages
  • Slow growing
  • Slow response to treatment
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58
Q

Desscribe the risk of TB reactivation after exposure?

A
  • 10% lifetime risk
  • Most in first two years then 0.1% per year

Increased risk in:

– Age (infants, young adults, elderly)
– Malnutrition
– Intensity of exposure
– Immunosuppression – e.g. HIV 10% per year

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59
Q

What would an induration of 5 or more millimetres indicate in tuberculosis?

A

A positive result in:

  • HIV infected persons
  • Recent contact with someone else with TB
  • Person with fibrotic change on radiograph
  • Immunosuppressed for any reason
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60
Q

What would an induration of 10 or more millimetres indicate in tuberculosis?

A

A positive result in:

  • Recent immigrants
  • Injection drug users
  • Mycobacteriology lab users
  • Children <4
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61
Q

What would an induration of 15 or more millimetres indicate in tuberculosis?

A

A positive result in persons with no know risk of TB

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62
Q

What are the different stages of tuberculosis?

A
  1. Primary Tuberculosis - bacilli takin in lymphatics to hilar lymph nodes
  2. Latent Tuberculosis - cell mediated immune response from T cells, primary infection
  3. Pulmonary Tuberculosis - granuloma forms around bacilli that settled in apex, CMI and necrosis results in abcess of bacilli forming and caseous material leaving cavity
  4. TB spreads beyond the lungs - Milliatry, TB meningitis, genito-urinary, bone TB
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63
Q

Whats makes up a primary complex in TB?

A

Granuloma + lymphatics + lymph nodes = primary complex

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64
Q

What is an enzyme inhibitor?

A

A molecule that binds to an enzyme and decreases its activity

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65
Q

What are the two types of enzyme inhibitors?

A
  • Irreversible inhibitors usually react with the enzyme and change it chemically (e.g. via covalent bond formation).
  • Reversible inhibitors bind non-covalently and different types of inhibition are produced depending on whether these inhibitors bind to the enzyme, the enzyme-substrate complex, or both.
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66
Q

What are the three main types of protein posts in cell membranes?

A
  1. Uniporters: use energy from ATP to pull molecules in.
  2. Symporters: use the movement in of one molecule to pull in another molecule against a concentration gradient
  3. Antiporters: one substance moves against its gradient, using energy from the second substance (mostly Na+, K+ or H+) moving down its gradient.
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67
Q

Give an example of a symporter?

A

The Na-K-Cl cotransporter (NKCC) is a protein that transports Na, K, and Cl into cells

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68
Q

What is transport?

A

Its when molecules move across a cell membrane

Needs energy (usually ATP)

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69
Q

Describe voltage-gated calcium channels?

A

Voltage-gated ion channels (VDCC) are found in the membrane of excitable cells (e.g., muscle, glial cells, neurones, etc.)

At physiologic or resting membrane potential, VDCCs are normally closed.

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70
Q

What is an action potential?

A

A momentary change in electrical potential on the surface of a cell, especially of a nerve or muscle cell, that occurs when it is stimulated, resulting in the transmission of an electrical impulse.

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71
Q

Give examples of irreversible enzyme inhibitors?

A

Omeprazole - proton pump inhibitor

Aspirin - COX inhibitor

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72
Q

What are xenobiotics?

A

are compounds foreign to an organism’s normal biochemistry, such any drug or poison

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73
Q

What are pharmokinetic principles of ADME?

A

Absorption
Metabolism
Distribution
Excretion

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74
Q

What is the study of drug metabolism?

A

Pharmokinetics

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75
Q

What are the three types of haemolysis?

A

α- partial, greening
– e.g. S.intermedius
– H2O2 reacts with Hb

β- complete lysis
– e.g. S.pyogenes
– Haemolysins O & S

non (or γ)
- no lysis
– e.g. some S.mutans

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76
Q

What are the three ways of classifying streptococci?

A
  1. Haemolysis
  2. Lancefield typing
  3. Biochemical properties
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77
Q

What is lancefield grouping

A

A method of grouping catalase negative, coagulase negative bacteria based on bacterial cell surface antigens

Antiserum to each group added to a supension of bacteria - clumping indicated recognition

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78
Q

Describe staphlyococcus?

A
  • Gram positive
  • 40 species coagulase+ve or -ve
  • S. aureus most important (coag -+e)
  • Normal habitat is nose and skin
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79
Q

How is staph aureus spread?

A

aerosol and touch - carriers and shedders

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80
Q

What is MRSA and what is it resistant to?

A

Methicillin Resistant Staphylococcus Aureus
Resistant to:
– β-lactams
– gentamicin, erythromycin, tetracycline

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81
Q

Describe the virulence factors of MRSA

A
  • Pore forming toxins
  • Proteases
  • Toxic shock syndrome toxin - cytokine release
  • Protein A
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82
Q

Describe some pyogenic associated conditions of staphylococci?

A
  • wound infections
  • abscesses
  • impetigo
  • septicaemia
  • pneumonia
  • endocardidis
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83
Q

Describe some toxin mediated associated conditions of staphylococci?

A
  • scaled skin syndrome
  • TSS
  • Food poisoning
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84
Q

Describe some coagulase negative associated conditions of staphylococci?

A
  • infected implant
  • endocarditis
  • septicaemia
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85
Q

What colour does Gram positive stain and why?

A

Purple because it contains peptidoglycan that is stained by crystal violet

86
Q

What colour does Gram negative stain and why?

A

Pink because it has a lot less pepidoglycan so is stained by safranin

87
Q

Difference between staphylococcus and streptococcus?

A

Staph - clusters

Strep - chains

88
Q

Describe the catalase test?

A

H2O2 + staphylococci = gas babbles

\+ve = staph 
-ve = non staph
89
Q

When would you use the catalase test?

A

To determine whether or not a bacteria is a staphylococcus or not

90
Q

Describe the coagulase test?

A

+ve = s.auereus because it produces coagulase that converts fibrinogen to fibrin

-ve = coagulase -ve staph

91
Q

When would you use the coagulase test

A

To determine wether no not a staphylococcus is staph. auereus

92
Q

If you saw clusters on a gram positive film what would this infer and what would you do next?

A

Staphylococcus

Do a coagulase test to determine whether or not it is s.aureus

93
Q

If you saw chains on a gram positive film what would this infer and what would you do next?

A

Streptococcus

Look at the type of haemolyis on a blood film

94
Q

What doe alpha haemolysis look like, what does it infer and what would you do next?

A

Alpha = partial

OPTOCHIN TEST:

Resistant = viridans strep
Sensitive = s.pneumoniae (+ve, clear ring around optochin disc)
95
Q

What does beta haemolysis look like, what does it infer and what would you do next?

A

Beta = complete lysis

LANCEFIELD TEST:

A: Streptococcus pyogenes
B: Streptococcus agalactiae
D: Enterococcus, Strep bovis (group D is not beta-haemolytic

96
Q

Name some importan Gramt +ve bacteria?

A

Listeria monocytogenes
Propionibacterium acne – acne
Clostridium difficile – diarrhoea from antibiotic overuse (those starting with C)

97
Q

What does MacConkey agar contain?

A

Contains bile salts, lactose and neutral red pH indicator

Identifies bacteria that can ferment lactose

Ferment lactose - produces acid - pH drop - <6.8 - pink

98
Q

Why doesnt Gram positive bacteria grow on MacConkey agar?

A

Because of the bile salts

99
Q

What grows on the yellow MacConkey agar?

A

Non fermentors e.g. salomella, shigella

100
Q

What grows on the pink MacConkey agar?

A

Fermenters e.g. e.coli

101
Q

What to do if the cultures growing on MacConkeys agar are yellow?

A

PERFORM OXIDASE TEST

Black/purple = +ve = pseudomonas or Neisseria(note it is cocci not bacilli)

Colourless = shigella, salmonella, proteus

102
Q

Describe proteus mirabillis?

A

Swarms on many agars, diffiicult to identifiy other bacteria growing

CLED is used to inhibit proteus
To identify - postitive urease test

103
Q

Give an example of gram -Ve cocci?

A

Any neisseria on microscopy: gram -ve diplococci

104
Q

Give some examples of Gram -ve rods?

A

Curved shaped: cholera
Helical shape: helicobacter pylori
Coccobacilli: haemphilus influenza

105
Q

What does fastidious bacteria need to grow?

A

Fastidious bacteria requires chocolate agar which is blood agar but with lysed RBCs due to heating to 80 degrees C

106
Q

Name the most important mycobacteria?

A

Tuberculosis

107
Q

How do you identify mycobacteria?

A

Mycolic acid in the cell wall does not absorb normal Gram staining

Requires Ziehl Neelsen stain to identify acid-fast bacilli

108
Q

Which antibiotics are used for the following:

  1. MRSA
  2. entamoeba histolytica, giardia
  3. PCP
  4. pneumonia
  5. C.difficile
A
  1. Vancomycin - MRSA
  2. Metronidazole - entamoeba histolytica, giardia
  3. Co-trimoxazole - PCP
  4. CURB65 score for pneumonia and their respective antibiotic regimens
  5. Vancomycin/metronidazole - C.difficile
109
Q

Which types of antibiotics inhibit cell wall synthesis?

A
  1. Glycopeptides - vancomycin, teicoplanin

2. Beta lactams - penicillins, cephalosporins, carbapenems

110
Q

Give some examples of penicillins

A

Penicillins (beta lactams)

  • Benzylpenicillin
  • Flucloxacillin
  • Ampicillin/amoxicillin
111
Q

Give some examples of cephalosporins?

A

Cephalosporins (beta lactams)

1st gen cephalexin
2nd gen cefuroxime
3rd gen ceftazidime

112
Q

Give some examples of carbapenems?

A

Imipenems

Ertapenem

113
Q

Which types of antibiotics inhibit protein synthesis?

A
  1. Chloramphenicol
  2. Macrolides
  3. Tetracyclines
  4. Aminoglycosides
114
Q

Give examples of macrolides?

A

Clarithromycin

Erythomycin

115
Q

Give some examples of tetracyclines?

A

Tetracycline

Doxycyline

116
Q

Give some examples of aminoglycosides?

A

Gentamycin

Streptomycin

117
Q

Give some examples of how some antibiotics inhibit nucleic acid synthesis?

A
  1. Inhibit folate synthesis - trimethoprim, sulphonamides, both = co-trimoxazole
  2. Inhibit DNA gyrase - fluroquinolones
  3. Binds to RNA polymerase - Rifampicin
  4. DNA strand breaks - Nitroidimazoles, metronidazole
118
Q

Where are fungal infects usually found and give some examples?

A

Usually in immunocompromised individuals

  • Candida albicans = treat with antifungal
  • Pnuemocystis pneumonia - treat with co-trimoxazole
  • Aspergillosis
119
Q

Name some helminths

A

Wucheria bancroftii – filariasis causing lymphoedema

Enterobius vermicularis – common in uk, itchy bum, spreads in household

Schistosomiasis – causes squamous cell bladder cancer

Hookworm - Worldwide cause of iron-deficiency anaemia
Treatment: normally mebendazole

120
Q

Name some protazoa?

A

Entamoeba histolytica: bloody diarrhoea, liver abscess
Treat with metronidazole

Malaria: learn in haematology, 5 types, plasmodium falciparum most important

Giardia: diarrhoea due to alteration of intestinal villi, reducing absorption
Treat with metronidazole

121
Q

Describe some routes of administration?

A
  • Oral
  • Intravenous
  • Intramuscular
  • Subcutaneous
  • Inhalation
  • Topical
  • Rectal
122
Q

Define pharacokinetics?

A

Pharmacokinetics is what the body does to a drug

123
Q

What are some mechanisms of absorption?

A
  • Passive diffusion
  • Facilitated diffusion
  • Active transport
  • Endocytosis
124
Q

Define bioavailiability?

A

Rate and extend to which an administered drug reaches the systemic circulation

(IV = 100% )

125
Q

What factors effect bioavailiability?

A
  • First pass hepatic metabolism
  • Solubility
  • Chemical instability
126
Q

What is first pass hepatic metabolism?

A

The hepatic transformation of drug to inactive metabolites

127
Q

What is the definition of distribution?

A

Drug reversibly leaves the bloodstream and enters the extracellular fluid and tissues

128
Q

What factors effect distribution?

A

Blood flow: e.g. brain>muscles

Capillary permeability

Plasma protein binding

Tissue protein binding

Lipophilicity (ability to cross cell membranes)

129
Q

Define: metabolism?

A

Process of elimination mainly through hepatic, renal and billary routes

130
Q

What is first order metabolism?

A

Catalysed by enzymes, rate of metabolism, directly proportional to drug concentration

131
Q

What is zero order metabolism?

A

Enzymes saturated by high drug doses, rate of metabolism is constant

132
Q

What is phase 1 metabolism?

A

Polarise lipophilic drugs, reduction / oxidation / hydrolysis, catalysed by cytochrome P450 system

133
Q

What is phase 2 metabolism?

A

Conjugation, e.g. glucuronic acid, polarisation of drugs to be excreted by renal or biliary systems

134
Q

What are some inducers and inhibitors of cytochrome P450

A

INDUCERS

Antiepileptics

Rifampicin

St Johns wort

Chronic alcohol intake

INHIBITORS

Cirproflaxin, erythromycin

Isoniazid

Amiodarone

Allopurinol

135
Q

Describe drug elimination?

A

Renal (excretion via urine, must be sufficiently polar, renal dysfunction = drug acumilation)

Intestines, bile, lungs, breast milk

136
Q

What is pharmacodynamics?

A

What the drug does to the body

Its effect on cellular receptors via signal transduction

137
Q

What is signal transduction?

A

Binding of drug to extracelluar or intracellular receptor

Via variery of receptors e.g. ligand gated ion channels and G protein coupled receptors

138
Q

What are the factors of drug effect?

A

Drug concentration (dose of drug + pharmacokinetic profile)

Receptor availability (maximal effect once receptors are saturated irrelevant of increasing dose)

139
Q

Describe the neurotransmitter pathways of sympathetic and parasympathetic systems?

A

Sympathetic =
Acetylcholine > nicotinic receptor > norepinephrine > adrenergic receptor

Parasympathetic =
Acetylcholine > nicotinic receptor > acetylcholine > muscarinic receptor

140
Q

What are some alpha 1 agonists and antagonists, and what are their effects?

A 
Agonists = decongestants 
Antagonists = tamsulosin, doxazosin 
Effects = 
- vasconstriction 
- increased peripheral resistance
- increased blood pressure 
- mydriasis 
- Increased closure of internal bladder sphincter
141
Q

What are the effects of alpha 2 receptors?

A
  • inhibiton of norepinephrine release
  • inihbition of acetylcholine release
  • inhibition of insulin release
142
Q

What are some beta 1 agonists, antagonists and what are their effects?

A 
Agonists = inotropes (epinephrine, dopamine) Antagonists = Selective / non selective beta blockers 
Effects = 
- tachycardia 
- increased lipolysis 
- increased myocardial contractility 
- increased release of renin
143
Q

What are some beta 2 agonists, anatgonists and what are their effects?

A 
Agonists = SABA / LABA 
Antagonists = non selective beta blockers 
Effects = 
- vasodilation 
- decreased peripheral resistance 
- bronchodilaton 
- increased muscle and liver glycogenolysis 
- increased release of glucagon 
- relaxed uterine smooth muscle
144
Q

Name some parasympathetic muscarinic receptor agonists and antagonists?

A 
Agonists = glaucoma, donepezil, rivastigmine 
Antagonists = atropine, SAMA/LAMA
145
Q

What are some CNS receptors

A

Dopamine (ant psychotics)
GABA (ag benzodiazepine)
Histamine-1 (ant certizine)
Histamine 2 ( ant ranitidine)

146
Q

What are the associated antibiotics for these common infections?

CAP 
Atypical CAP 
IECOPD 
HAP 
TB 
Cellulitis
UTI
A 
CAP - amoxicillin+/- clarithrmycin 
Atypical CAP - clarythromycin
IECOPD - amoxicillin 
HAP co-amoxiclav / cefuroxime /tazocin
TB - RIPE 
Cellulitis -flucloxacillin 
UTI - trimethoprim, nitrofurantoin
147
Q

What are the associated antibiotics for these common infections?

Gonorrhoea 
Chlamydia 
Syphilis 
Gastroeneritis 
C.Difficile 
Acute abdo infections (appendicitis)
A

Gonorrhoea - ceftriaxone (IM) + azithromycin (PO)

Chlamydia - doxycline /azithromycin (PO)

Syphilis - benzathine benzylpenicillin

Gastroeneritis -
Campylobacter - clarithromycin
Salmonella/shieglla - ciprofloxacin

C.Difficile
1st - metronidazole
2nd - vancomycin

Acute abdo infections (appendicitis)
Cef +met

148
Q

How do NSAIDs work?

A

Non selective competitive reversible COX inhibition

149
Q

How does heparin work?

A

Activates antithrombin (decreased thrombin and factor Xa), short half life

150
Q

How does warfarin work?

A

Anti-vitamin K = decreased FII (prothrombin) /VII/ IX/X and protein C/S

Reversal = vit K

151
Q

Give some examples of direct factor X inhibitors?

A

Apixaban, Rivaroxaban
Directly inhibit FXa
Side effect - bleeding

152
Q

How do thrombolytics work?

A

Activate plasminogen -> plasmin

E.g. strepokinase

side effect - bleeding

153
Q

What do juxtaglomerular cells release renin in response to?

A
  • DECREASED BP detected by barorecepotrs in afferent vascular walls
  • Decreased Na+ delivery to macula densa cells
  • Increased sympathetic stimulate (beta-1)
154
Q

What are the functions of ACE?

A
  • Catalyses conversion of angiotensin 1 to angiotensin 2

Degraded by bradykinin

155
Q

What are some of the effects of angiotensin 2?

A
  1. Systemic arteriole vasoconstriction
  2. Kidney efferent>afferent constriction = increased glomerular pressure = maintain GFR despite lowered overall kidney bloodflow
  3. Kidney PCT/thick ascending limb exchanged stimulation = increased Na+/HCO3/H2O reabsorption
  4. Adrenal cortex = aldosterone release
  5. Posterior pituitary = ADH release
156
Q

Describe how loop diuretics work?

A

e. g. Furosemide, bemetanide
- Inihibit Na/K/Cl cotransport of thick limb

IND: Oedematous States (HF, Cirrhosis, Nephrotic Syndrome, Pulmonary Oedema), HTN, Hypercalcaemia
SE: ototoxicity, hypokalaemia, dehydration, AKI, gout

157
Q

Describe how thiazide diuretics work?

A

e. g. Bendroflumethiazide
- Inhibit Na/Cl contransporter of distal tubule

IND: HTN, HF, Nephrogenic DI
SE: hypokalaemic metabolic alkalosis, hyponatraemia, hyperglycaemia, hypercalcaemia, hyperuricaemia

158
Q

Describe how spironolactone works?

A

Spironolactone = competitive aldosterone receptor antagonists in collecting tubules

IND: HF, Hyperaldosteronism, Hypokalaemia
SE: hyperkalaemia, antiandrogen effects, e.g. gynaecomastia, loss of libido, erectile dysfunction

159
Q

Give an example of a biguanide, mechanism and SE?

A

e.g. = Metformin

Mechanism = increased insulin sensitivity, decreased hepatic gluconeogenesis

SE = GI disturbance, lactice acidosis

160
Q

Give an example of a sulphonylurea, mechanism, and SE?

A

e.g. glicazide

mechanism = Increased insulin secretino

SE = hypoglycaemia, weight gain, SIADH

161
Q

Give an example of a gliptin, mechanism and SE?

A

e.g. sitagliptine

mechanism = decreased glucagon secretion

162
Q

Give an example of thiazolidinediones?

A

e.g. Pioglitazone

mechanism = increase adipogenesis

SE = weight gain, fluid retention

163
Q

Describe the pathology of a paracetamol overdose?

A
  • Phase 2 conjugation pathway saturated
  • Alternative pathway used - NAPQI = glutathione depletion
  • Glutathione depletion = liver/renal necrosis
164
Q

What are the risk factors of a paracetamol overdose?

A

Psychiatric Hx
Elderly/low weight
P450 inducers

165
Q

What investigation would be carried out for a paracetamol overdose?

A
  • Serum paracetamol level

- U and E, LFT, glucose clotting, ABG

166
Q

What is the management for a paracetamol overdose?

A

IV N-acetylcysteine

On/above nomogram line
Staggered overdose
Doubt over investigation time

Liver transplant

167
Q

What would be done for the following overdoses?

Aspirin 
Opioid 
Digoxin 
Carbon monoxide 
Organophosphate insecticide
A 
Aspirin  - haemodialysis 
Opioid - naloxone 
Digoxin - digoxin specific antibody fragments 
Carbon monoxide - 100% oxygen 
Organophosphate insecticide = atropine
168
Q

Define: antibiotic?

A

Antibiotics agents produced by micro organisms that kill or inhibit the growth of other micro organisms in high dilution - they work by binding to a target site on a bacteria

169
Q

Which antibiotics work by cell wall synthesis interference?

A

penicillins, cephalosporins, carbapenems

170
Q

Which antibiotics work by nucleic acid synthesis interference?

A

metronidazole, rifampicin

171
Q

Which antibiotics work by DNA gyrase interference?

A

Fluroquinolones

172
Q

Which antibiotics work by inhibition of ribosomal activity?

A

Aminoglycosides, tetracyclines, lincosamides, macrolides, chloramphenicol

173
Q

Which antibiotics work by inhibition of folate synthesis and carbon unit metabolism?

A

Sulphonamides and trimethoprim

174
Q

How do bacteriostatic antibiotics work?

A

Bacteriostatic antibiotics prevent bacteria multiplying

also reduce exotoxin production

175
Q

How do bactericidal antibiotics work?

A

Bactericial antibiotics kill the bacteria

Generally inhibit cell wall synthesis

176
Q

Does the lowest MIC = best antibiotic?

A

NO!

177
Q

What are the two major determinants of anti bacterial effects?

A

Concentration
(concentration dependent killing - key parameter is how high the concentration is above MIC)

Time
(time dependent killing - key parameter is the time that serum concentrations remain above the MIC during the dosing intervals)

178
Q

Define pharmacokinetics?

A

The movement of a drug from its administration site to its place of pharmacological activity

179
Q

What are the key considerations when choosing an antibiotic?

A
  • What is the appropriate or available route of administration?
  • Which antibiotics will penetrate that site?
  • What is the pH of the site?
  • Is the antibiotic lipid soluble?
  • Half life and elimination – What dosage interval / duration?
180
Q

How do bacteria resistant antibiotics?

A
  1. Change antibiotic target
  2. Destroy antibiotic
  3. Prevent antibiotic access
  4. Remove antibiotic from bacteria
181
Q

What does intrinsically resistant mean?

A

Naturally resistant

All subpopulations of a species will be equally resistant

182
Q

How do bacteria acquire resistance?

A
  1. Spontaneous gene mutation
  2. Horizontal gene transfer

In acquired a bacterium which was previously susceptible obtains the ability to resist

183
Q

What are the different types of horizontal gene transfer?

A

Conjugation > sharing of extra chromosomal DNA plasmids (bacterial sex)

Transduction > Insertion of DNA by bacteriophages

Transformation > Picking up naked DNA

184
Q

How do CRE infections work?

A
  1. Lots of germs, 1 or 2 are CRE
  2. Antibiotics kill off good germs
  3. CRE grow
  4. CRE share genetic defencces to make other bacteria resistant
185
Q

What are yeasts?

A

Small single celled organisms that divide by budding, account for less that 1% of fungi but include several highly medical ones

186
Q

What are moulds?

A

Moulds form multicellular hyphae and spores

187
Q

Describe the overall burden of fungus?

A

= enormous e.g. fungal asthma, fungal keratitis, nappy rash but life threatening fungus rare in healthy hosts

188
Q

How is fungal disease treated?

A

Selectvive toxicity: aim of antimicrobial drug therapy is to achieve inhibitory levels of agent at the site of the infection without host cell toxicity

189
Q

Describe the ideal vaccine?

A
  1. Safe - this could mean attenuated live if suitable or subunit if pathogen is lethal
  2. Should induce a suitable immune response - for example mucosal if pathogen uses this route, high antibody titre if antibody is most useful protective agent
  3. Generate T and B cell memory
  4. Stable and easy to transport - for use in remote areas
  5. Should not require repeated boosting
190
Q

What are the choices of antigen for vaccine design?

A

A. Whole organism (live attenuated or killed inactivated)

B. Subunits (toxoids or antigenic extracts)

C. Peptides

D. DNA vaccines

E. Engineered Virus

191
Q

Give some advantages and some disadvantages of using a whole organism for vaccines?

A

ADVANTAGES:
activation of full natural immune response
prolonged contact with immune system
memory response in T and B cell compartments
often only single is required

DISADVANTAGES:
immunocompromised could become infected
attenuated can revert to virulent e.g. polio sabin

192
Q

Give some examples of subunit vaccines?

A

ADVANTAGES:
safe
no risk of infection
easier to store and preserve

DISADVANTAGES
immune response less powerful
repeated vaccinations and adjuvants
consider genetic heterogeneity of the population

193
Q

Give some advantages and disadvantages of DNA vaccines?

A

ADVANTAGES:
safe - especially in immunocompromised
No requirement for complex storage and transportation
drug delivery can be simple and adaptable for widespread vaccination programs

DISADVANTAGES
DNA vaccines are likely to produce a mild response and require subsequent boosting
No transient infection
Limited to proteins, could induce tolerance or anti-DNA antibodies

194
Q

What is an adjuvant?

A

Any substance added to a vaccine to stimulate the immune system

195
Q

What are the four major groups of protozoa?

A

Protozoa - one celled eurkaryotic organisms

  1. Flagellates
  2. Amoebae
  3. Sporozoa > plasmodium
  4. Cilliated
196
Q

What are the 5 types of malaria?

A
  • Plasmodium falciparum > most severe
  • Plasmodium ovale
  • Plasmodium vivax
  • Plasmodium malariae
  • Plasmodium knowlesi
197
Q

How is malaria transmitted?

A

Bite of the female anopheles mosquito

198
Q

Describe the liver stage of malaria?

A
  1. Mosquito takes a blood meal and injects sporozoites
  2. These travel to the liver and infect the liver cells
  3. Mature into Shizonts
  4. Shizontes rupture into merozoites
199
Q

Describe the blood stage of malaria?

A
  1. Merozoites enter circulation and infect RBCs
  2. Enter the ring stage trophozoites mature into Schizonts
  3. Schizonts rupture releasing more merozoites
  4. Some immature trophozoites differentiate into sexual stage gametocytes
200
Q

Describe the vector stage?

A
  1. Another mosquito takes a blood meal ingesting gametocytes
  2. These mature into an oocyst which ruptures releasing sporozoites
  3. Sporozoites are injected into the next host
201
Q

What are the symptoms of malaria?

A 
FEVER but may also have 
Chills
Headache
Myalgia
Fatigue
Diarrhoea
Vomiting
Abdo pain
202
Q

What are some complications of malaria and how are they supported?

A
  • Cerebral: antiepileptics
  • ARDS: oxygen, diuretics, ventilation
  • Renal failure: fluids, dialysis
  • Sepsis: broad spectrum antibiotics
  • Bleeding/Anaemia: blood products
  • Exchange transfusion if huge parasite burden
203
Q

What is the treatment of complicated malaria?

A

IV artesunate

IV quinine + doxcycline

204
Q

Describe the natural history of a HIV infection?

A
  1. Acute primary infection
  2. (i) asymptomatic phase (years)
    (ii) early symptomatic HIV
  3. AIDS (CD4<200)
205
Q

What markers are used to measure HIV infection?

A
  1. CD4 T cell count /µl

2. HIV viral load (RNA copies/ml)

206
Q

What are some respiratory diseases associated with HIV?

A

Kaposi’s sarcoma

Pneumocystitis jeroveci

207
Q

How does HIV infect cells?

A

HIV infects cells that express CD4, the interaction between CD4 and gp120 is conserved among all primate lentiviruses

208
Q

Describe how HIV replicates?

A

HIV replication consists of 9 steps?

  1. Attachment
  2. Entry
  3. Uncoating
  4. Reverse transcription (error prone so genomic variability)
  5. Genome intergration
  6. Transcription of viral RBA
  7. Splicing of mRNA and translation into proteins
  8. Assembly of new virons
  9. Budding
209
Q

Describe the immune response to HIV?

A

Humoral immunity:

  • neutralising antibodies
  • poor /slow to develope effectively
  • envelpe glycoprotein is poorly immunogenic an has high genetic diversity

Cell mediated immunity:
CD8 = qualitatively and quantitatively poor, virus escapes CTL responses through mutations
CD4 = Failure of CD4+ proliferation

The lack of identification of protective immune responses remains a major barrier to development of an effective vaccine against HIV-1.

210
Q

What are the immune system consequences of HIV?

A

*HIV results in gradual damage to the immune system mainly through the depletion of CD4 T cells *

Progressive decline in number and function of CD4 T-lymphocyte characterises HIV infection and leads to susceptibility infection

Mechanisms of CD4+ T lymphocyte depletion

Phase 2a (13 decks)

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