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Cv Flashcards

1
Q
  1. Translational research

2. Translational circle

A
  1. Process of turning observations in the laboratory, clinic and community into intervention
  2. Unbiased approaches to identify candidate genes and pathways
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2
Q

Research exploration

A
  1. Molecular medicine (omics)
  2. Bioinformatics
  3. Hypothesis
  4. Main research question and specific aim. Inclusion criteria
  5. Ethical approval
  6. Testing and informed consent.
  7. Protocols and logistics
  8. Validation
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3
Q

Bioinformatics

A

Sub-discipline of biology involving computer science. Concerned with acquisition, storage and analysis

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4
Q

What to consider for data visualisation?

A
  1. Sample size
  2. Distribution
  3. Type of data
  4. Clarity and readability (not over plot)
  5. Consistency
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5
Q

Response to retention hypothesis

A
  1. LDL retention. + charged ApoB100 with the - charged proteoglycans. Limited amount of LDL receptors. High cholesterol content increase the affinity
  2. LDL modification. Become oxidized. Not recognised by LDL receptors. Recognised by scavenger receptors in macrophages.
  3. Endothelial activation. VCAM, ICAM, selection. Monocytes entering. M-CSF allows differentiation. Monocytes attracted by MCP-1 and IL-8.
  4. Foam cell formation. Lead to fatty streak and lesion.
  5. Fibrous plaque. Th1 and Th2 establish inflammation. Smooth muscle cell migration. Proliferate and secrete proteins that form fibrous plaque. Cytokines: IFNy, IL-4, IL-10, IL-13, TNF, IL-6
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6
Q

Transport of LDL in endothelial cells

A
  1. Endocytosis through LDL receptors

2. Trancytosia through Cav-1

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7
Q

Vulnerable plaque reasons

A
  1. Inflammatory response. MMP expression by macrophages and oxLDL
  2. VSMC apoptosis by TNF and INFy lead to decreased collagen synthesis
  3. Haemodynamic shear stress
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8
Q

Disrupted plaque characteristics

A
  1. Bigger lipid core
  2. High macrophage content
  3. Smaller cap thickness. Less collagen
  4. Fibrin rich thrombus
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9
Q

MMP regulation

A
  1. Activation by cleavage

2. Inactivation by TIMP bind to Zn and N-terminal

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10
Q

Eroded plaque

A

Fibrous cap is intact but a thrombus forms bead an area of endothelial denudation

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11
Q

Difference PE and PR

A
  1. Fibrous cap intact/ ruptured
  2. Morphology fibrotic/ lipid rich
  3. Inflammation min/max
  4. Smooth muscle abundant/ absent
  5. Platelet rich/ fibrin rich
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12
Q

Coronary angiogram

A

Use X ray imaging to o see heart blood vessel

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13
Q

Treat plaque rapture

A
  1. Cholesterol lowering. Statins and fibrates
  2. Antiplatelet: aspirin
  3. Lowering blood pressure: beta blockers and ace inhibitors
  4. Anti-inflammatory therapy
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14
Q

IP + and -

A 
\+ 
Beyond traditional way of thinking
Increase accessibility 
Sharing cost and knowledge 
Avoid silo effect
  • Time and energy
    Distraction
    Difficulties getting fining
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15
Q

CRISPR-Cas9 system

A

Clustered regularly interspaces short palindromic repeats

  1. Open up DNA. Cas9 enzyme.
  2. gRNA (tracr + cr) guides to the sequence.
  3. PAM + Cas9 binds
  4. Cas9 checks it’s bound gRNA to see if complementary and initiate and double-strand cut. Three base pairs upstream of 3’ edge of PAM sequence.
  5. Cell tries to repair: HDR OR NHEJ
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16
Q

Applications CRISPR

A
  1. Gene expression regulation
  2. Specific DNA integration. Knock in/out, GFP
  3. Chromosome manipulations. Deletion, insertion, translocation
  4. Genome wide functional screening. Repression, activation, enhancer
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17
Q

GWAS

A

Observational study of genome wide set of genetic variants to see if any variant is associated with a trait. Focuses on associations between single nucleotide polymorphism

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18
Q

How is a genome-wide association study performed?

A
  1. Blood sample
  2. Do Chip to get significant SNP
  3. Statistical test. Add covariates
  4. Chart Manhattan plot. Select significant SNP
  5. Validation test

Two groups of individuals: binary logistic (chi square). Allele frequency
Quantitative: anova/linear regression. Genotype frequency

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19
Q

RDT malaria

A

Histidine rich protein (HRP2)
Plasmodium antigen lactate dehydrogenase (pLDH)

  1. Can not distinguish species
  2. No information of parasitemia
  3. Ineffective if lack HRP gene
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20
Q

Conventional PCR vs quantitative

Nested PCR

A
  1. Gel vs real time
  2. Accuracy
  3. nested: two steps, risk of contamination, problematic visualisations of amplicon, increased specificity
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21
Q

ELISA malaria

A

Information about immune response, not parasite
Starts after days or week of infection
Can be long lasting
Which antigen to choose?

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22
Q

Mouse models

A
  1. ApoE. Develops atherosclerosis on ND. not human like lipid profile. ApoE influences plaque development
  2. LDLr. Human like profile, functional ApoE ( no impact on inflammation). Requires WD
  3. PCKS9. No generic modification. Require WD
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23
Q

Biomarker discovery

A
  1. Preclinical. Exploratory. Proof of concept
  2. Retrospective. Characterisation. Predict outcome?
  3. Prospective. How used in clinical setting?
  4. Cohort longitudinal studies. Cost efficacy?
  5. Clinical use
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24
Q

Different biochemical markers?

A
  1. ApoB elevated and ApoA1 decreased
  2. Remnant lipoprotein cholesterol.
  3. Lipoprotein analysis. Non-fasting glycerides
  4. ProBNP. Natriuretic peptide
  5. Cytokines
  6. CRP
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25
Q

What stimulate insulin?

A

Glucose, incretins/GLP (L cells) and gastric inhibitory peptides (K cells). Release of insulin from pancreas

26
Q

Glucagon secretion

A

From a cells, insulin regulated,

27
Q

Hepatic glucose production

A
  1. Provision of substrates
  2. Allosteric regulation by metabolites
  3. Balance of hormones
28
Q

Important enzymes in homeostasis

A
  1. Glucokinase. Phosphorylate glucose upon entry
  2. PKLR. convert pyruvate to PEP
  3. AKT. Activates glycogen synthesis
  4. Foxo1. Activate gluconeogenesis. Inhibited by insulin
29
Q

Hepatic steatosis

A

Non-physiological accumulation of TG inside hepatic droplets. Disturb metabolism. Promote inflammatory state imbalance between FA output and input

30
Q

DAG in insulin resistance

A

Impaired suppression of HGP. Hepatic levels of DAG mediate resistance. Activates PKC that impairs tyrosine activity of insulin receptor. No phosphorylation. Foxo1 will not be inhibited.

31
Q

T2D Treatment

A
  1. Metformin. Suppression of gluconeogenesis

2. Improve hepatic insulin sensitivity

32
Q

Insulin regulation of fat

A
  1. More FFA taken up by lipocytes
  2. Esterification of TGs
  3. Stop the release of FFA
33
Q

Adipokines

A

Act locally as a hormone

34
Q
  1. Leptin

2. Adiponectin

A
  1. Signal satiety. Dysregulated in obesity.

2. Anti- inflammatory. Protect from resistance.

35
Q

Measuring metabolic flexibility

A

Calorimetry. Measure oxygen/carbon dioxide out. RER ( respiratory exchange ratio) 1 or 0.7

36
Q

Hemostasis

A
  1. Sealing leaks
  2. Restoring normal vasculature
  3. Maintains composition and fluidity of the blood
37
Q

Players in hemostasis

A
  1. Endothelium. Contraction. Mediated by thromboxone.Antithrombotic properties. Negatively charged
  2. Platelets. Granules
    - a granules. Selection, fibrinogen, factor V and VIII, TGF
    - delta/dense. ATP, calcium, adenosine
  3. Inhibitors
  4. Fibrinolysis activators
38
Q

Secondary hemostasis players

A
  1. Procoagulant proteins. Form clot. vWF, TF. Adhere to Collagen
  2. Profibrinolytic system. Repair
  3. Anticoagulant proteins. Prostacyclin, TFPI, thrombomodulin, tPA
  4. Antifibeinolytic proteins
39
Q

Vitamin K dependent coagulation factors

A

Factor 9, 10, 7, 2, protein C and S

40
Q

Thrombin sensitive coagulation factors

A

Factor 5, 8, 11, 13

41
Q

Coagulation pathway

A
  1. Exposure of tissue factor. endothelium or released from monocytes. Binds factor 7
  2. Activate factor 9 and 10
  3. Factor 10 bind ( together with factor 5) factor 2 to form little bit of thrombin

!! factor 9 (together with 8)

  1. Thrombin activates arriving platelets. Release factor 5, convert factor 11 and release factor 8
  2. Factor 11 further activates 10 again that activate thrombin
  3. Thrombin cleaves circulating fibrinogen. Fibrin. D-dimers. Covalently crosslinks factor 13
42
Q

Tenase and prothrombinase complex

A

T: factor 10 + 9 + 8
P: factor 2+ 10 + 5

43
Q

Control of coagulation

A
  1. TFPI. Inhibition of TF-dependent coagulation. Synthesised by endothelial cells
  2. Protein C- system. Serine protease. Activated by thrombin and form APC. Inhibit 5 and 8. Protein C receptor help activating C. Protein S is a cofactors to APC.
  3. Thrombomodulin. Inhibits receptor that bind thrombin
  4. Fibrinolytic system. Dissolves clot. Into FDP. Release by endothelium. Turn plasminogen to plasmin. Reopen blood vessels
44
Q

What happens during cytokine storm

A
  1. Vasodilation
  2. Decreased tissue perfusion
  3. Endothelial dysfunction
  4. IL-B. Inflammatory ensamble
  5. IL- 6. Active IL-B
  6. TNF-a
  7. Jak-stat pathway
45
Q

Carotid restenosis components

A
  1. Remodelling. Negative. Increased collagen in ECM. Thickening. Adapatation to flow. Disturbed flow promote inflammation. No compensatory enlargement lead to restenosis.
  2. Intimate hyperplasia. Injury cause growth factor release, TGF, PDGF. Basement degradation. Migration of cells. Control: cytostatic, inhibitors of GF, heparin
    Re-endothelization. Proliferation and migration of smooth muscle cells
  3. Elastic recoil of media.
46
Q

How can we help a stroke patient?

A
  1. Stop the cause
  2. Save the brain
  3. Rehab
  4. Prevention
47
Q

Five types of malaria

A
  1. Falciparum
  2. Vivax
  3. Ovale
  4. Malariae
  5. Knowlesi
48
Q

Thick and thin smear

A

Thick: parasites on top. More blood. Determine if there is malaria

Thin: determine specie

Unfixed vs fixed
Several layers va one layers

49
Q

Parasite stage in blood

A
  1. Sporozoites injected. Travel to liver. Invade hepatocytes. Merozite invade blood cell.
  2. Ring shape in blood
  3. Trophozoite
  4. Schizont. Form merozoites. RBC bursts. Dotted in cells.
  5. Gametocytes. Banana or huge cell(vivax). Ovale. Will mate if taken up by mosquito.

Falciparum : not all stages present in blood

50
Q

Diabetes and malaria

A
  1. Alternated nutrient environment factor malaria
  2. Inflammation
  3. Increase rosetting
51
Q

Enteroviruses

A
  1. RNA, non-enveloped
  2. Encephalitis, meningitis, myopericarditis
  3. Beta-cell autoimmunity, antibody positive, destroy cells, auto reactive T cells,
52
Q

Aortic aneurysm

A
  • Progressive pathological widening of the aorta. First manifestation is often rapture. 1.5 timea bigger than usual.
  • Abdominal aneurysm most common.
  • disease of aortic media and adventitia (connective tissue and fibroblast). Loss of cells.
  • increased expression of proteases (EDP, MMP) Inflammatory cell recruitment
  • identified by chance
  • treatments: surgery, medical treatment unclear
  • thoracic form: monogenic ( mutation in ECM, TGF) , sporadic (inflammation), non-syndromic
  • bicupsid aortic valve is a risk factor. Migration, cell loosening, ETM
53
Q

different PRR

A
  1. TLR
  2. NLR
  3. CLR
  4. RIG like
54
Q

Pyropoptosis

A
  • Inflammatory lyric programmed cell death.
  • activation of NFKB
  • transcription of sensor and IL-1
  • activation of caspase and cytokines
55
Q

Pathways in recognition and what determines the response

A
  1. MAPK
  2. NFKB
  3. IRF

Expression of receptor, signalling pathway and cell prevalence

56
Q

Innate initiation

A
  1. Recognition DAMP/PAMP
  2. Cytokines
  3. Vasodilation and migration of cells
  4. Complement activation
  5. Fighting. Macrophages and neutrophils. IFN
  6. APC antigen uptake and migration. CCR7 expression
57
Q

Adaptive immune response initiation

A
  1. Activation of T cells
  2. Migration to lymph nodes or tissue
  3. B cell activation through T or by themselves
  4. Antibody secreting cells, flag for destruction
58
Q

Different Th cells

A

Th1. Bacteria. Viruses IFN, Il 2
Th2. Parasite. igE production, il4, il 10
Th17. Cytokine Il-17,
Regulatory

59
Q

GC role

A

Dark zone. Proliferation and somatic hypermutation. Affinity maturation. (Antigen binding, point mutation) Class switch. (Heavy chain). AID enzyme
Light zone. Interaction. Selection. FDC.

60
Q

GLP effects

A
  1. Insulin release
  2. Insulin transcription and biosynthesis
  3. Responsiveness of B cells
  4. Proliferation and and decreased apoptosis of B cells
61
Q

Insulin secretion in diabetes

A
  1. Less cells that secrete
  2. Impaired secretion (no 2nd phase). First spike short second spike should be longer and reach plateau
  3. GLP 1 low
  4. Downrefulation of GLUTs
    5.

CV (1 decks)

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