Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRR > cardiovascular 9-10 > Flashcards

cardiovascular 9-10 Flashcards

1
Q

Describe the activity of cardiac progenitor cells during the formation of the cardiogenic field during week 3.

(Hint - c migrate to s in A embryo)

A
  • cardiac progenitor cells of epiblast (positioned laterally to primitive streak) migrate
  • towards splanchnic mesoderm (peripheral to neural plate) in anterior region of embryo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the activity of pharyngeal endoderm cell during the formation of the cardiogenic field during week 3.

(Hint - P (PE cells) → CM cells)

A

underlying pharyngeal endoderm cells induce progenitor cells to form cardiac myoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the activity of angioblasts during the formation of the cardiogenic field during week 3.

(Hint - a-blasts origin → divide → a-cysts
THEN
a-cysts + a-cysts → form ⊃ tube which is CG-f)

A
  • angioblasts (embryonic vascular tissues) form and proliferate in mesoderm forming angiocysts
  • angiocysts unite and form a horseshoe endothelial tube surrounded by myoblasts → cardiogenic field
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the cardiogenic field overlaid by and what does this give rise to?

(Hint - IE cavity and then the p cavity)

A
  • overlaid by intraembryonic cavity

- which gives rise to pericardial cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the development of the primitive heart tube during cephalocaudal embryonic folding.

(Hint - bcph m pulled f → allow h + PC to move towards thorax)

A
  • the buccopharyngeal membrane pulled forward

- allowing developing heart + pericardial cavity to move towards thorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the development of the primitive heart tube caused by lateral folding on day 22 of embryonic development.

(Hint - caud angiog together → form endoc. tube)

A
  • brings caudal angiogenic regions into close proximity

- so they merge to form the endocardial tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does the primitive heart exist during the development of the primitive heart tube?

(Hint - e. tube hanging becoming suspended in PC by A+Vs at c + c ends)

A
  • as an expanding tube which becomes suspended in pericardial cavity
  • by blood vessels at cranial and caudal ends
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Whilst expanding, during the development of the primitive heart tube, what happens to the myocardium and what does this separate?

(Hint - more layers + secretes a jelly + myoc from endot)

A
  • myocardium thickens + secretes cardiac jelly

- separates myocardium from endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the myocardium formed surrounded by and what is this derived from?

(Hint - the outside type of cardium + SV cells)

A
  • epicardium

- sinus venosus cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the cardiac loop?

A
  • looping of the heart tube allows the straight heart tube to form a more complex structure
  • reminiscent of the adult heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens to the heart tube at week 4?

A

starts to bend

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens to the cephalic end and the more caudal section of the heart during the formation of the cardiac loop?

(Hint - one leads to the other:
• cephalic → c + R
• caudal → dc)

A
  • cephalic end bends caudally (near tail) + to the RHS

- more caudal section extends in a dorsocranial direction (towards head at the back)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

By what day is the bending of the cardiac loop complete by?

A

day 28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is a common enlarged atrium formed within a cavity following the formation of a cardiac loop?

(Hint - lower chambers of the heart get bigger so upper outside regions fuse)

A
  • ventricle enlarges

- and atrial region (initially a paired structure positioned outside cavity) fuses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How are the common atrium and ventricle connected and which structure exists here?

(Hint - connected by IV hole)

A
  • by a narrow atrioventricular canal

- primary intraventricular foramen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

By day 30 of embryological heart formation, in which direction does the conus cordia moves from the right hand side?

(HInt - inside as the upper heart valves move outside)

A
  • in the medial direction

- as atrium expands laterally on either side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

For each primitive region, state the fate in terms of formation of the heart:

a) sinus venosus (Hint - main node, main sinus and the correct upper chamber)
b) primitive atrium (Hint - part of both upper chambers and their individual ears)
c) primitive ventricle (Hint - the main ventricle)
d) bulbus cordis (Hint - the minor ventricle)
e) truncus arteriosus (Hint - 2 main trunks of the heart)

A

a) part of right atrium (posterior wall), coronary sinus and SA node
b) Part of R + L atrium (anterior wall), R + L auricle
c) left ventricle
d) right ventricle
e) ascending aorta and pulmonary trunk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

During week 4, what does the sinus venosus receive blood from and what do these structures receive blood from?

(Hint - L + R head structures of the devil, receive blood from vuc veins)

A
  • both right/left sinus horns

- these receive blood from L/R vitelline, umbilical and common cardinal veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

During weeks 5-10, how does the sinus venosus develop?

(Hint - L sinus horn retires and moves country, R sinus horn gets bigger and with SV becomes RA, SA orifice flanked by v. valves → form septum spurium, L v. valve + s spurium + developing atrial septum all fuse, superior R v. valve moves country inferior portion forms 2 valves → IVC + cs valves)

A
  • L sinus horn becomes redundant (week 10) → almost all horn disappears
  • R sinus horn enlarges + with sinus venosus → becomes incorporated into RA
  • sinoatrial orifice flanked on each side by L/R venous valves → fuse to form septum spurium
  • L venous valve + septum spurium fuse with developing atrial septum
  • at the same time, superior region of R venous valve disappears + inferior portion forms two valves → IVC valve + coronary sinus valve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

By days 27-37 by which 2 mechanisms do septal and valve formation occur?

(Hint - active masses growth across chamber cushioning + incomplete chamber partitioning due to small portion which won’t separate)

A
  1. formation of actively growing masses of cells (endocardial cushions) that grow across a chamber
  2. region of the wall failing to grow whilst regions either side continue to grow → prevents complete partitioning of chambers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do mechanisms function in septal and valve formation?

Hint - atrial ÷, AV canal creation, septum creation in TA, v. septum creation

A 
- by 4 divisional processes:
• division of atria 
• formation of atriovetricular canal 
• septum formation in the truncus arteriosus 
• formation of the ventricular septum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens as a part of division of the atria by the end of week 4?

(Hint - septum p created, down towards endoc. cushion in AV canal → op, cells of sup. endoc. → cushion towards op)

A
  • septum primum develops
  • extends down across the lumen towards endocardial cushion in atrioventricular canal, ostium primum
  • cells of superior surface of endocardial cushion extend upwards closing ostium primum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is the complete portioning of atria prevented by the end of week 4 and what does the anterior portion of the septum primum form?

(Hint - by the formation of a secondary structure (OS) and formation of a valve of OF which is constantly mentioned in CRR as a little oval on inside surface)

A
  • by formation of ostium secundum (oval foramen)

- forms the valve of oval foramen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

During the formation of the AV canal by the end of week 4 how are the atria connected to the left ventricle?

(Hint - how are A + V connected later on?)

A

via a single atrioventricular canal

25
Q

What happens to the AV canal in week 5 of its formation and why?

(Hint - more on the left side but needs enough BF on both sides)

A
  • enlarges to right

- so blood can enter both ventricles

26
Q

What do the superior and inferior AV cushions extend into during formation of the AV canal and what does it result in?

(Hint - into the named canal and results, formation of L+R so-named landmarks ‘o’)

A
  • extend into lumen of atrioventricular canal and fuse

- results in separation of atrioventricular canal into L + R atrioventricular orifices

27
Q

During the formation of the AV canal by week 5, what are the atrioventricular orifices bordered by and what do mesenchymal extensions form?

(Hint - bordered by ÷ of mes. tissue, formation of L + R main valves)

A
  • atrioventricular orifices are bordered by proliferation of mesenchymal tissue
  • mesenchymal extensions form L + R atrioventricular valves
28
Q

What does the septum of the truncus arteriosus divide the outflow of heart into?

(Hint - outflow of ?V → blood flow into AA/PA)

A

• 2 parts:

  • outflow of LV - blood flows into the aortic arch
  • outflow of RV - blood flows into the pulmonary artery
29
Q

When does septum formation occur?

Hint - over 30 days in and when t swellings start to grow

A

in week 5 when pairs of truncus swellings start to grow

30
Q

What do extensions of the superior and inferior truncus swellings fuse to form?

(Hint - 2 main vessels combined septum)

A

the aorticopulmonary septum

31
Q

Whilst truncus swelling extends, what also develops, what do they extend towards and what does this lead to the formation of?

(Hint - + swellings along L + R c.c. walls, one another + ACP septum, early moon valves)

A
  • additional swellings develop along L + R conus cordia walls
  • each other + then unite with aorticopulmonary septum
  • formation of primordial of semilunar valves
32
Q

When does the formation of the muscular interventricular septum occur?

(Hint - 40 days to create a habit like muscle-building in the gym)

A

end of week 4

33
Q

What does the muscular interventricular septum extend towards and which channel does this form to be closed by what?

(Hint - inf. endoc. cushion, IV foramen and extension of inf. endoc. cushion)

A
  • inferior endocardial cushion leaving a channel → forms interventricular foramen
  • closed by extension of inferior endocardial cushion
34
Q

Where does the pacemaker initially lies in the conducting system of the heart?

(Hint - L c. tube in c position)

A

in the left cardiac tube in a caudal position

35
Q

Where in the conducting system of the heart is the SA node initially positioned?

(Hint - opening of top, straight heart vessel )

A

near the opening of SVC

36
Q

From which 2 sources in the conducting system of the heart are the AV node and bundle of His initially derived from?

(Hint - ANV from left wall of sv, bundle of His from cells of AV bridge)

A
  • AV node → cells in left wall of sinus venosus

- bundle of His → cells of atrioventricular canal

37
Q

Summarise the development of the heart.

(Hint -
heart derived from meso c. field, heart tube c + l folding (22), bending (28), atrial separation and AV canal and ventricles and truncus and both types of valves formed (day 27-37), horns lost and RA formed and conduction system ready (week 10))

A
  • heart derived from mesodermal cardiogenic field positioned around neural plate
  • heart tube forms by cephlocaudal and lateral folding (day 22)
  • undergoes bending → formation of cardiac loop (day 28)
  • partitioning of atria, AV canal, truncus and ventricles → formation of AV + semilunar valves (days 27-37)
  • sinus venosus lost L sinus horns + incorporated into RA and conducting elements move into final position (week 10)
38
Q

What are most congenital heart defects related to and what do they lead to?

(Hint - abnormalities in cl, most common [atrial shunting] + serious ASDs [lack of AS] , VSD [atrial shunting] - how is blood shunted in each)

A
  • abnormalities in cardiac looping: arises as heart tube loops to L rather than R resulting in dextrocardia
  • atrial septal defects:
    • most common ASD is ostium secundum → shunting blood from LA to RA
    • most serious ASD is lack of atrial septa (common atrium or cortriloculare biventriculare) - defects of AV canal
  • ventricular septal defects: most common, occur in association with abnormal partitioning of aortic and pulmonary outflows → shunt of blood from LV to RV
39
Q

Give a basic review of coronary circulation.

A
  • heart has its own circulation - the coronary arteries
  • coronary arteries squeezed shut during contraction + fill during relaxation
  • coronary arteries:
    • L coronary artery → divides into LAD + circumflex branches
    • R coronary artery
    • coronary veins: great cardinal vein (drains anterior heart) + middle cardiac vein (drains posterior heart)
    → coronary sinus supplied with deoxygenated blood via great cardiac vein and the middle cardiac vein
40
Q

What is myocardial ischemia (referred pain) and what can it lead to?

A
  • partial obstruction of a coronary artery can cause myocardial ischemia
  • causes hypoxia which decreases the ability to produce ATP:
    • modifies actin/myosin muscular contraction
    • inhibits Na/K pump
    • inhibits ATP gated K channels
    • induces angina pectoralis
41
Q

What is angina pectoralis and what can it lead to?

Hint - pain associated with what referred where, sensation in chest, and what occurs a lot in geriatric ward

A
  • severe pain associated with myocardial ischemia referred to neck, chin or down left arm
  • patients feel squeezing sensation in chest
  • can lead to a MI
42
Q

What is myocardial infarction

A
  • caused by death of myocardial cells induced by blockade of blood supply
  • myocardium replaced by CT, forming scar tissue
  • heart muscle can:
    • lose some of its contractile strength
    • scar tissue may affect conductive system by isolation of AVN from atrial muscle and cause death by ventricular fibrillation
43
Q

What is ventricular fibrillation?

A

asynchronous (non-simultaneous) contraction of ventricles

44
Q

What does defibrillation result in?

A
  • depolarises sufficient cells

- to re-synchronise their activity

45
Q

What is coronary artery disease (CAD) caused by?

Hint - A for ‘a’ plaques

A

atherosclerotic plaques in coronary arteries

46
Q

State the five main risk factors of CAD.

Hint - the usual suspects, high c, high b, sootay, BMI, parents

A
  • high cholesterol
  • high BP
  • smoking
  • obesity
  • genetic factors
47
Q

Which apoproteins (Apo) can be found on atherosclerotic plaques?

(Hint - navigation C-2, E, B100)

A
  • Apo C-2
  • Apo E
  • Apo B100
48
Q

What is dyslipidaemia?

Hint - ‘dys’ means disruptions and ‘lipidaemia’ is those molecules being moved around

A

disruptions to lipid transport

49
Q

Describe lipoprotein transport in the blood.

A
  • lipids transported in blood complexed with proteins forming lipoproteins
  • consist of inner core of lipids and a hydrophobic coat consisting of phospholipids, cholesterol and apoproteins
50
Q

Classify each lipoprotein:

a) HDL
b) LDL
c) VLDL
d) chylomicrons

A

a) HDL: C particles (7-20 nm)
b) LDL: C particles (20-30 nm)
c) VLDL: particles (30-50 µm)
d) chylomicrons: (100-1000 nm)

51
Q

How are different lipoproteins transported?

Hint - lots of arrows and by apo-ps in outer lipid layer

A
  • via different pathways

- dictated by apoproteins incorporated into outer phospholipid layer

52
Q

What do apoproteins function as?

A

ligands for receptors enabling directed transport

53
Q

What are the two types of lipoprotein transport?

HInt - inside and outside

A
  • exogenous

- endogenous

54
Q

What occurs in exogenous lipid transport?

(Hint - c + TGs via cylms, m + a TGs via FAs and glycerol, cylms contain c-es pass to liver, bind and are endocytosed, c in liver oxidised to B acids and secreted in bile/endocytosis pathway)

A
  • cholesterol and TGs absorbed from ileum and transported via chylomicrons in lymph to blood
  • muscle + adipose TGs hydrolysed and tissues take up fatty acids and glycerol
  • chylomicrons still contain cholesterol esters- pass to liver, bind to the receptor and are endocytosed
  • cholesterol stored in liver, oxidised to bile acids and either secreted in bile or enter endogenous pathway
55
Q

Describe endogenous lipid transport.

Hint - VLDL, LDL and HDL

A
  • cholesterol transported by VLDL, LDL and HDL pathway
    • VLDL: cholesterol + newly-synthesised triglycerides
    • LDL: formed from VLDL via IDL particles and contain remaining cholesterol esters → cells take up LDL by endocytosis and use cholesterol in membrane and steroid synthesis
    • HDL: some cholesterol returned to plasma in HDL particles and transferred to VLDL or LDL particles by transfer protein (cholesterol ester transfer protein)
56
Q

What are the stages of the formation of an atherosclerotic clot?

(Hint - LDLs → monocytes, monocytes → foam cells + endothelial wall, foam cells → cytokines → TI replication + more monocytes, monocytes + SM + endothelial cells uptake lipoproteins = atherosclerotic plaque, gaps in endothelium + platelets → clot)

A
  • increased LDLs removed by circulating monocytes
  • monocytes form foam cells → attach to endothelial wall
  • foam cells release cytokines inducing replication of tunica intima attracting more monocytes
  • monocytes, SM and endothelial cells uptake lipoproteins resulting in atherosclerotic plaque
  • gaps form in endothelium and platelets attach to exposed collagen → clot
57
Q

How can hypercholesterolemia be treated?

Hint - SBF

A
  • statins → inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HGM-CoA) and mevalonate pathway
  • fibrates → increase hepatic LDL-C uptake
  • bile-acid-binding resins → reduce cholesterol absorption from intestines + stimulate up-regulation of LDL receptors, so increase LDL-C clearance from blood
58
Q

State how the following increase the risk of atherosclerosis:

a) high BP?
b) obesity?
c) smoking?
d) genetic factors?

A

a) extrapressure candamage arteries, so they are more vulnerable to the narrowing and plaque buildup
b) too much fat means the lining of your arteries doesn’t work as well as it should.
c) chemicals intobaccoharm blood cells, heart function and blood vessels
d) protein apolipoprotein E (with several different forms) is coded by a gene found on chromosome 19 - a lack of/faulty allele causes you to develop extremehypercholesterolemiawith a high-fat diet

CRR (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions