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Medicine - Phase 1 > Cardio > Flashcards

Cardio Flashcards

1
Q

what faci

Define Haematocrit (PCV)

A

ratio of volume of red blood cells to total volume (45%)

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2
Q

Define Haemopoiesis

A

formation of new blood cells and platelets

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3
Q

Define Anaemia

A

reduced haemoglobin or numbers of RBCs, often
due to iron deficiency

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4
Q

Define Haemostasis

A

the arrest of bleeding, involving blood coagulation and the contraction of damaged blood vessels.
1. vascular spasm
2. Primary- forms temporary platelet plug
3. Secondary- coagulation cascade forms permanent fibrin clot

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5
Q

Summarise how a platelet plug is formed

A
  1. Vessel damage and vWF secretion by endothelial cells
  2. vWF binds (adheses) platelets to exposed collagen in damaged vessel wall
  3. Platelet Activation: shape change and fibrinogen receptors (GPIIb/IIIa) expressed
  4. Secretions: alpha granules and dense granules
  5. Fibrinogen from liver binds to receptors on platelets = Aggregation
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6
Q
A
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7
Q

draw out the coagulation cascade on a whiteboard.

what is made by the liver?
what are witamin K dependent?

A

Liver makes all except VIII
Vit K dependent: X, IX, VII, II (thrombin)

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8
Q

what secreted von Willebrand factor?
what does it do?

A

endodthelial cells.
vWF bunds to exposed collagen which allows platelets to bind to collagen via (GP1B receptors)

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9
Q

What do alpha granules secrete?

alpha granules secreted by activated, anchored platelets

A

more vWF - platelet adherence and activation
PlateletDerivedGrowthFactor (PDGF) = assists in long term wound healing

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10
Q

what do dense granules secrete?

from activates, anchored platelets

A

Adenosine diphosphate (ADP) - binds to P2y12
Thromboxane (TXA2) - binds to TP

both promote more platelet activation

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11
Q

what enzyme promotes the synthesis of Thromboxane?

A

Cyclooxygenase (COX) and thromboxane synthase

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12
Q

Define Haemophillia

A

inability to make blood clots due to factor VIII
deficiency (Haemophilia A) or factor IX deficiency (Haemophilia B – Christmas disease). (Haemophilia A is more common.)

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13
Q

In adults, where are precursors of mature blood cells derived from?

A

Bone marrow of axial skeleton.
(all bones in children)

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14
Q

In embryos, where are the precursors of mature blood cells derived from?

A

yolk sac, liver, spleen bone marrow.

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15
Q

What is the production of RBCs called?
what is the hormone stimulating factor?
When is this hormone released?

A

Production = Erythropoiesis
Hormone = Erthyropoietin (EPO)
Released: low level continuously and in response to hypoxia

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16
Q

What is the production of WBCs called?
What is the hormone factor?

A

Production = myelopoiesis
Hormone factor=granulocyte-macrophege colony stimulating factor (GMCSF)
only stimulates myeloblastic WBCs not lymphoid cells

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17
Q

What is the production of platelets called?
What is the hormonal factor?
How does it work?

A

Thrombopoiesis
Hormonal factor = Thrombopoietin
works by increasing production of megakaryocytes which platelets bud off from.

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18
Q

what is the lifespan of an erythrocyte?

A

120 days

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19
Q

where are RBCs removed?

A

the reticuloendothelial system (spleen, liver, bonemarrow)
and blood loss

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20
Q

where is haemoglobin found?

A

in Erthythrocytes

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21
Q

describe the structure of haemoglobin

A

Tetrameric protein with 4 globin chains, each with a haem group with central ferrous iron. Capable of reversibly binding to oxygen.
HbA = 2 alpha chains 2 beta chains

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22
Q

Describe the structure of HbF

A

2alpha chains, 2 gamma chains

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23
Q

What levels of haemoglobin would count as anaemic

A

Male < 130g/L
Female <110g/L

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24
Q

Signs and symptoms of anaemia

A

pallor, tachycardia,
hyperventilation on exertion, malaise and angina

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25
Q

5 x causes of Anaemia?

A

*Acute blood loss
*Hypolastic production (not enough)
*Dyshaemotpoeitic prodcution (ineffective)
*Haemolytic anaemia (Increased removal of RBCs)
*Iron, folate or Vitamin B12 deficiencies.

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26
Q

White Cells (leucocytes) are made from Granulocytes, agranulocytes and platelets
Name the granulocytes.
Name the Agranulocytes

A

Granulocytes: Neutrophils, Eosinophils, Basophils,

Agranuloyctes: Lymphocytes, monocytes

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27
Q

What is a neutrophil and how to they work?

A

A type of granulocyte and the most abundant WBC.
multi-lobed nucleus
Phagocytic.
Contain 3 types of granuoles.
INFLAMMATORY response

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28
Q
A
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29
Q

What is a monocyte and how to they work?

A

A type of Agranulocyte.
Immature cells
Phagocytic and can be antigen presenting (pass antigen to lymphoctye)

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30
Q

what can a monocyte differentiate into?

A

Tissue Macrophages (everywhere)
Kupffer cells (liver)
Osteoclasts (bone)
Antigen presenting (everywhere)
Alveolar Macrophages (lung)

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31
Q

what is a basophil and how to they work?

A

a type of granulocyte (0.5% WBC)
Bi-lobed nucleus.
Blue staining histamine containing granules.
Inflammatory and prevent coag.
Immediate hypersensitivity reaction response.
IgE receptors

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32
Q

what is an eosinophil and how to they work?

A

a type of granulocyte (1% of WBC)
bi-lobed nucleus
neutralise histamine
particular role in fighting parasitic infections but also a wide range of regulatory functions

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33
Q

what are the two main groups of leukocytes?

A

Granulocytes (neurophil, monocyte, basophil, eosinophil)
Agranulocytes (Lymphocytes (T and B) and Monocytes)

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34
Q

Where are T lymphocytes matured?

A

Thymus Gland

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35
Q

where are B lymphocytes matured?

A

Bone marrow

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36
Q

what proportion of lymphocytes in blood are B lymphocytes?

A

20%

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37
Q

what are the functions of T Lymphocytes?

What are the 4 different types of T Lymphocytes?

A

involved in cell mediated immunity

T Helper: help B cells and activate macrophages
T Cytotoxic: kill marked target cells
T Supressor: supress TH and hence supress immune response
Natural Killer: mainly kill virus infected cells

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38
Q

what are the functions of B Lymphocytes?

A
  • Generation of antibodies (M, A, G,
    E, D)
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39
Q

what is the lifespan of a platelet (thrombocyte)?
how big is a platelet?
where do they come from?
How are they activated?

A

Size: anucleate, 2-4uM
Lifespan: 7-10 days
Origin: thrombopoesis from megakaryocytes
Activation: shape change from smooth discoid to spiculated with pseudopodia to increase surface area

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40
Q

what is haemostasis

A

keeping blood fluid in vessels and clotting when outside

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41
Q

how does blood remain a fluid inside vessels?

A
  • Platelets and proteins of the coagulation cascade
    circulate in an inactive state
  • endothelial cells, anticoagulant pathway & fibrinolytic pathways ensure fluidity
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42
Q

what is thrombosis?

A

clotting inside the vessel

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43
Q

platelets circulate in an […] form

A

inactive

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44
Q

platelets are:
a) anucleate
b) nucleate

A

a) anucleate

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45
Q

platelets orginate from:
a) monocyte
b) megakaryocytes
c) myoblast

A

b) megakaryocyte

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46
Q

why are platelets polyploidy?

A

Megakaryocytes enter endomitosis where the chromosomes
duplicate but the cells do not divide. Therefore more
chromosomes than normal

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47
Q

what is membrane blebbing?

A

platelets break off from the
megakaryocytes. 1 megakaryocyte can produce up to 4000 platelets.

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48
Q

Plasma is a transportation medium. What percentage of blood does plasma make up for?

A

55%

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49
Q

What proteins are present in plasma?

A
  • Albumin
  • Carrier proteins
  • Coagulation porteins
  • Immunoglobin (from B Lymphocytes)
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50
Q

Serum, is blood plasma without any […]

A

clotting factors

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51
Q

Where are elastic arteries found?

A

Closest to the heart

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52
Q

Label the image

A
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53
Q

The parietal pleura is on the […]
The visceral pleura is on the […]

A

outer
inner

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54
Q

how many lobes does the right lung have?

A

3

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55
Q

how many lobes does the left lung have?

A

2

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56
Q

label the lobes and fissures of the lung

A
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57
Q

what is the lifespan of a platelet?

A

7-10 days

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58
Q

where to platelets spawn from?

A

megakaryocytes

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59
Q

which germ layer does most of the cardiovascular system derive from?

A

mesoderm layer

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60
Q

Which of the heart fields give rise to the future left ventricle, and which give rise to the future right ventricle and artria?

A

first heart field = left
second heart field = right

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61
Q

blood islands form vessels in a process called […]

A

vasculogenesis

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62
Q

the development of the heart begins with the formation of the […]

A

primitive heart tube

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63
Q

The primitive heart tube is formed by a process called […] where two […] form a single heart tube

A

lateral folding
endocardial tubes

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64
Q

The bulbis cordis forms…?

A

right ventricle and outflow tracts

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65
Q

the primitive ventricle forms…?

A

the left ventricle

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66
Q

the primitive atrium forms…

A

anterior parts of left and right atrium

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67
Q

The sinus venosus forms…

A

the superior vena cava and right atrium

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68
Q

the truncus arteriosus forms…

A

aortic arches and arteries (aorta and pulmonary artery)

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69
Q

what happens if there is too much NKx2.5 transcription factor?

A

heart too large

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70
Q

what happens if you block Gata 4 transcription factor?

A

the fusion of two heart tubes into one doesnt happen

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71
Q

what happens if you block Fog1 transcription factor?

A

heart doesn’t loop

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72
Q

during cardiac embryonic development, how do cells know which way is left?

A

nodal secretions are circulated left by ciliary movement

this is recognised by transcription factors ie “lefty”

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73
Q

During Cardiac looping, the bulbis cordis moves:

A

inferiorly, anteriorly and to the embryo’s right

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74
Q

druing cardiac looping, the primitive ventricle moves:

A

to the embryo’s left

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75
Q

during cardiac looping, the primitive atrium and sinus venosus move

A

superiorly and posteriorly

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76
Q

what is formed during cardia septation?

A

endocardial cushion.

Grow on the sides of the atrioventricular canal to partition it into two separate openings (left and right)

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77
Q

what are the three types of capilaries?

A

continuous (most common)
fenestrated (kidney, SI, endocrine glands)
discontinuous (liver)

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78
Q

what is the purpose of vascular shunts in fetal circulation?

A

to bypass the pulmonary circulation
not needed inutero.

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79
Q

which heart shunt lies between the atria?

What does this become?

A

Foramen Ovale

becomes fossa ovalis

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80
Q

which heart shunt is between the pulmonary artery and aorta?
what does this become, and what can happen if ut doesnt become this>

A

Ductus Arteriosus
becomes : ligamentum arteriosum. If no then pulmonary hypertension which strains Right side of heart

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81
Q
  • First breaths of life -> lungs expand → the alveoli in the lungs are cleared of [a].
  • An increase in the baby’s [b] and a significant reduction in the [c] reduces the need for the [d] to shunt blood → closure of the shunt.
  • These changes increase the pressure in the [e] of the heart → decrease the pressure in the [f] -> [g] closes → newborn circulation.
A

[a] fluid
[b] BP
[c] pulmonary pressures
[d] ductus arteriosus
[e] left atrium
[f] right atrium
[g] foramen ovale

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82
Q

Embryology of Circulation:
Day 17 : formation of [a]
Day 17-21: vascularisation of [b]
Day 18: [c] commences in the [d]
Day 18+ : vasculogeneisis is added to by [e]

A

[a] blood vessels
[b] yolk sac, chorionic villus and stalk
[c] vasculogenesis
[d] lateral mesoderm
[e] angiogenesis

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83
Q

How does vasculogenesis work?

A

angioblasts combine to from angioblastic cords throughout the embryonic disc

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84
Q

1st Aortic arch =

A

part of maxillary

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85
Q

2nd aortic arch =

A

artery to stapedius

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86
Q

3rd aortic arch =

A

> common carotid arteries
proximal internal carotid arteries

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87
Q

4th aortic arch =

A

> Aortic arch
Right subclavian artery

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88
Q

6th aortic arch =

A

pulmonary trunk
ductus ateriosus

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89
Q

what drives embryonic vessel development? (3)

A

angiogenic growth factors (angiopoietin i & ii)
repulsive signals (plexin)
attractive signals (VEGF)

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90
Q

what does this xray show?

A

aortic coarctation

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91
Q

There are millions of erythrocyte antigens, what are the 4 most important

A

ABO and Rhesus

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92
Q

what blood group is universal acceptor?
Why?

A

AB
Has no antibodies

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93
Q

what blood group is universal donor?

A

O
Has no antigens

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94
Q

what are ABO antigens made from?

A

carbohydrates

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95
Q

What is meant by ABO being potently antigenic?

A

they occur naturally, i.e. you will have antibodies against other ABO without ever having been exposed to it.

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96
Q

when do humans start producing their own ABO antibodies?

A

after first 3 months of life. before this they are from mother.
amount decreases with age.

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97
Q

where is immunoglobin (IgM) produced?

A

spleen

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98
Q

which antibodies can cross the placenta?

A

Rhesus antibody (IgG)

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99
Q

How does Haemolytic Disease of the fetus occur?

A
  1. Rhesus positive father and rhesus negative mother = RhesusD positive baby
  2. Bleeding during birth = RhesusD positive baby blood passed to mother. Mother produces RhesusD antibodies.
  3. Later pregnancy = mother’s RhesusD antibodies attack blood cells of rhesus positive baby causing disease. (IgG anti-D can cross placenta)
    must test and treat with anti RhD
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100
Q

What blood type is this?

A

A+

A antigens have floated to the top = A type
B antibodies have floated to the top = A Type
D is floating

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101
Q

What test can be used for blood grouping for ABO and Rhesus D?

A

Indriect Antiglobulin Test:

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102
Q

What will permanently prevent you from giving blood?

A

Syphilis
HIV
Recieved blood products or organ transpants since 1980
notified risk of vCJD

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103
Q

Why is blood plasma only kept from male donors?

A

female plasma tends to be more antigenic.

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104
Q

Name some indications for transfusion of Red Cells

A

hypovolaemia due to blood loss
severe anaemia (not just ioron or b12 deficiency)

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105
Q

Why do Haemolytic reactions happen?

A

ABO incompatibility

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106
Q

what occurs during a haemolytic reaction?

A

Rapid intravascular haemolysis
cytokine release (inflammatory)
Acute renal failure and shock

rapidly/delay in fatality

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107
Q

what should you do during haemolytic reaction

A

stop transfusion immediately
fluid resuscitate

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108
Q

Name 4 hazards associated with blood transfusion

A
  1. Haemolytic reactions
  2. Bacterial contamination
  3. Transfusion-related lung injury (TRALI)
  4. Transfusion-associated circulatory overload (TACO
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109
Q

where to bacterial infections most commonly occur from? in blood transfusion?

A

platelets (kept at room temp)

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110
Q

What is TRALI and how does it occur?

A

Transfusion-related lung injury
Antibodies in donor blood react with recipients pulmonary epithelium = inflammation = plasma leaks into alveoli

SOB
cough frothy sputum
hypotension
fevers

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111
Q

What does TACO stand for and how does it occur?

A

Transfusion-Associated Circulatory Overload

too much blood transfused

acute pulmonary oedema

resp. dist, high bp

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112
Q

When would platelet transfusion be used

A

in thorombocytopaenia (low platelet count)
ABO anitbodies still present

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113
Q

give an example of an alternative to transfusion that would stimulate RBC production

A

Erthyropoietin

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114
Q

When would cryopreipitate be used in transfusion

A

in DIC and massive transfusion if there is a lack of fibrogen

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115
Q

when would fresh frozen plasma be used in transfusion?

A

multiple clotting factor deficiencies.
can be fractionated to produce
concentrates of specific components such as factor 8 or 9

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116
Q

When would albumin be transfused?

A

can be used in cases of oedema to correct the oncotic pressure of blood and keep fluid in. Used in liver disease or nephrotic syndrome

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117
Q

when would immunoglobin be transfused?

A

used in immunodeficiency, congenital or acquired and some auto- immune diseases

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118
Q

how do you calculate the rate (bpm) of this ECG at 24mm/s

A

(cycles in 10 seconds) x 6
12 x 6 = 72

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119
Q

Label the parts of the electrical conduction pathway

A

Where would this section of the Electrical Conduction pathway show up on an ECG?

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120
Q

Where would this section of the Electrical Conduction pathway show up on an ECG?

A

Sinoatrial node –> Left Atrium = p wave.

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121
Q

Where would this section of the Electrical Conduction pathway show up on an ECG?

A

Through the atrioventricular node (slower to wait for contraction of atrium) = after p wave

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122
Q

Where would this section of the Electrical Conduction pathway show up on an ECG?

A

Through the left and right bundle branches of ventricles = q wave

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123
Q

What is the QRS complex of an ECG wave indicating?

A

Ventricular depolarisation

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124
Q

what is the p wave of an ECG indicating?

A

atrial depolarisiation

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125
Q

what does the t wave of an ECG indicating?

A

ventricular repolarisation

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126
Q

what is depolarisation?
what is repolarisation?

A

depolarisation: influx of ions, contraction

repolarisation: efflux of ions, relaxation

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127
Q

What does this ECG show?

A

Atrial fibrillation
-random atrial activity
-irregulalry irregular rhythm

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128
Q

what does this ECG show?

A

atrial flutter
-organised atrial activity
-“razor claw”
-usually regular

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129
Q

what is the normal PR interval value on ECG?

A

120-200 millisquares
(3-5 small squares)

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130
Q

what is the normal p wave interval?

A

80ms

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131
Q

what would a PR interval of 220ms indicate?

A

Delayed AV conduction = a first degree heart block

normal PR = 120-200ms

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132
Q

What is the normal width of a QRS complex?

A

less than 120ms (3 small squares)

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133
Q

what is the normal value of a QT interval?

A

<440ms in Men
<460 ms in Women

134
Q

normal T wave?

A

160ms

135
Q

which is bipolar lead I, II, and III?

A
136
Q

what is the difference between bipolar and unipolar leads?

A

Bipolar (I II III) = triangle, can be +/ – in comparison with each other

Unipolar (aVR aVL aVF) = bisect the triangle. all positive,

137
Q

look at tleads I and II in this ECG…whats up

A

its normal…both QRS waves are positive

138
Q

This is wrong leads to look at babe…what does this ECG of leads I and II show?

A

I and II QRS waves are [L]eaving eachother = [L]eft axis deviation

139
Q

what does this ECG of Leads I and II show?

A

I and II QRS waves are [R]eaching towards eachother = [R]ight axis deviation

140
Q

which chest leads are anterior, lateral and septal?

A
141
Q

Which leads can you look at on an EVG to determine a normal axis?

A

Leads I and II/aVf
Reaching/leaving

142
Q

what are the anterior chest leads?

A

v1,2,3,4

143
Q

What are the lateral chest leads??

A

aVL, I, v6 v5

144
Q

label the parts of this ecg

A
145
Q

what does this ECG show and what might it indicate?

A

ST elevation = Blocked major artery (usually coronary)

there’s a total blockage of one of the heart’s main supply arteries. When that is happening during a heart attack, it can be a sign that the muscle of the ventricles is dying.

146
Q

What is happening at Phase 4 - the resting potential??

A

Na is forced out by Na/K ATPase (requires energy)
This generates a conc gradient = voltage.

The setup is now complete, everything from here on relies on passive movement of ions down their gradients.

147
Q

What is happening at phase 0?

A

Depolarisation:
Voltage gated Na Channel = Large number of Na+ ions enter the cell, causing the charge to increase

148
Q

What is happening in phase 1?

A

Initial repolarisation:
Transient outward Channel = K+ ions leaving the cell causing a small repolarization

149
Q

What is happening at phase 2?

A

Plateau:
Slow Calcium Channel = Calcium enters the cell and maintains depolarised state
(SOME K+ leaves too)

150
Q

what is happening at phase 3?

A

Repolarisation:
Ca2+ channels close
K+ leave cell
This efflux of K+ contributes to a rapid decrease of membrane potential from +10 mV to -60mV.
repolarisation

151
Q

what is happening in phase 4?

A

Resting Phase
* K+ channels open
* Maintained by Na+ and K+ATPase pumps
* 3NA+ inos out for every 2K+ ions in

152
Q

What does this graph show?

A

Cardiac action potential

153
Q

How does active potential propogation work?

A

Exits SAN and spreads to other cells through gap junctions called connexins which activates other myocytes (Na+ ions depolarise adjacent cells)

AV node and purkinje fibres have a similar action potential but generated at slower rate

154
Q

Contraction of the heart muscle requires (appropriately-timed) delivery of [a] ions to the cytoplasm. This is called [b]

A

[a] Ca2+
[b] Excitation-contraction coupling

155
Q

Step 1 of Excitation-Contraction Coupling

A

Calcium influx through surface ion channels

156
Q

Step 2 of Excitation-Contraction coupling:

A

Amplification of [Ca2+] - Calcium induced calcium release
The calcium entering the the cell through the surface channels is insufficient on its own to cause an action potential.

so calcium in the cell in the cell has two sources: ECF and SR

157
Q

w

A
157
Q

what facilitates calcium induced calcium release from the sarcoplasmic reticulum?

A

Ryanodine receptors.

This calcium-triggered calcium release is in contrast to skeletal muscle, where the action potential triggers calcium release directly.

158
Q

how does the influx of clacium cause contraction?

A

Calcium binds with troponinC on the actin filament, which frees up the binding site, allowing myosin to bind to actin.

Myosin Head rowing (using atp) pulls slides the thin filments closer together. Shortens sarcomere = contraction

159
Q

how is calcium removed from the sarcoplasm?

A

Calcium pumped OUT of sarcoplasm
INTO sarcoplasmic reticulum by:
1. SERCA 2

INTO ECF by:
2. Na/Ca/ATP pump (Na then removed)

muscle relaxation

160
Q

what is excitation-contraction coupling?

A

Cardiac myocytes have t tubules and entry of Ca++ leads to filaments contracting with actin-myosin coupled movement.

161
Q

what are the three specialist conduction tissues involved in excitation-contraction coupling?

A

SAN
AVN
His-Purkinje

162
Q

what is the role of the SAN in excitation-contraction coupling?

A

determines HR
Resting membrane potential is -60mV. Hyperpolarisation results in HCN opening and Ca++ entering which leads to depolarisation of cell.

NB HCN = for the SAN not the myocyte

163
Q

what is the role of the AVN in excitatino-contraction coupling?

A

slows down the exit of electrical impulses from atria to ventricle by 100-200ms - allows time for atria to contract and ventricles to fill

164
Q

what is the role of the His-Purkinkje system in exitation-electrical coupling?

A

rapid electrical conduction to the ventricles
-lots of gap junctions = rapid spread of conduction

165
Q

What is sympathetic stimulation of the heart controlled by?

A

Adrenaline and noradrenaline + type 1 beta adrenoreceptors
Increases adenylyl cyclase increases cAMP

166
Q

what does an increase in sympathetic stimulation lead to?

A

Increases heart rate (up to 180-250 bpm)
Increases force of contraction
Large increase in cardiac output (by up to 200%)

167
Q

what is parasympathetic stimulation controlled by?

A

Acetylcholine
M2 receptors – inhibit adenyl cyclase  reduced cAMP

168
Q

what would an increased parasympathetic stimulation lead to?

A

Decreased heart rate (temporary pause or as low as 30-40 bpm)
Decreased force of contraction
Decreased cardiac output (by up to 50%)

169
Q

What is the AV node’s role in excitation-contraction coupling?

A

Transmits cardiac impulse between atria and ventricles
Delays impulse
Allows atria to empty blood into ventricles
Fewer gap junctions
AV fibres are smaller than atrial fibres
Limits dangerous tachycardias

170
Q

where is the fastest conduction velocity in the heart?
where is the slowest?

A

fastest = purkinje fibres 4m/s
slowest = AV node 0.3-0.5m/s

Speed is dependent on;
* Ion movement in/out
* Interconnectedness – number of gap junctions

171
Q

what is the role of the his-purkinje system in excitation-contraction coupling?

A

rapid electrical conductions into ventricles.
=To allow coordinated ventricular contraction
Very large fibres
High permeability at gap junctions

172
Q

what is the refractory period?

A

Time in which myocardial cells cannot depolarise again

-Normal refractory period of ventricle approx 0.25s
(Less for atria than for ventricles)
-Prevents excessively frequent contraction
-Allows adequate time for heart to fill

173
Q

how does cell automaticity work?

A

Slow Na+ influx via ‘funny’ current
Automaticity varies throughout the heart but all tissues capable of automaticity

174
Q
A
175
Q

all patients take medicine

A

note which intercostal spaces 2, 2, 4, 5

176
Q

What are the 4 layers of the heart, from outermost to innermost

A

Pericardium, Epicardium, Myocardium, Endocardium

177
Q

Describe the two layers of the pericardium (sac)

bonus: what cells make up the fibrous sac?

A

Fibrous = Tough outer layer of connective tissue which anchors the heart to the mediastinum.
Serous = Simple squamous epithelial:
*Parietial = inner surface, secretes fluid
* Visceral = outer surface of the heart

fibrous sace = layer of squamous mesothelial cells resting on a thin layer of connective tissue

178
Q

Describe the epicardium

A

Layer of fatty connective tissue that covers the surface of the heart, and great vessels.

179
Q

Describe the myocardium

A

Muscular middle layer of the hearts, containing specialised cardiac muscle cells (myocytes)

180
Q

Describe specialised Cardiac myocytes

A

striated, branching, single central nuclei with intercalating discs

181
Q

what are the intercalated discs in myocytes?

A

specialised connections between myocytes that connect actin filaments.

182
Q

what junctions are present in intercalated discs of myocytes?
what are their functions?

A

gap junctions = allow cell to be electrically coupled (ion flow)
adhering junctions = bind cell together (bind cytoskeletons)
desmosomes = bind cell together (bind cytoskeletons)

183
Q

What is A pointing to?
What do they contain a small number of?

A

Endomysium
This is loos fibrous connective tissue that contain a small number of lymphocytes

184
Q

where are the largest myocytes found?

A

left ventricle

185
Q

What is N? What does it secrete?

A

neuroendocrine granule.
secretes atrial natriuretic peptide

186
Q

when is atrial natriuretic peptide secreted?

A

when cells in the heart are excessively stretched.

(decreased in r

(due to increase in H2O, Na and K secretion from kidney)

Atrial natriuretic peptide (ANP) is a cardiac hormone that regulates salt-water balance and blood pressure by promoting renal sodium and water excretion and stimulating vasodilation in glomerulus

187
Q

what is this? where are they found? what is this stained with?

A

Purkinje fibres
Found in ventricles
stained with PAS

188
Q

What is the innermost layer of the heart?
What is it made from?

A

Endocardium.
Thin layer of fibrous connective tissue + single flat layer of endothelial cells.

189
Q

What are the valves of the heart lined with?

A

endocardium

190
Q

What are the three layers of the valves?

A

Fibrosa, Spongiosa, Ventricularis

doesnt stain with h&e

191
Q

The Left Cx artery supplies…

A

Left Atrium and Left Ventricle

Posterior of heart (BACK)

192
Q

The Left Anterior Descending Artery supplies…

A

Right Ventricle, Left Ventricle, Interventricular Septum

Anterior heart

193
Q

RaceCarsrandomlyAggitateReallyViolentRodentsMakingRatatouillVioletApples

The Right Coronary Artery supplies…

A

the right atrium and right ventricle

194
Q

The left marginal Artery supplies…

A

The left ventricle

195
Q

the right marginal artery supplies…

A

the right ventricle and apex

196
Q

lol good luck

A
197
Q

OVERVIEW OF PLATELET PLUG FORMATION
1. Damage to blood vessel leads to exposure of [a]
2. [b] of platelets to collagen directly through [c] leads to exposure of [d]
3. [e] binds to collagen through [f] and increases platelet adhesion
4. Platelet contains 2 types on granules: [g]
5. Electron dense granules release [h x3] . ADP acts on [i x 2] which lead to further activation and ATP binds to [j]
6. [k] binds to PAR1 and PAR4 – resulting in platelet
activation
7. During activation, platelets [l] which increase surface area
8. Activation of platelets leads to increase expression of [m]
and [n] secreted from alpha granules bind to it which results in new platelets to adhere to old ones – This is [o]
9. Platelets produce [p] which play a part in vasoconstriction – reduced blood flow which aids in forming the primary haemostatic plug
[q x 2] stimulate vasoconstriction

A

[a] Collagen
[b] Adhesion
[c] GPIa
[d] GPIIb/IIIa
[e] Von Willebrand Factor
[f] GP IIb/IIIa
[g] electron dense & alpha
[h] ADP/ATP, serotonin and Calcium
[i] P2Y1 & P2Y12
[j] P2X1
[k] Thrombin
[l] change shape
[m] IIb/IIIa
[n] fibrogen
[o] platelet aggregation
[p] thromboxane A2
[q] thromboxane & serotonin

198
Q

where is Von Willebrand factor produced?

A

endothelium cells

199
Q

Platelet activation is caused by various factors:
* Binding of platelets to collagen fibre triggers the release of the contents of their secretory vesicles via [a]
* Platelets binding to collagen leads to release of [b]
* Thrombin binds to [c] which leads to release of [d] from dense granules and [e]
* [f] binds to TPα

A

[a] exocytosis
[b] Thromboxane A2
[c] PAR1
[d] ADP
[e] PAR4
[f] free thromboxane A2

200
Q

x4

What do alpha granules in platelets secrete?

A

PDGF, fibrinogen, heparin antagonist PF4 and vWF

201
Q

what enzyme enables the production of Thromboxane A2?

A

COX1 (Cyclooxygenase 1)

= key in platelet aggregation and stiumlates

Thromboxane A2 binds to TPα

202
Q

What is arachidonic acid converted to in the presence of COX1 alone?

A

Prostaglandin H2, which is then converted into Thromboxane A2

203
Q

In endothelial cells, the presence of COX! and COX2 convert arachidonic acid into…

A

prostaglandin H2 and Prostacyclin

this inhibits platelet aggregation and vasoconstriction.

204
Q

Low dose Aspirin inhibits [a] therefore….?

A

[a] Cox1
so less thromboxane A2 so less aggregation/activation

205
Q

high dose aspirin inhibits [a] which means….

A

[a] COX1 and COX2 in the endothelial cells
Which means there is inhibition of both processes…non-selectively mediating both pathways (increased aggregation and reduced aggregation}.

dangerous in patients with cardiovascular problems.

206
Q

What is the coagulation cascade?
What is its ultimate “goal”

A

process of blood clotting
goal = to convery soluble fibrinogen into fibrin

not to be confused with platelet plug formation which allows the bleedin

207
Q

What is the extrinsic pathway of the coagulation cascade?

A
  • damage to the endothelial cells => releases tissue factor VII (TFVII –> TFVIIa)
  • TFVIIa —> activates X = common cascade initiated
208
Q

What is the Intrinsic pathway of the coagulation cascade?

A

Blood contacts endothelial collagen outside the lumen –> activates XII –> XI –> IX +VIII + phospholipids + Ca2+ —> X

209
Q

What happens in the common pathway of the coagulation cascade?

A

Xa converts prothrombin (II) –> thrombin (IIa)
Thrombing converts Fibrogen (I) —> Fibrin (Ia) and activates XIII
Fibrin + XIIIa = crosslinking of fibrin = CLOT

XI

Thrombin also gives positive feedback on factors V, VII, VIII and

210
Q

How is Plasminogen converted to Plasmin?

A

via Intrinsic Activation Factor 7a
+
Extrinsic tissue Plasminogen Activator

Factor 7a is part of the

Plasmin then leads to the degradation of fibrin

211
Q

How is Fibring degraded in the fibrinolytic system?

A

Plasmin

212
Q

What Three things happen in a vessel injury?

A
  1. Vasoconstriction
  2. Platelet Plug Formation
  3. Blood Coagulation Cascade
213
Q

where is the sinoatrial node?

A

crista terminalis of right atrium

214
Q

At what voltage is the HCN channel opened?

Hyperpolarisiation Gated Nucleoside channels

A

-60mV

215
Q

What do HCN channels allow the passage of?

A

Na+ ions.
When open, Na+ move into cell = depolarisation from 60mV –> -40mV

216
Q

What is the primary pacemaker of the heart?
What can takeover if this is damaged?

A

Sinoatrial Node - spontaneously generates action potentials, modified by symp/para nerve fibres
Atrioventricular Node, Bundle of His and Purkinje Fibres can take over.

217
Q

what is the sinoatrial node’s rate of depolarisation

A

60-100 per minute

218
Q

what does catecholamine do?

A

has a positive chronotropic effect = faster repolarisation = reaches threshold faster = HR increase

219
Q

what does acetylchlorine do?

A

slows down the opening of HCN

(hyperpolarisation gated cyclic nucleoside channels)

220
Q

how does the activtion of myocadial cells differ from the activation of skeletal cells?

A

Myocardial = activated by adjacent cell (gap junctions, flow of ions)
Skeletal = activated by nervous system

myocyte contraction = 15x slower than skeletal (plateau phase of calcium channels)

221
Q

Explain the steps of the cardiac cycle

pressure, blood flow and valves (not polarisation and waves here)

A

1. Atrial Systole Begins
* After passive ventricluar filling (= 85% of blood in ventricle)
* Atrial contracts and completes ventricular filling

2. Isovolumetric Ventricular Contraction (V Systole 1)
* Ventricular systole = contraction. Pushes AV valve close. (Semilunar still closed so…)

3. Rapid Ventricular Ejection (V systole 2)
* Ventricular pressure > arterial pressure = semilunar valves open and blood ejected

4. Ventricular Diastole - Reduced Ventricular Ejection
* Pressure in ventricles drop, blood flows back against semi luncar valves which closes them.
* Blood flows into relaxed atria

5. Ventricular Diastole - Isovolumetric Ventricular Relaxation
* All chamers relaxed, ventricles fill passively

222
Q

What is the first heart sound?

A

Mitral valve closing

223
Q

what is the second heart sound?

A

aortic valve closing

224
Q

what is preload?
what factors might increase it?

A

load before ventricular contraction

increased by: hypervolemia
regurgitation of cardiac valves
heart failure

225
Q

what is afterload?
What factors increase it?

A

Resistance the Left Ventricle must overcome to circulate blood.

increased in : hypertension, vasoconstriction

226
Q

what occurs with a leaky mitral valvel

A

Blood leaks back into the atrium from the ventricle, decreasing preload. On the next beat the ventricle has normal fillin plus what went back to atrium. Ventricle needs greater pressure, must work harder = hypertrophy

227
Q

what is starling’s law?

A

the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles,

positive ionotropic effect

228
Q

what happens during left ventricular contraction?

systole

A
  • wave of depolarisation
  • L Calcium tube opens
  • Ca2+ arrives at the contractile proteins
  • LV pressure > LA pressure
  • Mitral valve closes (1st heart sound)
  • Isovolumic contraction = LV pressure>Aortic pressure
  • Aortic Valve opens…Rapid ejection

R peak on ECG

229
Q

What happens during ventricular relaxation?

Diastole

A
  • LV pressure peaks and then decreases due to ejection
  • Cytosolic Ca++ is taken up into the Sarcoplasmic reticulum
  • Reduced ejection phase
  • LV pressure < Aortic pressure : aortic valve closes (second Heart Sound A2)
  • Isovolumic relaxation and Mitral valve opens
230
Q

What happens during ventricular filling?

A
  • LVp<LAp : Mitral valve opens : passive filling
  • Ventrical suction also contributes to early filling (85%)
  • Diastasis LVp=LAp : filling temporarly stops
  • SAN depolarisation = Atrial depolarisation = contraction = remaining blood fills ventricle
231
Q

what is shortened when heart beats faster? diastole or systole?

A

diastole - relaxation time shorter

systole/contraction time always the same

232
Q

When is Systole physiologically vs cardiologically?

A

Physiologically: Isovlumic contraction and Maximal ejection
Cardiologically: M1 - A2 and a part of isovolumic contraction

233
Q

When is Diastole physiologically and cardiologically?

A

Physiologically: Reduced contraction, Isovolumic Relaxation and Filling
Cardiologically: A2 - M1

234
Q

What is the force-length interaction?

A

The force produced by the skeletal muscle declines when the sarcomere is less than the optimal length.

If cardiac sarcomere is at 80% of the optimal length, only 20% of maxima

235
Q

what is contractility?

A

the ability of the heart muscle to contract and thereby pump blood

236
Q

what is elasticity?

A

ability to recover normal shape after systolic stress

237
Q

what is compliance?

A

how easily a chamber of the heart or the lumen of a blood vessel expands when it is filled with a volume of blood.

238
Q

what is diastolic distensibility?

A

the pressure required to fill the ventricles to the same diastolic volume

239
Q

what are pressure volume loops?

A

reflects contractility in the ESV and compliance in the EDV.

240
Q

What are the main components of the myocardium?

A

Contractile tissue
Connective tissue
Fibrous frame
Specialised conduction system

242
Q

Why is a heart valve infection difficult to treat?

A

because there is no blood supply to valves - antibiotics can’t reach

243
Q

The pumping action of the heart depends on…

A

interactions between the contractile proteins in its muscular walls

244
Q

interactions between contractile proteins transform [a] into [b] which pumps blood.

A

[a] chemical energy derived from ATP
[b] mechanical work

245
Q

how are contractile proteins activated?

A

by a signally processs called excitation-contraction coupling.

an electrical impulse that induces a chemical change that induces a mech

246
Q

excitation-contraction coupling begins with [a] and ends with [b]

A

[a] depolarisation
[b] Ca2+ binding to the contractile apparatus

action potential depolarises the cell.
Ca2+ in cytosol binds to Ca2+ receptor of the contractile apparatus

247
Q

Contraction = Movement of Ca2+ [a] the cytosol is a [b] process (mediated by Ca2+ channels)

Relaxation = Movement of Ca2+ [c] the cytosol which is a [d] process
(mediated by ion exchangers and pumps)

A

[a] into
[b] downhill
[c] out of
[d] uphill (requires much energy!)

248
Q

Name the 4 main components of the myocardium

A
  1. Contractile tissue
  2. Connective tissue
  3. Fibrous frame
  4. Specialised conduction system
249
Q

what does the plasma membrane of the myocardial cell do?

A
  • regulates the excitation-contraction coupling and relaxation
  • Seperates the cytosol from the sarcoplasmic reticulum
250
Q

what is a sarcomere?

A

the contractile unit of a myocyte

251
Q

Contractile proteins are arranged in a regular array of…

A

thick and thin filaments

252
Q

What are the thick filaments of the sarcomere?
What bands are comprised of them?

A

Myosin
A-band

253
Q

What are the thin filaments of the Sarcomere?
What bands are compromised of them?

A

Actin, Troponin, Tropomyosin
I-band

254
Q

Sarcomeres are defined by a [a] on either side that bisect each [b]

A

[a] Z line
[b] I-band

255
Q

Contraction is the [a] action of [b] over [c]
which is fuelled by [d] by [e] found in [f]

A

[a] rowing/sliding/walking action
[b] myosin
[c] actin
[d] ATP hydrolysis
[e] ATPase
[f] myosin head

256
Q

How does the presence of calcium effect Myosin’s ability to bind to Actin?

A

TroponinC prevents blocks the myosin binding site of the actin, so they are not able to bind. When calcium is present, the troponinC moves away to bind to the calcium, opening up the binding site and allowing it to bind to the myosin again.

257
Q

what is the sarcolemma?

A

plasma membrane of the muscle

258
Q

what are the transveres tubules?

A

extensions of cell membrane that penetrates into the centre of muscle cells (skeletal and cardiac)

259
Q

What does the sarcoplasmic reticulum do?

A

Hydrolyse ATP in ADP+P
lets Ca2+ into organelle and releases it when activated

260
Q
  • Action potential arrives along the [a] and passes down the [b] and [c] the membrane.
  • Leads to release of [d] from [e] into the cytosol
  • Ca++ binds to TnC which [f]
  • This allows for the globular head of the myosin to interact with the groove of the thin-actin filament = [g]
  • [h] is required for the contraction and ATP hydrolysis (ATPase on myosin) breaks apart the the Ca++-TnC bond and the groove of the actin is partially blocked by the tropomyosin and TnI subunits.
  • The [i] action by the myosin leads to the sliding action of actin along myosin, thus shortening of the sarcomere and causes contraction.
A

[a] Sarcolmma
[b] t tubule
[c] depolarises
[d] Ca2+
[e] sarcoplasmic reticulum
[f] pulls the TnI and tropomyosin away and opens up the binding site
[g] Crossbridge formation
[h] ATP
[i] power stroke

261
Q
A
262
Q

Explain why after a certain length of sarcomere, tension/force drops

A

At the shortest length, the opposing actin/myosin relationships are distroted so minimal force is able to be generated.

There is optimal length for maximal myosin/actin interactions at 2.2um: increases Ca2+ sensitivity of troponin C, INcreases Ca2+ release from SR

With further lenghtening, the ends of actin filaments start moving beyond myosin heads to no interaction and no force generated.

263
Q

What is the name of this curve?
Explain the initial increase and the decrease.

A

Frank Starling Curve
Increase EDV = Increase Contraction = Increase SV
- this is because when a muscle is stretched, the distance between the myosin and actin filaments decreases so the cross bridge interactions increases so the muscle can generate more force.

+ED venous return = +EDV = +Muscle stretch = -Distance between actin and myosin = +cross-bridge interactions = +ED force = +Stroke Volume

Beyond this point is LV dysfuntion

264
Q

what is afterload and when does it occur?

A

the pressure that the heart must generate in order to eject blood out of the heart.
SYSTOLE

265
Q

what is preload and when does it occur?

A

the ventricular stretch at the end of the diastole.
depends on the amound of ventricular filling

266
Q

How do you calculate CO?

A

CO = HR x SV

267
Q

How do you calculate BP?

A

BP = CO x TPR

268
Q

what is TPR?

A

Total peripheral vascular resistance = the resistance to blood flow in the systemic vessels, specifically the arterioles, in the body
Increased TPR = reduced blood flow to tissues
Reduced TPR = increased blood flow to tissues

269
Q

How do you calculate PP?

pulse pressure

A

PP = Systolic - Diastolic

270
Q

How do you calculate MAP?

Mean arterial pressure?

A

MAP = Diastolic + (PP/3)

271
Q

How do you calculate SV?

A

SV = EDV - ESV

272
Q

what are the main controllers of blood pressure?

A

the arterioles.

Principle site if resistance to vascular flow.
Contract/relax in repsonse to: local, hormonal, neural fatcors

273
Q

What is Total Peripheral Resistance essentially?

A

Total Arteriolar Resistance…

Vascular smooth muscle, contractr and relaxes to adjust radius which has huge effect on the flow.

274
Q

Arteries provide [high/low] resistance due to the [x] properties.
Their media comprises layers of [x] which cushion systole.

A

Low resistance
elastic
smooth muscle and elastin

275
Q

Capillaries cover a large area and provide a [slow/fast] flow to allow time for nutrient and waste exchange.
[x] or [y] flow determine the distribution of ECF between these compartments.
Flow is also determined by [a] and [b]

A

slow flow.
[x] plasma
[y] interstitial fluid
[a] arteriolar resistance
[b] number of oopen pre-capiliary sphincters.

276
Q

Veins hold [a]% of blood but have a resistance of only [b]mmHg
[c] and [d] facilitate blood return
[e] aid venous return against gravity and prevent backflow
[f] - nervous system mediate vascoconstriction to maintain venous return/pressure.

A

[a] 70
[b] 10mmHg
[c] Skeletal muscle
[d] Respiratory pump
[e] valves
[f] Sympathetic

277
Q

Lymphatics drain [a] of excess fluid/proteins filtered from the capilliaries.
They return this fluid to the [b] System through the [c].
Unidirectional flow aided by : [d] [e] [f]

A

[a] interstitial
[b] Cardi Vascular
[c] thoracic ducts
[d] smooth muscle - lympatic vessels
[e] skeletal muscle - pumps
[f] Respiratory pumps

278
Q

the respiratory pump enable venous return by:

A

inhalation pushes diaphram down to increase abdominal pressure and decreases thoracic pressure.
this pressure difference allows venous return.

279
Q

What regulates blood volume?
why is its regukation important?

A

RAAS, ADH, Adrenals and Kidneys.

Important for beat to beat of heart (FS mechanism)
Important long term moderatory.

280
Q

what is blood pressure?

A

pressure of blood within and against the arteries.

281
Q

what are the 5 components of BP control?
(+ 1 bonus)

A

1. Autoregulation

2. Local humoral

3. Circulating humoral

4. Baroreceptors

5. Central neural

(6.Central chemoreceptors)

282
Q

Autoregulation controls BP by the stretching of [___ ____ ___ ]
This is [a] autoregulation which varies from excellent in the [a,b,c] moderate in the [d, e] and poor in the [f]

It is an intrinsic mechanism in the [?]

A

[–] Vasular smooth muscle
[a] immediate
[heart brain and renal]
[skeletal splanic]
[skin]

[heart brain skin]

283
Q

Give an example of a potent local vasoconstrictor.
Give and example of a potent local vasodilator (x2)

A

Local Vasocontrictor: Endothelian
Local Vasodilator: NO and Prostacyclin

284
Q

What are 3 circulating hormonal vasoconstrictor?

2 x dilators?

A
  • SKIN Epinephrine, Angiotensin II, Vasopressin
  • MUSCLE Epinephrine, Atrial Nateuretic Peptide
285
Q

where are primary baroreceptors found?

A

aortic arch (increase bp) and carotid sinus(increase and decrease BP)

286
Q

where are secondary barorecptors found?

A

veins, myocardium and pulmonary vessels

287
Q

Increased bp sensed by carotid baroreceptors which is then sent via the [a] to the medulla where there is increased firing which results in stimulation of [a] nerve and [c] in sympathetic stimulation.
Results in [d] CO and TPR.
BP=COxTPR

A

[a] glossopharyngeal (IX)
[b] parasympathetic (X)
[c] decrease
[d] decrease

288
Q

[–] baroreceptors = short term regulation of BP
If the baseline deviates for more than a few days, the base line is adapted –> [–]

A

[—] Arterial baroreceptors
[—] Hypertension

289
Q

when [—] baroreceptors are stimulated, [—] is secreted and you have decreased vasoconstriction and decreased BP, and therfore decreased release of [a] [b] [c] which leads to fluid loss.
Therefore key in blood volume regulation.

Maladaption of this would lead to… [d]

A

[—] cardiopulmonary
[—] ANP
[a b c] Angiotensin, aldesterone and vasopressin
[d] Heart failure

290
Q

what are the main neural influences on the medulla?

A
  • Baroreceptors
  • Chemorecpetors
  • HYpothalamus
  • Cerebral Cortex - stress
  • Skin - temp
  • O2 CO2
291
Q

Chemoreceptors are: [a]
High [b] –> vaso[c] –> increases [d] –> increases [e]
Similar changes with the [f]
[g] has less of an effect on medulla, (mainly peripheral)

A

[a] chemosensitive regions in th medulla
High CO2 = vasoconstriction = increased resistance = increased BP
[f] pH
[g] O2

292
Q

Peripheral chemoreceptors can be found where?
What are they mainly sensitive to?

Central chemoreceptors are found where?
what are they mainly sensitive to?

A

Peripheral
* Carotid and aortic bodies.
* mainly sensitive to O2

Central
* medulla
* mainly senstive to CO2 and pH

293
Q

short term BP control:

A

baroreceptors

294
Q

long term bp control

A

volume of blood

295
Q

how many axillary lymphg nodes are there?

A

5

296
Q

what are the branches of the subclavian artery?

A
  • axilliary artery —> lateral thoracic artery
  • internal thoracic artery
297
Q

at what level does CNX exit the diaphram.
what does it run alongside?

A

Vagus exits diaphram at T10
runs alongside Oesophagus in posterior mediastinum

298
Q

where does the phrenic nerve originate?
where does it exit the diaphram, and alongside what?

A

phrenic nerve orgintes at C3,4,5
descends in anterior mediastinum.
exits diaphram at T8 alongside vena cava (8 letters)

299
Q

how is pain in the ischeamic myocardium felt?

how is pain in the diaphram felt?

A
300
Q

which rib is continuous with the angle of louis/ sternal angle?

what else does thie angle of louis/sternal angle indicate?

A

2nd rib - T4/5
bifurcation of trachea
upper border of heart

301
Q

what does the manubrium articulate with

A

clavicle and first rib laterally

302
Q

how many pairs of ribs do we have?

A

12

303
Q

what ribs comprimise the:
costal margin?
True ribs?
False ribs?
floating ribs?

A

costal margin = 7-10
tru ribs = 1-7
false ribs = 8-10
floating ribs = 11 + 12

304
Q

by which joints do the ribs join to the vertebrae?

A

**COSTOVERTEBRAL joint: **
The HEAD of the RIB articulate with the vertebral BODY
**COSTOTRANSVERSE joint: **
The TUBERCLE of the rib articulate with the TRANSVERSE PROCESS of the vertebrae

305
Q

what are the three intercostal muscles?

bonus: where is the neurovascluar bundle found?

A

External - anteroinferior (inspiration, pulls rib up)
Internal - posteroinferior (expiration pulls rib down)
Innermost - postoinferior

neurovascular bundle between internal and innermost layer

306
Q
A
307
Q

what are the four borders of the heart?

A
308
Q

where is the apex of the heart located?

A

5th intercostal space - left midclavicular line

309
Q

how are artioventricular valves shut?

A

the chordae tendinae, held by papillary muscles are pulled by Trabeculae Carnae (irregular muscle ridges)

310
Q

draw the branches of the aortic arch

A
311
Q

draw out the coronary arteries and what they supply!!

A
312
Q

what is heart dominance?

A

whether the PDA (supply to the AV node) is supplied by the LCA or RCA

313
Q

what % of people or right heart dominent?
what % are left heart dominant?
what & are both?

A

70% Right
10% Left
20% both

314
Q

what is the Posterior Descending Artery (PDA) also known as?

what does it supply?

A

Posterior Inverventricular Artery (PDA = PIV)

AV node and posterior 1/3 of IV septum

315
Q

what is the SAN suplied by?

A

60% of people=RCA
40% of people=LCA

316
Q

what supplies the AVN?

A

Posterior Descending Artery (aka PIV)

this can be from LCA or RCA (90% RCA)

317
Q

where do the coronoary sinus (small and great cardiac veins) drain into?

A

directly into the right atrium

318
Q

what are the locations of valve ausculations?

A

All Patients Take Medicine
mitral at 5th IC space

319
Q

Why are incisions made in the middle to lower part of the intercostal space?

A

To avoid the neurovascular bundle which is found at the superior part of the intercostal space

320
Q

An occlusion in which coronary artery is most likely to be fatal?

A

LCA:
Since it branches into the Cx and LAD which supplies
left output to the body

321
Q

how many litres of blood can be found in the human body?

A

5L

322
Q

what are the constituents of blood?

A
323
Q

what is plasma?

A

Plasma is the liquid component of blood.
Proteins: Albumin, Globins, fibrinogen
Hormones
Clotting factors
Minerals
Water

324
Q

what is blood serum?

A

blood plasm without the clotting factors

325
Q

what is the lifespan of an erythrocyte?

A

4 months

326
Q

describe the shape of an erythrocyte

A

anucleate, biconcave, 6–8 µm

327
Q

where are erythrocytes produced?

A

Adult

328
Q

IgG is mostly involved in primary or secondary immune response?

A

secondary

329
Q

what does noradrenaline do?

A

stimulate sympathetic nervous system (fight/flight)

330
Q

what are metabolites, give some examples.
what do they do?

A

Tissues that undergo respiration (metabolically active) release metabolites
Most important: H+, CO2, K+, adenosine, lactate
These all cause vasodilation
Metabolite build up in tissues = vasodilation = reduced TPR = more blood flow to area

331
Q

Which ion channels are open during the plateau phase of the cardiac action potential?

Calcium channels and potassium channels.
Sodium channels only.
Calcium channels only.
Calcium channels and sodium channels.
Potassium channels only.

A

calcium and potassium channels

332
Q
A

Medicine - Phase 1 (16 decks)

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