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Cardiopulmonary I > Test 1 (Part 1) > Flashcards

Test 1 (Part 1) Flashcards

1
Q

The Muscle of the Gut, Vasculature, and Respiratory Tract must be able to:

A

1) Contract and maintain that contraction for a long period of time (ENERGY EFFICIENT)
2) Contract periodically to mix contents of Organ
3) Maintain SHAPE of Organ
4) Continue to GENERATE ACTIVE TENSION even when STRETCHED
5) Use relatively LITTLE ATP!!!!

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2
Q

Where is Smooth Muscle Found?

A

1) Vasculature (Arteries in Particular)
2) GI Tract
3) Urogenital Tract
4) Respiratory Tract
5) Eye

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3
Q

Innervation of Skeletal Muscle

A
  • Skeletal muscle is innervated by an ALPHA- MOTONEURON arising from the Spinal Cord
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4
Q

Innervation of Smooth Muscle

A

1) INTRINSIC INNERVATION:
- Gut, Trachea
- Neurons (Sensory and Motor)
- INDEPENDENT of CNS and PNS!!!!!!!

2) EXTRINSIC INNERVATION:
- the AUTONOMIC NERVOUS SYSTEM
- Allows CNS to Control Viscera

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5
Q

Neurotransmitters in Skeletal Muscle

A
  • Skeletal Muscle is activated by ACETYLCHOLINE, the only Neurotransmitter released at the NMJ!!!!
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6
Q

Neurotransmitters in Smooth Muscle

A

1) ACETYLCHOLINE:
- Excites Smooth Muscle (Gut)
- May INHIBIT other (Cause Relaxation)

2) NOREPINEPHRINE or EPINEPHRINE:
- Cause Contration of Vascular Smooth Muscle
- INHIBITS Gut Smooth Muscle

3) NITRIC OXIDE (NO)
- MAJOR INHIBITORY Influence on Smooth Muscle
- Don’t know any Smooth Muscle where a positive influence has been shown
- Acts vis cGMP Mechanism!!!!!

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7
Q

Major Difference between Skeletal Muscle and Smooth Muscle

A
  • Smooth Muscle can be DIRECTLY INHIBITED (Caused to RELAX)!!!!!!!!
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8
Q

Neuromuscular Contact in Skeletal Muscle

A

Motor End-Plate:
- Where we find the each Receptors

Presynaptic Terminal of Alpha Motor:
- Part that releases the Neurotransmitter!!!

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9
Q

Neuromuscular Contact in Smooth Muscle

A

VARICOSITIES: Swellings in Axons. Neurotransmitter is released from the VARICOSITY!!!!!!!!!!!!

** Varicosities are like the Pre-Synaptic Terminals!!!!

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10
Q

Neurotransmitter Receptors of Skeletal Muscle

A
  • Skeletal Muscle only has ACh Receptors!!!!!
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11
Q

Neurotransmitter Receptors of Smooth Muscle

A

1) MUSCARINIC Cholinergic
2) ADRENERGIC (Alpha and Beta)

**It is currently believed that NO does not require a membrane-bound receptor because it is extremely lipid soluble. It is believed that it diffuses through the cell membrane and has its action of the cGMP System

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12
Q

Compare and Contrast Activation/ Inhibition of Smooth Muscle with that in Skeletal Muscle

A

SKELETAL MUSCLE:
1) Alpha- MotorNeuron

2) Acetylcholine
3) Exclusively Positive
4) Specialized NMJ
5) ACh Receptors located at the Motor End-Plate
6) Only ACTIVATED vis NMJ!!!

SMOOTH MUSCLE:
1) Multiple Sources- Intrinsic, ANS, Sensory

2) ACh, Epinephrine/ Norepinephrine, Nitric Oxide, Others
3) May be Positive or Negative
4) VARICOSITIES, no Motor- End Plate
5) Multiple Receptor types located over Cell Membrane
6) May be activated by Blood-Borne Substances!!!!!!!

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13
Q

Hormonal Control of Smooth Muscle Contraction

A
  • Hormone Receptors are on the side of the Smooth Muscle cell that faces the Blood!!!!!
  • The Receptors for the Neurotransmitters are on the side of the cell closest to the Neurons!!!!!!

***Can have Hormones and Paracrine agents acting on the Smooth Muscle Cells as well

Examples of Hormones that can Elicit Smooth Muscle Contraction:!!!!!!!!!!!!!!!!!!

1) EPINEPHRINE
2) CHOLECYSTOKININ

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14
Q

Activation of Paracrine Agents in Control of Smooth Muscle Contraction

A
  • Endothelial Cells Secrete EDRF (Endothelium-derived Relaxing Factor) now know to be NITRIC OXIDE!!!!!!

**NO is produced by the Endothelial Cells and diffuses over to the Smooth Muscle cells and causes RELAXATION!

**Paracrine Agents can also ACTIVATE Smooth Muscle

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15
Q

Other Forms of Activation in Control of Smooth Muscle Contraction

A
  • Some smooth muscle cells can be activated by STRETCH!!!!!!!
  • Some of the Smooth Muscle in the VASCULATURE can be activated this way!!!!!
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16
Q

Compare and Contrast Activation/ Inhibition of Smooth Muscle with that in Skeletal Muscle

A

SKELETAL MUSCLE:
1) Innervation: Alpha- Motorneuron

2) Neurotransmitters: Acetylcholine
3) Action of NT: Exclusively EXCITATORY
4) Transmission Specializations: NMJ (Presynaptic terminal and specialized Motor End Plate)
5) NT Receptors: NICOTONIC CHOLINERGIC
6) Other forms of Activation: None

SMOOTH MUSCLE:
1) Innervation: Multiple- Including INTRINSIC and ANS

2) Neurotransmitters: Many- ACh, Norepo, NO, Others
3) Action of NT: May be Positive or Negative
4) Transmission Specializations: VARICOSITIES (presynaptic Swelling) with No end ORGAN SPECIALIZATIONS
5) NT Receptors: MUSCARINIC Cholinergic; Adrenergic, Others
6) Other forms of Activation: Blood-borne (Hormones). Paracrine (Ex: Nitric Oxide), and Intrinsic Mechanisms

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17
Q

Smooth Muscle Contraction Relaxation

A
  • The Pi can be REMOVED rom the Myosin Light Chain at any point in the Cycle. The Cycle will continue bet VERY SLOWLY!!!!!! A new Cycle cannot be started!
    • ***THIS IS HOW SM REDUCES Energy Consumption!!!

**Two ATPs are consumed in a cross bridge cycle for Smooth Muscle. With every cycle of a cross bridge of Smooth Muscle, it comes close to a 2nd ATP being consumed.

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18
Q

Smooth Muscle Contraction: the LATCH MECHANISM

A

1) Dephosphorylation of the Light Chain
2) Cycle preceding very SLOWLY
3) Any attached CROSSBRIDGES are still GENERATING TENSION!!!!
4) Way of INCREASING TENSION and DECREASING ATP Usage!!!!!

**Decreases ATP use because ATP cant get to the Myosin Head (Incredibly Slow) and when the Myosin head is Dephosphorylated, it will stay BOUND to the ACTIN (Generates TENSION) until the Myosin Head attaches to ATP again!!!

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19
Q

Energy Utilization of Skeletal Muscle vs Smooth Muscle

A

SKELETAL MUSCLE:
1) ATP Binding to Actomyosin Complex (To Separate): 1 ATP/ Cycle

2) Ion ATPases: Na/K; Ca2+ (SR); Other Membrane Bound
3) Addition During Cycle: None
4) ATP Savings: None

SMOOTH MUSCLE:
1) ATP Binding to Actomyosin Complex (To Separate): 1 ATP/Cycle

2) Ion ATPases: Na/K; Ca2+ (SR and Membrane); Others
3) Addition During Cycle: 1 ATP/ Cycle by MLCK

4) ATP Savings: Latch Mechanism and Slow Myosin ATPase
- These two mechanisms more than make up for the additional ATP used to Phosphorylate the Light Chain in each cycle of the Smooth Muscle Contraction

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20
Q

Length-Tension Relationship in Skeletal Muscle

A

ACTIVE TENSION:
- What the Cross Bridges do

PASSIVE TENSION:
- Comes from stretching the membranes (think of a rubber band)

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21
Q

Length-Tension Relationship in Smooth Muscle

A
  • So with EVERY STRETCH of the Muscle Cell, Passive Tension INCREASES a LITTLE, but as the Actin and Myosin REARRANGE, the Passive Tension DECREASES AGAIN!!!!!

***With time (even though the muscle is at the same length) the PASSIVE TENSION still goes back down to zero after the INITIAL STRETCH!!

***Passive Tension dissipates at any given length of the Smooth Muscle Cell. The reason it dissipates like this is because the Thick and Thin Filaments of the Smooth Muscle cell are NOT ARRANGED like in the Sarcomere!!!

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22
Q

Length-Tension Relationships in Smooth Muscle Cont.

A
  • REMEMBER that the Thick and Thin Filaments are not arranged in such a neat and organized manner like in the Skeletal Muscle
  • Instead the Thick and Thin Filaments are MUCH MORE “RANDOMLY” Arranged
  • As Smooth Muscle is Stretched, the Myosin Heads, once free from the Actin, will INTERACT with a DIFFERENT THIN FILAMENT!!!!!!!!
    * **Since the Thin Filaments are anchored and the Thick filaments are free to move around, the Myosin heads on the Thick Filaments can attach to different Thin Filaments. THIS EXPLAINS WHY THE PASSIVE TENSION DECREASES AFTER THE MYOSIN AND ACTIN ARE RELEASED FROM EACH OTHER!!!!!!

**Thin Filaments are Anchored to the Sarcoplasmic Reticulum of the Smooth Muscle Cell

**Thick Filaments are free to move around

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23
Q

Myosin interacting with different Actin Heads does two things:

A

1) It REDUCES the Passive Tension by Reducing the STRAIN on the points of attachment to the Membrane

2) It allows the Smooth Muscle cell to continue to GENERATE ACTIVE TENSION over a wide range of length. There is alway an ACTIN available for the Myosin Head
- The Active Tension in Smooth Muscle is maintained over a longer MUSCLE LENGTH compared to Smooth Muscle!!!!!!

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24
Q

General Purpose of the Cardiovascular System

A
  • The perfusion of capillary beds permeating all Organs with fresh blood over a narrow range of HYDROSTATIC Pressures
  • Local functional demands determine the structural nature of the wall surrounding the endothelial tubes
  • Divided into Systemic/ Peripheral Circulation and Pulmonary Circulation
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25
Q

Vascular Development

A

Blood Vessels for in two ways:

1) VASCULOGENESIS: blood vessels arise from Coalescence of HEMANGIOBLASTS, which arise from Blood Islands
- How we make most of the Blood Vessels in the Body

2) ANGIONGENESIS: Vessel formation via branches arising from existing vessels
- Major Vessels from VASCULOGENESIS
- An understanding of these processes is relevant to developing therapeutic strategies to produce revascularization of Ischemic Tissues or Inhibit Angiogenesis in Cancer and other disorders

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26
Q

Early Vasculogenesis

A
  • Begins is the XE SPLANCHNIC MESODERM surrounding the YOLK SAC (Week 3)
  • Formation then moves to LATERAL PLATE MESODERM
  • Yolk Sac is first see for formation of BLOOD ISLANDS
  • ISLANDS arise from MESODERM Cells that INDUCED to for HEMANGIOBLASTS, a common precursor for vessel and blood cell formation
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27
Q

Blood Islands

A
  • Blood Islands contain cells (Hemangioblasts) which are capable of DIFFERENTIATING into 2 Populations of Cells:
    1) ANGIONBLASTS (Vascular precursors)- form the ENDOTHELIAL CELLS aka the Tubing
    2) HEMATOPOIETIC STEM CELLS- made from the remaining Hemangioblasts
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28
Q

Molecular Regulation of Development

A
  • FGF2 binds to MESENCHYMAL CELLS (Mitogen)—> Hemangioblasts
  • Vascular Endothelial Growth Factor (VEGF) elicits regional change in Blood Islands (2 Receptors)
    a) Once Receptor makes tubing and the other makes the Hemangionblasts which make the Stem Cells
  • Signal to express VEGF may involve HOXB5, which up regulates the VEGF receptor FLK1!!!!!!!
  • CENTRAL CELLS become HEMATOPOIETIC STEM CELLS
  • PERIPHERAL CELLS differentiate into Angioblasts —> Endothelium of Blood Vessels!!!!!!
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29
Q

Angiogenesis

A
  • Once the Vascular Bed is established, VEGF their regulates formation of Additional Vasculature via Angiogenesis
    1) Angiopoietin 1 (ANG1(: Signals to other Pericytes to come into this newly forming vessels and form new SMOOTH MUSCLE CELLS
    2) Angiopoietin 2 (ANG2): Causes the loss of Endothelium cells and then allow the Branch to BUD OFF!!!!!!
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30
Q

Blood Circulation

A
  • Blood Circulation is established and Primary Plexi are remodeled into hierarchical network of Arterioles and Arteries (red), Capillaries (Grey), and Venues and Veins (Blue)

1) Aorta
2) Arteries
3) Arterioles
4) Capillaries
5) Venules
6) Veins
7) Vena Cava

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31
Q

Maturation and Remodeling of Vasculature

A
  • In addition to VEGF, regulated by Platelet-derived Growth Factor (PDGF) and TGF-Beta
  • Specification of occurs soon after ANGIOBLAST Induction
  • SHH from Notochord INDUCES Expression go VEGF (Mesoderm)
  • VEGF INDUCES Notch Pathway which specifies ARTERIAL DEVELOPMENT through expression of EphrinB2 (Ligand)!!!!!!
  • VEIN SPECIFIC Genes controlling Venous Development EphrinB4!!!!!!!!

***MASTER Gene for Lymphatic Vessel Differentiation is PROX1!!!!!!!!!!

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32
Q

Definitive Hematopoietic Stem Cells- AGM (Aorta-Gonad- Mesonephros Region)

A
  • In the fetus are derived from Mesoderm surrounding the AORTA in a site near the Developing Mesonephric KIDNEY
  • Called the AORT-GONAD-MESONEPHROS REGION (AGM)
  • These cells eventually colonize the LIVER, which becomes the MAJOR HEMATOPOIETIC ORGAN of the Embryo (2-7 Months)
  • HEMATOPOIESIS moves from LIVER to BONE MARROW (Month 7)
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33
Q

Hemangioma

A
  • ABNORMALLY DENSE collection of Capillary Vessels
  • Common TUMORS of Infancy (10%)
  • Focal or diffuse, more secondary complications

**Laser or surgical treatments available!!!!

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34
Q

Port Wine Stain

A

***NAEVUS FLAMMEUS

  • Superficial and Deep Dilated Capillaries in the Skin!!!!

***Some laser treatments have been Successful

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35
Q

Tumor Angiogenesis

A
  • There are today HUNDREDS of molecules know to Mediate or Regulate ANGIOGENESIS
  • Progressive Tumro Growth is DEPENDENT on Angiogenesis
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36
Q

Tumor Angiogenesis

A
  • When some of the Tumor Cells switch to an Angiogenic Phenotype, the local equilibrium between Positive and Negative ANGIOGENIC Regulators Changes
  • Tumor Growth begins, OFTEN RAPIDLY
  • Many molecules have been considered as POTENTIAL THERAPEUTIC targets or tools to inhibit Pathological Angiogenesis, in particular tumors!!!!!

***Tumors switch from a positive/ negative balance of VEGF, and then this causes for the tumors to produce NEW BLOOD VESSELS (Angiogenesis)

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37
Q

The Heart

A
  • The Heart is a folded Endothelial tube whose wall is thickened to act as a REGULATED PUMP

3 Cardiac Layers:
1) ENDOCARDIUM: Consisting of an Endothelial lining and sub endothelial Connective Tissue

2) MYOCARDIUM: a functional SYNCYTIUM of Striated Cardiac Muscle fibers forming three Major Types of Cardiac Muscle:
1) Atrial Muscle
2) Ventricular Muscle
3) Specialized Excitatory and Conductive Muscle Fibers

3) EPICARDIUM, the Visceral layer of the PERICARDIUM, is a LOW-FRICTION SURFACE lined by a MESOTHELIUM in contact with the PARIETAL PERICARDIAL SPACE!!!

***LARGE Vessels in the Heart have their own Blood Supply and Nerves!!!!!

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38
Q

Cardio (myo) cytes

A

1) CONTRACTILE: Contract to Move Blood
2) MYOENDOCRINE: Produce ATRIAL NATRIURETIC FACTOR that stimulates for DIURESIS and EXCRETION of SODIUM in Urine by Increasing the GLOMERULAR Filtration rate, Reduces Blood Volume!!!!!!!!!!
3) NODAL: Specialized to Regulate CONTRACTION of the Heart (Sinoatrial node and Atrioventricular Node)

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39
Q

Arteries

A
  • Arteries conduct blood from the heart to the Capillaries
  • They store some of the pumped blood during each CARDIAC SYSTOLE to ensure continued flow through the capillaries during CARDIAC DIASTOLE

Arteries are organized in three Major TUNICS or LAYERS:

1) TUNICA INTIMA
2) TUNICA MEDIA
3) TUNICA EXTERNA

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40
Q

Blood Bessel Tunics

A

1) TUNICA EXTERNA/ ADVENTITIA
- Outermost layer of the Blood Vessel Wall

  • Composed of a LOOSE CT that contains ELASTIC and COLLAGEN FIBERS
  • Helps ANCHOR the vessel to other tissues
  • An EXTERNAL ELASTIC LAMINA can be seen separating the Tunica Media from the ADVENTITIA
  • VASA VASORUM

2) TUNICA MEDIA
- Middel Layer of the Vessel Wall

  • Composed of CIRCULARLY ARRANGED layers of Smooth Muscle Cells
  • VASOCONTRICTION (Narrowing of the Blood Vessel Lumen)
  • VASODILATION (Widening of the Blood Vessel Lumen)

3) TUNICA INTIMA/ INTERNA
- Innermost Lyare of Blood Vessel Wall

  • Composed of an Endothelium and a Subendothelial layer
  • External layer of ELASTIC FIBERS, the INTERNAL ELASTIC LAMINA
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41
Q

Arteries

A

From the Heart to the Capillaries, Arteries can be classified into three major Groups:
1) LARGE Elastic Arteries

2) MEDIUM-SIZED Muscular Arteries
3) SMALL Arteries and Arterioles

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42
Q

Large Elastic (Conducting) Arteries

A

Two Major Characteristics:
1) RECEIVE Blood from the HEART under HIGH PRESSURE

2) Keep Blood circulating continuously while the heart is PUMPING INTERMITTENTLY
- DISTEND (Swell) during SYSTOLE and RECOIL during DIASTOLE
- Tunica Intima consists of the Endothelium and the Subendothelial Connective Tissue
- LARGE AMOUNTS of Fenestrated ELASTIC SHEATHS are found in the TUNICA MEDIA, with bundles of Smooth Muscle cells PERMEATING the Narrow Gaps between the ELASTIC LAMELLAE!!!

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43
Q

Large Elastic (Conducting) Arteries

A
  • BLOOD VESSELS (Vasa Vasorum), NERVES (Nervi Vasorum), and LYMPHATICS can be recognized in the TUNICA ADVENTITIA of Large Elastic Arteries
  • AORTA and its largest branches (the Brachiocephalic, Common Carotid, Subclavian, and Common Iliac Arteries)
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44
Q

Musculature or Distributing Arteries

A
  • Allow a Selective Distribution of Blood to Different organs in response to FUNCTIONAL NEEDS. Diameter about 3 mm or Greater
  • Tunica Intima consists of Three Layers:
    1) The Endothelium
    2) The Subendothelium
    3) The Internal Elastic Lamina (IEL)
  • In the larger vessels of this group, a fenestrated EXTERNAL ELASTIC LAMINA can be seen at the junction of the Tunica Media and the Adventitia.
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45
Q

Muscular or Distributing Arteries Cont.

A
  • The TUNICA MEDIA shows a SIGNIFICANT REDUCTION in Elastic Components and an INCREASE in Smooth Muscle Fibers
  • Examples of Medium sized Arteries include the Radial, Tibial, Popliteal, Axillary, Splenic, Mesenteric, and Intercostal Arteries
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46
Q

Arterioles or Resistance Vessels

A
  • Final Branches of the Arterial System
  • Regulate the DISTRIBUTION of Blood to different capillary beds by Vasoconstriction/ Vasodilation
  • Structural adaption is walls with Circularly arranged Smooth Muscle
  • PARTIAL CONTRACTION (known as Tone) of the Vascular Smooth Muscle exists in ARTERIOLES!!!

**Arterioles are regarded as RESISTANCE VESSELS and are the MAJOR Determinants of SYSTEMIC BLOOD PRESSURE

***Lined by SQUAMOUS ENDOTHELIAL CELLS with SMOOTH MUSCLE CELLS in the Wall

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47
Q

Microcirculation

A
  • The Microvascular bed, the sire of the Microcirculation, is composed of the TERMINAL ARTERIOLE (An Metarteriole), the Capillary Bed, and the Postcapillary Venues
  • The capillary bed consists of slightly large capillaries (Called Preferential or THOROUGHFARE CHANNELS), where Blood Flow is CONTINUOUS, and the Small Capillaries, called the TRUE CAPILLARIES, where Blood Flow is INTERMITTENT!!!!!!
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48
Q

Capillaries

A

***The FUNCTION UNITS of the CARDIOVASCULAR SYSTEM!!!!!!

  • Small Blood Vessels, CONNECT Arterioles to Venues
  • The diameter range of a capillary is about 5 to 10 micrometers, large enough to accommodate ONE RED BLOOD CELL, and thin enough (0.5 micrometers) for GAS DIFFUSION
  • Contain only the TUNICA INTIMA, but this layer consists of a Basement Membrane and Endothelium ONLY!!!!!
  • CAPILLARY BED: group of capillaries (10-100) FUNCTION TOGETHER!!!
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49
Q

3 Kinds of Capillaries

A

1) CONTINUOUS Capillaries: lined by Endothelium with TIGHT JUNCTIONS and a Basal Lamina with PERICYTES (Contractile Cells)
2) FENESTRATED Capillaries: have PORES or Fenestrae (GI and Kidney)

3) SINUSOIDS, or Discontinuous Capillaries, are characterized by an Incomplete Endothelial Lining and Basal Lamina, with Gaps or Holes between and WITHIN ENDOTHELIAL CELLS (Liver and Spleen)
* **Designed to facilitate something going forma he Capillary to the tissue or picking something from the tissue to the Capillary

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50
Q

Veins are Capacitance (Reservoir) Vessels

A
  • The Venous system starts at the end of the Capillary bed with a Postcapilary Venule that structurally resembles Continuous Capillaries but with a WIDER LUMEN
  • POSTCAPILLARY VENUES are the preferred site of Migration of Blood Cells into Tissues (DIAPEDESIS!!!!!)
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51
Q

Venous System

A
  • Postcapillar venues converge to form muscular Venues, which converge and lead to a series of Veins of Progressively Larger diameter
  • Veins have a relatively thin wall in comparison with Arteries of the same size
  • The high CAPACITANCE of veins is attributable to the distensibility of their wall (Compliance Vessels) and, therefore, the content of Blood is LARGE relative to the VOLUME of the Veins
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52
Q

Venous System Cont.

A
  • Similar to Arteries, Veins consist of TUNICS
  • However, the DISTINCTION of TM from a TA is OFTEN NOT CLEAR
  • A distinct INTERNAL ELASTIC LAMIN is NOT SEEN!!!!!!
  • the Muscular Tunica Media is THINNER than in Arteries and Smooth Muscle cells have an IRREGULAR ORIENTATION Approximately Circular
  • a typical characteristic of veins is the presence of VALVES to PREVENT REFLUX of BLOOD!!!
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53
Q

Large Veins

A
  • A typical characteristic of veins is the presence of VALVES to PREVENT REFLUX OF BLOOD
  • You get VARICOSE VEINS when the VALVES IN YOUR VEINS DO NOT CLOSE PROPERLY
  • HEMORRHOIDS are dilations of the Internal or External Rectal Venous Plexuses
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54
Q

Vasculities

A
  • Vasculitis is an INFLAMMATION of you Blood Vessels
  • Causes changes in the walls of Blood Vessels, including THICKENING, WEAKENING, NARROWING, and SCARRING!!!!
  • Changes RESTRICT Blood Flow, resulting in ORGAN and TISSUE DAMAGE
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55
Q

Lymphatic Vessels

A
  • Conduct Immune Cells and LYMPH to Lymph Nodes
  • Remove EXCESS FLUID accumulated in Interstitial Spaces
  • Transport CHYLOMICRONS, LIPID-containing Particles, through LACTEAL Lymphatic Vessels inside the INTERSTINAL VILLI

***Lympahtic Vessels have “FLAPLIKE” Minivalves that allow for the fluid from the Capillaries to flow into the Lymphatic Vessels

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56
Q

Lymphatic Capillaries

A
  • Begin as DILATED TUBES with closed ends in Proximity to Blood Capillaries and Collect Tissue Fluid (LYMPH)
  • Wall is an Endothelium Lacking a complete Basal Lamina
  • Lymphatic Capillaries can be found in most tissues!!!
    - EXCEPTIONS:
    1) Cartilage
    2) Bone
    3) Epithelia
    4) CNS
    5) Placenta
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57
Q

Lymphatic Drainage

A

By INTRINSIC CONTRACTION:
- When vessels become expanded by Lymph, the Smooth Muscle of the wall Contracts. Each segment of the Lymphatic vessel between successive valves, called LYMPHANGIONS, behave like an AUTOMATIC PUMP

By EXTRINSIC CONTRACTION:
- External factors such as Contraction of the surrounding muscles during Exercise, Arterial Pulsations, and Compression of tissues by Force OUTSIDE the body, which COMPRESS the Lymph Vessels and cause PUMPING!!!

***When Lymph Drainage is Impaired, excess FLUID accumulated in the Tissue Spaces (EDEMA!!!!!)

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58
Q

Edema

A

1) LYMPHEDEMA:
- Caused by a DEFECT in the Transport of Lymph because of abnormal vessel development or damaged Lymphatic Vessels

2) FILARIASIS (Elephantiasis):
- A PARASITIC INFECTION of Lymphatic Vessels by WUCHERERIA BANCROFTI or BRUGIA malayo worms, transmitted by Mosquito Bites. This condition causes DAMAGE to the LYMPHATIC VESSELS with CHRONIC LYMPHEDEMA of Legs and Genitals!!!!!
* **Filaris Occurs in TROPICAL COUNTRIES!!!!!

3) CHYLOUS ASCITES and CHYLOTHORAX:
- Caused by the accumulation of HIGH FAT contains Fluid, or Chyle, in the Abdomen or Thorax as a result of TRAUMA, OBSTRUCTION, or ABNORMAL Development of Lymphatic Vessels

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59
Q

Endothelial Cell- Mediated Regulation of Blood Flow

A
  • Endothelial cells produce Vasoactive substances that can induce Contraction and Relaxation of the Smooth Muscle Vascular Wall
  • NITRIC OXIDE (NO) and PROSTACYCLIN: Relaxation of Smooth Muscle
  • Prostacyclin also PREVENTS Platelet Adhesion and Clumping leading to BLOOD CLOTTING
  • ENDOTHELIN 1 is a very Potent VASOCONSTRICTOR Peptide
  • The permeability of Capillary Endothelial cells is tissue specific. Also TOPOGRAPHIC PERMEABILITY: the Endothelial cells at the Venous end are MORE PERMEABLE than those at the ARTERIAL END.
    - Postcapillaru Venules HAVE THE GREATEST PERMEABILITY to LEUKOCYTES
  • Endothelial cells also pay a role in the process of cell homie and Inflammation
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60
Q

Artherosclerosis

A
  • The THICKENING and HARDENING of the walls of Arteries caused by ATHEROSCLEROTIC PLAQUES of Lipids, Cells, and Connective Tissue deposited in the TUNICA INTIMA
  • Artherosclerosis is frequently seen in arteries sustaining HIGH BLOOD PRESSURE, it does not affect veins and is the cause of MYOCARDIAL INFACTION, Stroke, and Ischemic Gangrene
  • Artherosclerosis is now recognized as a CHRONIC INFLAMMATORY DISEASE, characterized by features of Inflammation at all stages of its Development
  • Artherosclerosis correlates with the Serum levels of CHOLESTEROL or Low-Desity Lipoprotein (LDL). A genetic defect in Lipoprotein metabolism (Familial Hypercholesterolemia) is associated with Artherosclerosis and Myocardial Infarction before Patients reach 20 years of age!!!
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61
Q

Thorax Region

A
  • Region between the Neck and Abdomen, the superior portion of the trunk
62
Q

Thoracic Aperture

A

1) Superior Thoracic Aperture

2) Inferior Thoracic Aperture

63
Q

Superior Thoracic Aperture

A
  • Communication between the Neck and Thorax

Contents:

1) Trachea and Esophagus
2) Nerves and Vessels that supply and drain the Head
3) Neck and Upper Extremities

Boundaries:

1) T1 Vertebral Segment
2) Paired 1st Ribs
3) Superior Manubrium

64
Q

Inferior Thoracic Aperture

A
  • Irregular Communication between the Thorax and Abdomen

Contents:

1) Esophagus
2) Inferior Vena Cava
3) Aorta

Boundaries:

1) T12 Vertebral Segment
2) 11th and 12th Ribs
3) 7th through 10th Costal Cartilages
4) Xiphisternal Joint

65
Q

Thoracic Cavity Helpful Note

A
  • The thoracic cavity is surrounded by an OSTEOCARTILAGINOUS THORACIC CAGE and contains three Primary Divisions:
    1) Two Pulmonary Cavities
    - Located Laterally which contain the funds and Pleurae

2) Mediastinum
- Located Centrally containing the Heart, Thoracic Great Vessels, Trachea, Thoracic Esophagus, and Thymus

66
Q

Sternum Osteology

A

1) Manubrium (Superior Portion)
2) Body of Sternum (Middle portion, longer, narrow and thinner than the Manubrium)
3) Ziphoid Process (Inferior Portion)

67
Q

Manubrium

A
  • Suprasternal Notch (Superior Border of Manubrium)
  • Sternal Angle (Junction of Manubrium and Body)
  • Clavicular Notch (Articulates with Sternal End of Clavicle
  • Costal Notches (1st and held of 2nd)
68
Q

Body of Sternum

A
  • Xiphoid/ Sternal Joint (Junction of Body and Xiphoid Process)
  • Costal Notches (Half of the 2nd, 3rd through 6th and half of the 7th)
  • Transverse Ridges (Anterior Surface, between Costal Notches
69
Q

Xiphoid Process

A
  • Costal Notch (Half of 7th)

- Ribs

70
Q

Ribs Helpful Note

A
  • There are three types of Ribs:
    1) TRUE (Vertebrocostal) Ribs—-> (1st-7th)
    • Attaching directly from Vertebral segments to the Sternum via their own Costal Cartilage

2) FALSE (Vertobrochondral) Ribs —> (8th-10th)
- Attaching from vertebral segments to join the Costal Cartilage immediately superior to that segment

3) FLOATING (Vertebral) Ribs —> (11th-12th)
- Do not attach to the Sternum AT ALL!!!!

71
Q

Typical Ribs (3rd-9th)

A

1) HEAD (Articulates with THORACIC VERTEBRAE)
A) SUPERIOR ARTICULAR FACET: Articulates with Inferior Costal Demifacet of Thoracic Vertebral body one numeric segment Superiorly)

  B) INFERIOR ARTICULAR FACET: Articulates with Super Costal Demifacet on Thoracic Vertebral Body of the Same numeric segment

   C) Crest of the Head (Separates the two Articular Facets)

2) NECK (Stretch of Bone between Head an Tubercle)
3) TUBERCLE (Possesses an Articular Part with an Articular Facet and a Nonarticular Part that is the attachment point for the LATERAL COSTOTRANSVERSE Ligament)

4) BODY (Shaft)
A) Costal Groove (Houses Intercostal Nerve and Vessels)
B) Costal Angle (Anterolateral turning point of the Rib)

72
Q

Atypical Ribs (1st, 2nd, 10th-12th)

A

1) FIRST RIB (Broad, Flat, and Wide)
A) HEAD (Posses only a single FACET)

 B) SCLALENE TUBERCLE (Insertion point for the Anterior Scalene Muscle)

 C) GROOVE for the SUBCLAVIAN ARTERY (Superior aspect, Posterior to the Groove for the Subclavian Vein

 D) GROOVE for the SUBCLAVIAN VEIN (Superior aspect, Anterior to the Groove for the Subclavian Artery)

2) SECOND RIB (Longer than 1st Rib)
A) TUBEROSITY of SERRATES ANTERIOR Muscle (Insertion for the Serrates Anterior Muscle)

3) TENTH RIB
A) HEAD (Possesses only a SINGLE FACET)

4) ELEVENTH RIB (Short, does not attach tot he STERNUM)
A) HEAD (Possesses only a SINGLE FACET

  B) TUBERCLE (Not Present)

  C) NECK (Not Present)

4) TWELFTH RIB (Short, Does not attach to the Sternum)
A) HEAD (Possesses only a SINGLE FACET)

  B) TUBERCLE (Not Present)

  C) NECK (Not Present)
73
Q

Rib Fractures, Clinical Note

A
  • Most commonly fractures Ribs are the middle Ribs, at their weakest locus, just ANTERIOR to the COSTAL ANGLE.
  • Rib fracture CAN DAMAGE internal organs and produce severe pain with RESPIRATION, COUGHING, LAUGHING, and SNEEZING
74
Q

Supernumerary Ribs, Clinical Note

A
  • Extra Ribs either in the Cervical Region or Lumbar Region.
  • Cervical Ribs typically produce no Symptoms; However, can produce Neural and Circulatory problems with based on their PROXIMITY to the Brachial Plexus and Subclavian Artery.
  • Lumbar Ribs also often produce NO SYMPTOMS; however, can result in confusion when reading Radiographs and other Diagnostic Images
75
Q

Thoracic Vertebrae (12)

A

1) Vertebral Body (Articulates with 12 Ribs)
A) Superior Costal Facet
B) Inferior Costal Facet

2) Vertebral Foramen (Transmits Spinal Cord)

3) Vertebral Arch
A) Pedicle
B) Lamina (Well pronounced in the Superior to Inferior Direction)

4) Spinous Process (Protrude predominantly INFERIORLY)

5) Transverse Process
A) Transverse Costal Facet

6) Superior Articular Process (Articulates with the Inferior Articular Process of the Vertebral Segment above)
A) Articular Facet

7) Inferior Articular Process (Articulates with the Superior Articular Process of the Vertebral segment below)
A) Articular Facet

76
Q

Chondrology

A 
Costal Cartilages (Connect the Anterior portion of the Ribs to the Sternum)
   A) 1st-7th (Individually connect Ribs to the Sternum)

B) 8th-10th (Articulate with the Costal Cartilage superior to them before Articulating with the Sternum)

77
Q

Joints Helpful Note

A
  • Three Types of joints are:
    1) Synovial Joints (Diarthrosis; United by an ARTICULAR CAPSULE)2) Fibrous Joint (Synarthrosis; United by FIBROUS TISSUE)
    3) Cartilaginous Joint (Amphiarthrosis; United by HYALINE CARTILAGE or FIBROUS CARTILAGE)
78
Q

Synovial Joints

A
  • Diarthoris, Freely Movable, Characterized by a Fibrous Capsule lined with a Synovial Membrane, a Joint Space, HYALINE CARTILAGE lining the Articular Surfaces and Synovium)

1) PLANAR:
- Flat Arthodial, Non-Axial Gliding Movement
- Ex: Acromioclavicular Joint

2) GINGLYMUS:
- Hinge, Uniaxial
- Ex: Humeroulnar Joint

3) TROCHOID:
- Pivot, Uniaxial, Rotation
- Ex: Atlantoaxial Joint

4) CONDYLAR:
- One or two CONCAVE Surfaces articulating with one or two CONVEX Surfaces, Biaxial
- Ex: Metacarpophalangeal Joint

5) SELLAR:
- Saddle, Both surfaces are CONVEX and CONCAVE, Biaxial, Allowing false Circumduction without rotation
- Ex: Carpometacarpal Joint

6) SPHERODIAL:
- Ball and Socket, Triaxial, Allowing Circumduction in all three planes
- Ex: Femoroacetabular Joint

7) COMPOUND SYNOVIAL:
- Any combination of the above Joints

79
Q

Fibrous Joints

A
  • SYNARTHROSIS, Characterized by Bone, Fibrous Connective Tissue and Bone

1) SUTURES:
- Interlocked Bone
- Ex: Skull Sutures

2) SCHINDYLESIS:
- Tongue-In-Groove
- Ex: Vomer B./ Perpendicular Plate of the Ethmoid Bone into the Nasal Crest

3) GOMPHOSIS:
- Peg-In-Socket
- Ex: Dentoalveolar Joint

4) Syndesmosis:
- Bone-Ligament-Bone
- Ex: Radioulnar Joint by Interosseous Membrane

80
Q

Cartilaginous Joints

A
  • AMPHIARTHOROSIS, Characterized by Bone, Cartilage, Bone

1) Synchondrosis:
- Primary Cartilaginous Joints, Characterized by Temporary cartilaginous union of Hyaline Cartilage, Usually between the Diaphysis and Epiphysis of Growing Bone

2) Symphysis:
- Secondary Cartilaginous Joints, Characterized by Strong slightly moveable Joints united by Fribrocartilage

81
Q

Sternum

A

1) Manubriosternal (SYMPHYSIS)
A) Sternal Angle
B) 2nd Costal Notch

2) Xiphisternal (SYNCHONDROSIS)
A) Inferior Limit of Thorax
B) 7th Costal Notch

82
Q

Sternocostal

A
  • Junction of Costal Cartilages with Sternum
    1) Rib 1 (SYNCHONDROSIS)

2) Ribs 2-7 (SYNOVIAL PLANAR)
A) Anterior Radiate Sternocostal Ligament

B) Posterior Radiate Sternocostal Ligament

83
Q

Costovertebral

A
  • SYNOVIAL PLANAR
    1) Radiate Ligament (Head of the Rib to Vertebral Body)
    2) Intraairticular Ligament (Head of the Rib to the Intervertebral Disc)
    3) Articular Capsule (Strongest Anteriorly as the Radiate Ligament
84
Q

Head of Rib Helpful Note

A
  • The Head of Each Rib articulates with the Inferior Costal Facet of the SUPERIOR Numeric Thoracic Vertebral Segment and the Superior Costal Facet of the SAME Numeric Thoracic Vertebral Segment.
  • The articulating Facet of the Costal Tubercle articulates with the same Numeric Vertebral Segment
85
Q

Costotransverse

A
  • Synovial Planar
    1) Lateral Costotransverse Ligament (Tubercle of the Rib to the Transverse Process)
    2) Superior Costotransverse Ligament (Neck of the Rib to the Transverse Process of One Vertebral Segment Superiorly
86
Q

Forms of Movement in Costovertebral Joint Helpful Note

A
  • Two forms of Movement occur at the Costovertebral Joint, both function to INCREASE the Thoracic Volume, thereby DECREASING Thoracic Pressure producing INSPIRATION:
    1) BUCKET HANDLING MOVEMENT: Elevation of the LATERAL MOST PORTION of the Rib, Increasing the TRANSVERSE DIAMETER of the THORAX
    2) PUMP HANDLE MOVEMENT: Elevation of the STERNAL END of the Rib, Increasing the ANTERIOR to POSTERIOR diameter of the Thorax
87
Q

Costochondral

A
  • Articulation between Ribs and Costal Cartilages

- SYNCHONDROSIS

88
Q

Dislocation of Ribs Clinical Note

A
  • DISLOCATION of ribs refers to a dislocation at the STERNOCOSTAL Joint.
  • SEPARATION of Ribs refers to a separation at the COSTOCHONDRAL Joint
89
Q

Interchondral Joint

A
  • Between 6th/7th, 7th/8th, 8th/9th Costal Cartilages: PLANAR SYNOVIAL
  • Between 9th/10th Costal Cartilages: FIBROUS JOINT

1) Interchondral Ligament
- Strengthen the Interchondral Joint

90
Q

Thoracic Vertebral Joints

A
  • Intervertebral Joint: SYNPHYSIS
  • Zygopophyseal Joint: PLANAR SYNOVIAL

1) ANTERIOR LONGITUDINAL LIGAMENT
- Travels ont he Posterior surface of the Vertebral Bodies, Inside the Vertebral Canal

2) POSTERIOR LONGITUDINAL LIGAMENT
- Travels on the Posterior surface of the Vertebral bodies, inside the Vertebral Canal

3) LIGAMENTYM FLAVUM
- Pale yellow fibers which travel on the Ventral surfaces of Vertebral Laminae, inside the Vertebral Canal

4) INTERSPINOUS LIGAMENT
- Travels between adjacent Spinous Processes

5) INTERTRANSVERSE LIGAMENT
- Exist as Fibrous Cords in the Thoracic Region

6) SUPRASPINOUS LIGAMENT
- Travels on the Dorsal Surface of the Spinous Process

7) INTERVERTEBRAL DISCS
A) Annulus Fibrosis (Tough fibrosis Outer Region)

B) Nucleus Pulposus (Soft Gelatinous Inner Portion)

91
Q

Intercostal Muscles

A

1) External Intercostal Muscles
2) Internal Intercostal Muscles
3) Innermost Intercostal Muscles

92
Q

External Intercostal Muscles

A
  • 11 pair; Anteriorly Muscle Fibers are replaced by the EXTERNAL INTERCOSTAL MEMBRANE which overlies the Internal Intercostal Muscle
  • Inferiorly the External Intercostal Muscle is continuous with the External Abdominal Oblique Muscle

Origin: Inferior Border of the Ribs (Posteriorly)

Insertion: Superior Border of Ribs below (Anteriorly)

Action: Elevate Ribs

Innervation: Intercostal Nerve

93
Q

Internal Intercostal Muscle

A
  • 11 pair; Posteriorly Muscle Fibers are replaced by the Internal Intercostal membrane which is visible in the Posterior Mediastinum immediately lateral to the Vertebral Column
  • Inferiorly the Internal Intercostal Muscle is continuous with the Internal Abdominal Oblique Muscle

Origin: Inferior Border of Ribs (Anteriorly)

Insertion: Superior Border of Ribs below (Posteriorly)

Action: Depress Ribs (Interchondral Part Elevates Ribs)

Innervation: Intercostal Nerves

94
Q

Innermost Intercostal Muscle

A
  • 11 pair; the deepest fibers of the Internal Intercostal Muscle, separated from the Internal Intercostal Muscles by the Intercostal nerve and Vessels

Origin: Inferior Border of Ribs

Insertion: Superior Border of Ribs

Action: Undermined, probably the same as Internal Intercostal Muscle

Innervation: Intercostal Nerves

95
Q

Thoracentisis

A
  • Insertion of a HYPODERMIC Needle through the Intercostal musculature between ribs to obtain a fluid sample or drain small amounts of blood or fluid for the Pleural Cavity.
  • The needle is inserted between ribs Inferior to the Intercostal Neuromuscular bundle, but Superior to the Collateral Branches
96
Q

Insertion of a Chest Tube

A
  • Insertion of a tube to remove Large amounts of Air, Fluid, Blood, or Pus from the Pleural Cavity.
  • tube is typically inserted in the 5th or 6th Intercostal Space
97
Q

Thoroscopy

A
  • Insertion of a Throrscope into the Pleural Cavity through small incisions for visualizing and biassing the space inside the Pleural Cavity
98
Q

Internal Thoracic Wall Muscles

A

1) Transverse Thoracic Muscle

2) Subcostal Muscle

99
Q

Transverse Thoracic Muscle

A

Origin: Posterior Surface of the Lower part of the Sternal Body and Xiphoid Process

Insertion: Internal Surface of the 2nd-6th Costal Cartilages

Action: Depress Ribs

Innervation: Intercostal Nerves

100
Q

Subcostal Muscle

A
  • Typically appear her the Innermost Intercostal Muscle on the Internal surface of the Posterior Thoracic Wall, near the Angles of the Ribs

Origin: Inferior Border of Rib

Insertion: Superior Border of Rib (1 to 2 Segments)

Action: Probably ct as the Internal Intercostal Muscle

Innervation: Intercostal Nerve

101
Q

Lungs

A

1) Left Lung (two Lobes separated by OBLIQUE FISSURE):
A) SUPERIOR LOBE

B) INFERIOR LOBE

C) Oblique Fisure (Separating Superior and Inferior Lobes)

2) Right Lung (Three Lobes separated by OBLIQUE and HORIZONTAL FISSURES)
A) Superior Lobe

B) Middle Lobe

C) Inferior Lobe

D) Oblique Fissure (Separating Superior and Middle Lobes from Inferior Lobe)

E) Horizontal Fissure (Separating Superior and Middle Lobes)

102
Q

Lung Apex

A
  • Superior aspect of the Lungs
103
Q

Surfaces of the Lung

A

1) Costal Surface (Opposes the Rib Cage)
2) Mediastinal Surface (Opposes the Mediastinum)
3) Diaphragmatic Surface (opposes the Diaphragm)

104
Q

Costal Surface

A
  • Opposes the Rib Cage
105
Q

Mediastinal Surface (Opposes the Mediastinum)

A

1) Hilum
A) Pulmonary Artery
- Typically MORE SUPERIOR, THICKER-Walled of the Blood Vessels at the Pulmonary hilum

B) Pulmonary Vein
- Typically more ANTEROINFERIOR, THINNEST-walled structure at the Pulmonary Hilum

C) MAIN BRONCHI
- Typically more POSTERIOINFERIOR, THICKEST-Walled Structure at the Pulmonary Hilum

D) PULMONARY LIGAMENT
- Hanging Pleura from the Root of the Lung

2) RIGHT LUNG
3) LEFT LUNG

106
Q

Right Lung Impressions

A

1) Cardiac Impression
2) Groove of the Azygous Vein
3) Groove for the Esophagus
4) Groove for the Superior Vena Cava
5) Groove for the Inferior Vena Cava
6) Groove for the 1st Rib
7) Groove for the Brachiocephalic Vein

107
Q

Left Lung Impressions

A

1) Cardiac Impression
2) Groove for the Aortic Arch
3) Groove for the Descending Aorta
4) Groove for the 1st Rib
5) Groove for the Subclavian Artery

108
Q

Diaphragmatic Surface

A
  • Opposes the Diaphragm
109
Q

Borders

A

1) Anterior Border
- Left Lung:
A) CARDIAC NOTCH: Indentation of the Anteroinferior aspect of the Superior Lobe

     B) LINGULA: Thin process of the Superior Lobe created by the Cardiac Notch

2) Posterior Border
3) Inferior Border: Projects into the Costodiaphragmatic and Costomediastinal Recesses

110
Q

Lung Cancer

A
  • Can derive from actual lung tissue, or from the Bronchi (Bronchogenic Carcinoma).
  • Lung cancer can involved the PHRENIC Nerve, Vagus Nerve, and Recurrent Laryngeal Nerve, due to the proximity of those nerve to the Lung
  • Treatment can include removal of a Lung (PNEUMONECTOMY), a lobe of a lung (LOBECTOMY) or a specific Bronchopulmonary Segment (SEGMENTECTOMY) through a procedure called LUNG RESCECTION!!!!!
111
Q

Pleura

A
  • Paired serous membranes surrounding the Lungs

1) PARIETAL PLEURA: Adherent to the Thoracic Wall, the Mediastinum and the Diaphragm
A) Costal Pleura (Internal Surface of the Thoracic Wall)

B) Mediastinal Pleura (Lateral Mediastinum)

C) Diaphragmatic Pleura (Superior Diaphragm)

D) Cervical Pleura (Dome shaped over the apex of the fissures)

2) VISCERAL PLEURA (Adherent to the lungs, extends into the fissures)
- Innermost Pleura!!!!

112
Q

Pleuritis (Pleurisy)

A
  • an Inflammation of the Pleura producing a roughness on the lungs making breathing difficult
  • PLEURAL CAVITY (Potential space between the two layers of the Pleura that contains a Serous Lubricating fluid that reduces friction and produces cohesion through Surface Tension)—-> SURFACTANT!!!!
113
Q

Pulmonary Collapse

A
  • Occurs when enough air enters the Pleural Cavity to break the surface tension between the two laters of the Pleura. The ELASTICITY of the lungs causes them to COLLAPSE
114
Q

Pneumothorax

A
  • Entry of air into the Pleural Cavity from a PENETRATING WOUND to the Thoracic Wall or a rupture of a Pulmonary Lesion into the Pleural Cavity, which results in a COLLAPSE of the Lung
115
Q

Hydrothorax

A
  • Accumulation of excess fluid in the PLEURAL CAVITY, usually the result of fluid escape into the Pleural Cavity, or Pleural Effusion
116
Q

Hemothroax

A
  • Accumulation of blood in the Pleural Cavity, usually the result of a chest wound, usually the result of a laceration of an Intercostal vessel or Internal Thoracic Vessel rather than laceration of the lung
117
Q

Lines of Pleural Reflection

A
  • Abrupt changes in the direction of parietal Pleura

1) Sternal Line of Pleural Reflection
- Costal Pleura becomes Mediastinal Pleura ANTERIORLY

2) Costal Line of Pleural Reflection
- Costal Pleura becomes Diaphragmatic Pleura

3) Vertebral Line of Pleural Reflection
- Costal Pleura becomes Mediastinal Pleura POSTERIORLY

118
Q

Trachea (Right)

A
  • Entends from the LARYNX to its first Branch Point LEFT and RIGHT Bronchi, exists in the Posterior Mediastinum

1) RIGHT MAIN BRONCHUS:
- PRIMARY Bronchus; Wider, Shorter, and runs more vertical than the Left Main Bronchus

A) Right Superior Lobar Bronchus (Secondary Bronchus):

     1) Segmental Bronchi:
         - Tertiary Bronchi, associated with corresponding Bronchopulmonary Segment; Branches into Conducting Bronchioles

      2) Conducting Bronchiole:
          - Devoid of Cartilage; Branches into Terminal Bronchioles

      3) Terminal Bronchiole:
           - Devoid of Cartilage; Branches into Respiratory Bronchioles

      4) Respiratory Bronchiole:
            - Devoid of Cartilage, capable of GAS EXCHANGE; Branches into Alveolar Ducts

      5) Alveolar Duct:
             - Ending at a Alveolus, the functional unit of the Lung, the PRIMARY site of GAS EXCHANGE

 B) Right Middle Lobar Bronchus (Secondary Bronchus):

      1) Segmental Bronchi:
         - Tertiary Bronchi, associated with corresponding Bronchopulmonary Segment; Branches into Conducting Bronchioles

      2) Conducting Bronchiole:
          - Devoid of Cartilage; Branches into Terminal Bronchioles

      3) Terminal Bronchiole:
           - Devoid of Cartilage; Branches into Respiratory Bronchioles

      4) Respiratory Bronchiole:
            - Devoid of Cartilage, capable of GAS EXCHANGE; Branches into Alveolar Ducts

      5) Alveolar Duct:
             - Ending at a Alveolus, the functional unit of the Lung, the PRIMARY site of GAS EXCHANGE

 C) Right Inferior Lobar Bronchus (Secondary Bronchus):

      1) Segmental Bronchi:
         - Tertiary Bronchi, associated with corresponding Bronchopulmonary Segment; Branches into Conducting Bronchioles

      2) Conducting Bronchiole:
          - Devoid of Cartilage; Branches into Terminal Bronchioles

      3) Terminal Bronchiole:
           - Devoid of Cartilage; Branches into Respiratory Bronchioles

       4) Respiratory Bronchiole:
            - Devoid of Cartilage, capable of GAS EXCHANGE; Branches into Alveolar Ducts

       5) Alveolar Duct:
             - Ending at a Alveolus, the functional unit of the Lung, the PRIMARY site of GAS EXCHANGE
119
Q

Bronchoscopy

A
  • Insertion of a Bronchoscope into the Trachea to visualize the Main Bronchi
120
Q

Bronchial Asthma

A
  • Widespread narrowing of the airways produced by CONTRACTION of Smooth Muscle, Edema of the Mucosa and Mucus in the Lumen of the Bronchi and Bronchioles
121
Q

Trachea (Left)

A

2) Left Main Bronchus (Primary Bronchus; Travels INFEROLATERALLY)

 A) Left Superior Lobar Bronchus (Secondary Bronchus):

      1) Segmental Bronchi:
         - Tertiary Bronchi, associated with corresponding Bronchopulmonary Segment; Branches into Conducting Bronchioles

      2) Conducting Bronchiole:
          - Devoid of Cartilage; Branches into Terminal Bronchioles

      3) Terminal Bronchiole:
           - Devoid of Cartilage; Branches into Respiratory Bronchioles

       4) Respiratory Bronchiole:
            - Devoid of Cartilage, capable of GAS EXCHANGE; Branches into Alveolar Ducts

       5) Alveolar Duct:
             - Ending at a Alveolus, the functional unit of the Lung, the PRIMARY site of GAS EXCHANGE

 B) Left Inferior Lobar Bronchus (Secondary Bronchus)

      1) Segmental Bronchi:
         - Tertiary Bronchi, associated with corresponding Bronchopulmonary Segment; Branches into Conducting Bronchioles

      2) Conducting Bronchiole:
          - Devoid of Cartilage; Branches into Terminal Bronchioles

      3) Terminal Bronchiole:
           - Devoid of Cartilage; Branches into Respiratory Bronchioles

       4) Respiratory Bronchiole:
            - Devoid of Cartilage, capable of GAS EXCHANGE; Branches into Alveolar Ducts

       5) Alveolar Duct:
             - Ending at a Alveolus, the functional unit of the Lung, the PRIMARY site of GAS EXCHANGE
122
Q

Trachea (Bronchopulmonary Segments)

A

Bronchopulmonary Segments:
- Pyramid-shaped segment with Apex at the HILUM and base at the PULMONARY SURFACE, separated by Connective Tissue SEPTA, Supplied by and named for the Single Segmental Bronchus, Surgically Recectable

1) RIGHT LUNG
   A) Superior Lobe:
        1) Apical
        2) Posterior
        3) Anterior

B) Middle Lobe:

    1) Lateral
    2) Medial

C) Inferior Lobe:

    1) Superior
    2) Anterior Basal
    3) Medial basal
    4) Lateral Basal
    5) Posterior Basal

2) LEFT LUNG
A) Superior Lobe:
1) Apical (Usually combined as Apicoposterior)
2) Posterior (Usually combined as Apicoposterior)
3) Anterior
4) Superior (Lingular)
5) Inferior (Lingular)

 B) Inferior Lobe:

      1) Superior
      2) Anterior Basal (Usually combined as Anteromedial Basal)
      3) Medial Basal (Usually combined as Anteromedial basal)
      4) Lateral Basal
      5) Posterior Basal
123
Q

Triacylglycerosl

A
  • Major storage form of Fatty Acids

- Contains Three Fatty Acids and a Glycerol molecule

124
Q

Source of Triacylglycerol

A

1) DIETARY TG (processed in Intestinal Cells)
2) DE NOVO TG (In LIVER Hepatocytes)
3) DE NOVO TG (In ADIPOCYTES)

125
Q

TG Synthesis in Intestinal Cells

A

1) Dietary Triacylglycerols enter the Intestinal Cell
2) Fatty Acids come from the Triacylglycerol
3) The Fatty Acids are absorbed into the Intestinal Cell
4) The FA adds to Acetyl CoA and ATP to make Fatty Acyl CoA
5) Monoglycerol adds to the Fatty Acyl Glycerol to form Diacylglycerol (Acylglycerol Acyltransferase)
6) Another Fatty Acid is added to the Diacylglycerol to make Tiacylglycerol + Apolipoproteins + other Lipids
7) The Triacylglycerols are released as Chylomicrons from the Intestinal Cells!!!

126
Q

TG Synthesis in Liver Hepatocytes

A

1) Glucose (Glycerol 3-Phosphate Dehydrogenase) or Glycerol (Glycerol Kinase) can be broken down into Glycerol 3-P
2) Fatty acids add a CoA to become Fatty Acyl CoA
3) The Fatty Acyl CoA and Glycerol 3-P add together to make Lysphosphophatidic Acid
4) 2 more Fatty Acyl CoAs are added along the way until the Triacylglycerol + Apolipoproteins + other lipids are formed
5) The Triacylglycerol is released at VLDL

127
Q

TG Synthesis in Adipocytes

A

1) The VLDL and Chylomicrons are broken down by CAPILLARY LIPOPROTEIN LIPASE to make Fatty Acid that is absorbed into the Adipocyte
2) Glucose (Through GLUT4) is broken down to DHAP then to Glycerol 3-P
3) The Glycerol 3-P is added to Fatty Acyl CoA to make Lypophosphatidic Acid
4) Two more Fatty Acyl CoAs are added along the wan and then the Triacylglycerol is formed and stored in the Adipoctyre!!!

***Capillary Lipoprotein Liapse: Acts extracellularly and is present in the Capillaries and degrades the TG (VLDL and Chylomicron) to form Fatty Acids which are used by the Adipocytes and make TG

  • *The hormone INSULIN has a stimulatory effect on the Capillary lipoprotein Lipase which helps form the TG in the Adipocytes
    • Insulin also supports the Transport of Glucose through GLUT4 which leads to more TG
128
Q

Breakdown of TGs

A
  • HYDROLYSIS of Acylglycerols

3 Major Lipases:

1) Hormone Sensitive Lipase (HSL)
- Positively regulated by Glucagon, Epinephrine, and Norepinephrine
- Negatively regulated by Insulin

2) Lipoprotein Lipase
- Takes the Diacylglycerol and makes Monoacylglycerol and a Fatty Acid

3) Monoacylglycerol Lipase
- Takes the Monoacylglycerol and form Glycerol and a Fatty Acid

  • Release of Fatty Acids
  • Transport of Fatty Acids
    1) Short Chain Fatty Acids are SOLUBLE2) Long Chain complexed with ALBUMIN for Transport
129
Q

Mechanism of Hormone-Sensitive Lipase (HSL) Regulation

A
  • Key first step in TG DEGRADATION in Adipocytes
  • HSL ACTIVATED by PHOSPHORYLATION by PKA
  • PKA activated by GLUCAGON and EPINEPHRINE vis cAMP and the GCPR Signaling Cascade
  • HSL INACTIVATED by DEPHOSPHORYLATION by PROTEIN PHOSPHATASE 1 (PP1)
  • PP1 ACTIVATED by Insulin

Bottom Line:
- GLUCAGON (Secreted in response to hunger) and EPINEPHRINE (Secreted in response to Exercise) promote LIPOLYSIS in Adipocytes

  • INSULIN (Secreted in response to a High Carb Meal) INHIBITS LIPOLYSIS
130
Q

Perilipin

A
  • Family of proteins that coat lipid droplets in Adipocytes and Muscle Cells
  • Regulate Lipolysis by CONTROLLING Physical access to HSL
  • Humans have 5 members in the family
  • PERILIPIN 1 Overexpression INHIBITS Lipolysis and its KNOCK OUT have CONVERSE Effects
  • Regulated by PKA, Phosphorylation allows association with HSL and promotes Lipolysis
  • Target of OBESITY TREATMENT

***Perilipins can leave the surface of the molecule when it is Phosphorylated by PKA

131
Q

Synthetic Fats- Olestra

A
  • SYNTHETIC Fats made of Sucrose backbone with 6-8 Fatty Acids
  • Not ABSORBED in Small Intestine
  • Absorbs Vitamins A, D, E, and K
  • High amounts of OLESTRA cause DEFICIENCY in these Vitamins
  • Abdominal cramps, bloating, and Diarrhea
132
Q

Lipoproteins

A
  • Serve as transport vehicle for Cholesterol, TGs, and Fat Soluble Vitamins
  • Contribute to the METABOLISM of Lipids

Structure:
- OUTER SHELL: Monolayer of Phospholipids, free Cholesterol, and Apolipoproteins

  • INNER SHELL: Packed with Hydrophobic TGs, Cholesterol Esters
133
Q

Acyl CoA Acyl Transferase (ACAT)

A
  • Transfers a Fatty Acyl to a Cholesterol molecule to make CHOLESTEROL ESTER (Extremely HYDROPHOBIC and stored in LIPID DROPLETS)
134
Q

Lipoproteins

A
  • Five different Types
  • Differ based on Size, Density, and Composition
  • Various disorders arise due to Abnormalities in Synthesis and Processing

Different Types:

1) Chylomicrons
2) VLDL
3) IDL
4) LDL (Bad)
5) HDL (Good)

135
Q

Chylomicron

A
  • Exogenous
  • Formed from DIETARY FATS
  • Really big and the LEAST DENSE (High TG Content)

Chylomicron Properties:

  • Largest
  • Least Dense
  • High Triacylglycerol Content

Apo:

1) ApoB-48
2) ApoC-II
3) ApoE

136
Q

VLDL

A

Contains:

1) ApoB-100
2) ApoC-II
3) ApoE

137
Q

IDL

A

Contains:

1) ApoB-100
2) ApoE

  • Have comparative less TG and more Cholesterol Ester
138
Q

LDL

A

Contains:
1) ApoB-100

  • Heavily packed with CHOLESTEROL
139
Q

HDL “Good Cholesterol”

A

Contains:

1) ApoA-I
2) ApoC-II
3) ApoE

Properties:

  • Smallest
  • Most Dense
  • High PROTEIN and PHOSPHOLIPID Content

***Collect CHOLESTEROL from the PERIPHERY

140
Q

Lymphatic System

A
  • Lymph is a clear fluid- Recycled Plasma
  • Lymphatic system consists of lymph vessels and lymphoid tissue (Thymus, Bone Marrow, Lymph Nodes)
  • Plays an important role in DIGESTIVE and IMMUNE FUNCTIONS
  • Lymph circulation removes Interstitial fluid from tissues, transport RECONSTITUTED Lipids Chylomicrons from the Small Intestine and Transport Lymphocytes and Antigen Presenting Cells
  • Lymph nodes trap and destroy circulating cancer cells
  • When overwhelmed may help to spread cancer cells (Metastasis)
  • Swelling of Lymph nodes found in Infections and Cancer (non-Hodgkin Lymphoma)
141
Q

Apolipoprotein Functions

A

Three Main Functions:

1) STRUCTURAL (Stabilize Lipoproteins)
- Ex: Apo B in LDL, Apo A-1 in HDL, and Apo E in VLDL and some HDL

2) TRANSPORT (Redistribution of Lipids between Tissues)

3) COFACTORS for ENZYMES
- Ex: Activation of LPL by Apo-CII

142
Q

Type I (Familial Hyperchylomicronemia)

A

Cause:
- Deficiency in ApoC-II or defective Lipoprotein Lipase

Effects:

  • Increase in Chylomicrons
  • Increase in Triacylglycerol
143
Q

Type IIa and IIb (Familial Hypercholesterolemia)

A

Cause:
- LDL Receptor is completely (IIa) or partially defective (IIb)

Effects:

  • Increase in Cholesterol
  • Tryglycerol: IIa Normal
  • Tryglycerol: IIb Increase
  • Increase in LDL
  • Increase in VLDL (IIb)
144
Q

Type I Hyperlipoproteinemia

A
  • HYPERCHYLOMICRONEMIA
  • Inability to Hyrolyze TAGs in Chylomicrons and VLDL
  • Cause: either a DEFICIENCY in LIPOPROTEIN LIAPSE (LPL) or Apo C-II, an essential part of LPL Complex and necessary for activity
  • Primary LPL Deficiency: Manifests in INFANCY
  • Apo C-II Deficiency: POST-ADOLESCENCE
  • PLASMA TAG Levels > 100 mg/ dL
  • Creamy appearance of Blood Sample
  • Overnight at 4 Degrees C, the plasma separates into a Creamy Layer and a Clear Layer
  • BOTH AUTOSOMAL RECESSIVE
  • CLINICAL SYMPTOMS: Abdominal pain, Acute Pancreatitis, Cutaneous Eruptive Xanthomas
  • TREATMENT: Low Fat Diet
145
Q

Type II Hyperlipoproteinemia

A
  • HYPERCHOLESTEROLEMIA (FH)
  • CAUSE: Defects in UPTAKE of LDL via LDL RECEPTOR
  • Receptors mediated ENDOCYTOSIS contributes to 75% Clearance of LDL in Plasma
  • Defects causes increased Cholesterol in Blood and subsequent ATHEROSCLEROSIS
  • Over 1000 Mutations reported
  • Impaired ability to recognize ApoB 100 on LDL
  • AUTOSOMAL DOMINANT INHERITANCE
  • Normal Cholesterol: 130-200 mg/dL
  • Heterozygous: 300-500 mg/dL
  • Homozygous: >800 mg/dL
  • Untreated Homozygous die of CORONARY ARTERY DISEASE (CAD) before teenage years
  • Heterozygous Develop CAD by age 40
  • Physical Symptoms: Xanthomas, Arcus Senilis, or Corneal Deposits in eye, and Angina Pectoris
  • HETEROZYGOUS respond to diet, Statins, and Bile Acid Binding Resins
  • HOMOZYGOUS need LDL Aphaeresis and Liver transplantation
146
Q

Chylomicron Processing

A
  • Chylomicrons are formed in the Intestinal Cells (Nascent Chylomicrons)
  • They are released into the Lymphatic System and then into the Blood where they add ApoE and ApoC-II from HDL, and then they are considered Mature Chylomicrons. Then they are acted upon by the CAPILLARY LIPOPROTEIN LIPASE

***A Defect in CPL can cause Type I Hyperlipoprotenemia

147
Q

VLD, IDL, and LDL Processin

A

1) VDL turns into IDL by the Capillary Lipoprotein Lipase and also removes an ApoC-II
2) IDL turns into LDL by the Hepatic Lipoprotein Lipase and removes an ApoE
3) The LDL is either absorbed in the Liver or the Peripheral Tissue (Muscle) by the LDL Receptor

148
Q

HDL Processing

A
  • Made in the Liver and Small Intestine
  • Go from tissue to tissue and collect the CHOLESTEROL
  • They then add on the Apoproteins and form MATURE HDL
  • HDL gives CHOLESTEROLS to VLDL, IDL, and LDL!!!
149
Q

Integration of Lipoprotein Processing

A

**SLIDE 34 of Lipid Lecture!!!!!!

150
Q

Beneficial Effects of HDL

A
  • HDL Cholesterol levels correlate positively with reduced risk of CAD
  • Due to its ability to reverse Cholesterol Transport from Peripheral Tissue to Liver
  • ANTIOXIDANT and ANTI-INFLAMMATORY Properties
  • HDL Levels increased by Weight Loss, Exercise, Smoking Cessation, and Moderate Consumption of Alcohol
  • Antihypercholesteremic drugs, Fibrates, Niacin, Anti-diabetic Thiazolidine drugs, Estrogens, Omega-3 Fatty Acids, and Increase HDL-C
  • HDL levels low in Smoking, Progestins, Androgens, Beta Blockers, and High Intake of PUFA (Omega-6)
151
Q

Cholesterol-Lowering Drugs (Statins)

A
  • Statins mimic the structure of HMG CoA and Mevalonate (Substrate and product of HMG CoA Reductase)
  • Rate limiting Enzyme in Cholesterol Biosynthesis!!!!!
  • Potent COMPETITIVE INHIBITORS
  • Cholesterol levels fall
  • Enhances Transcription of LDL Receptor
  • More uptake into Hepatocytes, lowering of Plasma Levels

*****LOVASTATIN targets HMG- CoA REDUCTASE!!!!!

Cardiopulmonary I (12 decks)

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