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
TB staining
ZN stain. Heating sample with carb fuschin- goes pink. | Acid fast
26
Candida albicans
Vaginal and oral infections Sepsis Catheter infections Fungi. Can kill
27
Aspergillus fumigatus
Predominantly lung infections - allergic disease. Poor prognosis. Kills slowly
28
HIV treatment
HAART
29
Severe herpes treatment
IV acyclovir
30
Neisseria &HI evasion
Secrete protease that lysis IgA
31
N. Gonorrhoea evasion
Pili. Antigenic variation.
32
B. Pertussis evasion
Secrete adhesion molecules
33
S. Pneumonia evasion.
Polysaccharide capsule prevents phagocytosis
34
Staph evasion
Coagulase- forms fibrin coat around organism
35
Mycobacterium evasion
Escapes phagolysosome and lives in cytoplasm
36
What shape is tb
Rod
37
What does s. Pyogenes cause
Wound infections, tonsillitis & pharyngitis. Otitis media. Impetigo etc. Can lead to rheumatic fever and glomerulonelhritis
38
Colonies of s. Pneumoniae
Draughtsman colonies
39
Bacrericidal
Kills >99.9% - inhibit cell wall synthesis usually. Used in difficult to treat infections etc
40
Bacteriostatic
Inhibits growth of bacteria (and kills a lot) | Minimum bactericidal concentration: minimum inhibitorqy concentration >4
41
HIV tests
CD4 count. Normal >500. Bad <200 | Viral load - mount of HIV in blood
42
Post exposure prophylaxis
Combination antiretroviral therapy for 28 days within 72 hours of exposure. Not as effective as PrEP
43
Pre exposure prophylaxis
1 tablet containing 2 drugs taken daily. If at high risk
44
AIDS
CD4 <200 or when aids defining illness is present
45
AIDS defining illness
``` Pneumocystis pneumonia Mycobacterium TB Candidiasis Non TB mycobacterium CMV/HSV pneumonitis Kaposi sarcoma Lymphoma Recurrent pneumonia’s ```
46
What does JC virus cause
Progressive multi focal leukencephalopathy
47
HAART drugs
Usually 2NRTIs (pyrimidine analogues, purine analogues) & 1 other
48
Malaria treatment
``` 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
Primaquine side effects
Can cause haemolytic anaemia if G6PD deficient - check first
50
Pharmacokinetics
Absorption Distribution Metabolism (cyp450 increase metabolism) Excretion (pH dependent, weak acids are cleared faster if urine is alkali and vice verse)
51
Triple whammy
NSAID or cox-2 inhibitor ACEI Dehydration/furusemide =renal failure
52
Potency
Concentration/dose required to produce 50% of the drugs maximal effect Very potent = small dose needed
53
Efficacy
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
Intrinsic activity
Maximal efficacy as a fraction of maximal efficacy produced by a full agonist of the same type
55
Affinity
How well a ligand binds to a receptor | Agonists and antagonists
56
Tolerance
Slow process - reduction in effect over time | When receptor is activated continuously repeatedly and in high concentrations
57
Desensitisation
Rapid process. E.g. Irreversible antagonist binds
58
Bioavailability
Fraction of a drug that reaches the systemic circulation
59
Muscarinic receptors
Parasympathetic M1- brain. M2- heart, slows heart (blocked with atropine). M3- glandular and smooth muscle- bronchoconstriftion & invreases secretions. M4/5 CNS
60
Nicotinic receptors
Sympathetic and parasympathetic
61
Opioid antagonist
Naloxone
62
Codeine
Pro drug that gets converted to morphine
63
Type 1 hypersensitivity
Antigen reacts with IgE bound to mast cells (they have bound to mast cells following first exposure) Anaphylaxis & atopy
64
Type 2 hypersensitivity
Cell bound. IgG or IgM binds to antigen on cell surface. | Autoimmune haemolytic anaemia, goodpastures, pernicious anaemia, rheumatic fever
65
Type 3 hypersensitivity
Free antigen and antibody combine to form an immune complex | SLE, hypersensitivity pneumonitis. Post strep glomerulonephritis
66
Type 4 hypersensitivity
Delayed. T cell mediated (th1 activated macrophages, th2 activated eosinophils) TB, graft vs host disease, MS, GBS
67
Anaphylaxis
CV: vasodilation, increased permeability, lowered BP - shock- arrest Resp; bronchial smooth muscle constricts, mucus, wheeze
68
Anaphylaxis management t
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
ADRs
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
Rawlings Thompson ADR classification
``` 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
Yellow card what to write
Suspected drug and reactions. Patients details. Reported details. Additional useful info
72
Yellow card must report
Reactions for herbal medicines Black triangle drugs Serious reavtions
73
Drugs commonly implicated in hypersensitivity
Aspirin. Penicilli. Cephalosporins. TB drugs nitrofurans. Anti malarials. Anti convulsants. Anaesthetics etc
74
Non immune anaphylaxis
Direct mast cell degrabulation with no prior exposure needed
75
Acute inflammation cells
Neutrophils
76
Chronic inflammation cells
Macrophages and lymphocytes
77
Papilloma
Benign tumour of non glandular non secretory epithelium
78
Adenoma
Benign tumour of glandular or secretory epithelium
79
Carcinoma
Malignant tumour of epithelial cells
80
Adenocarcinoma
Carcinoma of glandular epithelium
81
Sarcoma
Malignant connective tissue neoplasm
82
Teratoma
Contain elements of all 3 term cell lwyers
83
Blastoma
Embryonal tumour
84
Common myeloid progenitor
Megakaryocytes, erythrocytes, mast cells, myeloblasts | Myeloblasts differentiate into basophils, neutrophils, eosinophils and monocytes (macrophages)
85
Common lymphoid progenitor
Natural killer cell and small lymphocyte | Small lymphocyte -> t and b
86
CD4 vs CD8
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
Fab vs fc on antibodies
Fc- constant across whole class. Binds to self cell receptors. fab binds antigens.
88
Toll like receptors
Membrane bound
89
Nod like receptors
In cytoplasm
90
Whole organism attenuated vaccine
TB, typhoid, polio, Sabin, mmr
91
Recombinant vaccines
Engineered virus - non pathogenic | Vaccina virus and canary pox
92
DNA vaccines
Mild response as no transient infection
93
Subunit vaccines
Purified parts of pathogen that are antigenic Anthrax, cholera, pertussis, plague, hep A, polio salk, rabies, influenza Less infection risk
94
Adjuvants in vaccines
Aluminium salts - boost immune response. Saponins, tlr agonists etc Antibiotics to prevent contamination during manufacture
95
…mab
Monoclonal antibody
96
…sone or …lone
Corticosteroids
97
…terol
Bronchodilators
98
…nib
Kinase inhibitor
99
Nebulisers
Give medication in form of aerosols
100
Beta adrenofeptor agonists
Smooth muscle relaxation and bronchodilaton. And inhibit histamine release from lung mast cells Salbutamol (Saba) salmeterol (LABA)
101
Muscarinic receptor antagonists
Block muscarinic receptors preventing contraction & gland secretion E.g. atropine. Ipratropium bromide
102
How do ICS reduce inflammation
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
Antifibrotic (lungs)
Pirfenidone | Reduced fibroblast proliferation and collagen production
104
Nintedanib
Tyrosine kinase inhibitor Inhibits vegfr Idiopathic pulmonary fibrosis
105
Autosomal dominant disorders
``` 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 ```