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FOM > Christmas Exam bits & pieces > Flashcards

Christmas Exam bits & pieces Flashcards

1
Q

Define a tumour

A

An abnormal growing mass of tissue, growth is uncoordinated with surrounding tissue & continues after the external stimulus is removed

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2
Q

What is the prefix for glandular epithelial tumorus?

A

Adeno-

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3
Q

What do we call Epithelial malignant tumours?

A

Carcinomas

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4
Q

What is differentiation like in benign/malignant tumours?

A

Benign are well differentiated

Malignant tumours are poorly differnetiated

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5
Q

What are the 2 types of neural malignant tumour?

A

Astrocytoma in the CNS

Schwannoma in the PNS

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6
Q

How does invasion work?

A

multi-step process
Proteolytic enzymes degrade ECM
Cells lose cell-cell & cell-matrix adhesion

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7
Q

What are the 4 types of Tumour spreaD?

A

Lymph
Blood
Local
Trans-coleimic

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8
Q

Examples of a diagnostic tumour biomarker:

A

ALpha-fetoprotein

Marker for hepatocellular carcinoma & Testicular Teratoma.

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9
Q

Common metastasis sites:

A
  • Axial Skeleton
  • Adrenal Gland
  • Liver
  • Lung
  • Brain
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10
Q

Example of a predictive biomarker:

A

OEstrogen receptors are monitored in breast cancer as theyre prescence/type can indicate the specific type of cancer & therefore the best treatment

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11
Q

Common metastasis for breast, prostate & colorectal cancer?

A

Breast/Prostate -> Bone

Colorectal - > Liver

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12
Q

Whats the abnormal morphology of cancer cells speciically?

A

Cellular & Nuclear Pleomorphism

MArked difference in cell & nucleus size/shape

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13
Q

Dysplasia?

A

Uncontrolled growth of abnormal cell type

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14
Q

Characteristics of Dysplasia:

A
  • Graded (high/low)
  • Disorganised (Increased nuclear size & mitotic activity + abnormal mitosis)
  • No invasion
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15
Q

Example of abnormal hormone secretion by a tumour?

A

Lung Carcinoma can secrete ADH & ACTH

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16
Q

Systemic effects of malignant tumours:

A

Weight loss cachexia
PAraneoplasstic syndrome
Abnormal hormones
Treatments effects

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17
Q

Causes of pain in cancer:

A

Commonly:
= Perineural infiltration
- Pathological fractures
- Ulceration/haemorrhage

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18
Q

External stimuli/inhibitors of cell growth:

A
  • Growth facors
  • Hormones
  • Cytokines
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19
Q

Define cell cycles?

A

Time between mitotic division

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20
Q

3 types of enviromental carcinogens?

A

Radiation
Chemical
Oncogenic viruses

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21
Q

How do enviromental cacinogens cause cancer?

A
  • Radiation mutates bases
  • Chemical binds to DNA fomrming adducts which eventually causes oncogenesis
  • Oncogenic viruses either isnert oncogenes into cells ( Retrovirals) or viral promoters cause proto-oncogene overexpression
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22
Q

Difference between inherited & sporadic oncogenesis?

A

Inherited involves being born with atleast one mutated allele
Sporadic involves both hits occuring as sporadic point mutations

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23
Q

Difference between inherited cancer syndromes & familial cancers?

A
  • Inherited is autosomal dominent of a single mutant gene

- Familial has multifactorial inheritence with no clear predisposing gene

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24
Q

Some inherited/ familial cancers:

A

Inherited - MEN, FAP, Familial retinoblastoma

Familial - Some breast/ovarians

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25
Q

How do proto-oncogenes becomeoncogenes?

A

Overexpresssion or mutation

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26
Q

Some common oncogenic viruses and their cancers?

A

HEP B - > LIver
EBV and herpes -> Burkitts lymphoma
HPV -> Cervical

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27
Q

What is the henderson-hasselbach equation and what do we use it for/

A

pH = pKa + log10 (conjugate base/unionised acid)

Determing the relationship between local pH and a drugs ionisation

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28
Q

What 4 thins affect bioavailiabilty & what is it?

A

Bioavaliability is the amount of drug reachin the systemic circulation acitive and useable.

  • GI factors
  • Ability to cross physiologicak barriers
  • Formulation
  • First Pass MEtabolism
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29
Q

How do GI factors affect bioavailability?

A

Increased gut motility improves time to the site of absorption
Food & diseases can both impair/enhance the amount of drug absorbed

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30
Q

How does fomrulation affect bioavailiabitly?

A

Some durgs are slow-release formualtions

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31
Q

What effects a dugs ability to cross barriers?

A
  • Ionisation/pH
  • Lipid solubility
  • Particle Size
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32
Q

What is taken up by Active transport?

A
  • Levidopa in brain (for parkinsonism)
  • Iron
  • Calcium
  • Sodium
  • Potassium
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33
Q

What is taken up by facilitated diffusion?

A
  • Monosacchrides
  • AMino acids
  • Vitamins
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34
Q

What drives filtration/bulk flow?

A

Hydrostatic and/or osmotic pressure

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35
Q

What is the aparent volume of distributio?

A

Vd

Volume is which a durg needs ot be distributed to produce observed blood conc.

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36
Q

What does an increased Vd tell us?

A

The drug is better at crossing membranes

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37
Q

What is drug clearence?

A

Cl
Volume of fluid cleared of drug every unit time
e.g. ml/min

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38
Q

What is clearnece dependant on?

A

Renal clearence - Conc. urine flow rate

Hepatic clearence - Metabolism & biliary excretion

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39
Q

Where does most drug excretion occur?

A

Kidneys

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40
Q

What other places can du excretion occur?

A
  • lung
  • milk
  • liver
    yadda yadda
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41
Q

What are the 3 types of renal excretion emchanisms?

A
  • Active tubular secreiton
  • Passive tubular reabsorbtion
  • Glomerular filtraion
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42
Q

What occurs in active tubular secretion?

A

Acid/alkali drugs (often protein bound) are secreted into urine

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43
Q

What occurs in passive tubular reabsorption?

A

Small unionised drugs are reabsorbed into circulation

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44
Q

What occurs in Glomerular filtration?

A

All unbound drugs are filtered from the blood and excreted

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45
Q

How does the liver deactivate metabolsied drugs?

A

by conjugating them

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46
Q

What happends to non-conjugated drugs after theyre secreted into bile?

A

Theyre reabsorbed (entero-hepatic cirulation)

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47
Q

What happens to conjugated drugs secreted into bilE?

A

They cant be reabsorbed so they are shat out

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48
Q

What effects bound drug levels?

A
  • Renal failure
  • Hypoalbumineia
  • Pregnancy
  • Other drugs
  • Sturability of bindin
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49
Q

What affects tissue distribution of drugs:

A
  • Plasma binding protein
  • Membrane characteristics
  • Tissue perfusion
  • Transport mechanisms
  • ELimnation
  • Siseas/otherdrugs
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50
Q

What would make a drug unable to be filteerd out at the glomerulus?

A

LArge particles or large charges

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51
Q

Whats the difference in metabolism at different ages?

A

Infants have reduced renal funciton & fewer enzymes

Pubescent kids have the highest metbolic rate of all ages

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52
Q

Waht 3 reactions could occur in phase 1 metabolism?

A

Hydrolysis
Oxidation
or reduction

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53
Q

What is the purpose of phase 1 metabolism?

A

To increase polrity & provide ana ctive site for phase 2

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54
Q

What family of enzymes act in phase 1 and examples:

A

Cytochrome P-450s
CYP1A2
CYP3A4
CYP2D6

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55
Q

What CYP1A2 metabolize?

A

Theophylline

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56
Q

What does CYP2D6 metabolixe? What about CYP2C9

A

Cyp2d6;
- Anti-depressents
- Anti-psychotics
- Codeine->morphine

Vs Cyp2c9 :
-warfarin

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57
Q

Which cytochrome p-450s are smoking induced

A

CYP1A2

CYP2D6

58
Q

Where is CYP1A2 found?

A

Liver

59
Q

Some common enzyme inhibitors?

A

Grapefurit
Clarythromycin
Erythromycin

60
Q

What occurs in phase 2 metabolism?

A

Conjugation

Makes drugs more water soluble & inactive

61
Q

What are common conjugates in phase 2 metabolism?

A

GLucuronic acid
Glutathione
Suplahte
Acetate

62
Q

How does metabolism vary between race?

A

Races have different Cytocrhome P-450 expression

63
Q

How does pregnancy affect metabolism?

A

in 2nd/3rd timerseter hormonal changes induce enzymes

64
Q

What drug do we enteric coat to protect itt form the stomach?

A

Omeprazole

65
Q

Why do enteric coated drugs survive the stomach?

A

They only break down in high pHs like small intestine

66
Q

What delivery modes are prolonged release

A
  • Intramuscular
  • Subcutanoues Pellet
  • Tablet
67
Q

What has a systemic effect in inhalation?

A

Inhalation anesthetics

68
Q

What kind of drugs are Intramuscular?

A

Insoluble or formulated in an oil base

69
Q

How Many inpateitns suffer ADRS?
Admissions are ADR relateD?
hospital deaths are due to ADRS?

A
  • 10-20% of inpatients
  • 6.5% of admission
  • 0.2-3% deaths (5-10k/yr)
70
Q

Examples of TYPE A ADRs?

A

Beta-blockers causing bradycardia

Insulin causin hypoglycaemia

71
Q

Examples of Type C ADRs?

A

long term Excess cortisol causing iatrogenic cushings

72
Q

Examples of Type E ADRs?

A

Stopping Beta blockers causing unstable angina/Myocardial infarction

73
Q

Examples of Type D ADRs?

A

Isotretinoin causing kids born with craniofacial deformation

74
Q

What do loop diuretics do?

A

Increase tubular reabsorbtion

75
Q

What are the characteristics of the most serious drug interactions?

A

Drugs involved have:

  • Steep dose-respponse curves
  • Narrow therapeutic indexes
  • Very high protien binding
  • Can affect renal function
  • Induce/inhibit hepatic enzymes
76
Q

How do drug interactions affect absorption?

A
  • Insoluble complexes
  • Alter pH cauing ionisation
  • Affect gut motility
  • Alter gut bacteria
77
Q

What proto-oncoene is mutated to cause MEN2?

A

The RET gene

78
Q

What mutation predisposses you to breast/ovarian canceR?

A

Tumour supressor genes BRCA1 & BRCA2

79
Q

wHAT KIND OF defect leads to HNPCC?

A

Defective DNA repair genes

80
Q

What mutation cuases colon cancer?

A
  • APC tumour supressor gene (adenomatous polyposis COli)
81
Q

What can a Kras mutation cause?

A

Lung cancer

Or Colorectal cancer if following an APC mutation

82
Q

What shapes does the secondary protein struction take?

A

Alpha helices

Beta-pleated sheets

83
Q

What bonds stabilise protein alpha helixes?

A

H bonds between CO & NH in adjacent turns

84
Q

What bonds stabilize protein beta-pleated sheets?

A

H bonds between amide groups

85
Q

What do hydrophobic interactions need?

A

A water free enviroment internal to the protein

86
Q

What do disulphide bridges bind?

A

Cysteine residues

87
Q

Caues of protein denaturation?

A
  • Acid
  • Heat
  • Chaotrophic agents (Urea)
  • Cross-linking reagent (Formaldehyde)
  • Disulphide-Bond Reducers (2-mercaptoethanol)
88
Q

Where does glycosylation occcur?

A

Endplasmic Reticulum

Golgi Apparatus

89
Q

Main glycoproteins?

A

Immunoglobulins

90
Q

Using of metalloproteins?

A
  • Storage
  • Transport
  • Enzymes
  • Signalling
91
Q

What change in proteins causes sickle cell anaemia?

A

Hydrophilic glutamte is replaced by hydrophobic valine

92
Q

What causes scurvy?

A

Vitamin C deficiency
Less STable collagen cross links
Weaker collagen

93
Q

What does osteogenesis imperfecta cause?

A

Amino acid substitution
Collagen polypeptides cant coil tightly
Loses secondary/tertiary strucutre
Weak/brittle collagen

94
Q

What does an LDL receptor mutation cause & how?

A

Familial Hypercholesterolemia -> early cardiovascular disease

The cells have a glycoprotein LDL receptor that detects apoB, when its mutated LDL cant be internalized. This leads to an excess in the blood.

95
Q

Whats the difference between central & peripheral tolerance?

A

Central tolerance involves destroying auto-reactive lymphocytes in the primary lymhoid organs
Peripheraltolerance involves inhibiting auto-reactive lymphocytes that slip thorugh central tolerance

96
Q

Whats the difference between +ve & -ve selection in T cell educaiton?

A

Positive selection removes an T cells that ail to recognize MHC1
NEgative selection removes any T cells that recognise & bind to self-antigen

97
Q

What are the 5 chemo drugs?

A

SPindle poisons - Vinca Alkaloids & taxanes
Alkylating Agents
Anitmitotic antibiotics
Anti metabolites

98
Q

How do vinca alkaloid work?

A

They bind to tubuli preventing microtube/spindle formation, this arrests mitosis at the metaphase

99
Q

How do taxanes work?

A

Taxanes inhibit spindle dissaelmbly, freezing the cell at that stage

100
Q

How do alkylating agents wokr?

A

The alkyl group causes DNA to cross link between free guanines in adjacent strands at the N6 level preventin unzipping

101
Q

At what stages of the cell cycle do alkylating agents work?

A

All of them

102
Q

What are the 2 types of antimitotic antibiotic?

A

Anthracycline or non-anthracyclines

103
Q

How do antimitotic antibiotics work?

A
  • Metal ion chelation produces cytotoxic agents
  • Increasing the membrane permeability to ions
  • Alkylation
104
Q

Hw do anti-metabolites work?

A
  • Nucleoside analogues stop DNA synthesis

- Some bind ireversibly to viral enzymes

105
Q

What can we taret in targeted cancer treatments?

A

Epidermal growth factor receptor (EGFR)

Vascular Endothelial Growth Factor (VEGF)

106
Q

What do we target VEGF with?

A

aVastin

107
Q

What do we target EGFR with?

A

Erlotinib E for E 💋

108
Q

What drugs can be used to target hormones in breast & prostate canceR?

A

Prostate - Anti-androgens like CPA

Breast - Anti-oestrogens like tamoxifen & aromatase inhibitors

109
Q

What is cystisis?

A

Bladder inflammation

110
Q

What is myelosuppresion?

A

Bone marrow suppression

111
Q

Hair loss?

A

Alopecia

112
Q

Phlebitis?

A

Clots causing vein inflammation

113
Q

What food are linked to cancers?

A

Red meat to CRC

Saturated fat to breast cancer

114
Q

What are the 5 Rs of radiology?

A 
Radiosensitivity
Repair
Re-population
Re-oxygenation
Re-assortment
115
Q

Is hormones therapy treatment or prophylactic?

A

Both

116
Q

What re the 4 stages of staging?

A

Examination
Imaging
Genomics
Classification

117
Q

Do cancer cells have contact inhibition?

A

No they lose it when they beocme malignant

118
Q

What are the most common chemical carcinogens?

A

SMoking & alcohol

119
Q

What chemical carcinogen causes liver cancer?

A

Aflatoxin in peanuts

120
Q

What are the initiation, promotion, progression stages?

A

Inititation is a carcinogen induced mutation
PRomotion is growth promoted by oncogenes, mutant anti-oncogenes & growth factors
Progression is spread

121
Q

What ways does ionising radiation cause cancer?

A
  • Translocates chromosomes
  • Amplifies certain genes
  • Activates oncogenes
122
Q

When are tumour supressor genes normally activated?

A

By DNA damage or hypoxia

123
Q

What would you use to treat an unkown gram -ve infection?

A

Gentamicin

124
Q

WHat would you use to treat a Staph. Aureus strain thats producing B-lactamasE?

A

Flucloxacillin

125
Q

Whats the best IV treatment for serious pneumococcal, meningicoccal & strep. Pyogene infections?

A

IV Benzyl Penicillin

126
Q

What is ciprofloxacin?

A

A flouroquinolone that inhibits nucliec acid synthesis

127
Q

Which DNA analysis system doesnt need an electric field?

A

PCR

128
Q

In what direction do strands form in DNA replication?

A

5’ to 3’

129
Q

What enzymes form new DNA strands & which bind okizake fragments together?

A

DNA polymerase forms DNA
DNA ligase binds okizake fragments
(more are involved)

130
Q

Does mitosis involve recombination?

A

It can but not always

131
Q

What does nitrofurantoin treat?

A

Just UTIs

132
Q

What are the main eukaryotic histones

A

H1, H2A dimer, H2B dimer, 2x H3, 2x H4

133
Q

Which eukaryotic histoens isnt the DNA wrapped around?

A

H1

134
Q

What do you use to treat all chlamydia infections?

A

Azithromycin (macrolide)

135
Q

What would treat Chlamydia psittacci, Coxiella burnetti and Mycoplasma pneumoniae

A

Erythromycin
Clarithromicin
Levofloxacin

136
Q

Treating pseudomonas?

A

Ciprofloxacin

137
Q

Describe cephalosporin generations

A

Gram -ve activity increase from 1st generation to 3rd
Gram +ve activity increases from 3rd to 1st generation One of the 4Cs!
(examples of cephalosporins- Cephradine, cefuroxime, ceftriaxone [1st-3rd generation])

138
Q

Name a first gen cephalosporin

A

Cephradine

Gram +ve

139
Q

Name a 2nd Gen cephalosporin

A

Cefuroxime

Even

140
Q

NAme a 3rd gen cephalosporin

A

Ceftriaxone

Gram -ve

141
Q

What are the 4 Cs that cause C.diff infection?

A

Cephalosporins
Clindamycin
Ciprofloxacin
Co-Amoxiclav

142
Q

What commonly causes pseudomembranous colitis?

A

Clindamycin

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