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DDT > Trigger 3 > Flashcards

Trigger 3 Flashcards

1
Q

What is hypertrophic cardiomyopathy?

A

overgrowth of the heart muscle and thickening of the spetum

result in smaller chambers

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2
Q

How is it caused?

A

some hypertrophy occurs with cardiovascular exercise

Genetic disease causing mutations in the proteins of the sarcomere

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3
Q

What type of mutations occur in the proteins

A

42% occur in cardiac myosin binding protein C

40% occur in cardiac beta myosin heavy chain

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4
Q

What is Arrhythmogenic right ventricular cardimyopthy

A

enlargement of the right ventricle

disease of the desomosomes proteins

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5
Q

what are the stages of ARVC

A

Concealed - small change in right ventricle
Overt - noticable structural changes in the heart muscle, affecting pumping action and cause abnormal rhythms
Weakening - right ventricle becomes stretched, pumping weaker
left ventricle also affected

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6
Q

What are cardiomyocyte intercalacted discs

A

structures that connect the myosites together

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7
Q

what are cardiomyocyte intercalacted discs made up of

A

Desmosomes
Gap junctions
Adhere Junctions

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8
Q

What are Desmosomes

A

structure that holds cells together
made up of proteins
gives structural intergrity
link to intermediate filament cytoskeleton

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9
Q

Gap junctions

A

form direct pores between myocytes
continous electrical and metabolic connection between the cells
allows them to contract together
made of kenxin

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10
Q

Adhere junctions

A

anchors thin filament of the sacromere to the sarcolemma

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11
Q

describe direct immunohistochemistry

A

slice tissue using a chiroscat and fix in formalin
Insert primary antibodies which are against the antigen/protein of interest
Label antibody with reporting system - enzyme or flourscent congulated to antibody

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12
Q

Benefits of direct method

A

specific

quciker

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13
Q

disadvantage of direct

A

only one antibody for each protein

more expensive

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14
Q

describe indirect immunohistochemistry

A

slice tissue using a chiroscat and fix in formalin
Insert primary antibodies which are against the antigen/protien of intrest
Insert secondary antiobies which ahve been raised in another species against original IGg antibody
secondary antibody is coagulated to reporting system

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15
Q

Benfits of indirect method

A 
sensitive 
can bind to more reporter antiobodies 
can bind more than one 2nd antibody to each 1st antibody 
allows applicfication 
useful when antigen is in low abundance
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16
Q

Disadvantage of indirect method

A

slower

can get non specific binding

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17
Q

steps of immunohistochemistry

A

slice tissue and fix slides in formalin 10 minutes
Block slide in serum, stops non-specific binding when you add antibodies later 30min - 1 hr
Wash in saline, removes anything that is not bound to tissue
Incubate with pirmary antibody 30min- 2hr
Wash
Incubate with secondary antibody 30min - 2hr
Enzymatic detection - Reveale antigen

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18
Q

What is pentrance

A

is the probabilty that a person carrying a diseas-assocaited genotype will develop that disease whithin a give time period

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19
Q

pentrance calcualtion

A

no. individuals displaying conditions/ no. with the mutation x 100

20
Q

What is incomplete/reduced penetrance

A

when it has been demostrated that individauls who possess a disease associated genotype show absolutley no manifestion of that condition
- number of individuals who display the condition is less than those who carry

21
Q

What is complete pentrance

A

if a person carrying a disease assocaited genotype always develops the condition
-number of individuals who display clinical features of the condition is equal to those who carry the mutaution

22
Q

What is cost-effcetive analysis

A

cost of health care related to the net outcomes
assigns a value to the outcome
meaured in £ per life year saved
uses QALYs

23
Q

what is cost benefit analysis

A

rescourse cost relative to the possible medical benefit

effectiveness measured in £

24
Q

why does a myocyte action potential have a plateau

A

due to the inflow of Ca2+ through L-type channels

25
Q

describe the myoctye exctiation contraction

A

AP deploarises membrane
Ca2+ flow through voltage gated channels
depolaristation of dihydropyridine receptor causing transformatonal change of L type channel
causes ryanodine receptor to open
CA2+ unbinds from calsequestin and pours into intracellular space
binds to troponin C
cross bridge cycling

26
Q

order of heart muscle

A 
Endothelium 
-lines inside of ventricles, thin 
Myocardium 
-thickest layer 
Pericardium 
-outside layer 
-visercal and partietal pericardium
27
Q

What are GPCRS

A

membrane bound plasma proteins that couple hormone receptors to effector enzymes
7 transmemebrane domains

28
Q

Describe the steps of the adenyly cylase mechanism

A

Hormones binds to receptor on membrane, cause conformational changes of the alpha s subunit
GDP released, GTP binds
Alpha subunit detaches
Alpha s -GTP complex migrates and binds to adenylyl cylase
activated adenylyl cyclase catalyses conversions of ATP to cAMP
cAMP activates protein kinase A
phosphorylates intracellular proteins

29
Q

Describe steps of smooth muscle signalling

A

Hormone binds to receptor on membrane, cause conformational changes of the alpha q subunit
GDP released, GTP binds
Alpha subunit detaches
Alpha q -GTP complex migrates and binds to phopsplipase C
activated phospgolipase C, catalyses the liberation DAG and IP3 from PIP2
IP3 causes the release of Ca2+ from intracellular stores in the ER/SR
Ca2+ and DAG activate Protein Kinase C
CA2+ binds to calmodlin, activating MLC kinase
Kinase phosphorlyates light chain of myosin
ATP –> ADP
contraction

30
Q

What does the Gq-R vasopressin cause

A

vasoconstriction

31
Q

What does the Gs-R adrenaline cause

A

Vasodilation

32
Q

What does the Gi-R adrenalin/noradrenline cause

A

vasoconstriction

33
Q

Function of Gs

A

activates adenylyl cylase, increase cAMP

activates PKA, phophorylates downstream target prtoeins

34
Q

Examples of Gs

A

beta adrenoceptor

35
Q

Function of Gi

A

inhibits adenylate cyclase, decrease cAMP

36
Q

Examples of Gi

A

muscarinic AChR

37
Q

Function of Gq

A

activates phospholipase C, increase IP3, Ca2+, DAG

PKC activation, phosphorylates downstream proteins

38
Q

Examples of Gq

A

muscarinic AChR

39
Q

What is diagnostic sensitivty

A

% of patients with disease correctly test positive for disease

true positive/ true positive + false negative

40
Q

What is diagnostic specificty

A

% of healthy people who have a negative test

true neagtive/ true negative + fasle positive

41
Q

describe the vector preparation satge of recombinant dna technology

A

create an insertion site by restriction digestion
dephosphorylation of the vector may be necessary to prevent self-ligation
alkaline phosphate removes the 5’ phosphate groups, prevents self-ligation

42
Q

describe the insert preparation satge of recombinant dna technology

A

perform restriction digestion to generate compatiable ends from subsequent slicing into the vector
the desired fragement can be purtified by running on agrose

43
Q

describe the ligation preparation satge of recombinant dna technology

A 
joining of vector and insert 
common enzymes (T4DNA ligase) links DNA ends between 5' phosphate ans 3' OH group
44
Q

describe the tranformation preparation satge of recombinant dna technology

A

naturally occruing process in which bacterial cells take up foreign DNA at a low frequency

45
Q

describe the colony screnning satge of recombinant dna technology

A

the transformational reaction contains a mix of cells with no vector, the vector with no insert, the insert alone and succesful vector and insert
bacteria without the vecor will not grow, where as bacteria with will grow due to anitbiotic resistance

46
Q

What is recombinant dna technology

A

joining together of DNA molecules from two different species that are inserted into a host organism to produce new genetic combinations that are of value to science, medicine, agriculture, and industry.

DDT (10 decks)

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