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Year 1 Incorrect Questions > Basic Science/Principles > Flashcards

Basic Science/Principles Flashcards

1
Q

Antibio for leprosy that works in same way as sulphanomide

A

Dapsone

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2
Q

Which antibio inhibits p450 liver enzymes and causes drug interactions/toxicity?

A

Ciprofloaxacin

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3
Q

Common combo with sulphonamide

A

Trimethoprim

co-trimoxazole

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4
Q

Role of penicillin/beta-lactams

A

Inhibits a transpeptidation reaction involved in peptidoglycan utilization in the cell wall

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5
Q

Polymixin action

A

Disrupts bacterial membr in gm-bacteria

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6
Q

Ethambol and Isoniazid target … and … of mycolic acid

A

Incorporation and synthesis

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7
Q

Macrolide action

A

Binds to P-site, preventing the translocation step of the growing polypeptide chain

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8
Q

Clavulanic acid

A

Combo w beta-lactam antibios to inhibit beta-lactamase

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9
Q

Atypical pneumonia treatment

A

Azithromycin

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10
Q

Sulphonamide action

A

Inhibition of folic acid synthesis by acting as a p-aminobenzoic acid analogue

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11
Q

Why is metronidazole for anaerobics?

A

Only active when reduced by anaerobic cell enzymes

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12
Q

Why are cephalosporins useful in meningitis?

A

Penetrate blood-brain barrier well

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13
Q

Ototoxicity from which drugs?

A

Aminoglycosides e.g. gentamicin

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14
Q

Role of albumin

A

Regulates oncotic pressure of blood

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15
Q

Nine essential AAs

A 
My (methionine)
Tall (threonine)
Handsome (histidine)
Vegan (valine)
Friend (phenylalanine)
Is (isoleucine)
Watering (tryptophan)
Kale (lysine)
Leaves (leucine)
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16
Q

Apolipo spec to chylomicrons

A

Apo B48

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17
Q

Where are bile salts formed?

A

Liver

From glycine or taurine

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18
Q

Role of NK cells

A

Recognise virus-infected/malignant cells without interacting w thymus

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19
Q

Cohort study vs case-control

A

Cohort -
Two groups are selected according to their exposure to a particular agent and followed up to see how many develop a disease or other outcome

Case-control - Compares a group with a disease to a group without, looking at past exposure to a possible causal agent for the condition

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20
Q

Immunoglobulin types

A

IgG - phagocytosis of bac/virus, passes to fetal circ
IgA - sweat and tears
IgM - first released
IgD - unknown role, activ B cells
IgE - least common, parasites, hypersensitivity

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21
Q

Metformin action

A

Activation of AMP-activated protein kinase (AMPK)

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22
Q

Fructose intolerance enzyme

A

Aldolase B

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23
Q

Noradrenaline binds to…

A

Alpha 1 receptors

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24
Q

Lincomycin action

A

Inhibit protein synthesis

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25
Q

Th1 vs Th2

A

Th1 - cell-mediated

Th2 - humoral

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26
Q

What happens to rate of excretion if you incr conc of drug in plasma kinetcs?

A

Rate is unchanged

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27
Q

Assoc gene in neuroblastoma

A

N-MYC proto-oncogene

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28
Q

Phases of drug metabolism

A

Phase I: oxidation, reduction, hydrolysis

Phase II: conjugation

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29
Q

What type of receptor do insulin and oestrogen bind to?

A

Insulin - tyrosine kinase receptor

Oestrogen - nuclear receptor

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30
Q

Down’s syndrome characteristics

A

Single palmar crease, prominent supra-orbital ridge, brush spots, slanted ears and hypotonia

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31
Q

Neurotransmitter in pre/post-ganglionic neurones

A 
Symp
- pre = ACh
- post = NA
Parasymp
- pre + post = ACh
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32
Q

Order of potency of agonists in adrenoceptors

A
  • ⍺-adrenoceptor: noradrenaline > adrenaline > isoprenaline
  • β-adrenoceptor: isoprenaline > adrenaline > noradrenaline
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33
Q

Function of beta adrenoceptor subtypes

A

b1 - stim ad cyclase - incr HR and contraction force
b2 - “” - relax bronch/vasc SM
a1 - stim phospho C - contract vasc SM
a2 - “” - inhibit NA release

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34
Q

Muscarinic cholinoceptor functions

A

M1 - stim phos C - incr stomahc acid
M2 - inhib ad cyclase, opening of K channels - decr HR
M3 - stim phos C - incr saliva and visc SM contraction in bronch

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35
Q

Action of atenolol

A

Selective competitive B2 antagonist

angina, HT

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36
Q

Salbutamol action

A

Selective B2 antagonist

asthma bronchodila

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37
Q

Atropine action

A

Comp antag of musc ACh receptors

reverse bradycardia after MI and anticholinesterase poisoning

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38
Q

How does a G protein work when there’s no signalling?

A
  1. Receptor unoccupied
  2. ⍺ subunit binding site occupied by GDP
  3. Effector is not modulated
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39
Q

How does G protein receptor work with signal turning on?

A
  1. Agonist activates receptor, causing a conformational change
  2. G protein couples with receptor
  3. ⍺ subunit releases GDP and GTP binds in its place (guanine nucleotide exchange)
  4. ⍺ subunit dissociates from receptor and β𝛾 dimer
    1. ⍺ subunit and β𝛾 dimer are both signaling units
  5. ⍺ subunit combines with effector and modifies its activity
  6. Agonist may dissociate from receptor but signaling can persist because G protein and receptor are now separate
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40
Q

How does G protein receptor work in turning signal off?

A
  1. ⍺ subunit acts as an enzyme - hydrolyses GTP to GDP and Pi (signal is now off)
  2. ⍺ subunit recombines with β𝛾 subunit
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41
Q

Kinase-linked receptor

A

Hydrophillic protein mediators in plasma membrane that works in hour timescale
e.g. insulin

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42
Q

Nuclear receptor

A

Hydrophobic signalling molecules e.g. steroid hormones in nucleus/cytoplasm
Ligan-gated trans. factors

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43
Q

Driving force for Na (in) and K (out)

A

Na+ influx = Vm - ENa

K+ influx = Vm - EK+

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44
Q

Phases of membr potential

A 
Resting potetial
Depol stimulus to reach threshold
Upstroke to overshoot (depol)
Downstroke (repol) to undershoot (hyperpol)
Resting
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45
Q

Depol vs repol vs hyperpol

A

D - opening of Na channels (pos feed)
R - closure of Na, opening of K (neg feed)
H - K remains open

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46
Q

WHat is saltatory conduction?

A

Action potential jumps from one node of Ranvier to the next

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47
Q

Pharmacology vs pharmakinetics

A
  • Pharmacology: what a drug does to the body

- Pharmacokinetics: what the body does to a drug

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48
Q

Potency vs efficacy

A
  • Potency: amount of drug required to produce a desired effect
  • Efficacy: maximum response achievable from drug
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49
Q

EC50

A

Concentration of agonist that elicits half maximal effect

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50
Q

Phase 1 vs 2 metabolism

A

Phase 1: change in the drug by oxidation, reduction or hydrolysis
Phase 2: involve the combination of the drug with one of several polar molecules to form a water-soluble metabolite - conjugation

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51
Q

Drug that can go directly to phase 2

A

Codeine (pharmaco active metabolites)

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52
Q

Glucuronidation

A
  • Enzyme - uridine disphosphate-glucoronosyltransferases

- Cofactor - uridine diphosphate glucuronic acid

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53
Q

Definition for fates of drug abs in body

A

Absorption: drug is absorbed from site of administration, entry into the plasma

Distribution: drug leaves bloodstream and is distributed into interstitial and intracellular fluids

Metabolism: drug transformation by metabolism - liver and other tissues

Excretion: drug and/drug metabolites excreted in urine, faeces or bile

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54
Q

pKa

A

pH at which 50% of the drug is ionized and 50% is unionised
HH equation
pKa = pH + log(AH/A)

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55
Q

What does lower pKa and higher Ka mean?

A

Stronger acid (lower pH)

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56
Q

pH trapping

A

Weak bases accumulate in compartments with low pH (+ reverse)

57
Q

Apparent vol of distribution (Vd)

A

Vd: extent to which a drug partitions between the plasma and tissue compartments

- Low Vd = drugs retained in vascular compartments
- High Vd = drugs retained in non-vascular compartments – adipose, muscle etc.
58
Q

Effect of albumin on Vd

A
  • Reduces the ability of the drug for diffusion to target organ
  • May also reduce transport of the drug to non-vascular components
59
Q

Factors influencing drug elim

A

Abs>elim before optimum conc (first order)

Abs

60
Q

Clearance def

A

An expression of the elimination of a drug from the body - the volume of blood removed of a drug per unit time
CLR, CLH, CHO, CLT

61
Q

Equation for CL

A

CL = rate of drug elimination/[D] plasma

62
Q

Steady state

A

When rate of drug admin=rate of elim (R0=RE)

63
Q

Elim half-life equation

A

t½ = (0.693 x Vd)/CL

64
Q

Gm + vs gm -

A

Gm + thick peptidoglycan, purple

Gm- thin peptidoglycan, pink

65
Q

What are biofilms more resistant to?

A

Antimicrobials

66
Q

Aerobes vs anaerobes

A
  • Aerobic: grow in oxygen
  • Obligate aerobes: require oxygen
  • Obligate anaerobes: killed by oxygen
  • Facultative anaerobes: tolerate oxygen
67
Q

Coagulase vs haemolysis

A

Coag - stah aureus (+) vs - staph

Haemolysis - diff between strep

68
Q

Why do gm - sepsis patients deteriorate so quickly?

A

Gram-negative sepsis get very unwell very quickly due to endotoxin released when Gram-negative bacteria die

69
Q

Process of fever

A
  1. Antigen/LPS interacts with macrophages
  2. Macrophages release cytokines into bloodstream
  3. Cytokines travel to anterior hypothalamus
  4. Prostaglandin E released - increases body’s thermal set point
  5. Body perceives it as cold - starts to ‘shiver’
  6. FEVER
70
Q

Examples of each bac type

A

Gm- cocci - neisseria men and gonn

Gm+ cocci - strep, GAS, staph epi and aureus, enterococcus, clostridium

71
Q

Symmetry of viruses

A
  • Icosahedral symmetry: virus consists of repeated subunits that make up equilateral triangles arranged in a symmetrical fashion
  • Helical symmetry: made up of a single repeated unit
72
Q

Process of viral infection

A 
Replication
Attachment
ENtry
Uncoating
NA and protein synth
Assembly
Release
73
Q

How do they become resistant?

A

Genetic mutation

Transfer of bac DNA (transformation, conjugation, transduction)

74
Q

Empirical antibios

A
  • Staph aureus: flucloxacillin IV
  • Staph epidermidis: vancomycin IV
  • Strep pyrogenes: doxycycline
  • Gram negatives: clindamycin
  • Anaerobes: metronidazole, cotriomazol
75
Q

Mechs of resistance to antibiotics

A

Altered binding site
Destruction of antibio (ESBLs*****)
Incr efflux

76
Q

Bacteriostatic vs cidal

A
  • Bacteriostatic: inhibit growth of bacteria

- Bactericidal: kill bacteria

77
Q

ANtibiotics acting on cell wall

A

Penicillins (fluclox, amox)
Cephalosporins (cefaclor, cefadroxil)
Glycopeptides (vancomycin)

78
Q

Antibios inhibiting protein synth

A

Macrolides (erythro, azithro)
Aminoglycocides (gentamicin)
Clindamycin, tetracycline, cholarmphenicol

79
Q

Antibios on bac DNA

A

Metronidazole
Trimethoprim
Fluoroquinolones - c diff (ciprofloxacin, levofloxacin)

80
Q

Cell cycle

A

G1
S (DNA synth)
G2
M

81
Q

SNPs and CVNs

A

SNP - single nucleotide polymorph, most have no effect

CVN - extra/missing stretches of DNA; deletions or duplications

82
Q

Unbalanced chromosome rearragement

A
  • Extra or missing chromosomal material, usually 1 or 3 copies of gene
  • Causes major developmental problems
83
Q

Aneuploidy

A

Whole extra/ missing
X chromosome is better tolerated
Monosomy - lack of one
Trisomy - 3 copies (trisomy 21 - downs)

84
Q

Turner’s

A

Female w only one X

85
Q

Specific aneuplodies

A
  • 47XY +21 (trisomy 21) - Down’s syndrome
  • 47 XY +14 (trisomy 14) - miscarriage
  • 47 XY +18 - Edward syndrome, trisomy 18
  • 45 X - Turner syndrome
  • 47 XXY - Klinefelter syndrome
86
Q

Somatic mosaicism

A

Two genetically distinct populations of cells within an individual, derived from a post-zygotic mutation

87
Q

Robertsonian vs reciprocal

A

Rob

  • Two acrocentric chromosomes stuck end to end
  • Increased risk of trisomy in pregnancy

Recip
- Two broken off chromosome pieces of non-homologous chromosomes are exchanged

88
Q

Gene analysis tests

A 
aCGH - 1st line, detects missing/dup chroms
FISH - fluorescent probs
PCR - amp small piece
Whole genome seq - all exons
Genetic filter
89
Q

Types of mutations

A

Missense (change to single AA, most likely activate oncogene)
Change to AA seq
Insertion/deletion (frameshift)
Promoter and splice site change

90
Q

How is mitochondrial disease transmitted?

A

Mitochondrial DNA is transmitted maternally, in the ovum

90
Q

How is mitochondrial disease transmitted?

A

Mitochondrial DNA is transmitted maternally, in the ovum

91
Q

DNA methylation

A
  • Usually occurs on cytosine bases just before guanine bases

- Prevents transcription (leads to modification of histones)

92
Q

How are proto-oncogenes activated?

A 
Point mutation (BRAF)
AMplification (HER2)
Translocation (Philadelphia)
93
Q

Lynch syndrome

A

Hereditary form of cancer due to mutation in mismatch repair gene

94
Q

Incidence vs prevalence

A
  • Incidence rate: (number of NEW cases of a disease occurring in a population during a specific time period/number of persons exposed to the risk of developing the disease during that time period) x 1000
  • Prevalence rate: (number of cases of a disease present in a population at a given time/number of persons at risk of the disease at that point in time) x 1000
95
Q

Cytokines

A
  • Interferons released by virally infected cells signal to neighbouring uninfected cells:
    • Destroy RNA and reduce protein synthesis
    • Undergo apoptosis
96
Q

Macrophages and mast cells

A

Macro - Phagocytose bacteria

Mast - deal w pathogens too large for phagocytosis

97
Q

Transendothelial migration

A

Recruitment of neutrophils to the site of infection/damage during acute inflammation

98
Q

Killing pathogen mechanisms

A
  • Phagocytosis: phagolysosomal killing (like macrophages) via production of reaction oxygen species (ROS)
  • Degranulation: release of anti-bacterial granules
  • NETs: release of a net-like structure that traps pathogens, leading to phagocytosis
99
Q

Pinocytosis

A

ingestion of fluid of surrounding cells

100
Q

Acute phase proteins

A
  • C3 - involved in complement
  • CRP - activates complement via classical pathway (incr in inflam)
  • MBL - activates complement via MBL pathway
101
Q

Classical pathway activated by which Ig

A

IgM and IgG

102
Q

What signals do B cells require to become active and proliferate?

A

Antigen

Helpr signals

103
Q

T cell types

A
  • CD4+ Helper T cells: activate B cells & stimulate production of memory B cells
  • CD8+ Killer T cells: kill infected cells via perforin/granzymes/granulysin
  • Regulatory T cells: lymphocyte suppression
  • Memory T cells: involved in the adaptive immune response
104
Q

Class 1 and 2 MHC

A
  • Class I MHC: expressed on all nucleated cells, present peptide antigens to CD8+ killer T cells
  • Class II MHC: expressed only on antigen presenting cells (e.g. dendrites, macrophages), present peptide antigens to CD4+ helper T cells
105
Q

CD4+ cells and CD8+ cells diff into which cells?

A

CD4+ T cells → T helper cells

CD8+ T cells → CTLs (TC cells)

106
Q

Fick’s law of diffusion

A
  • ↑ concentration gradient (𝝙C) = ↑ rate of diffusion (Q)
  • ↑ surface area of membrane (A) = ↑ rate of diffusion
  • ↑ lipid solubility = ↑ rate of diffusion
  • ↑ molecular weight of substance = ↓ rate of diffusion
  • ↑ distance (thickness) = ↓ rate of diffusion
107
Q

Fick’s law of diffusion

A
  • ↑ concentration gradient (𝝙C) = ↑ rate of diffusion (Q)
  • ↑ surface area of membrane (A) = ↑ rate of diffusion
  • ↑ lipid solubility = ↑ rate of diffusion
  • ↑ molecular weight of substance = ↓ rate of diffusion
  • ↑ distance (thickness) = ↓ rate of diffusion
108
Q

Secondary active transport

A
  • Symport: solute and Na+ move in the same directio

- Antiport: solute and Na+ move in opposite directions (Na+ in, solute out)

109
Q

Exo vs endocytosis

A
  • Exocytosis: vesicle fuses with plasma membrane, releasing its contents to the ECF
  • Endocytosis: ‘pinching off’ of membrane to engulf substance
110
Q

Exer vs endergonic reactions

A

Exer - Total free energy of products is less than total free energy of reactants
Ender - Total free energy of products is more than total free energy of reactants

111
Q

When does pH = pKa?

A

When the concentration of acid is equal to the concentration of the conjugate base

112
Q

Structures of RNA and DNA

A
  • Nucleoside: base and 5 carbon sugar
  • Nucleotide: nucleoside and phosphate group
  • Purines: adenine and guanine
  • Pyrimidines: cytosine, thymine, uracil
  • Phosphodiester bonds: form between 3’ OH group and 5’ triphosphate, link nucleotides
113
Q

How is DNA synthesised?

A

5->3 direction

114
Q

Stages of translation

A

Initiation
Elongation
Peptide bond formation and translocation
Termination

115
Q

Apo vs holoenzyme

A
  • Apoenzyme: enzyme without cofactor (metal ion req)

- Holoenzyme: enzyme with cofactor

116
Q

Michaelis-Menten Kinetics

A
  • S: solute concentration
  • V0: initial rate (velocity) of reaction
  • VMAX: the maximum rate of reaction when all enzyme active sites are saturated with substrate velocity
  • Km (Michaelis constant): the substrate concentration that gives half maximal velocity
117
Q

Km = ?

A 
Km = [S] at 0.5(VMAX)
Km = (k-1+k2)k1

Low Km (only need little substrate to work at half max velocity and vice versa)

118
Q

k1, k-1, k2

A
  • k1 = forward rate for enzyme association with substrate
  • k-1 = backwards rate for enzyme dissociation with substrate
  • k2 = forward rate of enzyme conversion from energy to product
119
Q

Control points of glycolysis

A

Phosphofructokinase
Glyceraldehyde 3-phosphate
Pyruvate kinase
H+

120
Q

Warburg effect

A

Cancer cells produce energy by high rate of glucose metabolism to lactate - anaerobic glycolysis
(low Km hexokinase)

121
Q

How is NAD regenerated?

A

Krebs cycle

122
Q

Stages of TCA cycle (krebs)

A
  1. pyruvate enter
  2. pyruvate -> acetyl coA
  3. acetyl coA + oxaloacetate -> citrate
  4. citrate decarboxylated twice (yields 2 CO2)
  5. 4 ox reactions to yield NADH, H, FADh
  6. GTP formed
  7. oxaloacetate reformed
123
Q

What is generated from each acetyl-coA?

A
  • 3 NADH + H+
  • 1 FADH2
  • 1 GTP
  • 2 CO2
124
Q

Per glucose how many NADH etc are yielded?

A
  • 10 NADH and 10 H+
  • 2 FADH2
    (eac one has 2 high energy electrons for ETC/ox phosph)
125
Q

Process of oxidative phosph

A
  1. resp chain where electrons are handed down incr pos potentials (O2 is final accepto -> H2O)
  2. coupled to H transport from matrix
  3. 4 resp complexes pump H into IM space
  4. H flows back into matrix through ATP synthase
126
Q

Inhibition of ox phosph

A

Cyanide
Azide
CO

127
Q

How many ATP?

A

Net 30-32 from ETC

128
Q

Types of plasia

A

Dys - abnorm growing w/o stm
Meta - reversible change between cell types
Hyper - incr in number from stim

129
Q

Hallmarks of cancer

A
  • Resisting apoptosis
  • Sustained proliferative signaling
  • Evading growth suppressors
  • Activating invasion and metastasis
  • Inducing angiogenesis
130
Q

Stage vs grade in caner

A

Stage - how far

Grade - how bad

131
Q

Mechs of disease mnemonic

A

VINDICATE

132
Q

Types of necrosis

A

Coag - MI
Liquefactive - Bac/fung/brain
Caseous - TB

133
Q

Cell changes in resp to injury

A 
Stasis
Margination
Rolling
Adhesions
Transendo migration
134
Q

What are the 4C antibiotics most likely to cause C. diff?

A

Co-amoxiclave
Clindamycin
Ciprofloxacin
Cefuroxime

135
Q

Which immunoglobulin is transported across placenta for foetal immune protection?

A

IgG

136
Q

Group A strep shows what type of haemolysis?

A

Complete haemolysis

137
Q

Function of oligodendrocytes

A

Secretion of insulating material in CNS

Year 1 Incorrect Questions (7 decks)

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