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BRS/POM MOCKS > POM HARD QUESTIONS > Flashcards

POM HARD QUESTIONS Flashcards

1
Q

Haem structure?

A

The haem group consists of a ferrous iron ion (Fe2+) bound by a porphyrin ring.

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2
Q

How is 2,3 dpg made?

A

Conversion of 1,3 bpg made in glycolysis to 2,3 bpg via Rapoport- Luebering shuttle.

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3
Q

Why does haemoglobin F have a greater affinity that haemoglobin A?

A

Single amino acid substitution in gamma chain of haemoglobin F results in reduced affinity for 2,3 bpg and so increased affinity for oxygen.

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4
Q

What can spectrophotometry be used for in relation to haemoglobin?

A

Can be used to follow changes in oxygen binding by haemoglobin - absorbance changes when oxygen is bound. Checking the respiratory status of newborn infants.

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5
Q

What causes methaemoglobin to be present in blood?

A

Lack of methemoglobin reductase or production of a mutant form of haemoglobin known as haemoglobin M, which is resistant to reduction. Exposure to chemicals such as p-chloroaniline, nitrates, and local anaesthetics such as benzocaine.

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6
Q

Why does haemoglobin A travel further in electrophoresis that haemoglobin S?

A

HbA is more negatively charged than HbS.Due to a point mutation occurring in one amino acid of the β-chain. In this mutation, the amino acid glutamate in the normal protein (hydrophilic, negatively charged) is replaced by valine (hydrophobic, uncharged).

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7
Q

Stains used for blood film?

A

Haematoxylin and Eosin. Leishman’s stain

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8
Q

What contributes to validity of dataset?

A

A standard operating procedure (SOP) for data collection and analysis
Small proportion of missing data
Explicit inclusion and exclusion criteria
A large and diverse sample

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9
Q

Why is diagnostics important?

A

Prevent misuse of treatment - reduce use of antibiotics when they’re not necessary. Identify and prevent outbreaks.

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10
Q

What is the antimicrobial breakpoint?

A

An antimicrobial breakpoint is the agreed concentration of an agent at which bacteria can, and cannot, be treated with the antimicrobial agent in question.

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11
Q

What are hemolysins?

A

Enzymes that damage red blood cells.

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12
Q

How is a catalase test performed?

A

Application of bacteria to glass slide. Application of hydrogen peroxide to slide. Observation for generation of bubbles.

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13
Q

How to perform coagulase test?

A

Application of bacteria to glass slide. Application of plasma to slide. Incubate for 15 seconds and gently rotate. Observe for clumps.

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14
Q

What bacterium produces coagulase?

A

S.aureus

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15
Q

What does HTLV-1 cause?

A

Adult T- cell leukemia (ATL). Adult T-cell leukaemia/lymphoma (ATLL).

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16
Q

What do you call the DNA stain that is used to see how far the DNA fragments have migrated in electrophoresis?

A

DNA loading dye.

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17
Q

For a positive HTLV diagnosis what antibodies need to be present on western blot method?

A

MTA-1, p53, p24, p19 and gd21(recombinant glycoprotein).

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18
Q

How do you know if someone is positive for HTLV in QPCR?

A

Increase in fluorescence above a certain threshold. Negative HTLV patients the fluorescence doesn’t increase above threshold.

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19
Q

How is DNA probe based method done?

A

DNA Oligonucleotide probe added. Probe binds to specific gene that is amplified on template strand. Probe contains fluorophore at 5 prime and quencher at 3 prime sides. Fluorescence increases when fluorophore and quencher are seperated which happens when DNA polymerase synthesises new DNA stand and degrades probe. Fluorescence is proportional to amount of the specific gene in sample.

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20
Q

What does chymotrypsin target?

A

Hydrophobic side chains.

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21
Q

Treatment for autosomal dominant disease caused by a point mutation?

A

Knockdown (antisense) approach.

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22
Q

Treatment for nonsense mutation caused by the change of a single nucleotide.

A

Stop codon read through

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23
Q

Treatment for mutation affecting hematopoietic cells?

A

Ex vivo gene therapy.

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24
Q

Types of knockdown (antisense) approach?

A

antisense oligonucleotides (ASOs) and RNA interference (RNAi)

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25
Q

What in a trinucleotide repeat expansion affects phenotype severity?

A

More repeats more severe phenotype.

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26
Q

What are cancer risk gene normally involved in?

A

Normally correct DNA damage that naturally happens when a cell divides.

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27
Q

What occurs in the first step of cholesterol synthesis?

A

Synthesis of isopentyl pyrophosphate. Condensation of 3 acetyl CoA molecules to form HMG-CoA. HMG-CoA is converted into mevalonate. Mevalonate is phosphorylated and decarboxylated to produce 3-isopentyl pyrophosphate.

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28
Q

What is the rate limiting step of cholesterol synthesis?

A

HMG-CoA to Mevalonate. Reduced by NADPH and catalysed by HMG-CoA reductase.

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29
Q

How is HMG-CoA reductase under negative feedback control?

A

Inhibited by mevalonate, cholesterol and bile salts.

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30
Q

Whats happens to mevalonate?

A

Phosphorylated and decarboxylated to produce 3-isopentyl pyrophosphate.

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31
Q

What happens in the second step of cholesterol synthesis?

A

Condensation of 6 isopentyl pyrophosphate molecules to form squalene.

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32
Q

What happens in the third step of cholesterol synthesis?

A

Cyclisation and demethylation of squalene by monooxygenases.

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33
Q

Where does cyclisation and demethylation of squalene occur?

A

Endoplasmic reticulum.

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34
Q

How can creatine kinase activity in serum be detected?

A

A coupled assay. Absorption spectra of NADP+ and NADPH. Rate of NADPH formation is proportional to creatine kinase activity.

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35
Q

What are the two types of stratified squamous epithelium? Can you explain the two types.

A

Keratinising and non keratinising. Keratinising produce keratin and die but become strong protective structures. Non keratinising don’t die and so retain nuclei and organelles.

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36
Q

What kind of transport occurs at apical domain?

A

Passive transport with ion channels while on basolateral domain active transport occurs. This ensures directionality.

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37
Q

How long do biopsies take to get a result from the histopathology lab?

A

2-3 days.

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38
Q

Pros and cons of a fine needle aspirate?

A

Can penetrate inaccessible tissues. No information on tissue architecture.

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39
Q

When using manufactured antibodies, what is indirect activation?

A

Use of secondary antibodies that bind to an antibody (primary) that is bound to an antigen.

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40
Q

When is immunodiagnosis useful for?

A

Useful for infection or myeloma diagnosis.

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41
Q

Stain for diagnosis of tuberculosis?

A

Ziehl-Neelsen stain

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42
Q

Stain for lipids?

A

Oil red O

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43
Q

Stain for ECM components such as elastin and collagen?

A

Congo red

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44
Q

What malignant tumours end in ‘oma’?

A

Lymphoma, Melanoma, Hepatoma and Teratoma (not all malignant).

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45
Q

What blood vessels to malignant tumours usually spread by?

A

Veins or capillaries as they have thinner walls.

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46
Q

Malignant vs benign tumour differences?

A

Malignant tumours metastasise to distant sites whereas benign tumours do not. Malignant tumours have a less well defined architecture than benign tumours.

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47
Q

What cells predominantly produces type 1 interferons such as IF-alpha and IF-beta?

A

Virally infected cells.

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48
Q

What do interferons do?

A

Promote transcription of anti viral genes. Enhances t cell response by higher MHC expression and tissue repair.

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49
Q

What do anti viral genes promoted by interferons code for?

A

Nucleases, viral entry/exit inhibitors, viral uncoating inhibitors, protein translation inhibitors.

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50
Q

What activates innate immune cells?

A

Detection of microbial ligands (PAMPS). Gene expression changes driven by specific combination of cytokines

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51
Q

What is the R number?

A

Number of cases one case generates on average over the course of infectious period.

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52
Q

Advantages of inactivated toxoid vaccine?

A

Cheap and safe.

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53
Q

Advantages of recombinant protein vaccines?

A

Safe.

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54
Q

Disadvantages of live attenuated vaccines?

A

Can affect immunocompromised badly and could revert to virulence. Attenuation may lose key antigens.

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55
Q

Vaccines against viruses are usually of what type?

A

Either live-attenuated or killed.

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56
Q

What cytokines cause B cells to produce IgE (class switch) in type 1 hypersensitivity?

A

IL-4 and IL-13.

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57
Q

What antibodies does type II hypersensitivity involve?

A

IgG and IgM.

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58
Q

What antibodies does type III hypersensitivity involve?

A

IgG and IgM.

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59
Q

What causes contraction of pulmonary smooth muscle?

A

Leukotrienes and prostaglandins.

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60
Q

What is a hapten? Give an example

A

A small molecule which on its own is not antigenic, but when associated with a large carrier such as a protein can form an antigen. Penicillin binding to surface antigen on red blood cells causing haemolysis.

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61
Q

What are the steps for inflammation?

A

Change in local blood flow, structural changes in microvascalature, recruitment of immune cells and proteins.

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62
Q

After damage to tissue occurs and inflammatory signals are released, what happens?

A

Vasodilators are released - histamines and nitric oxide.

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63
Q

How do neutrophils directly clear pathogens?

A

Phagocytosis. Netosis.

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64
Q

How do neutrophils indirectly clear pathogens?

A

Release cytokines which recruits and activates other immune system cells.

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65
Q

Explain phagocytosis process

A

Microbe engulfed into phagosome. Phagosome fuses with lysosome to form phagolysosome. Reactive oxygen species and antimicrobial peptides kill microbe in phagolysosome.

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66
Q

What is the first step of neutrophil extravasation?

A

Leukocyte such as a macrophage releases cytokines that activate adhesion molecules (selectins) on endothelial surface.

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67
Q

What is the second step of neutrophil extravasation?

A

Integrins in low affinity state on neutrophils bind to selectins. This is referred to as rolling adhesion.

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68
Q

What is the third step of neutrophil extravasation?

A

Chemokines promote low to high affinity switch integrin switch.

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69
Q

What is the fourth step of neutrophil extravasation?

A

Cytoskeletal rearrangement to migrate out of endothelium.

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70
Q

What do macrophages do to resolve inflammation?

A

Clear apoptotic cells. Produce anti inflammatory mediators.

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71
Q

What can cause chronic inflammation?

A

Autoimmunity, prolonged infection, persistent toxic stimuli and unclearable particulates.

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72
Q

What cells do you see in chronic inflammation?

A

Lymphocytes, macrophages, and plasma cells

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73
Q

Key macrophage features?

A

Phagocytic, cytotoxic, anti-inflammatory and involved in wound repair.

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74
Q

What is granulomatous inflammation?

A

Chronic inflammation with formation of granulomas.

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75
Q

Why are granulomas formed?

A

To act as a barrier. To contain an area of bacterial, viral or fungal infection so it can try to keep it from spreading.

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76
Q

Characteristics of chronic inflammation?

A

Persistent inflammation, monocytes and macrophages are the dominant cell type present, ongoing cytokine release and scarring. T cells and B cells also present.

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77
Q

Characteristics of acute inflammation?

A

Vasodilation, increased vascular permeability, neutrophils dominant cell type present, histamine release and necrosis.

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78
Q

Consequences of long term inflammation?

A

Tissue damage, scarring, loss of function which can lead to organ failure.

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79
Q

Explain what leads to swelling in inflammation?

A

Vascular leakage increases blood flow into the inflamed tissue, leading to fluid build-up.

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80
Q

Explain what leads to redness in inflammation?

A

Accumulation of blood contents including red blood cells near surface of skin.

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81
Q

Explain what leads to heat in inflammation?

A

Heat results from the increased presence of fluid at core body temperature at a site that would otherwise have a limited exposure to this. During inflammation infiltrating immune cells are also highly metabolically active, which may also contribute to the generation of heat as a by-product.

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82
Q

Explain what leads to pain in inflammation?

A

Inflammatory mediators signalling on local nerve cells.

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83
Q

What is osmolarity?

A

Number of solute particles per 1 L of solvent.

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84
Q

What is pharmacogenomics?

A

The study of variability in drug response due to genetic differences.

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85
Q

What do serum tubes contain?

A

Silica coating to induce clotting. Gel to form physical barrier between serum and red blood cells.

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86
Q

What does albumin do?

A

Transports lipids, hormones and ions. Maintains osmotic pressure of plasma. Transports fatty acids released from adipocytes so they can be used in cells in the process of beta oxidation.

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87
Q

Intravenous Immunoglobulin G is used for what?

A

Treatment of auto immune disorders by clearing immune complexes. Protects against most of the common pathogens

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88
Q

How is hyperimmune globulin created?

A

Donors are screened for high levels of IgG against a particular pathogen by using ELISA. The IgG fraction is isolated from the plasma of these donors and concentrated.

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89
Q

What causes hypertrophy?

A

Increased functional demand or hormonal stimulation.

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90
Q

What is the common cause of physiological hyperplasia?

A

Hormonal or compensatory.

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91
Q

What kind of cell death causes coagulative necrosis?

A

Hypoxia.

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92
Q

What organ/tissue would you find fat necrosis?

A

Breast and pancreas.

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93
Q

Ballooning degeneration is considered a hallmark of what disease?

A

Steatohepatitis

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94
Q

What is non disjunction?

A

Uneven number of chromosomes in meiosis daughter cells. Results in +1 or -1 leading to trisomy and monosomy.

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95
Q

Most common form of aneuploidy?

A

Sex chromosome aneuploidy.

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96
Q

How would you write the karyotype of an individual with trisomy 21?

A

47 +21 or 47,XX +21

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97
Q

What causes unequal crossover of chromatids?

A

Misalignment of homologous chromosomes.

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98
Q

What can unequal crossover of chromatids cause?

A

Trinucleotide expansion.

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99
Q

What is philadelphia chromosome?

A

Chromosome 9 and 22 break and exchange portions.

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100
Q

What is a metacentric chromosome?

A

Short arm and long arm are the same length.

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101
Q

What is a submetacentric chromosome?

A

Short arm is shorter than long arm.

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102
Q

What is an acrocentric chromosome?

A

Short arm encodes no genes.

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103
Q

When does a Robertsonian translocation cause problems?

A

If its unbalanced. Can cause problems in offspring.

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104
Q

What is a dominant negative mutation?

A

The mutant form interferes with the activity of proteins it binds to.

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105
Q

What is an insufficient mutation?

A

Mutant in one gene results in half the amount of protein which is not enough for normal function.

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106
Q

What are the characteristics of y linked disorders?

A

Affects only males. All sons of affected father. Vertical degree of pattern.

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107
Q

What causes mitochondrial disease variability?

A

Number of mutant mitochondria in cell. Develop with age due to accumulation of mutant mitochondria.

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108
Q

What can streptococcus pyogenes cause?

A

Pharyngitis, skin infection, scarlet fever and sepsis.

109
Q

How does a capsule polysaccharide evade the immune system?

A

Hides antigenic structures. Antibodies or complement proteins can’t bind.

110
Q

What do proteases that are released do to evade immune system and what proteases does s.pyogenes release?

A

They cleave antibodies. Prevents normal opsonisation and so neutrophils can’t detect. S.pyogenes = Ides.

111
Q

What does C3b do?

A

Opsonisation and formation of C5 convertase (produces c5a and c5b).

112
Q

What do s.aureus and s.pyogenes produce that degrades complement protein C3?

A

Aur and SpeB.

113
Q

Explain how s.aureus inhibits C3 and C5 convertases?

A

S. aureus produces SCIN protein which binds to C3bBb and inhibits formation of C3 convertase and C5 convertase.

114
Q

What does S.pyogenes do to inhibit chemotaxis?

A

Releases SpyCEP which cleaves CXCL8. CXCL8 can’t bind to CXCR1/2 and so migration to site of infection doesn’t occur.

115
Q

How does S.aureus prevent antibody mediated phagocytosis?

A

They release molecules that bind to Fc receptors on neutrophils and prevent detection of opsonised bacteria. FLIPR targets IgG Fc receptor and SSL5 target IgA Fc Receptor.

116
Q

What complement negative regulator does s.pyogenes recruit?

A

Factor H and C4BP.

117
Q

What does s.pyogenes protease SpyCEP do?

A

Cleaves CXCL8 and so prevents binding to CXCR1/2. Neutrophils do not migrate to sites of infection.

118
Q

What toxins cause skin peeling? What bacteria produces these?

A

Exfoliative toxins A and B. S.aureus

119
Q

What toxin can mediate multiorgan pathology? What bacteria produces these?

A

Toxic shock syndrome toxin. S.aureus

120
Q

What are some diseases s.aureus can cause?

A

Pneumonia, Endocarditis and Septic arthritis.

121
Q

How do antibodies neutralise extracellular virus?

A

It blocks viral attachment proteins. It destabilises viral structure.

122
Q

Why does a new influenza vaccine need to be created each year?

A

Antigenic drift. Influenza viruses mutate and evolve to change year on year. A new influenza vaccine is required each year to reflect the circulating virus types.

123
Q

How do influenza viruses undergo antigenic shift?

A

Acquire completely new antigens by reassortment with animal viruses.

124
Q

How do rhinoviruses evade antibody recognition?

A

Exist as hundreds of antigenically distinct serotypes.

125
Q

How do Hepatitis B virus (HBV) and Ebola virus evade antibody recognition?

A

Secrete surface antigens that mop up antibody, stopping it reaching virus particles or infected cells.

126
Q

What does previous infection with one serotype of Dengue Virus followed by infection with a different serotype lead to?

A

Leads to antibody dependent enhancement of disease as virus enters immune cells via antibody and the Fc-Receptor. This triggers Dengue Haemorrhagic Fever.

127
Q

What cells are specialised for secreting IFN-α?

A

Plasmacytoid dendritic cells.

128
Q

What cells secrete interferon gamma?

A

Activated NK cells, CD4+ Th1 cells and CD8+ cytotoxic T cells.

129
Q

What proteins block viral replication?

A

2’5’ oligoadenylate synthetase and protein kinase R.

130
Q

What molecules activates NK cells?

A

IFN-α and interleukin-12.

131
Q

How does NK detect infected cells?

A

If a is cell displaying fewer than normal MHC molecules.

132
Q

How does herpes simplex HSV and cytomegalovirus CMV evade immune system?

A

Encode proteins that interfere with the MHC antigen processing pathway.

133
Q

Examples of enveloped viruses?

A

Measles virus and ebola virus.

134
Q

How does influenza replicate?

A

Influenza enter cell by endocytosis. Single strand of RNA enters nucleus. RNA is replicated and mRNA is produced. mRNA leaves nucleus and is translated into viral proteins. RNA genomes and viral proteins go to cell surface join together and bud off.

135
Q

What does remdesivir treat?

A

Hepatitis C and SARS-COV-2

136
Q

How does amantadine work?

A

Blocks M2 channel protein. Influenza is locked in the endosome as H+ ions can’t enter M2 channel protein and so no uncoating of virus.

137
Q

What does baloxavir treat and how?

A

Influenza. Inhibits PA endonuclease.

138
Q

Anti IL6 drug?

A

Tocilizumab

139
Q

Monoclonal antibody for RSV?

A

Palivizumab.

140
Q

What occurs as the pathogen is eliminated?

A

Apoptosis of lymphocytes that lose their survival signals (antigen). Formation of memory cells.

141
Q

What can lead to apoptosis of t cell in thymus?

A

If the t cell doesn’t bind or binds too strongly to self mhc.

142
Q

What is it called when T cell doesn’t bind to self MHC at all?

A

Death by neglect.

143
Q

What is anergy (deactivation of t cell)?

A

Type of peripheral tolerance. T cell binding to mhc but antigen presenting cell doesn’t have co stimulation proteins. Engagement of inhibitory receptors on T cell. T cell less likely to be stimulated in the future even if co stimulatory proteins are present.

144
Q

What is antigen induced cell death?

A

Activation of t cell receptor leads to apoptosis. Binding of fas ligand to fas receptor causes apoptosis of t cell.

145
Q

How do Treg cells regulate immune response?

A

Inactivate dendritic cells so naive T cells aren’t activated. Inhibition of T cell effector functions.

146
Q

How do Treg cells regulate immune response if lymphocytes bind to self antigen?

A

T lymphocytes are activated by binding to self antigen on MHC in thymus or peripheral tissues. Activated lymphocytes release IL2. IL2 binds to IL2 receptor on Treg cells and foxp3 is expressed. Release of anti inflammatory cytokines such as IL-10. Inhibition of T cell activation or effector functions.

147
Q

Role of cytokines?

A

Level of immune response. Cytokines shape transcription factor pathways. Transcription factor pathways result in different t helper cell types.

148
Q

Inducible regulatory T cells development?

A

Develop from mature CD4 T cells that are exposed to antigen in the periphery.

149
Q

Natural regulatory t cells development?

A

Recognition of self antigen during maturation in thymus. Reside in peripheral tissues to prevent harmful reactions against self.

150
Q

How do sulphonamide antibiotics work?

A

Competitive inhibitors of folic acid synthesis in bacteria. Inhibits DNA replication.

151
Q

What enzyme do sulphonamide antibiotics target?

A

Dihydropteroate synthase.

152
Q

What gram positive bacterium is associated with Pseudomembranous colitis, antibiotic-associated diarrhoea?

A

Clostridium difficle.

153
Q

What gram positive bacterium can cause a UTI?

A

Enterococcus spp (VRE).

154
Q

What gram negative bacterium is common in cystic fibrosis lung infections and survives on abiotic surfaces?

A

Pseudomonas aeruginosa.

155
Q

What gram negative bacterium can cause GI infect., neonatal meningitis, UTI?

A

E.coli

156
Q

What gram negative bacterium can cause GI infect and typhoid fever?

A

Salmonella

157
Q

What gram negative bacterium can cause UTI and pneumonia?

A

Acinetobacter baumannii.

158
Q

What gram negative bacterium can cause gonorrhoea?

A

Neisseria gonorrhoeae.

159
Q

How do aminoglycosides work?

A

They target protein synthesis, RNA proofreading and damage cell membranes.

160
Q

Examples of aminoglycosides?

A

gentamicin and streptomycin

161
Q

What is Rifampicin?

A

Bactericidal that targets RNA polymerase.

162
Q

What is vancomycin?

A

Bactericidal. Targets lipid II component of cell wall synthesis, as well as wall crosslinking.

163
Q

What is linezolid?

A

Bacteriostatic. Inhibits initiation of protein synthesis by binding to the 50s ribosomal RNA subunit. Only works on gram positive.

164
Q

What drug class is linezolid?

A

Oxazolidinones.

165
Q

What is daptomycin?

A

Bactericidal. Targets bacterial cell membrane. Only works in gram positive.

166
Q

State a glycopeptide?

A

Vancomycin.

167
Q

State a lipopeptide?

A

Daptomycin.

168
Q

What is the resistance mechanism in streptococcus pneumoniae?

A

Acquires gene that encodes an enzyme that causes Methylation of AB target site in 50s ribosomal subunit leads to resistance to erythromycin.

169
Q

How do macrolides work?

A

Target 50s ribosomal subunit preventing amino-acyl transfer and thus truncation of polypeptides.

170
Q

Name 2 macrolides?

A

erythromycin and azithromycin

171
Q

How do quinolones work?

A

Bactericidal. Target bacterial enzymes involved in DNA. Leads to DNA damage.

172
Q

Reasons for why antibiotic course may fail?

A

Presence of AB resistance within commensal flora. Inappropriate dose. Bacterial spores.

173
Q

How to deal with antibiotic resistance?

A

Knowledge of local strains / resistance patterns. Reduce use of broad spectrum antibiotics. Quicker identification of infection caused by resistant strains. Combination therapy

174
Q

How does chloramphenicol acetyl transferase work?

A

Transfers acetyl group from acetyl CoA to chloramphenicol. Chloramphenicol can’t bind to ribosomes.

175
Q

What are mycoses?

A

Fungal infections.

176
Q

Classes of mycoses?

A

Superficial, cutaneous, subcutaneous or systemic.

177
Q

What are Mycotoxicoses?

A

Ingestion of fungi and their toxic products

178
Q

Antifungal treatment targets?

A

Cell membrane - Fungi use ergosterol instead of cholesterol. Cell wall (mammalian cells don’t have).

179
Q

Gram positive antibiotics?

A

Linezolid, Daptomycin.

180
Q

Why do IgG ABO antibodies that cross the placenta not cause HDFN?

A

Fetal red cells have poorly developed ABO antigens which are unable to support binding of the IgG antibodies. ABO antigens are found on numerous other cells (not just red cells) so any IgG ABO antibodies that have crossed the placenta can be ‘mopped-up’ by these cells.

181
Q

When can IgG ABO mediated HDFN occur?

A

Mothers who have especially high levels (‘high-titre’) of IgG anti-A and anti-B antibodies.

182
Q

When is an antibody screen test done?

A

To see if a patient has acquired alloantibodies.

183
Q

How is HTLV screened for?

A

Antibody in blood.

184
Q

How is syphillis screened for?

A

Antibody test.

185
Q

What is FFP used to treat?

A

Bleeding, multiple clotting factor deficiencies, dilutional coagulopathy, disseminated intravascular coagulation.

186
Q

When is cryoprecipitate used?

A

To treat haemophilia A or VWF disease. Liver disease (low fibrinogen).

187
Q

What are the viral inactivation steps to produce plasma derived medicines?

A

Heat treatment and use of solvent detergent.

188
Q

What are the two types of immunoglobulin solutions?

A

Normal and specific.

189
Q

Why are prothrombin complex concentrates better for treating patients with major bleeding than FFP?

A

Administering PCCs takes less time than FFP as FFP needs to be thawed.

190
Q

How to avoid dilutional coagulopathy?

A

Transfusing red cells and FPP in either a 1:1 or 1:2 ratio (1 FFP for every 2 units of red cells given).

191
Q

What does autocrine signalling generally lead to?

A

Negative feedback.

192
Q

What is an ionotropic receptor?

A

Ligand gated ion channel. Ligand binds and ion permeable pores open to allow ion to travel down the channel.

193
Q

How does a g protein coupled receptor specifically work?

A

Ligand binding causes conformational change in 7tm receptor. This allows heterotrimeric g protein to bind to 7tm receptor. GDP is exchanged for GTP and g protein is seperated into alpha and beta sub unit. Each sub unit binds to its target protein.

194
Q

How can g protein be deactivated?

A

Dephosphorylation of GTP to form GDP. Alpha unit leaves target protein and rejoins with beta unit.

195
Q

What deactivates 7tm receptor?

A

Unbinding of ligand. Receptor remains active as long as ligand is bound and can activate further heterotrimeric g proteins.

196
Q

How do enzyme linked receptors work specifically?

A

Ligand binding causes receptors to cluster. This leads to enzyme activity within the cell. Enzymes phosphorylate the receptor. This leads to binding of signalling proteins to cytoplasmic domain of receptor. These signalling proteins lead to a signal cascade within the cell.

197
Q

How do type 1 intracellular receptors work specifically?

A

Receptor located in cytoplasm. Hormone passes through cell membrane and bind to receptor which leads to heat shock protein dissociation which results in 2 hormone bound receptors join together and form a hormodimer that passes through nucleus and bind to DNA.

198
Q

How do type 2 intracellular receptors work?

A

Binding of hormone to DNA receptor. Transcriptional regulation induced.

199
Q

What happens in the amplification step?

A

Small amount of thrombin mediates the activation of the co-factors V and VIII, the zymogen factor XI and platelets.

200
Q

What happens in the propagation phase?

A

Factor XI converts more factor IX to IXa, which in concert with factor VIIIa,amplifies the conversion of factor X to Xa, and there is consequently a rapid burst in thrombin generation which cleaves the circulating fibrinogen (soluble) to form the insoluble fibrin clot.

201
Q

How is prothrombin time done?

A

A source of TF and phospholipid is added to the citrated plasma sample, together with calcium to start the reaction; the length of time taken for the mixture to clot is recorded.

202
Q

How is APTT done?

A

Contact activator, together with phospholipid, is added to the citrated plasmasample followed by calcium; the time taken for this mixture to clot is measured

203
Q

What is disseminated intravascular coagulation (DIC)?

A

Generalised and uncontrolled activation of coagulation followed by marked activation of the fibrinolytic system. This activation results from the expression of TF within the circulation.

204
Q

Causes of reduction of clotting factors?

A

Liver disease, Disseminated intravascular coagulation

205
Q

Increased fibrinolysis causes?

A

Disseminated intravascular coagulation or use of t-PA.

206
Q

Why can’t anti thrombin activated by low molecular weight heparin inhibit thrombin (factor IIa), but can only inhibit clotting factor Xa?

A

Inactivation of IIa (thrombin)
requires longer chains of heparin
chains, which are able to wrap
around both the antithrombin and
thrombin. LMW heparin mainly
inactivates Xa.

207
Q

What factor is increased in pregnancy?

A

Factor VIII

208
Q

What does the single point mutation causing factor V Leiden result in?

A

Factor V Leiden makes factor V more resistant to inactivation by protein C. Type of inherited thrombophilia.

209
Q

How is mitochondria adapted for oxidative phosphorylation?

A

Folds in the cristae provide a larger surface area for the membrane-bound components of the electron transport chain.

210
Q

Why does FADH2 produce less ATP than NADH?

A

FADH2 bypasses complex I when it is reoxidised. NADH therefore pumps more H+ ions into the intermembrane space and so produces more ATP.

211
Q

How does ketoacidosis and high triglycerides cause coma?

A

The levels of ketone bodies (and fatty acids) will significantly lower the plasma pH disrupting ion transport in the CNS, leading to coma.

212
Q

Why does hyperglycemia lead to coma?

A

Hyperglycaemia leads to coma as it can make you dehydrated which can cause you to lose consciousness.

213
Q

What is needed for oxygen consumption in oxygen electrode?

A

Citrate/succinate/malanate, ADP and mitochondrial suspension.

214
Q

What glucose transporter do cancer cells express?

A

GLUT1.

215
Q

What amino acids give rise to α-ketoglutarate and aspartate in transamination?

A

Glutamate and oxaloacetate.

216
Q

Which family of enzymes catalyses the first oxidation step in the β-oxidation of fatty acids?

A

Acyl-CoA-dehydrogenases

217
Q

What are the three ketone bodies?

A

Acetone, acetoacetate and D-3-Hydroxybutyrate.

218
Q

What enzymez catalyse the irreversible reactions?

A

Hexokinase, phosphofructokinase and pyruvate kinase.

219
Q

What does it mean if a redox couple has a negative standard redox potential?

A

More reducing power than hydrogen. Has a tendency to donate electrons.

220
Q

What do you see in β
thalassemia electrophoresis and why?

A

Raised Haemoglobin A2 is found where there is a reduction in beta globin chains, caused by β
thalassemia (or trait). Allows more delta chains to be incorporated into hemoglobin and so raised HbA2.

221
Q

What is haemolytic anaemia

A

Premature destruction of red blood cells.

222
Q

What are the consequences of red blood cell sickling?

A

Haemolysis and vaso-occlusion.

223
Q

What causes ‘sickling’ in sickle cell disease?

A

Polymerization of hemoglobin S that make red blood cells less flexible.

224
Q

What is seen on the blood film of a patient with Infectious Mononucleosis?

A

Scalloped margins and ‘hugging’ of the surrounding red blood cells. Lymphocytes that have intensely basophilic (blue) cytoplasm.

225
Q

What do we see on the blood film of a patient with CLL?

A

Smear cells. Lymphocytes.

226
Q

Why does the philadelphia chromosome leads to CML?

A

BCR::ABL1 gene on philadelphia chromosome encodes a protein with uncontrolled tyrosine kinase activity, which gives rise to leukaemic clone.

227
Q

CML key symptom?

A

Splenomegaly.

228
Q

How do you differentiate acute lymphoblastic leukaemia and acute myeloid leukaemia on a blood film?

A

Cytoplasm in blasts of AML contain
granules. Very irregular shape of the nuclei seen in acute lymphoblastic leukaemia.

229
Q

What kind of cells do you see on blood film of acute myeloid leukaemia?

A

Myeloblasts, Nucleated red blood cell

230
Q

What kind of cells do you see on blood film of chronic myeloid leukaemia?

A

Increased granulocyte precursors

231
Q

Test for infectious mononucleosis?

A

Monospot test or looking for IgM antibodies to Epstein-Barr Virus (EBV).

232
Q

Metabolic effects of leukaemia?

A

High levels of uric acid and renal failure

233
Q

What is a specific indicator of bacterial infection seen in neutrophils on blood film?

A

Presence of clear vacuoles within the cytoplasm of the neutrophils.

234
Q

How to optimise image when using a light microscope?

A

Step 1: Focus the image. Step 2: Focus the condenser. Step 3: Adjust the field iris. Step 4: Adjust the condenser iris.

235
Q

Lymphatic system components?

A

Lymphatic vessels and secondary lymphoid tissue.

236
Q

Explain somatic hypermutation?

A

An enzyme called activation-induced cytidine deaminase (AID) makes random mutations in the antibody variable region genes. If the mutations result in an antibody that more strongly binds to their targets then these B cells will survive and may differentiate into antibody-producing plasma cells with the new specificity.

237
Q

Example of fungi?

A

Candida albicans.

238
Q

What are protozoa?

A

Unicellular eukaryotes.

239
Q

When is erythropoietin produced?

A

In response to hypoxia to boost red blood cell production in order to carry oxygen to tissues. In response to anaemia.

240
Q

What does hepcidin do?

A

Blocks absorption of iron and blocks release of storage iron from the liver.

241
Q

What happens when iron storage is low?

A

Hepcidin production is downregulated. More iron is absorbed and released from iron storage in liver.

242
Q

How is megaloblastic anaemia caused?

A

Vitamin b12 and folic acid are required for DNA synthesis. Needed for Deoxythymidine triphosphate. One of the four nucleoside triphosphates in DNA.

243
Q

Spherocyte feature on blood film?

A

Lack central pallor. Round, regular outline.

244
Q

What can G6PD deficiency cause? What can you see in a blood film?

A

Severe intravascular haemolysis. Bite cells.

245
Q

What are heinz bodies?

A

Clumps of irreversibly denatured hemoglobin seen in bite cells when you stain with methylene blue.

246
Q

Normocytic anaemia causes?

A

Gastrointestinal haemorrhage, bone marrow failure or hypersplenism.

247
Q

What are leukocytes derived from?

A

Myeloblast.

248
Q

What may neutrophilia be accompanied with?

A

Left shift (increase in non segmented neutrophils). Toxic granulation.

249
Q

Neutropenia causes?

A

Chemotherapy, radiotherapy, autoimmune disorders or severe infection.

250
Q

Persistent high lymphocyte cause?

A

Chronic lymphocytic leukaemia.

251
Q

What is reduced in acute myelod leukaemia?

A

Platelets.

252
Q

What term is used to describe the positive effect of an anti-viral drug on reducing the amount of virus in a patient?

A

Sustained virological response.

253
Q

Buffy coat consist of what in blood after centrifuge?

A

Leukocytes and plasma

254
Q

Inactivation of x chromosome nature?

A

random and permanently inactivated

255
Q

Why does the rate of mitochondrial respiration increase with the addition of ADP?

A

ADP is key for respiratory control in mitochondria. Uptake of oxygen by mitochondria is controlled by the components of ATP production:Inorganic phosphate (Pi), and ADP.

256
Q

What can resume oxygen consumption after adding oligomycin?

A

Addition of DNP

257
Q

Why does cyanide block oxygen consumption?

A

Stops flow of electrons and so electrons can’t be transferred to oxygen.

258
Q

What affects severity of mitochondrial inherited disorders?

A

Percentage of mutated mtDNA inherited. mtDNA is present within cells in multiple copies, some of which are mutated and some which are not

259
Q

What intercept changes with non competitive inhibitors?

A

Y intercept

260
Q

What intercept changes with competitive inhibitors?

A

X intercept

261
Q

What is keeps glutathione reduced?

A

The pentose phosphate pathway (aka hexose monophosphate shunt) G6PD generates NADPH which is key in keeping glutathione reduced

262
Q

Setting up a light microscope steps?

A

Focus the image. Focus the condenser. Adjust the field iris. Adjust the condenser iris.

263
Q

What antibiotic resistance should be checked with enterococcus?

A

Vancomycin.

264
Q

What antibiotic resistance should be checked with s.aureus?

A

Methicillin or vancomycin.

265
Q

Carbapenase producing bacteria?

A

E.coli

266
Q

What is the reverse primer complementary to?

A

Top strand of DNA.

267
Q

What is the forward primer complementary to?

A

Bottom strand of DNA.

268
Q

Explain when PCR can be used to determine if a specific bacterial strain is resistance to an antibiotic and explain when PCR cannot be used?

A

PCR is useful if resistance is conferred by the introduction of a specific additional gene. PCR is not used to detect resistance due to point mutations in house-keeping or existing genes

269
Q

What chromosomes can robertsonian translocations take place?

A

13, 14, 15, 21 and 22,

BRS/POM MOCKS (23 decks)

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