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2a > ICS > Flashcards

ICS Flashcards

1
Q

Spirochetes

A

Gram negative
Leptospira
Treponema pallidum (syphilis)
Borrelia (Lymes)

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2
Q

Other gram negative

A

Vibrio cholerae
Legionella
Campylobacter
Helicobacter pylori

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3
Q

Obligate intracellular

A

C. Trachomatis (chlamydia)

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4
Q

Mollecutes

A

Absent cell wall

Mycoplasma pneumoniae

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5
Q

Antibiotics that target cell wall synthesis

A 
Beta lactams
Vancomycin 
Bacitracin
Glycopeptides
Polymyxins (cell membrane)
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6
Q

Beta lactams

A

Penicillins
Cephalosporins
Carbapenems e.g. meropenem (resistant stuff)
Monobactams

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7
Q

Antibiotics targeting nucleic acid synthesis

A

Quinolones (e.g. ciprofloxacin) - dna gyrase
Rifampin - rna polymerase
Sulfonamides & trimethoprim - folate synthesis
Metronidazole

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8
Q

Antibiotics targeting protein synthesis

A 
Macrolides (clarithromyfin & erythromycin - gram positive & atypical pneumonia)
Clindamycin
Linezolid 
Tetracyclines
Aminoglycosides (gentamicin)
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9
Q

Which malaria’s persist in liver as hypnozoites

A

P. Ovale. P. Vivax

Treated with 14 days of primaquine

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10
Q

What cell does HIV infect

A

CD4+

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11
Q

Typical staph treatment

A

Flucloxacilin

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12
Q

MRSA antibiotic

A

Vancomycin

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13
Q

Macrolide example

A

Clarithromycin

Erithromycin

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14
Q

Staph and strep drugs

A

Mostly beta lactams or vancomycin

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15
Q

Klebsiella antibiotics

A

So sensitivity testing

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16
Q

Neisseria antibiotics

A

Cephalosporins

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17
Q

Blood agar uses

A

Strep and other

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18
Q

Chocolate agar

A

Neisseria

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19
Q

MacConkey agar

A

Lactose status

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20
Q

CLED agar

A

Proteus

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21
Q

XLD agar

A

Salmonella and shigella

Both lactose ferment & go red but salmonella then gets black dots

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22
Q

Gram positive

A

Prefer dry and dusty environments. Great skin colonisers

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23
Q

Gram negative

A

Prefer wet and damp environments. Majority prefer to colonise mucus membranes
Have an outer membrane but less peptidogkycan

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24
Q

What can cdiff lead to

A

Toxin a&b mucosal injury & inflammation -> pseudomembranous colitis -> toxic megacolon -> perforation and death

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25
Q

TB staining

A

ZN stain. Heating sample with carb fuschin- goes pink.

Acid fast

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26
Q

Candida albicans

A

Vaginal and oral infections
Sepsis
Catheter infections
Fungi. Can kill

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27
Q

Aspergillus fumigatus

A

Predominantly lung infections - allergic disease. Poor prognosis. Kills slowly

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28
Q

HIV treatment

A

HAART

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29
Q

Severe herpes treatment

A

IV acyclovir

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30
Q

Neisseria &HI evasion

A

Secrete protease that lysis IgA

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31
Q

N. Gonorrhoea evasion

A

Pili. Antigenic variation.

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32
Q

B. Pertussis evasion

A

Secrete adhesion molecules

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33
Q

S. Pneumonia evasion.

A

Polysaccharide capsule prevents phagocytosis

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34
Q

Staph evasion

A

Coagulase- forms fibrin coat around organism

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35
Q

Mycobacterium evasion

A

Escapes phagolysosome and lives in cytoplasm

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36
Q

What shape is tb

A

Rod

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37
Q

What does s. Pyogenes cause

A

Wound infections, tonsillitis & pharyngitis. Otitis media. Impetigo etc. Can lead to rheumatic fever and glomerulonelhritis

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38
Q

Colonies of s. Pneumoniae

A

Draughtsman colonies

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39
Q

Bacrericidal

A

Kills >99.9% - inhibit cell wall synthesis usually. Used in difficult to treat infections etc

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40
Q

Bacteriostatic

A

Inhibits growth of bacteria (and kills a lot)

Minimum bactericidal concentration: minimum inhibitorqy concentration >4

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41
Q

HIV tests

A

CD4 count. Normal >500. Bad <200

Viral load - mount of HIV in blood

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42
Q

Post exposure prophylaxis

A

Combination antiretroviral therapy for 28 days within 72 hours of exposure. Not as effective as PrEP

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43
Q

Pre exposure prophylaxis

A

1 tablet containing 2 drugs taken daily. If at high risk

44
Q

AIDS

A

CD4 <200 or when aids defining illness is present

45
Q

AIDS defining illness

A 
Pneumocystis pneumonia 
Mycobacterium TB
Candidiasis 
Non TB mycobacterium 
CMV/HSV pneumonitis 
Kaposi sarcoma 
Lymphoma 
Recurrent pneumonia’s
46
Q

What does JC virus cause

A

Progressive multi focal leukencephalopathy

47
Q

HAART drugs

A

Usually 2NRTIs (pyrimidine analogues, purine analogues) & 1 other

48
Q

Malaria treatment

A 
IV artesunate (only treats blood forms); IV quinine. IV doxycycline 
If not severe or not falciparum can be treated orally with artemisinin based combination therapy
49
Q

Primaquine side effects

A

Can cause haemolytic anaemia if G6PD deficient - check first

50
Q

Pharmacokinetics

A

Absorption
Distribution
Metabolism (cyp450 increase metabolism)
Excretion (pH dependent, weak acids are cleared faster if urine is alkali and vice verse)

51
Q

Triple whammy

A

NSAID or cox-2 inhibitor
ACEI
Dehydration/furusemide
=renal failure

52
Q

Potency

A

Concentration/dose required to produce 50% of the drugs maximal effect
Very potent = small dose needed

53
Q

Efficacy

A

Maximum effect which can be expected from the drug
(Point at which increasing dose further doesn’t make any difference)
How well it activates the receptor (only agonists)

54
Q

Intrinsic activity

A

Maximal efficacy as a fraction of maximal efficacy produced by a full agonist of the same type

55
Q

Affinity

A

How well a ligand binds to a receptor

Agonists and antagonists

56
Q

Tolerance

A

Slow process - reduction in effect over time

When receptor is activated continuously repeatedly and in high concentrations

57
Q

Desensitisation

A

Rapid process. E.g. Irreversible antagonist binds

58
Q

Bioavailability

A

Fraction of a drug that reaches the systemic circulation

59
Q

Muscarinic receptors

A

Parasympathetic
M1- brain. M2- heart, slows heart (blocked with atropine). M3- glandular and smooth muscle- bronchoconstriftion & invreases secretions. M4/5 CNS

60
Q

Nicotinic receptors

A

Sympathetic and parasympathetic

61
Q

Opioid antagonist

A

Naloxone

62
Q

Codeine

A

Pro drug that gets converted to morphine

63
Q

Type 1 hypersensitivity

A

Antigen reacts with IgE bound to mast cells (they have bound to mast cells following first exposure)
Anaphylaxis & atopy

64
Q

Type 2 hypersensitivity

A

Cell bound. IgG or IgM binds to antigen on cell surface.

Autoimmune haemolytic anaemia, goodpastures, pernicious anaemia, rheumatic fever

65
Q

Type 3 hypersensitivity

A

Free antigen and antibody combine to form an immune complex

SLE, hypersensitivity pneumonitis. Post strep glomerulonephritis

66
Q

Type 4 hypersensitivity

A

Delayed. T cell mediated (th1 activated macrophages, th2 activated eosinophils)
TB, graft vs host disease, MS, GBS

67
Q

Anaphylaxis

A

CV: vasodilation, increased permeability, lowered BP - shock- arrest
Resp; bronchial smooth muscle constricts, mucus, wheeze

68
Q

Anaphylaxis management t

A

Abcde
Remove trigger
IM adrenaline (500 micrograms (epipens has 300)
Oxygen, if no response fluid bolus and repeat adrenaline. Steroids for refractory. Antihistamine to treat skin stuff later. Shock may need IV adrenaline

69
Q

ADRs

A

Collateral effect - when normal dose given. E.g. antibiotics causing c diff
Toxic effect- when dose too high/impaired excretion e.g. dysarthria & ataxia with lithium
Hyper susceptible effect - below therapeutic range e.g. anaphylaxis in tiny dose penicillin

70
Q

Rawlings Thompson ADR classification

A 
A) augmented - secondary effect or extension of normal effect
B) bizarre - nor predictable 
C) continuous - due to cumulative dose 
D) delayed e.g. teratogenesis 
E) ending of drug use 
F) failure of therapy
71
Q

Yellow card what to write

A

Suspected drug and reactions. Patients details. Reported details. Additional useful info

72
Q

Yellow card must report

A

Reactions for herbal medicines
Black triangle drugs
Serious reavtions

73
Q

Drugs commonly implicated in hypersensitivity

A

Aspirin. Penicilli. Cephalosporins. TB drugs nitrofurans. Anti malarials. Anti convulsants. Anaesthetics etc

74
Q

Non immune anaphylaxis

A

Direct mast cell degrabulation with no prior exposure needed

75
Q

Acute inflammation cells

A

Neutrophils

76
Q

Chronic inflammation cells

A

Macrophages and lymphocytes

77
Q

Papilloma

A

Benign tumour of non glandular non secretory epithelium

78
Q

Adenoma

A

Benign tumour of glandular or secretory epithelium

79
Q

Carcinoma

A

Malignant tumour of epithelial cells

80
Q

Adenocarcinoma

A

Carcinoma of glandular epithelium

81
Q

Sarcoma

A

Malignant connective tissue neoplasm

82
Q

Teratoma

A

Contain elements of all 3 term cell lwyers

83
Q

Blastoma

A

Embryonal tumour

84
Q

Common myeloid progenitor

A

Megakaryocytes, erythrocytes, mast cells, myeloblasts

Myeloblasts differentiate into basophils, neutrophils, eosinophils and monocytes (macrophages)

85
Q

Common lymphoid progenitor

A

Natural killer cell and small lymphocyte

Small lymphocyte -> t and b

86
Q

CD4 vs CD8

A

CD8 = killer. CD4 goes to th1(high levels of IL12) or th2.
Th1: secreted il2 and ifn y - kills intracellular pathogens
TH2: contribute to antibody production

87
Q

Fab vs fc on antibodies

A

Fc- constant across whole class. Binds to self cell receptors.
fab binds antigens.

88
Q

Toll like receptors

A

Membrane bound

89
Q

Nod like receptors

A

In cytoplasm

90
Q

Whole organism attenuated vaccine

A

TB, typhoid, polio, Sabin, mmr

91
Q

Recombinant vaccines

A

Engineered virus - non pathogenic

Vaccina virus and canary pox

92
Q

DNA vaccines

A

Mild response as no transient infection

93
Q

Subunit vaccines

A

Purified parts of pathogen that are antigenic
Anthrax, cholera, pertussis, plague, hep A, polio salk, rabies, influenza
Less infection risk

94
Q

Adjuvants in vaccines

A

Aluminium salts - boost immune response. Saponins, tlr agonists etc
Antibiotics to prevent contamination during manufacture

95
Q

…mab

A

Monoclonal antibody

96
Q

…sone or …lone

A

Corticosteroids

97
Q

…terol

A

Bronchodilators

98
Q

…nib

A

Kinase inhibitor

99
Q

Nebulisers

A

Give medication in form of aerosols

100
Q

Beta adrenofeptor agonists

A

Smooth muscle relaxation and bronchodilaton. And inhibit histamine release from lung mast cells
Salbutamol (Saba) salmeterol (LABA)

101
Q

Muscarinic receptor antagonists

A

Block muscarinic receptors preventing contraction & gland secretion
E.g. atropine. Ipratropium bromide

102
Q

How do ICS reduce inflammation

A

Suppress production of chemo tactic mediators. Reduce adhesion molecule expression. Inhibit inflammatory cell survival in airway. Suppress inflammatory gene expression
Also increase transcription of beta 2 receptor gene for sabas etc

103
Q

Antifibrotic (lungs)

A

Pirfenidone

Reduced fibroblast proliferation and collagen production

104
Q

Nintedanib

A

Tyrosine kinase inhibitor
Inhibits vegfr
Idiopathic pulmonary fibrosis

105
Q

Autosomal dominant disorders

A 
Very Powerful DOMINANT Humans 
Von willebrand/Von hippel-lindau 
Pseudo hypo parathyroidism
Dystrophia myotonica
Osteogenesis imperfecta 
Marfan 
Intermittent porphyria
Neurofibromatosis
Achondroplasia/Adult poly cystic kidney disease
Noonan syndrome 
Tuberous Sclerosis
Hyper cholesterolaemia 
Huntington’s 
Hypertrophic obstructive cardiomyopathy 
Hereditary spheroxytosis 
Hereditary non polyposis coli
Hereditary haemorrhagic telangiectasia

2a (10 decks)

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