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Medicine > CP > Flashcards

CP Flashcards

1
Q

Notifiable Diseases

A
  1. Acute Meningitis
  2. Measles
  3. Mumps
  4. Rubella
  5. Acute Polymyelitis
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2
Q

Which Immunoglobulin is produced in acute infection

A

IgM

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3
Q

Which Immunoglobulin is produced in long term immunity

A

IgG

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4
Q

Differential diagnoses for a child with a rash

A 
Parvovirus
Measles
Chickenpox
Rubella
Non-polio enterovirus infection
(bacterial e.g Staphylococcus aureus, N. meningitidis)
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5
Q

Definitive signs of measles (most infective)

A

Buccal mucosa bluish white spots with red base
Florrid rash macupapular rash they join up as the disease progress
Starts face and neck and spreads to extremities

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6
Q

What virus causes measles

A

Paramyxovirus

Droplet transmission person to person

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7
Q

Virus in Rubella

A

Togavirus

Droplet transmission

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8
Q

Treatment of chickenpox/varicella zoster

A

Oral or IV Acyclovir depending on severity

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9
Q

What virus causes “slapped cheek syndrome”?

A

Parvovirus B-19

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10
Q

Differential diagnosis for a child with respiratory symptoms

A 
Respiratory Syncytial Virus 
Parainfluenza
Influenza
Adenovirus
Metapneumovirus
Rhinovirus
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11
Q

What does respiratory syncitial virus/pneumovirus cause

A

Bronchiolitis: SOB, wheezing, fever, in under 1s.

Can be fatal, winter epidemics

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12
Q

Treatment of RSV/pneumovirus

A

O2, steroids, bronchodilators
IV Ribavarin
(immunoglobulin and monoclonal abs - Palivizumab)

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13
Q

What is metapneumovirus

A

Paramyxovirus

Causes respiratory illness similar to RSV (same treatment) – ranges from URTI to pneumonia.

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14
Q

What virus causes parainfluenza

A

Paramyxovirus

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15
Q

Viruses that cause diarrhoea in children

A

Rotavirus

Norovirus

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16
Q

Rotavirus: virus, symptoms and treatment

A

Caused by reovirus
Cause diarrhoea and vomiting
Can be fatal in young children
Treatment: rehydration

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17
Q

What is mumps

A

Caused by paramyxoviridae family

Bilateral gross parotitis (can be unilateral)

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18
Q

What are the two main groups of parasites

A

Microparasites: protozoa
Macroparasites: helminths

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19
Q

4 main groups of protozoa

A

Flagellates e.g. giardia
Amoeboids e.g. acanthamoeba
Sporozoans e.g. plasmodium, toxoplasma
Trypanosomes e.g. leishmania

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20
Q

2 main groups of helminths

A

Nematodes e.g. ascaris, trichuris

Platyhelminths/flatworms e.g. schistosoma

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21
Q

What causes ascariasis

A

Intestinal nematode: Ascaris lumbricoides
Acquired by ingesting worm eggs
3-8 years old, poor hygiene
1 billion people affected worldwide

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22
Q

What is Loeffler’s syndrome

A

Migration of ascariasis to lung

dry cough, dyspnea, wheeze, haemoptysis, eosinophilic pneumonitis

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23
Q

Treatment of ascariasis

A

Albendazole/Benzimidazole
Prevents glucose absorption by worm
Worm starves-detaches-passed PR
(Improve sanitation to control spread)

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24
Q

What is schistosomiasis/bilharzia disease

A

Caused by a trematode/fluke worm (carried by snails in water)
Causes chronic disease resulting in bladder cancer (S. haematobium) and liver cirrhosis (S. Japonicum)

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25
Q

Treatment of schistosomiasis

A

Praziquantel

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26
Q

What causes hydatid disease

A

Caused by a Tapeworm Echinococcus sp
Humans are accidental host- Usual hosts are sheep and dogs
Found all over the world wherever sheep are farmed

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27
Q

What are the symptoms of hydatid disease

A 
Cysts: 70% liver, 20% lungs
May remain asymptomatic for years
Mass effect
Secondary bacterial infection
Cyst rupture- hypersensitivity
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28
Q

What are the 4 species of sporozoans that cause malaria

A 
Plasmodium falciparum (most common)
P. vivax
P. ovale
P. Malariae
Carried by female anopheles mosquitos
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29
Q

Mechanism of disease and symptoms of malaria

A

Parasites rupture red cells, block capillaries and cause inflammatory reaction
Fever, rigors, renal failure, hypoglycaemia, headaches, coma, pulmonary oedema, DIC etc

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30
Q

What causes cryptosporidiosis/ diarrhoeal disease

A

Cryptosporidium parvum and hominis (micro-parasite, sporozoan)
Faecal-oral route
human- human (cattle, sheep, goats)

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31
Q

Treatment of cryptosporidiosis

A 
Rehydration etc.
For immunocompromised:
Nitazoxanide
Paromomycin (to kill parasite)
Octreotide (reduce cramps and frequency)
HIV patients, HAART should be quickly initiated
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32
Q

Enteroviral infections

A

Coxsackie, enterovirus, echovirus

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33
Q

Rarer clinical manifestations of mumps

A

CNS involvement is the most common extrasalivary gland manifestation of mumps
Epididymo-orchitis is the most common extrasalivary gland manifestation in the adult

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34
Q

What are dimorphic fungi

A

Fungi that can grow as unicellular yeast or multicellular mould e.g. penicillium marneffei or histoplasma

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35
Q

What causes dutch elm disease

A

plant parasitic fungi

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36
Q

Examples of superficial fungal infections

A

Thrush, ringworm etc.

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37
Q

Examples of subcutaneous fungal infections

A

sporotrichosis, chromoblastomycosis etc

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38
Q

Examples of systemic fungal infections

A

Pneumocystis, Aspergillosis, Systemic candidosis, Histoplasmosis

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39
Q

Main classes of anti-fungal agents

A 
Pyrimidine (1)
Polyenes (2)
Allyamine (1)
Azoles (4)
Echinocandins (3)
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40
Q

What is the active component of pyrimidine/5-fluorocytosine

A

Taken up by fungal specific cytosine permease

Deaminated into active component is 5-fluorouracil

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41
Q

2 modes of action of 5-fluorouracil

A
  1. fluorodeoxyuridine monophosphate (FdUMP) inhibits thymidylate synthetase inhibiting DNA synthesis
  2. fluorouridine triphosphate affects RNA incorporation disrupting translation
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42
Q

What is 5-fluorocytosine spectrum of activity

A

limited spectrum of activity
Active against: Cryptococcus neoformans, Candida species (most)
Inactive against: Candida krusei, Most moulds

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43
Q

Why is 5-fluorocytosine usually used in combination therapy rather than mono therapy

A

Resistance to 5FC develops quickly in Candida and Cryptococcus spp. when used as monotherapy
Now used mainly as combination therapy with Amphotericin B to treat cryptococcal meningitis

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44
Q

What can high levels of 5-flurocytosine for an extended period cause

A

bone marrow supression

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45
Q

What is the main side effect of IV Amphotericin B

A

Nephrotoxicity

Can use liposomal forms of Amphotericin which have reduced side effects

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46
Q

2 examples of polyenes and what they are derived from

A

natural products of Streptomyces sp.
Nystatin
Amphotericin B

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47
Q

What is the mode of action of polyenes

A

Increase cell permeability e.g. measured by K+ release
Polyenes bind sterols, particularly ergosterol a fungal membrane sterol
Oxidative damage via auto-oxidation of amphotericin B

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48
Q

Spectrum of activity of Amphotericin B

A

Broad spectrum
Most yeasts and moulds are sensitive
Some notable exceptions : Aspergillus terreus is resistant

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49
Q

Spectrum of activity of nystatin

A

Most yeasts are sensitive

e.g. Treatment of oral or vaginal candidosis

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50
Q

Why is Nystatin administered as topical cream

A

Not absorbed orally and too toxic to give IV

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51
Q

What is terbinafine

A

Only oral allyamine

Inhibits ergosterol synthesis and disrupts cell membrane synthesis by inhibiting squalene epoxidase

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52
Q

Spectrum of activity of terbinafine

A

Dermatophyte fungi: cause of ringworm e.g. Trichophyton rubrum
Aspergillus sp.
Many filamentous fungi
Variable activity against most yeasts
Some species of yeast e.g. Candida krusei resistant

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53
Q

How is terbinafine administered and what for

A

Oral tablet
Official Licensed indication:infections of the skin, hair and nails caused by dermatophytes
Can be fungicidal or fungistatic

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54
Q

2 subclasses of Azoles

A

Imidazoles – older group 2 nitrogens in azole ring. E.g. clotrimazole
Triazoles – newer group 3 nitrogens in azole ring e.g. Fluconazole

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55
Q

What enzyme do Azoles inhibit

A

C14alpha- demethylase

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56
Q

Mode of action of Azoles

A

Accumulation of 14alpha methyl sterols and disruption of structure and function of membrane
Affect on membrane leads to disruption of cell wall biosynthesis and growth

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57
Q

Are Azoles fungistatic or fungicidal

A

Azoles generally fungistatic

Itraconazole and voriconazole may be fungicidal when fungus is exposed to high concentrations for extended periods

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58
Q

Spectrum of activity of azoles

A

Fluconazole: Most yeasts, Some yeasts e.g. Candida krusei and most moulds intrinsically resistant
Itraconazole and Voriconazole: Most yeasts including C. krusei and moulds, Zygomycetes resistant
Posaconazole: Most yeasts and moulds, Some activity against zygomycetes

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59
Q

Primary side effects of Azoles

A

Primary- Rash, raised liver function tests, nausea

Secondary- inhibition of cytochrome P450 enzymes, increasing concentration of drugs metabolised by such enzymes

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60
Q

Examples of echinocandins

A

Caspofungin
Anidulafungin
Micafungin

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61
Q

Mode of action of echinocandins

A

Inhibition of cell wall beta1-3 glucan biosynthesis
Echinocandins bind product of Fsk1 gene which is part of a membrane complex producing beta1-3 glucan
beta1-3 glucan is important part of most fungal cell walls

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62
Q

What organisms are echinocandins effective against

A

Most yeasts
Aspergillus and some moulds
Pneumocystis jirovecii – protozoan-like fungus causing pneumonia – not licensed indication

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63
Q

What organisms are echinocandins ineffective against

A

Cryptococcus
Zygomycetes
Fusarium and Scedosporium

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64
Q

Clinical uses of Azoles

A

Fluconazole: Candida and Cryptococcus infections
Itraconazole: Aspergillus infections in immunocompetent patients, some mould infections, Prophylaxis for immunocompromised patients
Voriconazole: Aspergillus infections in any patient, other mould infections
Posaconazole: Prophylaxis for immunocompromised patients, Treatment of serious fungal infections where other approaches fail, Zygomycosis

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65
Q

What route are echinocandins administered as

A

All IV

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66
Q

Clinical uses of echinocandins

A

systemic candidosis
For some Treatment of unresponsive aspergillosis
and Empiric treatment of suspected infection

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67
Q

What is the only immunoglobulin that can pass through the placenta

A

IgG

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68
Q

Examples of inactivated/dead vaccine

A

Flu, cholera, plague, and hepatitis A. Most vaccines of this type are likely to require booster shots.

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69
Q

Examples of live attenuated vaccines

A

Yellow fever, measles, rubella, and mumps (MMR), varicella, rotavirus. Responses are more durable and do not generally require booster shots.

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70
Q

Why is a cocktail of anti viral HIV drug therapy used instead of just one drug

A

Approx 3 diff drugs as one is not usually enough to suppress viral load as they can mutate and become resistant to one drug

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71
Q

Treatment of Hep C and B

A

Interferons

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72
Q

Stages of viral replication

A 
Virus attachment to cell (via receptor)
Cell Entry
Virus Uncoating
Early proteins produced – viral enzymes
Replication
Late transcription/translation  – viral structural proteins
Virus assembly
Virus release
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73
Q

How do viruses leave the cell once they have replicated

A

Reverse endocytosis or kill the cells

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74
Q

What is AZT (azidothymidine)

A

Inhibits HIV replication
Nucleoside Reverse Transcriptase Inhibitor (NRTI)
Nh3 group prevents polymerase from working as there is no longer a free 3’ OH group

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75
Q

2 main groups of NRTIs

A 
Pyrimidine analogues: 
Thymidine analogues: Zidovudine
Cytosine analogues: Lamivudine
Purine analogues (Adenine and Guanidine)
Abacavir and Tenofovir
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76
Q

What viruses use Reverse transcriptase to convert their RNA sequences into DNA sequences in the host

A

HIV and Hep B Virus/HBV

some NRTIs work on HBV too e.g. Lamividine + Tenofovir

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77
Q

What are NNRTIs

A

Non-nucleotide reverse transcription inhibitors

e.g. Nevirapine, Efavirenz

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78
Q

What are protease inhibitors

A

Antiviral drugs used to treat HIV/AIDS and hepatitis C virus. Protease inhibitors prevent viral replication by selectively binding to viral proteases (e.g. HIV-1 protease) and blocking proteolytic cleavage of protein precursors that are necessary for the production of infectious viral particles.

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79
Q

Examples of protease inhibitors

A

Atazanavir, Darunavir, Fospamprenavir, Lopinavir, Nelfinavir

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80
Q

What is HAART

A

Highly Active Anti-Retroviral Therapy
2 NRTIs + NNRTI or
2 NRTIs + boosted PI

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81
Q

When is HAART started

A

when CD4 count falls

Taken lifelong to suppress viral replication

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82
Q

What HIV mutation leads to resistance to Lamivudine

A

M184V

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83
Q

What are the only sexually transmitted infections which commonly cause epididymitis

A

chlamydia and gonorrhoea

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84
Q

Which antibiotic carries a high-risk for patients to develop C.difficile infections after use

A

Cephalosporins

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85
Q

What are bacteristatic antibiotics

A

Inhibit bacterial growth
Protein synthesis inhibitors
e.g Tetracyclines, Sulfonamides

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86
Q

What are bactericidal antibiotics

A

Kill bacteria
Cell wall-active agents
Beta-lactam antibiotics (penicillin derivatives (penams), cephalosporins (cephems), monobactams, and carbapenems) and vancomycin.

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87
Q

What is the Minimum inhibitory concentration

A

Minimum concentration of antibiotic at which visible growth is inhibited e.g. testing antifungal activity

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88
Q

What are the 3 main antibiotic interactions

A

Synergism: Activity of two antimicrobials given together is greater than the sum of their activity if given separately
Antagonism: One agent diminishes the activity of another
Indifference: Activity unaffected by the addition of another agent

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89
Q

An example of synergistic interaction of antibiotics

A

β-lactam/aminoglycoside combination therapy of streptococcal endocarditis

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90
Q

Targets of antibiotics

A 
Cell wall
Protein synthesis 
DNA synthesis
RNA synthesis
Plasma membrane
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91
Q

What was the first true antibiotic used in clinical practice

A

Benzylpenicillin (β-lactam)

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92
Q

What are β-lactams

A

All contain β-lactam ring: Structural analogue of D-alanyl-D-alanine so taken up into cell wall
They act by interfering with penicillin binding proteins: enzymes (Transpeptidases) involved in the synthesis and maintenance of peptidoglycan.

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93
Q

4 main subclasses of β-lactams

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

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94
Q

Examples of Penicillins

A

Benzylpenicillin (PEN), amoxicillin, flucloxacillin

Relatively narrow spectrum

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95
Q

Examples of Cephalosporins

A

chemically modified Cefuroxime (CXM), ceftazidime pseudomonas originosus etc.
Broad spectrum- prone to C.Diff infection post use

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96
Q

Examples of Carbapenems

A

Meropenem (MER), imipenem, ertapenem

Extremely broad spectrum

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97
Q

Examples of Monobactams

A

Aztreonam (AZT)
Gram-negative activity only
Used when patients have allergies to other b-lactam antibiotics

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98
Q

Deficiency of which of the following complement proteins is most likely to result in recurrent Neisserial infection?

A

C5-C9 (MAC)

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99
Q

A staphylococcus aureus infection that is not methicillin resistant is best treated with what antibiotic?

A

Flucloxacillin
Staph. aureus is a gram positive, coccus. It produces ß-lactamases which break down the ß-lactam ring in penicillins. Flucloxacillin is resistant to ß-lactamases. Vancomycin would be the next option and also used if the bacteria was methicillin resistant.

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100
Q

What are Negative Acute Phase Proteins

A

Albumin, transferrin, antithrombin levels, along with several other molecules, are decreased during inflammation
The physiological role of decreased synthesis of such proteins is generally to save amino acids for producing “positive” acute-phase proteins more efficiently.

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101
Q

Examples of Positive Acute Phase Proteins

A

CRP
Fibrinogen (leads to elevated ESR)
Complement proteins

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102
Q

Why is CRP a more accurate indicator of inflammation that ESR

A

ESR is dependent on elevation of fibrinogen, an acute phase reactant with a half-life of approx one week. This protein will therefore remain higher for longer despite removal of the inflammatory stimuli.
CRP (with a half-life of 6-8 hours) rises rapidly and can quickly return to within the normal range if treatment is employed.
E.g. in active systemic lupus erythematosus, one may find a raised ESR but normal C-reactive protein.

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103
Q

Which drug is used extensively in organ transplantation?

A

Cyclosporin

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104
Q

Temperature-dependent pruritis, following a hot bath typically, is a characteristic symptom of what

A

Polycythaemia vera

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105
Q

What type of acidosis is a recognised complication of uncontrolled diabetes mellitus

A

Metabolic Acidosis

106
Q

What is the usual treatment for viral meningitis

A

Aciclovir

107
Q

What is the usual treatment for bacterial meningitis

A

Cefotaxime

108
Q

What do NRTIs inhibit

A

Inhibits the viral reverse transcriptase, stopping the viral RNA from being reverse transcripted into DNA.

109
Q

What do protease inhibitors do

A

Act upon the aspartyl protease enzyme within HIV.

110
Q

What do fusion inhibitors do

A

Prevent the HIV virus from entering the healthy T-cell

111
Q

What do Integrase inhibitors do

A

Inhibit the integration of the proviral DNA into the host DNA, which is the step after reverse transcription of RNA into proviral DNA

112
Q

What is used as a marker of Glomerular Filtration Rate in the clinical setting

A

Creatinine clearance

113
Q

The clinical features of painless jaundice, steatorrhoea, pale stools, loss of weight and appetite are strongly suggestive of what

A

Pancreatic carcinoma

Raised CA 19-9 marker levels

114
Q

Which bacterium is the usually commonest cause of community-acquired pneumonia in healthy adults in the UK

A

Streptococcus Pneumoniae

115
Q

Which antibiotic should be avoided for use in pregnancy

A

Ciprofloxacin

A form of quinolone antibiotic and should be avoided in pregnancy as they have been shown to cause arthropathy

116
Q

Where are Class II antigens (HLA-DR, DQ, DP) PRIMARILY expressed

A

B lymphocytes

117
Q

What are glycopeptide antibiotics

A

Bind directly to terminal D-Alanyl-D-Alanine on NAM pentapeptides- inhibiting peptidogylcan synthesis
Gram-positive activity- Unable to penetrate Gram-negative outer membrane porins
e.g. Vancomycin, teicoplanin etc

118
Q

Under what circumstances would you use glycopeptide antibiotics (even though they can be toxic)

A

Patients who are critically ill,
who have a demonstrated hypersensitivity to the β-lactams, or who are infected with β-lactam-resistant species (MRSA)
They exhibit a narrow spectrum of action, and are bactericidal only against the enterococci.

119
Q

What are amino glycosides

A

Protein synthesis inhibitor antibiotics
Gentamicin, amikacin
Bind to 30S ribosomal subunit

120
Q

What are Macrolides, Lincosamides etc

A 
Protein synthesis inhibitor antibiotics
Erythromycin, clarithromycin (macrolides)
Clindamycin (lincosamide)
Bind to 50S ribosomal subunit1
Inhibit protein elongation
121
Q

What are tetracyclines

A

Protein synthesis inhibitor antibiotics
e.g. tetracycline, doxytetracycline)
Bind to 30S ribosomal subunit
Inhibit RNA translation/ Interfere with binding of tRNA to rRNA

122
Q

What are Oxazolidinones

A 
Protein synthesis inhibitor antibiotics e.g. Linezolid
Inhibits initiation of protein synthesis
Binds to 50S ribosomal subunit
Inhibits assembly of initiation complex
May also bind to 70S subunit
123
Q

What protein synthesis inhibitor is used topically to reduce mrsa up nose

A

Mupirocin

124
Q

What protein synthesis inhibitor is used topically for skin and systemic infections

A

Fusidic Acid

125
Q

What is a precursor of purine synthesis

A

Folic Acid

Therefore inhibiting folic acid synthesis inhibits DNA synthesis

126
Q

What do many bacteria make folic acid from

A

Para-aminobenzoic acid

127
Q

What enzyme do sulphonamides inhibit

A

inhibit dihydropteroate synthetase, the enzyme that catalyses the first step in folic acid synthesis

128
Q

What enzyme does trimethoprim inhibit

A

Dihydrofolate reductase
Inhibiting folate acid synthesis
Used to treat UTIs

129
Q

What is co-trimoxazole

A

Trimethoprim-sulfamethoxazole
Combination of trimethoprim and sulphonamides
Used to treat resistant bacterial infections, Pneumocystis jirovecii, and some protozoal infections

130
Q

Why are sulphonamides rarely used as a mono therapy

A

Toxicity problems and high levels of resistance

131
Q

What are Fluoroquinolones and quinolones

A

DNA synthesis inhibitors
Inhibit DNA gyrase and topoisomerase IV involved in remodelling of DNA during DNA replication
Supercoiling/strand separation
e.g. Nalidixic acid, ciprofloxacin, levofloxacin etc

132
Q

An example of an RNA synthesis inhibitor antibiotic

A 
Rifampicin 
RNA polymerase inhibitor
Prevents synthesis of mRNA
Antistaphylococcal 
Treats TB
Combined with flucloxacillin etc as resistance is quite high
133
Q

Example of a plasma membrane agent antibiotic

A

Daptomycin
Cyclic lipopeptide
Inserts lipophilic tail into cell membrane resulting in depolarisation and ion loss
Effective in Gram-positives only

134
Q

Adverse effects of amino glycosides

A

Reversible renal impairment on accumulation
Therapeutic drug monitoring indicated
Irreversible ototoxicity

135
Q

Main adverse effect of β-lactams

A

Allergic reaction: generalised rash or rarely anaphylaxis

136
Q

Main adverse effect of Linezolid

A

Bone marrow depression reversible on stopping use

137
Q

What beta-lactams can you use in a patient with non-severe penicillin allergy

A

Cephalosporins and carbapenems

138
Q

What drug can be used in patients with any penicillin allergy

A

Aztreonam (Monobactam)

Aztreonam does not contain a bicyclic nucleus

139
Q

Key antibiotic/bacteria combinations

A

Flucloxacillin - Staphylococcus aureus (not MRSA)
Benzylpenicillin – Streptococcus pyogenes
Cephalosporins (avoid in elderly) – Gram-negative bacilli
Metronidazole – anaerobes
Vancomycin – Gram-positives (MRSA)
Meropenem – most clinically-relevant bacteria

140
Q

How do bacteria become resistant to β-lactams

A

By synthesizing a β-lactamase, an enzyme that attacks the β-lactam ring.
To overcome this resistance, β-lactam antibiotics are often given with β-lactamase inhibitors such as clavulanic acid.

141
Q

Adverse effects of gentamicin

A

Nephrotoxicity and ototoxicity, vestibulotoxicity

142
Q

4 methods of sterilising equipment

A

Heat: Moist (Autoclave), dry (oven)
Chemical: Gas, liquid
Filtration
Ionising radiation: Used for single use disposable equipment

143
Q

How are mycobacterium different to other bacteria

A

Unusual waxy cell wall:High lipid content
Slow growing: Different media requirements
Poor take up of standard Gram’s stains: (Gram positive: Ghost cells)
Retain certain stains without decolourisation by acid / alcohol: “acid fast bacilli” (AFBs), Ziehl Neelsen stain (ZN)

144
Q

What organism causes tuberculosis

A

Mycobacterium tuberculosis and bovis

145
Q

What organism causes leprosy

A

Mycobacterum leprae

146
Q

What condition are atypical Mycobacterium associated with e.g. M. Marinarum

A

HIV (opportunistic infections)

147
Q

What is the disease process of TB

A

Usually affects lung- apices esp. (highest oxygen tension)

Often latent infection (asymptomatic) that can become active later in life

148
Q

What is the body’s response to TB

A

Forms tubercles/Granuloma
Cell - mediated immune response
Central area of epithelioid cells, giant cells, Surrounding lymphocytic cell infiltration.
Central area caseous necrosis.
Fibrosis / calcification of lesions
Bacilli slowly die / may remain viable 20 years

149
Q

What causes a latent TB infection to be reactivated

A

Lowered immunity
Western countries : over 50 year old, men
Malnutrition
Alcoholism
HIV infection.
Silicosis, chronic renal failure, gastrectomy..
Anti TNFα blockade (e.g. infliximab)

150
Q

Symptoms of active TB

A

Chronic productive cough: Haemoptysis

Weight loss, fever, night sweats.

151
Q

What is disseminated/miliary TB

A

Extra-pulmonary TB
Very young / old; immunocompromised
Primary disease
Secondary erosion of necrotic tubercle into blood vessel
Widespread infection, including meningitis.

152
Q

What causes an IgE mediated allergic reaction

A

IgE Ab mediated mast cell and basophil degranulation- release of inflammatory mediators

153
Q

Features of IgE mediated allergic reaction

A

Fast onset (15-30 min)
Weal and flare
Late phase response: Leukotrienes, Prostaglandins, Eosinophils
Central role for Th2 T cell

154
Q

What causes Type4 delayed-type hypersensitivity (chronic inflammation and cytokine release).

A

Th1 overactivation against autoantigens

155
Q

What are the main effector cells for Th2 cells

A

Eosinophils, basophils, and mast cells as well as B cells

156
Q

Allergic rhinitis, atopic dermatitis, and asthma belong to which category of autoimmunity

A

Th2 autoimmunity

157
Q

What are the main effector cells of Th1 immunity

A

Macrophages, CD8 T cells, IgG B cells, and IFN-γ CD4 T cells

158
Q

80% of what type of food allergies resolve by the age of 16

A

Milk and eggs

159
Q

What is the atopic triad

A

Excema, Rhinitis, Asthma

160
Q

What causes cytotoxic/Type 2 hypersensitivity reactions

A

IgG/IgM Ab response against combined self/foreign antigen at the cell surface- complement activation/phagocytosis/ADCC

161
Q

Clinical features and common antigens of type 2 hypersensitivity reactions

A

Onset minutes to hours
Cell lysis and necrosis
Penicillin!!

162
Q

Conditions associated with Type 2 hypersensitivity reactions

A

Erythroblastosis fetalis,

Goodpasture’s nephritis

163
Q

What causes immune complex/type 3 hypersensitivity reactions

A

IgG/IgM Ab against soluble antigen- immune complex deposition
e.g. SLE

164
Q

Clinical features of Type 3 hypersensitivity reactions

A

Onset 3-8h

Vasculitis

165
Q

What causes delayed/Type 4 hypersensitivity reactions

A

Antigen specific T-cell mediated cytotoxicity (Th1)

e.g. contact dermatitis

166
Q

Clinical features of Type 4 hypersensitivity reactions

A

Delayed onset 48-72h

Erythema induration

167
Q

Common antigens causing type 4 hypersensitivity

A

Metals-e.g nickel

tuberculin reaction

168
Q

Organ specific autoimmune diseases

A

Type 1 diabetes
Graves Disease
Multiple Sclerosis

169
Q

Systemic autoimmune diseases

A

SLE

Rheumatoid arthritis

170
Q

What is the most common causative organism in cases of osteomyelitis

A

Staphylococcus Aureus

171
Q

Actinic keratoses are most commonly precursors to which skin condition

A

Squamous cell carcinoma

172
Q

During a Mantoux or Heaf test in order to determine immunity to tubercle bacilli a positive reaction is indicative of what type of hypersensitivity reaction?

A

Type 4

173
Q

Which antifungal class contains an agent which can cause unwanted inhibitory effects on CYP450

A

Azoles- bind to cytochrome P450 enzyme and inhibit it from normal metabolic functions. Drugs which are usually metabolised by CYP450 will be in higher concentration as a result of azole-induced inhibition

174
Q

Which of the 4 pathological classifications of Hodgkin’s lymphoma (HL) is NOT a classification of Classical Hodgkin’s lymphoma?

A

Nodular lymphocyte-predominant HL
HL is caused by the malignancy of Reed-Stenberg cells in lymph nodes or (rarely) extra-nodal tissue. Reed-Stenberg cells are derived from germinal centre B cells or (rarely) peripheral T cells. To be classified as Classical HL, CD30 and CD15 antigens are usually expressed. However, nodular lymphocyte-predominant HL does not express CD30 and CD15, and alternatively expresses CD20.

175
Q

Orphan Annie eye nuclei and psammoma bodies are characteristic of what thyroid condition

A

Papillary carcinoma of the thyroid
Most common thyroid cancer
Excellent prognosis

176
Q

Of which autoimmune disease are anti-neutrophil cytoplasmic antibodies (ANCAs) most characteristic

A

Wegener’s granulomatosis

177
Q

What syndrome syndrome consists of a triad of protenuria, hypoalbuminaemia and oedema, often accompanied by hyperlipidaemia and lipiduria

A

Nephrotic Syndrome

178
Q

How many types of IgG are there

A

4
IgG1 is the most common circulating IgG
The main difference in structure between the subtypes is the structure of the hinge region

179
Q

The nephritic syndrome is composed of what symptoms

A

proteinuria, haematuria and hypertension
Causes hypertension
post-streptococcal glomerulonephritis
crescentic glomerulonephritis

180
Q

Difference between nephritic syndrome and nephrotic syndrome

A

thin glomerular basement membrane and small pores in the podocytes of the glomerulus, large enough to permit proteins (proteinuria) and red blood cells (hematuria) to pass into the urine. By contrast, nephrotic syndrome is characterized by only proteins (proteinuria) moving into the urine.

181
Q

Pathophysiology of Autoreactive B cells and autoantibodies

A

Directly cytotoxic
Activation of complement
Interfere with normal physiological function

182
Q

Pathophysiology of auto reactive T Cells

A

Directly cytotoxic

Inflammatory cytokine production

183
Q

What is Hashimoto’s thyroiditis

A

Destruction of thyroid follicles by autoimmune process
Associated with autoantibodies to thyroglobulin and to thyroid peroxidase
Leads to hypothyrodism

184
Q

What is Grave’s disease

A

Inappropriate stimulation of thyroid gland by anti-TSH-autoantibody
Leads to hyperthyrodism

185
Q

What is myasthenia gravis

A

Muscle weakness caused by antibodies that block nicotinic acetylcholine receptors at the postsynaptic neuromuscular junction.
Muscles become progressively weaker during periods of activity, and improve after periods of rest.
Muscles that control eye and eyelid movement, facial expressions, chewing, talking, and swallowing are especially susceptible

186
Q

What causes SLE

A

Anti-nuclear antibodies causing inflammation and apoptosis

Type 3 hypersensitivity

187
Q

What is Rheumatoid Factor

A

Antibody (IgM, IgG or IgA) directed against the Fc portion of IgG
Commonly found in rheumatoid arthritis but not diagnostic of the disease

188
Q

What antibody is most specific for Rheumatoid arthritis

A

Anti-CCP (ACPA) more specific (95%) for RA than RF
Citrullination happens when the cells are dying-
The citrulline is detected by the anti-ccp

189
Q

What are Anti-neutrophilic cytoplasmic antibodies (ANCA)

A

An autoantibody mainly of the IgG type, against antigens in the cytoplasm of neutrophil granulocytes.
specific for Wegeners granulomatosis/ granulamatosis with polyangitis

190
Q

What are the targets of the 2 different types of ANCAs

A

2 types

perinuclear targets MPO protein (found in Churg Strauss) cytoplasmic targets PR3 (found in Wegeners)

191
Q

What autoimmune condition is Anti-mitochondrial Ab specific for

A

Primary biliary sclerosis

192
Q

What antibodies are found in autoimmune hepatitis

A

Anti-smooth muscle and anti-liver/kidney/microsomal (LKS) Abs

193
Q

What are immunomodulators

A

Medicinal products produced using molecular biology techniques including recombinant DNA technology
e.g. monoclonal antibodies

194
Q

Which organism is the most common cause of urinary tract infections (UTIs)

A

E.Coli

195
Q

What are the most common type of skin cancers.

A

Basal cell carcinomas
Very invasive and locally destructive but they rarely metastasise
Good Prognosis

196
Q

What is the name of the bacterium that causes syphilis

A

Treponema pallidum

197
Q

What condition is Hydroxychloroquine used to treat

A

Lupus
Interferes with production of cytokine
Used for joint and skin complaints in CTD
Caution: may cause haemolytic anemia in G6PD def

198
Q

What condition is Sulphasalazine used to treat

A

Used in inflammatory bowel disease and RA

Caution: regular FBC monitoring required

199
Q

What conditions is colchicine used to treat

A

Used in Familial Mediterranean fever (FMF) and Behcet’s, gout
Interferes with microtubule assembly/neutrophil chemotaxis
Caution: causes GI problems

200
Q

What conditions is Dapsone used to treat

A

Dermatitis herpetiformis
Inhibits neutrophil adherence to endothelium
Caution: haemolysis in G6PD def

201
Q

What conditions is thalidomide used to treat

A

Several effects on immune system: anti-TNF, decreases expression
of adhesion molecules, favors Th2 T cell responses
Used in Rx of Behcets’s disease and myeloma
Caution: birth defects, peripheral neuropathy

202
Q

Actions of corticosteroid use

A

Decreased neutrophil margination
Reduced production of inflammatory cytokines
Inhibition phospholipase A2 (reduced arachidonic acid metabolites production)
Lymphopenia
Decreased T cells proliferation
Reduced immunoglobulins production

203
Q

Side effects of corticosteroid use

A

Carbohydrate and lipid metabolism: Diabetes, Hyperlipidaemia
Reduced protein synthesis: Poor wound healing
Osteoporosis
Glaucoma and cataracts
Psychiatric complications

204
Q

Which combination of antibiotics is used in the treatment of intra-abdominal infections caused by an intestinal source in patients less than 65 years of age

A

Metronidazole and Cefuroxime
They target aerobic enteric bacteria, therefore providing a clinically effective treatment.
These drugs are used in patients under 65 due to an increased risk of developing Clostridium Difficile infection in individuals over 65.

205
Q

The malignant blood disorder which can result in extramedullary hematopoiesis of the liver and the spleen is

A

Myelofibrosis
bone morrow is replaced by scar/fibrous tissue. This results in a decrease in the numbers of blood cells being produced and a pancytopaenia. Extramedullary hematopoiesis (creation of new blood cells from stem cells OUTSIDE the bone marrow) in one mechanism which attempts to compensate for this.

206
Q

Which chromosomal translocations causes the formation of the “Philadelphia chromosome” in Acute Lymphoblastic Leukaemia

A

t(9;22)

forms BCR-abl fusion gene

207
Q

4 classes of drugs targeting lymphocytes

A

M-TOR inhibitors: Sirolimus
IL-2 receptor mABs: Basiliximab, Daclizumab
Antimetabolites: Azathioprine (AZA), Mycophenolate mofetil (MMF)
Calcineurin inhibitors: Ciclosporin A (CyA), Tacrolimus (FK506)

208
Q

Mode of action of calcineurin inhibitors and effect on T cells

A

Prevents activation of NFAT nuclear factor activated t cell
Factors which stimulate cytokines (i.e IL-2 and INFγ) gene transcription
Reversible inhibition of T-cell activation, proliferation and clonal expansion

209
Q

Mode of action of Sirolimus (M-TOR inhibitor) and effect on T cells

A

Macrolide antibiotic
Also binds to FKBP12 but different effects
Inhibits mammalian target of rapamycin (mTOR)
Inhibits response to IL-2
T Cell cycle arrest at G1-S phase

210
Q

Side effects of calcineurin/M-TOR inhibitors

A 
Hypertension
Hirsutism
Nephrotoxicity
Hepatotoxicity
Lymphomas
Opportunistic infections
Neurotoxicity
Multiple drug interactions (induce P450)
211
Q

What are calcineurin/M-TOR inhibitors used to treat

A

Transplantation (allograft rejection)

Autoimmune disease

212
Q

What is the most common cause of croup in children

A

Parainfluenza viruses

Distinctive Barking cough

213
Q

What antibiotic does Legionella not respond to

A

Beta Lactams e.g. penicillin

Similar symptoms to pneumonia

214
Q

What is the most common organism to cause opportunistic pneumonia (especially in AIDS)

A

Pneumocystic jiroveci

215
Q

What are the symptoms of Herpes Simplex

A

Herpes Simplex is a peri-oral, weeping, vesicular rash preceded by tingling and precipitated by fever and stress.

216
Q

In what condition is M. Avium Complex likely to cause an opportunistic infection

A

HIV
MAC causes disseminated disease in up to 40% of patients (HIV)
Fever, sweats, weight loss, and anemia

217
Q

Is Leprosy culturable in vitro?

A

No

218
Q

2 different types of leprotic presentations

A

Tuberculoid: Th1 mediated

Lepromatous(more severe): Th2 mediated

219
Q

What is the action of calcineurin inhibitors

A

CyA- Binds to intracellular protein cyclophilin
Tacrolimus (FK506)- Binds to intracellular protein FKBP-12
Mode of action:
Prevents activation of NFAT nuclear factor activated t cell
Factors which stimulate cytokines (i.e IL-2 and INFγ) gene transcription
T cell effects:
Reversible inhibition of T-cell activation, proliferation and clonal expansion

220
Q

Why are children and elderly are much more sensitive to infection

A

Immaturity or senescence of the immune system

221
Q

What are primary immunodeficiencies

A

Genetic defects in individual components of the immune system.

222
Q

In what ways are an infants immune system immature

A 
Maternal Antibodies
Ab production from 5 - 6 months
No response to bacterial polysaccharides
Lower complement levels
Poor cell-mediated immunity
Poor macrophage function
Poor neutrophil function
223
Q

Immunodeficiency conditions in lymphocytes

A 
T & B CELL:
SCID subtypes
Omenn’s
Wiskott-Aldrich
X-linked Hyper IgM

B cell:
XL & AR hypogammaglobulinaemia
CVID
CSR defects

224
Q

What are the two inheritance patterns of SCID

A

Mainly autosomal recessive but can be Xlinked

225
Q

Presentation of chickenpox in SCID

A

Fulminant disease

Haemorrhagic lesions

226
Q

What is Wiskott-Aldrich syndrome

A

X-linked immunodeficiency
Mainly affects T cells
Eczema, Thrombocytopenia, Immunodeficiency
Antibody deficiency first, then cellular
Complications – Autoimmunity, haematological malignancy
Low Mean Platelet Volume

227
Q

Infection patterns in immunodeficiency

A

T Cell: Opportunistic infections
Virus
Intracellular bacteria
Protozoa

Antibody: Respiratory problems
Encapsulated bacteria

Neutropenia: bacterial sepsis
IgA deficiency: upper respiratory tract infections
Asplenia: encapsulated bacteria

228
Q

SIGNALS POINTING TO POSSIBLE IMMUNODEFICIENCY

A

Infectious signals:
>4 (proven) bacterial infections per year

SPUR checklist:
Severe infections
Persistent infections
Unusual causative organism
Recurrent infections
229
Q

Where are Class 1 and 2 HLA proteins expressed

A

Class I antigens (HLA-A, B, Cw) found on all nucleated cells

Class II antigens (HLA-DR, DQ, DP) primarily expressed on B lymphocytes but expression can be induced on T lymphocytes and other cells

230
Q

Symptoms of Pneumonia

A 
Cough, fever
Dyspnoea
Pleuritic pain
Production of purulent sputum
Tachypnoea
New focal chest sign
231
Q

Normal viral causes of pneumonia in adults and children

A

Adults: Influenza A and B, adenovirus
Children: RSV, parainfluenza

232
Q

Differences in presentation of typical and atypical pneumonia

A

Typical: Alveolar inflammation, Peripheral/pleuritic chest pain, copious purulent sputum, Elevated WBC

Atypical: Tracheobronchial-interstitial inflammation, central substernal pain, scanty non-purulent sputum, normal WBC

233
Q

Bacterial and viral causes of atypical pneumonia

A

Bacterial: Legionella sp. Chlamydia pneumoniae Chlamydia psittaci Mycoplasma pneumoniae

Viral: Measles, HSV, CMV

234
Q

Predisposing conditions for pneumococcal pneumonia

A 
Sickle cell disease
Asplenia/ splenic dysfunction 
IgG disorders: agammaglobulinemia, myeloma, chronic lymphocytic leukemia
Nephrotic syndrome
Cirrhosis
Alcoholism
235
Q

What is legionella pneumophila

A

Water borne infection (aerosolisation)
Failure to respond to beta-lactam antimicrobials
Severe pneumonia, often associated with non-pulmonary symptoms such as mental confusion, diarrhoea and renal failure
Rapid urinary antigen testing should be available in at least one laboratory per region.
Legionella cultures should be performed on all invasive respiratory samples (bronchoscopy)

236
Q

Treatment of pneumonia

A 
Usually amoxillin (+clarithromycin)
If severe then Co-amoxiclav
Alternatively use doxyclycline or if severe benzylpenicillin and a flueorquinolone
237
Q

What are charcot-leyden crystals indicative of

A

Eosinophilic inflamtiion e.g. after an asthma attack

238
Q

Changes in airways during an asthma attack

A

Increased mucus production and increased goblet cells
Smooth muscle hypertrophy
Thickened Basement membrane
Lots of inflammatory cells e.g. macrophages and neutrophils in lamina propria

239
Q

What are Curschmann spirals

A

Stringy condensed mucin found in asthma attacks

240
Q

What 2 components make up COPD

A

Chronic bronchitis

Emphysema

241
Q

Clinical definition of chronic bronchitis

A

Cough with sputum for three months in 2 consecutive years

242
Q

Pathological findings in COPD

A

Hyperinflated lungs with air trapping and bullae
Dilated airspaces, both macro and microscopically
Enlarged right ventricle due to cor pulmonale
Atheromatous coronary arteries

243
Q

Types of pneumothorax

A

Primary spontaneous pneumothorax (idiopathic)

  • Male
  • Tall and thin
  • Age 20-40s

Secondary spontaneous pneumothorax

  • Emphysema, cystic fibrosis, asthma
  • High altitude, scuba diving

Traumatic pneumothorax, including as a complication of a medical procedure

  • Insertion of a central venous catheter
  • Thoracoscopy
  • Mechanical ventilation

Tension pneumothorax
- Due to trauma, chronic lung disease, medical complication

244
Q

How is rheumatic fever contracted

A

A disease that affects the joints, kidneys, and heart valves, is a consequence of untreated strep A (S.Pyogenes) infection caused not by the bacterium itself. Rheumatic fever is caused by the antibodies created by the immune system to fight off the infection cross-reacting with other proteins in the body. This “cross-reaction” causes the body to essentially attack itself and leads to the damage above.

245
Q

What is pharyngitis and a grey pseudmembrane indicative of

A

Diptheria

V rare- treat with erythromycin

246
Q

How to treat Strep A throat

A

Penicillin

247
Q

What is quinsy

A

Peritonsilar abscess
Mostly caused by Strep esp Viridans and anaerobes
Requires drainage and antibiotics

248
Q

What is the main cause of infectious mononucleosis/ glandular fever

A

EBV

sometimes CMV

249
Q

What is epiglottitis

A

MEDICAL EMERGENCY
Cellulitis of epiglottis (“cherry red”) – airway obstruction
Child (2-4 yrs), fever, irritable, difficulty speaking (“hot potato”) and swallowing. Leans forward, drools. Stridor, hoarse.

250
Q

What is otitis media

A

Middle ear inflammation. Fluid present in the middle ear.
V common in children
Fever, pain, impaired hearing. Red bulging tympanic membrane.
Usually viral
H influenzae, S. pneumoniae, M. catarrhalis
Antibiotics: amoxicillin or clarithromycin
Complications= Mastoiditis

251
Q

Risk factors for Gastro oesophageal reflux

A

Defective lower oesophageal sphincter
Hiatus hernia
Increased intra-abdominal pressure
Increased gastric fluid volume due to gastric outflow stenosis

252
Q

Types of columnar mucosa in Barrett’s oesophagus

A

Gastric cardia type
Gastric body type
Intestinal type = “specialised Barrett’s mucosa” more common containing goblet cells with mucin in it.. Diagnostic

253
Q

Complications of Barretts’ oesophagus

A

Premalignant condition with an increased risk of developing adenocarcinoma (as they contain glandular structures)
Regular endoscopic surveillance is recommended for early detection of neoplasia

254
Q

Risk factors for peptic ulcer disease

A 
Hyperacidity
H. pylori infection
Duodeno-gastric reflux
Drugs (NSAIDs)
Smoking
255
Q

Major sites of Peptic ulcer disease

A

First part of duodenum
GOJ
Junction of antrum and body mucosa

256
Q

What mutation causes Hereditary diffuse type gastric cancer (HDGC)

A

Germline CDH1/E-cadherin mutation
Epithelial cells lose adhesions and migrate
Signet ring cell

257
Q

Pathogenesis of coeliac disease

A

GLIADIN- Alcohol soluble component of gluten
Contains most of the disease-producing components
Induces epithelial cells to express IL-15

CD8+ Intraepithelial lymphocytes (IELs)
IL15 produced by the epithelium = activation / proliferation of CD8+ IELs
These are cytotoxic and kill enterocytes
CD8+ IELs do not recognise gliadin directly

258
Q

Coeliac disease and cancer

A

Enteropathy-associated T-cell lymphoma

Small intestinal adenocarcinoma

259
Q

Where do diverticular occur most frequently

A

Mainly sigmoid colon
Weak points occur at sites where blood vessels (vasa recta) penetrate the circular layer of the bowel wall
These points occur in between strips of smooth muscle called TAENIA COLI
These weak points are where diverticula occur due to increased intra-lumenal pressure

260
Q

What is the pathology go diverticulosis

A

Thickening of the muscular wall (muscularis propria)
Elastosis / thickening of the teniae coli
Muscosal redundancy
Infolding of mucosa
Sacculation / diverticula formation

261
Q

What are the symptoms of diverticulosis

A 
Usually asymptomatic 
Typically elderly (>60)
Abdominal pain
Left lower quadrant
Constant 
Nausea & vomiting
262
Q

What are the consequences of diverticulitis

A 
OBSTRUCTION
PERFORATION
ABCESS FORMATION
PERITONITIS
FISTULA FORMATION

Medicine (7 decks)

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