Week 2 Flashcards

(175 cards)

1
Q

Three general layers of vessels

A

Tunica intima

Tunica medical

Tunica adventitia

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2
Q

Endothelium

What types of epithelium is it? Exception?

What is the function of endothelium?

What signalling molecules does it secrete?

What is stored in endothelium (in arterioles and larger vessels)?

Enzymes?

A

Simple squamous (exception **cuboidal **in high venous endothelium in lymph node)

Smooth surface (promote flow/prevent clothing), Trasnport (H2O, electrolytes, O2, CO2)

NO (vasodilation), Endothelin (vasoconstrictor), Collagen and laminin (extra cellular matrix)

Wiebel-Palade bodies store vWF

Angiotensin-converting enzyme (ACE) AI→ AII

Inactivate bradykinin, serotonin, prostaglandin

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3
Q

Basal lamina of endothelial cells

What is it between?

A

Endothelium and Subendothelial tissue

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4
Q

What is the subendothelial connective tissue made of?

A

Loose CT with scattered smooth muscle cells

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5
Q

Internal elastic fiber?

What is it made of and in what arrangement?

What may pass through internal elastic fibers? Purpose?

A

Fenestrated sheet of elastin

Processes of endothelial cells (to form gap junctions with smooth muscle in tunica media)

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6
Q

Cell layers from inside of the blood vessel to outside

Which layer TI/TM/TA do they belong to?

A

Endothelium (TI)

Basal lamina (TI)

Subendothelial connective tissue (TI)

Internal elastic membrane (TI)

Smooth muscle (TM)

External elastic membrane (TM)

Adventitia (TA)

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7
Q

Tunica media

Composition?

Large vessels vs. small vessels?

Where this layer is not present?

A

Smooth muscle, elastin, collagen (varies)

Small vessels: pericytes (contractile)

Large vessels: external elastic laima

Capillaries / post capillary venules

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8
Q

Tunica adventitia

Composition?

Unique structures?

A

Fibroblasts, collagen, elastic fibers

Vasa vasorum, nerves

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9
Q

Where are the post-synaptic nerves?

How do they reach smooth muscle?

When stimulated by sympathetic which vessels dilate and which contract?

A

Tunica adventitia

Release norepinephrine and it diffusses through EEL. Propagation through gap junction.

Vessels assocaited with skeletal muscle dilate, and all others contract

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10
Q

Blood supply to blood vessels

Small vessels vs. large vessels?

In which blood vessels the blood supply to blood vessels more prevalent? Why?

A

Vasa vasorum supplies the elastic and muscular arteries.

Small vessels receive O2 by diffusion, while large vessels have capillary beds in tunica media

Veins, less oxygen

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11
Q

Three types of artiers?

A

Elastic, Muscular, and Arteriole

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12
Q

Elastic artery

Location of these arteries?

Prominent structure in tunica media? Function?

Prominent structure in tunica adventitia? Function?

A

Conduction of blood from heart

40-70 fenestrated layers of elastin alternating with smooth muscle – allow to strech and recoil

Loose fibroelastic tissue allows movement and distention

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13
Q

Muscular artery

Location of these arteries?

What structures are prominent about layers?

Vasa vasorum?

A

Distributing arteries (most named down to 0.1 mm)

Internal elastic lamina (with endothelium / gap junctions)

Thick tunica media with smooth muscle. Gap junctions connect all layers of smooth muscle.

Extenal elastic lamina (fenestrated for neutrotransmitters from unmyelinated neurons)

Vasa vasorum less prominent

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14
Q

Arteriole

Layers?

Which layers cannot be distinguished?

A

Tunica intima and media

Adventitia cannot be distinguished from CT

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15
Q

Corresponding Arteries vs. Veins

Size?

Tunica media?

Shape?

Where blood cells are usually not found?

A

Size: Veins > Arteries

Tunica media: Arteries > Veins

Shape: Arteries circular

Where blood cells are usually not found: arteries

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16
Q

Luminal diameter defintion

A

Width of arteriole wall approx

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17
Q

Capillaries

Size?

Tunica media / adventitia?

Function?

Three types?

A

8-10 uM (diameter of single RBC)

No

Provide oxygen and control temperature

Continuous, fenestrated, sinusoidal

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18
Q

Capillaries types characterstiics

Location?

Characteristic?

A

Location:

Continuous: nervous (modified in brain to limit passage), muscle, and connective tissue

Fenestrated: pancreas, renal glomerulus (without diaphgram)

Sinusoidal: Spleen, liver, bone marrow of lymphoid organs

Layer charactersitics:

Continuous: Diaphram with endothelial cells with tight junctions

Fenestrated: Diiaphagram covering pores (

Sinusoidal: Discontinuous endothelial wall with basal lamina forming irregular channels

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19
Q

Are veins or arteries more numerous?

Which one is more permeable? Importance?

A

Veins

Veins (high endothelial venules)

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20
Q

Veins

Characteristic of large veins?

Sizes?

Characteristics of pulmonary/leg veins?

Charactersitic structure of veins?

A

More developed tunica adventitia than tunica media

venules >20um, medium vein >1cm, sm >1mm

Veins in legs/pulmonary system have smooth muscle

Valves (extensions of tunica intima)

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21
Q

Three heart layers

Component of endocadrium?

Subendocardial layer?

Myocardial cells function?

What is another name for epicardium?

What travels through epicardium?

A

Endocardium, Myocardium, Epicardium

Endothelial cells (continuous with vessels), CT, smooth muscle cells

Suendocardial contain CT, nerves, blood vessels, purkinje fibers

Attach to fibrous skeleton, contraction, secrete hormones

Visceral layer of pericardium

Coronary arteries

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22
Q

Where does the signal travel from AV?

A

AV node

bundle of His

bundle branches

Purkinje fibers

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23
Q

Lymphatic System

How does it differ from cardiovascular?

Strcuture of the wall?

Layers?

A

No pump, one way flow (to heart)

Endothelial cells anchored by fillaments

In ducts, there are three similar layers to blood vessels

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24
Q

Shortness of breath when lying flat (manifestation of heart failure)

A

Orthopnea

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25
Removal of appendix
Appendectomy
26
Systolic sound heard over the carotid artery area during auscultation
Carotid bruit
27
Increasing and decreasing in sound murmur
crescendo decrescendo
28
Grading of heart murmurs
Scale 1-6 Stage of cardiac cycle Systolic murmurs can be of ejection type (aortic stenosis), holosystolic (mitral regurgitation -- not closing fully), late systolic (mitral valve prolapse -- not closing properly) Diastolic murmurs can be early type (aortic regurgitation) or mid-late diastole (mitral stenosis)
29
Sounds from heart
**S1** Mitrial / Tricuspid valve closing **S2** Aortic / Pulmonary valve closing Splitting because of pulmonary low pressure (inspiration) Heard during expiration during atrial septal block **S3** (diastole) Chordae tendineae relaxing during diastole \* Present in young individuals Pathological in adults (CHF or pregnancy) **S4** (diastole) Caused by noncompliant ventricle
30
Heart tests
Lipid Panel Beta natriuretic protein (secreted in resposne to excessive streeching) Troponins (released when heart muscle is damaged) Echocardiograms (image e.g. valves) EKG Coronary Angiogram
31
What is the name of cells that will form heart? Where are they located? Where do they go to? Whey these cells are programmed to become progenitors?
**Cardiac progenitor** cells lie in epiblast immediately adjacent to the cranial end of the primitive streak They **migrate through** the **streak** and **into** the **splanchnic layer** forming primary heart field (PHF). They are **determined already** before the process starts.
32
How endocardial tube is formed from angiogenic cells?
**Angiogenic cells** clusters **form** right and left **endocardial tubes** **Endocardial tubes fuse** by **apoptosis**
33
What are the four layers of endocardial tubes?
**Endocardium** (endothelial cells) **Cardiac jelly** (acellular material made by myocardium) **Myocardium** **Epicardium** (mesothelial migrates in form septum transversum -- the location of diaphgram; forms coronary arteries)
34
What folding causes the heart to move into thorax region?
Cranial-caudal folding due to fast nervous system growth
35
Three main veins in embryo and their destination
Cardinal [anterior,posterior,common] → Body Vitelline → Yolk Sac Umbilical → Placenta
36
Are inflow or outflow tracks conntected to the heart tube before or after any cardiac folding takes place? What is the imporance of that?
They are connected **before** any folding Arterial and venous ends anatomically fixed in place
37
Four dialations of the heart tube
1. Sinus venosus 2. Primitive atrium 3. Primitive ventricle 4. Bulbus cordis / Conus cordis - truncus arteriosus
38
What is created by cardiac loop formation?
Normal position of heart chambers Single circuit becomes asymmetrical system
39
Which direction is the cephalic porition of heart tube is folded?
Ventral, lateral, and caudal
40
How these strctures form? Atriventricular canal? Trabeculated part of the right ventricle? Outflow tracks? Trunkus arteriosus?
**Atrioventricular junction** → Atriventricular canal **Proximal third of bulbus cordis** → Trabeculated right ventricle **Midpoint of bulbus cordis** → Outflow tracks **Distal part of bulbus cordis** → Trunkus arteriosus
41
Development of inferior and superior vena cava What are initial three veins? Which side does the venous return shifts? What becomes inferior vena cava? What becomes superior vena cava? What becomes coronary sinus? What fuses with atrium?
Vitelline, Cardinal, and Umbilical Right right vitelline → inferior vena cava right anterior cardinal → superior vena cava left sinus horn → coronary sinus right sinus horn → fuses with atrium
42
How are trabeculae formed in atrium and ventricle?
Parts of bulbus cordis develops trabeculae
43
What is formed after the sinus venosus fuses with right atrium? What opens into this region? What important structure is along the lateral side of sinus venarum?
Sinus venarum IVC, SVC, and coronary sinus crista terminalis (conducting fiber tract SA node to AV node)
44
What becomes pulmonary veins?
Smooth portion in the left atrium
45
What is the name of structure that will form septum? Which layer of endocardial tube does it come from? What are the components of this strcture? Clinical importance?
Endocardial cushions Cardiac gelly Splachnic mesoderm + neural crests Septal defects
46
Steps in formation of foramen ovale
Formation of **septum primum** (thin **membranous** septum) Programmed cell death forms **ostium secundum** (**superior** aspect) Thick **muscular** **septum secundum** forms to **right** of septum primum contains **foramen** **ovale** on its **inferior** surface.
47
What is an importance of foramen ovale? When and why does it close? When does the functional and anatomic closure occurs? Clinical importance?
Right to left shunt During birth when the pressure builds up in right atrium Functional closure occurs at birth and anatomical closure occurs at 3 month Incomplete fusion of septum primum and septum secundum (25% of population, usually no clinical importance)
48
Where does the smooth part of left atrium come from? Where does the smooth part of right atrium come from? What does the primitive atrias become?
Growth of pulmonary veins Sinus venarum (sinus venosus) Atrial appendages
49
Endocardial Cushions Where are they come from? Function? Associated heart Defects (examples)?
they originate from **splachnic mesoderm** from **cardiac jelly** and **neural crest cells** in the conotruncal area Forming **septa** and **valves** **ASD**, **VSD**, **transposition** of great vessels, and **tetralogy of Fallot**
50
ASD More prevalent in female or male? Most significat ASD defect? Cor triloculare biventriculare? How is it often detected?
Female 2:1 Osteum segundum Common atrium Problems in athletic individuals and wierd blood cells in a blood smear
51
How chordae tendinae and papillary muscles are formed?
By degeneration of trabeculae in ventricles
52
What forms septum? What forms bicuspid and tricuspid valves?
4 endocardial tissues
53
What are the things that can go wrong with division of truncus arteriosus and bulbus cordis?
Persistent common atriventricular atria Abnormal division
54
What assists truncus arteriossu and the bulbus cordis in the formation of aorticopulmonary septum?
Neural crest cells contribute to swelling (cushions) They form CT and smooth muscle of the aorticopulmonary septum Divided into pulmonary and aortic part
55
How is the truncus arteriosus and bulbus cordis partitioned?
Spiraling lines up the correct outflow tract with the correct ventricle Neural crests cells are required If neural crests are removed, this lead to a persistent truncus arteriosus
56
Persistent Tuncus Arteriosus Structure? Error? Sign/Symptoms? Rate?
Persistent Truncus Arteriosus No formation of septum Cyanosis, blood buildup in lungs and less flow = difficulty to breathe 1/10,000
57
Transposition of the Great Vessels Structure? Error? Sign/Symptoms? How infants survive? Occurence rate?
Aorta/right ventricle and pulmonary trunk/left ventricle Failure of septa to develop in a spiral fashion Strong cyanosis ASD/VSD/ductus arteriossu 2 or 3 per 10,000
58
Tetralogy of Fallot Structure? Error? Symptoms/SIgns?
Misaligned septum - VSD Large right ventrcile and pressure on pulmonary artery, and lack of blood in lungs -\> acidosis (preventing by squatting) Failure of outflow tract opening to align with ventricles Cyanosis
59
Partitoning of Primitive ventricle Where does the muscular septum come from? What does it fuse with? Where does the membranous septum come from?
**muscular** interventricular (IV) septum develops midline **on** the **floor** of primitive ventricle **AV cushions** right and left **bulbar** ridges and inferior AV cushions
60
Clinical importance of Ventricular Septum Defect Reasons? Importance/Significance? Occurence?
Failure of septum to form (most common) VSD are most cardiac congential defect Occurs in 30% of children with congential heart disease 2 to 6 per 1,000
61
Where do semilunar valves come from?
Truncus swelling during end of partitioning
62
What happens to vitelline veins (system)? What happens to umbilical veins?
The vitelline system gives rise to the **liver sinusoids** (including the **ductus venous**) The **right umbilical vein disappears** and the left **umbilical vein anastomoses** with the **ductus venous**.
63
Where do aortic arches crome from?
Aortic sac, the most distal part of the truncus arteriosus
64
How many aortic arches are there? Where do they originate and where do they terminate? Which vessels contibute to adult arterial system? Arch 1 & 2? Arch 6 importance?
6 Aortic sac (distal to trunkus arteriosus) -- right/left dorsal aortae Aortic arch 3, 4, and 6 as well as dorsal aortae arch 1 maxillary artery arch 2 stapedial artery 6 remains on left side and forms pulmonary vessels and the ductus arteriosus
65
Three right to left shunts How they are shut down during birth?
Ductus venosus (constriction) Foramen ovale (closing septa) Ductus arteriosus (constriction)
66
Fetal criculation What vein carries oxygenated blood to heart? Where most oxygenated blood goes to? What returns blood for re-oxygenation?
Left umbilical vein Head, neck, and upper limbs Umbilical arteries
67
Fetal remnants Umbilical arteries Umbilical vein Ductus venosus Ductus arteriosus Foramen ovale
Umbilical arteries → Internal iliac arteries and medial umbilical ligaments Umbilical vein → ligamentum teres of liver Ductus venosus → ligamentum venosum Ductus arteriosus → ligamentum arteriosum Foramen ovale → becomes oliterated
68
Patent Ductus Arteriosus Reason? Occurence rate? Male vs. Female? What can be used to treat? Complications?
Not closing ductus arteriosus 2 out of 1,000 Female 2:1 Prostaglanding inhibitors such as indomethacin or obuprofen can close small PDAs Enlargement of the heart (future failure) and possible endocarditis (1/8 patients develop) increase mortality by 50%
69
Paradoxical splitting
**Paradoxical splitting** occurs when **splitting** increases during **expiration**. It often be caused by the **setback** of the **aortic valve**. It can be also seen in patients with mechanical delay of LV ejection in **aortic stenosis**.
70
BNP test
BNP in an acronym used for B-type natriuretic peptide marker for cardiac overload due to volume expansion and increased ventricular pressure
71
edema "water pills"
hydrochlorothiazide or lasix
72
Why Calcium overload leads to DADs?
Increase Na+ by Na+/Ca++ exchanger
73
Smooth muscle vs. Skeletal muscle Force? Speed?
Force same Skeletal is faster
74
Two locations of multiunit smooth muscle?
Iris Vas deferens
75
Dimensions of smooth muscle cell Diameter? Length? SA/V raio?
3-6 um 100-500 um 1.5-2.5 um2 per every 1 um3
76
Dense bands vs. Dense bodies? What dense bands can be connected to?
Dense bodies are dense bands found in cytoplasm. Other cells (adherens type), extracellular matrix, actin filaments
77
Caveolae Size? How many per cell? How much plasma membrane is taken by these caveolae? Positioning? Important protein in caveolae?
70-120 nm pokets 170,000 (increases 70% plasma membrane) 50% (interposed wbetween dense bands) Close to the tubules of the sacroplasmic reticulum Ca-pump ATPase
78
How smooth muscle are connected? What protein is involved in formation of these connections? What is so special about gap junctions?
Gap junctions (low resistance pathway) Connexon 43 made of connexins They penetrate two membranes and they are made of two hemichannels (connexons)
79
How smooth muscle are regulated?
**Myogenic mechanisms** (selft-regulation = spontaneous in absence of signals) *e.g. membrane potential sets Ca2+ entry* **Neural regulation** (motor neurons innervate smooth muscle) *e.g.* *alter conductance of Ca2+* **Hormonal** *e.g. similar to neurotransmitters* **Humoral or paracrine** (No or prostaglandins) *e.g. NO and prostaglandins* **Inflammatory mediators** (inflamatory agents lead to contraction) *e.g. rlease of cytokines and inflammatory agents*
80
How smooth muscle cell is activated? How it is deactivated?
**Ca2+** binds to **calmodulin** and **activates** myosin light chain kinease (**MLCK**). MLCK **phosphorylates** light chain of **myosin**, and facilitates actin binding and cross-bridge cycle. **Myosin phosphatase** (MLCP) reduces cross-bridge cycling leads to relaxation.
81
How is electric gradient maintained in smooth muscle cells? What establishes resting membrane potential in smooth muscle? Resting membrane potential in smooth muscle?
ATP pumps K+ channels -40mV to -80 mV
82
Calcium dependent ion channels in smooth muscle Channels that permit calcium in smooth muscle cells
Channels that permit calcium into a cell: voltage-dependent, dihydropyridine-sensistive (L-Type) Ca2+ channels (VDCC) ROCs are typically non-selective cation channels (NSCC; allow Na+/Ca2+ entry) IP3 mediated G-protein-coupled receptors (GPCR)
83
Smooth muscle transport Primary active transport Secondary active transport Channels that excite smooth muscle? Channels that release calcium from sacroplasmic reticulum?
**Primary** sarcoplasmic reticulum Ca2+ ATPase (SERCA) plasma membrane Ca2+ ATPase Na+/K+ ATPase **Secondary** Na+/Ca2+ exchanger (NCX) **Excite** Na+/Ca2+ non-selective cation channels (NSCC) Ca2+ VDCC GPCR **SR Ca2+ release** IP3 receptor-operated channels (IP3) ryanodine-sensitive (RYR)
84
Interplay of K+ and Ca2+ in exitation
A major theme in smooth muscle is that **Ca2+ entry** (i.e. **excitation**) tends to be **controlled by K+** channels, **because these** channels set or **regulate membrane potential**, and it is **membrane potential** that **determines** Ca2+ entry via voltage-dependent **Ca2+** **voltage gated** channels.
85
4 types of K+ channels in smooth muscle
**Voltage gated channels** (6 transmembrane domains + 1 pore doamin) **Ca2+ activated K+ channels** (six or seven transmembrane segments) **e.g. BK, IK and SK** (two transmembrane channels and one pore doamin) **e.g KATP, KIR, GIRK channels** (has four transmembrane segments and two-pore domains ) **e.g.** **K2P**
86
What channels in smooth muscle are activated by the change in membrane potential?
voltage-dependent Ca2+ channels, typically L-type Ca2+ channels all smooth muscle express them
87
What molecule is required for action potential in smooth muscle?
Ca2+
88
Ca2+ effect on K+ (BK) channels in vascular smooth muscle cells
**Ca2+ sparks** **activated** large-conductance Ca2+-activated **K+ (BK)** channels in vascular smooth muscle cells Thus, **localized Ca2+** **release** events typically **cause hyperpolarization** and tend to cause **relaxation** in vascular smooth muscle cells.
89
How neurotrasmitters control/activate smooth muscle
Neuronal action potentials (**AP**) **promote** the **release** of **ATP** and norepinephrine (**NE**) from perivascular nerve terminals. **Norepinephrine** stimulates **α1** adrenergic receptors (α1R) and **ATP** binds to **P2X** receptors (P2XR) giving rise to [Ca2+]i. **Inward current** through P2X receptors also **depolarizes** cells and increases Ca2+ entry through **L-type Ca2+ channels**.
90
5 receptors that regulate smooth muscle Their secondary messengers?
Gq (PLC) - PLCb - DAG/IP3 / G12 - (RhoK) Gs - AC (+) Gi - AC (-) sGC - NO NSCC - +++
91
Two major pathway leading to sensitization to Ca2+? Desensitization to Ca2+?
DAG -\> PKC -\> CPI-17-(P) that inhibits MLCP G12 -\> Rho-GEF -\> RhoA -\> RhoK (kinease) -\> inactivate MLCP by phosphorylation mediated by cAMP -\> PKA -\> (+) MLCP NO -\> PKG as well both K+ hyperpolarization
92
No-mediated dialation mechanism in smooth muscle
93
Laplace's law
o = Pr/n o = wall stress (dynes/cm^2) P = pressure in chamber r = radius n = wall thickness
94
Muscle contraction cycles diagram With load? Without load?
Top with load Bottom without load
95
Term that describes a pressure at which the aortic valves open
Afterload
96
The Pressure-Volume (PV) Loop
97
Ejection Fraction (EF)
EF (%) = SV/EDV The normal human heart has an EF value ranging from ~ 55-75%
98
Starling’s Law
* *heart** is its **ability** to **increase** its **contractility** in response to an * *increase** in **blood volume**
99
Effect of a change in a preload on heart pressure volume loop of the heart
Increases preload increases Pressure and stroke volume
100
Effect of a change in a afterload on heart pressure volume loop of the heart
Higher afterload (possibly due to the higher BP) results in lower cardiac output This may lead to first hypertrophy and then heart failure
101
Effect of a change in cardiac contractiliy on the pressure volume loop
Sympathetic stimulation decreases EDV (EF up) In heart failure, EDV increases (EF down)
102
Stroke Work
StrokeWork = P x SV ejection pressure is 105 mm Hg and a normal stroke volume is 70 ml 7,000 mm Hg ml or ~ 9.3 x 106 dyne cm
103
Cardiac output
CO = SV \* HR CO = Mean Arterial Pressure / Total Peripheral Resistance 5.6 L/min for male and 4.9 L/min for female
104
Cardiac index
CI = CO / Body surface 3 L/min/m^2
105
(2) Factors that can increase CO? Factors that decrease CO?
**Increase** Sympathetic stimulation Cardiac hypertrophy **Decrease** (pathological) inhibition of nervous excitation conditions leading to irregular heart rhythms valvular heart disease hypertension congenital heart disease myocarditis cardiac anoxia diphtheria other types of myocardial damage or toxicity.
106
How graph x: right atrial pressure y: cardiac outpur can be affected by: changes in intrapleural pressure? changes in heart efficiency?
107
What is the relationship between x: right atrial pressure y: venous return
Pleateau: veins tend to collapse Down slope: downward gradient
108
Mean systemic filling pressure
A pressure in the right atrium when venous return = 0
109
What drives the preload?
The difference between **right atrial pressure** and **mean systemic filling pressure**
110
Venous return equation
Venous Return = (MSFP - RAP)/RVR MSFP = mean systemic filling pressure RAP = the right atrial pressure RVR = resistance to venous return
111
How the graph x: right atrial pressure y: venous return is affected by gain or loss of blood (changes in mean systemic filling pressure)? is affected by change is resistance to venous return?
Left or right shift beacuse of **changes** in **means systemic atrial pressure**
112
How is the VR / CO is affected by: increase in venous return? increase in contractility?
venous return: CO because of preload (Starling's law) & gradient between veins and atrium contractility: more blood pumped and less pressure in atrium
113
How HR affects CO?
Main mechanism to increase CO during exercise too low: can only pump so much too high: incomplete stroke volume
114
Methods for measuring cardiac output
**Direct** Doppler flow probe **Indirect** Oxygen Fick Method CO = O2 lung uptake / (aterial O2 - venous O2) Indicator dilution method CO = mg of Dye injected / (average dye concentration \* duration of first passage) Thermodiluytion Saline injected in right atrium Temperature changes measured in pulmonary artery
115
Atrial pressure vs CO Right vs. left ventricle effect of intrapleural pressure? effect of cardiac tamponade?
116
How End-Diastolic Pressure affect P-V loop?
117
All variables that affect CO
118
Arteries Type of flow? Pressure?
Have **rapid pulsatile blood flow** High pressure
119
Arterioles Imporance? Major function? Prominent layer? Have ... ?
**Most important** in **control blood flow** = hign in number and smooth muscle / diameter ratio Are **major resistance vessels (biggest pressure drop) **of the whole peripheral circulation and regulate blood flow to capillary beds Have thick smooth muscle layer The smooth muscle is partially contracted under normal conditions (**basal tone**)
120
Basal tone
Degree of **contractile tension** remaining in blood vessels after complete **without externalexcitatory influences** In contrast to skeletal muscle, smooth muscle have basal tone probably **from** **intrinsic** and **local factors** CO2?
121
Venules Can venules exchange fluid? Why?
Also **participate in exchange** Only have endothelial layer
122
Veins Importance for reservior? Any muscles in veins?
**Major capacitance vessels** = major collection and storage site for blood (**major controllable reservoir**) have thin but **muscular walls**
123
Velocity of blood equation why speed of the blood speed drops?
V=Q/A Greater distance = friction Smaller radii = more resistance surface are increases = slower flow
124
Blood pressure definition
The force exerted by the blood against any unit area of the vessel wall
125
Pulse pressure definition Why is it decreased over distance?
The **difference** between the peak **systole** and **diastole ** **Dampened** due to **Compliance** of the **arterial vessel** walls **Resistance** to flow as vessel **diameter** become **smaller**
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Graves’ disease Casue? Effect on cardivascular system?
* **hyperthyroidism** * elevated basal metabolism * **arteriolar vasodilation** * **reduced** arteriolar **resistance** * the dampening effect on the pulsatile arteial pressure is diminished * **pulsatile flow** in the **capillaries** is observed in the finger nail beds
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Mean arterial pressure
Diastole + Systole + 1/3 (Systole - Diastole)
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Arterial pulse pressure in congestive heart failure/hemmorage? aortic regurgitation (incomplete closing of the valve)? athletes?
Low High large SV =\> High pulse pressure
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How atrial pressure is calculated?
**estimated by pulmonary wedge pressure** **catheter**, **inserted** into the smallest branches of the **pulmonary artery**, makes almost direct contact with the pulmonary capillaries. The **measured** pulmonary capillary pressure is **approximately equal** to the left **atrial pressure**.
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Blood flow equation
Q = dP/R Q = blood flow (ml/min) dP = pressure gradient (mm Hg) R = resistance (mm Hg/ml/min)
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Capacitance (complicance) equation (distensibility)
"distensibility" C = dV / dP C = capacitance or compliance (ml/mm Hg) V = volume (ml) P = pressure (mm Hg)
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Relationship of complicance vs. volume vs. age
As a person ages, the arteries become stiffer and less distensible.
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Resistance equation (poiseuille's law)
R = 8nI / PI r^4 viscosity \* vessel length / radius R - resistance h - blood viscosity (e.g. hematocrit) l - blood vessel length r - radius of the vessel
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How blood flow is affected by increase in blood pressure?
It is not linear beacuse: Higher pressure gradient Vessels are streched
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Total peripheral resistance
The complete resistance that blood encounters as it flows from the arterial to the venous side of the circulation.
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venous resistance
The resistance that the blood encounters as it flows from the capillaries back to the heart.
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Polyctemia vera effect on blood flow
**polycytemia vera** (**increased** number of **red blood **cells). The apparent **viscosity** in this condition is **increased** more than **twofold**.
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Blood viscosity vs. Water viscosity
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Laminar flow
Laminar flow is streamlined (on a straight line), with each layer of blood remaining the same distance from the wall.
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How the arrangement of blood cells changes from slow flow to fast flow? What is the term that describes particular red blood cells arrangement?
**Axial streaming** of red blood cells **lowers** the **apparent viscosity** of blood
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Critical velocity increased by?
defined by the Reynolds number velocity at which the flow becomes turbulent * *decreased blood viscosity** (e.g., reduced hematocrit, anemia) * *increased blood velocity** (e.g., narrowing of a blood vessel followed by a precipitous increase in internal diameter)
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Diagram comparing arteries, capillaries, and veins
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Arrangement of smooth muscle in arteries and veins
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Resistance definition
is the force that impedes blood through the system.
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Distensibility Which vessels are more distensible?
Ability to strech Veins
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Relationship between compliance and distensibility
Compliance = Distensibility x Volume
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What is the relationship of compliance in veins and arteries on volume/pressure graph?
Veins have higher compliance
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Delayed compliance Importance?
**exposed** to **increased volume** will at **first** exhibit a large **increase** in **pressure**, **but delayed stretch** of the vessel Blood transfusion Hemmorage
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What happens when compliance of arteries fails?
When arteries are rigid (**arteriosclerosis**) blood **flow** through the capillaries during **systol**, but **flow ceases** during **diastole**.
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Where is tyrosin hydroxylase localized in muscle?
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Which blood vessels are supplies by nervous system?
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Which blood vessels are more responisve to the sympathetic stimulation?
Veins more NE is released for the same singal
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Venous pressure Peripheral venous pressure Central venous pressure
**Venous pressure** is the average blood pressure within the venous compartment **Peripheral venous pressure** is the average blood pressure within the peripheral venous pool. **Central venous pressure** is the pressure in the thoracic vena cava near the right atrium (CVP = right atrial pressure). the filling pressure of the right heart. = preload
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How central venous pressure be increased (2)?
Increased volume Decreased compliance
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How these variables affect preload: Ventricular failure Heart rate Outflow resistance & afterload (pulmonic valve stenosis) Inflow resistance (tricuspid valve stenosis) Venous volume Venous Pressure Venous Compliance Ventricular Compliance Atrial Contractility
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Hydrostatic pressure Toricceli law
**Hydrostatic pressure:** the pressure that results from the weight of water **Toricceli law: **in any body of water, the pressure at the surface of the water is equal to the atmospheric pressure, but the pressure rises below the surface.
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How Venous valve incompetence affects preload?
Decreases
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How position affects arterial and venous pressure?
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How long does RBs spend in capillaries?
1-3 seconds
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What shunts the blood from arteriole to venule? Structure that controls the flow?
Metarteriole Precapillary sphincter
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How stuff moves across cappilary?
**Diffsuion**: glocuse, O2, CO2, steriod hormones **Water-soluble substances ** Glucose and electrolytes must pass through **filtration pores** **Pinocytosis/Transcytosis**
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Hydrostatic pressure in capillary vs. intersistial fluid
Hydrostatic capillary pressure always \> IF
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Arteriolar dialation/constriction effect on the pressure curve over vessels
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Most important protein in determining colloid osmotic pressure
Albumin
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How capillary blood pressure and IF blood pressure varies over the capillary? Exceptions?
166
Starling equation
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Causes for endema?
168
How much fluid is reabsorbed by venules and lymph
85% (16-18L/day) venules and 15% (2-4L/day) lymph
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Importance of lymph bulb
The **contraction-relaxation** cycle o**f lymph bulbs i**s the fundamental process that **removes excess water** and **plasma proteins** from the **interstitial spaces**. **Propells**
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What aids flow of lymph?
Peristalic contractions One way valves Movement of skeletal muscle Respiratory diaphragm (decrease interpleural pressure)
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Lymphedema
Obstruction of lymph vessel
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Is lymphatic tissue present in the brain? Replacement?
No (BBB) Channels
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Name the structure in lymphatic vessels that elps to keep lymphatic vessel open
Lymphatic anchoring filaments
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What two components make membranous IV septum? What makes bicuspid and tricuspid valves?
Right and left bulbar ridges AND inferior AV cushions Endocardial cushions
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Active tension vs. resting tension in Skeletal muscle vs. Cardiac muscle