I. BASIC SCIENCES

ANATOMY AND PHYSIOLOGY

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CARDIOVASCULAR

RESPIRATORY

CENTRAL NERVOUS SYSTEM

MUSCULOSKELETAL

ENDOCRINE

HEPATIC AND RENAL

HEMATOLOGIC

GASTROINTESTINAL

IMMUNE

QUESTIONS

QUESTIONS

QUESTIONS

QUESTIONS

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CARDIOVASCULAR

The cardiac cycle involves movement of blood through the heart and the body as a result of a series of pressure changes and muscle contractions within the heart.

The Cardiac Cycle

  • Sodium channels of cardiac muscle do not completely close. Rather, they constantly leak sodium inside the cell and excitation occurs by electrical stimulation. This repetitive discharge is described as rhythmicity. The usual resting membrane potential is -60 to -70 mV.
  • The closure of the aortic valve to the opening of the mitral valve on the left ventricular pressure-volume loop is the isovolumetric relaxation.
  • On the left ventricular pressure-volume loop, the period from the mitral valve closure to the opening of the aortic valve is the isovolumetric contraction.
  •  

Circulation

  • The heart, lungs, brain, kidneys, and liver are the highly perfused organs. This group receives about 75% of normal cardiac output even though it constitutes about 1/10th of the body mass.

The coronary arteries receive 5% of cardiac output.

  • In the presence of hypercarbia, pulmonary vascular resistance is INCREASED. This is noteworthy because this is the opposite of systemic and cerebral vasculature.
  • Cardiac output depends upon preload, afterload, contractility, left ventricular compliance, and heart rate.
    • Increases in HR and/or SV increases blood flow
    • Cardiac output decreases by 25% when a person experiences new-onset atrial fibrillation.
    • The most useful measure of coronary perfusion in the clinical setting is mean arterial pressure.

Myocardial Blood Flow and Oxygen Consumption

  • The resting oxygen consumption of the heart is 10 mL/100 g/min.
  • Coronary blood flow is the greatest during diastole.
  • The right ventricular coronary flow is sustained throughout both systole and diastole. However, the left ventricular coronary flow is briefly halted during systole because of compression.
  • Subendocardium is exposed to the highest left ventricular end diastolic pressure, specifically at peak systole.
  • The metabolite- adenosine- causes the greatest degree of vasodilation in cardiac cells of any substance.
  • Myocardial oxygen demand:
    • Heart rate (greatest effect)
    •  Preload
    •  Afterload
    • Contractility
  • Events leading to myocardial ischemia due to supply issues:
    • Increase in ventricular compliance
    • Eccentric hypertrophy
        •  
  • Alpha-1 and beta-2 receptors are dispersed throughout the heart. Alpha-1 is responsible for vasoconstriction and beta-2 is vasodilation.
  • Myocardial preconditioning is when the heart is subjected to an ischemic insult and allows the heart to better handle future events that are more severe in nature.
    • Volatile anesthetics, adenosine, and opioids mimic this.
    • Ketamine is antagonistic.
      •  

Conduction pathway through the heart

  1. Sinoatrial node is the pacemaker (60 – 100 bpm)
  2. Internodal tracts
    • Atrioventricular node
    • Bachmann’s bundle to left atrium
  1.  
  2. Atrioventricular node (40 – 60 bpm)
  3. Bundle of His
  4. Bundle branches
  5. Purkinje fibers (20 – 40 bpm)
  6. Ventricular muscle

The QRS complex correlates with atrial repolarization in the cardiac electrical conduction.

  • Right and left ventricular contractions are coordinated by the Purkinje fibers.

 

  • An S3 heart sound (gallop rhythm)
    • Occurs during mid-diastole
    • CHF
    • Reflects a flaccid/inelastic diastolic condition
    • Oscillation of blood between the ventricular walls caused by blood from the atria rushing in.

 

  • The slowest conduction of the heart is through the AV node.
  • The fastest conduction of the heart is through the Purkinje fibers.

 

  • Intrinsic firing rates
    • SA node- 60-100
    • AV node- 40-60
    • Ventricles/Purkinje fibers- 20-40
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Action Potentials and Ions

Ventricular action potential

    • Depolarization caused by an influx of sodium
    • Repolarized by Na+-K+ pump
    • Phase 0- sodium influx
    • Phase 2- calcium influx (calcium channel blockers)
    • Phase 3- potassium efflux
    • Phase 4- Na+-K+ pump

 

Sinoatrial node action potential

    • Calcium influx causes depolarization
    • Heart rate is effected by controlling phase 4; slowing phase 4 causes a lower heart rate and vice versa
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  • A change in membrane potential from -70 mV to 0 is called depolarization.
  • CALCIUM causes relaxation of the cardiac muscle during diastole. Calcium in leads to contraction. Calcium out leads to diastole.

When intracellular calcium reaches a certain point in the plateau phase, potassium exits the cell after the K+ channel opens. This causes the cell to repolarize. Until this point, the gated Na+ channel is in an absolute refractory period.

Once repolarization is complete, the gated Na+ channel returns to its original form. Therefore, intracellular calcium determines the length of the cardiac cycle.

  • The normal resting potential of the ventricular cell is largely the result of the extracellular movement of potassium.
    • The movement of K+ out of the cell and down its concentration gradient results in a net loss of positive charge from inside the cell. An electrical potential is established across the membrane with the inside of the cell being negative because anions do not accompany the K+.
  • During depolarization of the ventricular cell, activation of the slow calcium channels occurs during phase 2.
    • Contraction of the cardiac myocyte occurs when intracellular calcium levels rise and the calcium binds to troponin C.
  • Calcium entering the cell increases the duration of action in cardiac muscle relaxation.

 

Preload

Afterload

Contractility

Determined by:

Volume

Pressure

Chemical

Measured by:

CVP

SVR

Stroke volume

 

Blood Pressure Control

  • When the carotid sinus (more important) and aortic arch stretch from increased arterial blood pressure, afferent action potentials increase in the glossopharyngeal nerve (carotid) and the vagus nerve (aortic arch). Signals are then transmitted back to the heart via the efferents of the vagus nerve causing:
    • Decreases heart rate and cardiac output
    • Decreased sympathetic activity in the nerves of the ventricles and systemic vasculature
      • Less sympathetic activity leads to decreases in:
        • contractility
        • stroke volume
        • cardiac output
  • This leads to:
    • venodilation
    • decreased preload
    • decreased SVR
  • Stretching the carotid sinus leads to increased afferent action potentials to Hering’s nerve. This is known as baroreceptor reflex.
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  • Coronary perfusion pressure (CorPP) = aortic diastolic pressure (AoDP) – left ventricular end-diastolic pressure (LVEDP).

       AoDP – LVEDP = CorPP

  • LVEDP is estimated by the PCWP.

       CorPP = AoDP – PCWP

  • If the aortic diastolic pressure increases OR if the PCWP decreases, the coronary perfusion pressure will increase.
    • Pulmonary capillary wedge pressure (PCWP) assesses the left ventricular end-diastolic pressure.
  • Diastolic function of the left ventricle is assessed by examining left ventricular compliance. The best indicator of diastolic dysfunction is a decrease in left ventricular compliance.

 

  • The two determinants of pulse pressure:
    • arterial compliance
    • stroke volume
  • Hypotension following spinal anesthesia is due to sympathetic preganglionic blockade.

Coronary Blood Flow

  • The subendocardium of the left ventricle has the most capillaries.
  • After perfusing the myocardium, most of the blood returns to the right atrium via the coronary sinus. Lesser amounts of blood also return via the anterior cardiac veins and the Thebesian veins.

 

  • Because it is subjected to the greatest intramural pressures during systole, the endocardium tends to be most vulnerable to ischemia during decreases in coronary perfusion pressure.

 

  • Factors causing an increase in cardiac oxygen consumption:
    • Heart rate> afterload > preload

 

  • Increases in heart rate are likely to increase oxygen consumption more than increases in blood pressure (afterload). Increasing venous return (increasing preload) increases oxygen consumption less than increases in either heart rate or afterload. Increasing preload is the least costly means of increasing cardiac output.

 

  • The mixed venous oxygen tension (or saturation) is the best measurement for determining adequacy of cardiac output.
    • A decrease in mixed venous oxygen saturation in response to increased demand usually reflects inadequate tissue perfusion. Thus, in the absence of hypoxia or severe anemia, the mixed venous oxygen tension (or saturation) is the best measurement for detecting adequacy of cardiac output.

ALPHA-1

ALPHA-2

BETA-1

BETA-2

Vasoconstriction

Inhibition of norepinephrine release

Tachycardia

Vasodilation

Increased peripheral resistance

Inhibition of acetylcholine release

Increased lipolysis

Slightly decreased peripheral resistance

Increased blood pressure

Inhibition of insulin release

Increased myocardial contractility

Bronchodilation

Mydriasis

 

Increased release of renin

Increased muscle and liver glycogenolysis

Increased closure of bladder internal sphincter

 

 

Increased release of glucagon

 

 

 

Relaxed uterine smooth muscle

  • Beta-Adrenergic receptors are responsible for:
    • mediating activation of the cardiovascular system
    • vascular and respiratory smooth muscle relaxation
    • renin secretion by the kidneys
    • metabolic functions
      • lipolysis
      • glycogenolysis
      • insulin secretion
  • Beta1-Adrenergic receptors primarily mediate cardiac effects
    • heart rate
    • contractility
    • conduction velocity
    • release of fatty acids from adipose tissue
  • Beta2-receptors primarily mediate:
    • vascular smooth muscle tone
    • airway smooth muscle tone
    • uterine smooth muscle tone
    • glycogenolysis
  • Alpha-Adrenergic receptors mediate intestinal and urinary bladder-sphincter tone.
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RESPIRATORY

The respiratory system extracts oxygen from atmospheric air and delivers it to the cells of the body  while simultaneously removing  carbon dioxide waste. This is accomplished through respiration and gas exchange between alveoli and capillaries.

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Anatomy and Physiology

  • The recurrent laryngeal nerve, which is a branch of the vagus, provides sensation below the cords.

 

  • The internal branch of the superior laryngeal nerve, which also is a branch of the vagus, provides sensations above the cords.

 

  • Superior laryngeal nerve stimulation can cause laryngospasm.

 

  • The cricothyroids are the muscles involved in laryngospasm.
    • adduct and tense the true vocal cords
  • Laryngospasm is mediated by the external branch of the superior laryngeal nerve.
    • The external branch of superior laryngeal nerve provides motor innervation to the cricothyroid muscle.
  • The posterior cricoarytenoids abduct (open) the cords.
  • Dead Space is the tidal volume portion that does not participate in gas exchange.
    • Increased with:
      • Age
      • Positive-pressure ventilation
      • PE
      • Respiratory disease or compromise
  • Anatomic dead space is the volume of air in the conducting airways.
      • 2 mL/kg in adult
  • Alveolar dead space is the air that enters the poorly perfused alveoli.

 

  • Physiologic dead space = anatomic dead space + alveolar dead space

 

  • Alveolar dead space = physiologic dead space – anatomic dead space

 

  • Minute ventilation (MV) = tidal volume (VT) + respiratory rate (RR)

 

  • KEY- Increasing the respiratory rate increases DEAD SPACE as well as minute ventilation.
    • An increase in VT only increases minute ventilation.
  • Increased alveolar ventilation = Increased PAO2.
      • Increased alveolar ventilation = decreased PACO2 
        • inverse relationship 
        • doubling of alveolar ventilation will decrease PACO2 by half.
  • Compliance is the change in volume that occurs in response to a change in pressure.

 

  • Resistance is the change in pressure along a tube divided by flow.

 

  • Surfactant is a substance secreted by type II alveolar epithelial cells that decrease surface tension. This reduces the work of breathing and increases pulmonary compliance.

 

  • Functional reserve capacity = expiratory reserve volume + residual volume
    • FRC is the amount of air left in the lungs after a normal exhalation.
    • The chest wall normally wants to pull itself outward while the lungs want to retract inward.
  • When the chest and lungs recoil are equal, this is also FRC.

 

  • Intrapleural pressure is never positive.
    • Negative to start inspiration, becomes more negative during the breath.
    • During exhalation, the pressure becomes less negative.
    • Intrapleural pressure is the least negative at:
      • Lung bases
      • Dependent lung
    • Intrapleural pressure is the most negative at:
      • Lung apices
      • Nondependent lung

Pulmonary Blood Flow

  • The lungs blood supply is delivered by the:
    • Bronchial arteries
      • 1 on right; 2 on left
      • Do not participate in fresh gas exchange
      • Follow the bronchial divisions down to the respiratory bronchioles
    • Pulmonary arteries
      • Bring unoxygenated blood to the lungs from the right ventricle
      • Provides blood flow past the terminal bronchioles

 

  • Pulmonary vascular resistance is 1/8th that of systemic vascular resistance.

 

    • PVR is increased by:
      • Hypoxia
      • hypercapnia
      • norepinephrine
      • histamine

 

    • PVR is decreased by:
      • Acetylcholine
      • phosphodiesterase type 5 inhibitors

 

  • Dual lung ventilation:
    • In the left lateral position, the dependent lung receives 65% of blood flow and the nondependent lung receives 35%.
    • In the right lateral position, the dependent lung receives 55% and the nondependent lung receives 45%.
    • The nondependent lung averages 60% blood flow.
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Hypoxic Pulmonary Vasoconstriction

  • Pulmonary vessels vasodilate in the presence of increased oxygen and decreased carbon dioxide. This is the opposite for systemic circulation.
    • Important because areas with a high oxygen content receive more blood and are able to oxygenate more.
    • Hypoxic areas become vasoconstricted and preferentially divert oxygen away.
  • Hypoxic pulmonary vasoconstriction is initiated in less than 1 minute.
  • On average, the dependent lung receives 60% of blood flow. Once one-lung ventilation is initiated, a shunt develops and alveolar hypoxemia triggers hypoxic pulmonary vasoconstriction.
    • Diverts half of the blood from the nondependent lung to the dependent lung resulting in 80% of the total blood flow.
  • HPV is initiated by alveolar hypoxemia.
    • Purpose is to divert shunted blood towards the better ventilated lung or part of lung.
    • Conditions that oppose HPV are:
      • alkalosis/hypocapnia
      • high Vt or PEEP
      • hypervolemia (LAP > 25 mm Hg
      • atrial natriuretic peptide)
      • hypothermia
      • drugs
        • nitroglycerin
        • nitroprusside
        • dopamine
        • nifedipine
  • Chemoreceptor agonists, like Almitrine, augment HPV.
        •  
  • Vital capacity = 60 mL/kg

 

  • Carbon dioxide tension will most accurately assess alveolar ventilation.

 

  • Gravity is the main reason for increase in blood distribution to dependent lung.

 

  • The carotid and aortic bodies are most sensitive to a PaCO2 < 50 mm Hg.

 

  • Central chemoreceptors are most sensitive to increased PaCO2.

 

  • Hypercapnia can be caused by:
    • increased dead space ventilation
    • opioids
    • malignant hyperthermia
  • The most important ion to alveolar ventilation regulation is carbon dioxide.

 

  • Mixed venous oxygen content is determined by oxygen delivery and oxygen consumption.

 

  • The PO2 is 50 mm Hg when the hemoglobin oxygen saturation is 80%.

 

  • A saturated gram of hemoglobin will contain 1.34 mL of oxygen.

 

  • The normal partial pressure of oxygen when the hemoglobin is 50% saturated is 26 mm Hg.

 

  • A normal bicarbonate value EXCLUDES carbon dioxide retention.

 

  • Upper end of the Pa02 ventilatory drive is 60 mm Hg.

 

  • Hypoxic pulmonary vasoconstriction is most evident during one-lung ventilation.
    • In response to alveolar hypoxia, as well as low oxygen concentration in pulmonary venous blood, pulmonary arteries will vasoconstrict. This helps to:
      • Maintain V/Q matching
      • Preserve PaO2.
  • The larynx serves to protect the airway and aid in respiration and phonation.

 

  • Valsalva maneuver increases pleural pressure the greatest amount.

 

  • Vagus nerve triggers the Hering-Breuer reflex.

 

  • 34 mL of CO2 is dissolved in blood if the PaCO2 is 35 mm Hg (in mL CO2/100 mL).
  • Upright (3 zones) Arterial -Pa  Alveolar -PA  Venous -PV
    • Zone 1: PA > Pa > PV
      • Alveolar pressure exceeds arterial pressure so the collapsible vessels are held closed with no blood flow.
    • Zone 2: Pa > PA > PV
      • Arterial pressure exceeds alveolar pressure but alveolar pressure exceeds venous pressure. Therefore, a constriction occurs downstream to each collapsible vessel, and the pressure inside the vessel is equal to the alveolar pressure. Meaning, the pressure gradient causing flow is arterial-alveolar.
      • Blood flow increases linearly with distance down the lung.
    • Zone 3: Pa > PV > PA
      • Venous pressure exceeds alveolar pressure and collapsible vessels are held open. The pressure gradient is arteriovenous, and there is constant perfusion of alveoli.
      • Lung perfusion depends on gravity related to the level of the heart.
      • In a spontaneously breathing, upright patient, perfusion increases from apex to base. Due to downward traction from gravity, negative pleural pressure is greatest at the apex and this keeps alveoli distended.
      • Most of the tidal volume breath is distributed to the dependent alveoli.
    • Zone 4: PA > PISF > PV > Pa
      • Gravitational compression of the lung parenchyma or interstitial edema fluid causes a decrease in blood flow.

 

  • Awake Lateral
    • More of the tidal volume fills the dependent lung because of diaphragm contraction and displacement in this position.
    • Perfusion is greater in the dependent lung as well, so the relationship between ventilation and perfusion is unchanged.

 

  • Anesthetized lateral position, chest closed, with spontaneous ventilation
    • FRC decreases due to:
      • Induction of anesthesia
      • Mediastinum weight
      • Abdominal contents displacing the diaphragm cephalad
    • Lungs are less compliant when at a very high volume (distended alveoli) or a very low volume (atelectasis).
    • There is an overall net loss of FRC in this situation; however, the nondependent lung slightly increases FRC.
    • Ventilation is preferentially distributed to the nondependent lung, whereas gravity-dependent blood flow preferentially goes to the dependent lung = V/Q mismatch.

 

  • Anesthetized, paralyzed, mechanically ventilated
    • FRC further declines because the diaphragm does not contribute to the lower lung ventilation.
    • V/Q mismatch worsens.
    • PEEP may help restore FRC and improve V/Q ratio.

 

  • Anesthetized, open chest
    • Resistance to gas flow is released in the nondependent lung. This leads to further preference for the nondependent lung.
    • Even spontaneous respiration becomes very inefficient.
    • This patient grouping exhibits significant regional areas of V/Q mismatching.

Respiratory / Cranial Interplay

  • Cranial nerve IX- glossopharyngeal– is responsible for the transfer of afferent information from the carotid bodies.
  • Cranial nerve X- vagus– transmits afferent information from the aortic bodies and lung stretch receptors.

 

  • Pulmonary vascular congestion or an increase in pulmonary interstitial fluid volume stimulates the Juxtapulmonary-capillary (or J) receptors. This will lead to tachypnea.
    • These receptors are involved in the dyspnea encountered with pulmonary vascular congestion and left ventricular failure-related edema.
    • C-fibers innervate the pulmonary J receptors. The c-fibers are slow-conducting nonmyelinated fibers of the vagus. This pathway is afferent from the J receptors.

 

  • Chronic smoking makes the ETCO2 and PaCO2 gradient larger because of the ventilation: perfusion mismatch.
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Central Nervous System

Neurophysiology

Anatomy and Physiology

  • Mean arterial pressure minus intracranial pressure (ICP)- or CVP if greater- equals cerebral perfusion pressure (CPP).
    • MAP – ICP (or CVP if greater than ICP) = CPP
  • The brain can autoregulate blood flow within a wide range of blood pressures.
    • With chronic hypertension, the autoregulation curve is shifted to the right. Also, the upper and lower limits are shifted.
  • PaCO2 has the most influence on cerebral blood flow.
    • CBF is directly proportional to PaCO2 between 20-80 mm Hg.
  • The blood-brain barrier (BBB) allows lipid-soluble substances through but not those that are ionized or larger in size.
    • CO2 and O2 freely pass the BBB, but proteins, large substances, and ions do not.
  • Situations in which the BBB can be altered and movement of substances across it is dependent on hydrostatic pressure:
    • severe hypertension
    • tumors
    • trauma
    • CVA
    • infection
    • very high PaCO2
    • very low PaO2
    • seizures

 

  • Ketamine is the only intravenous anesthetic that has any substantive effect on CMR and/or CBF

 

  • Vasopressors increase CBF only when mean arterial blood pressure is below 50- 60 mm Hg or above 150-160 mm Hg.

Anterior  pituitary

Negative-feedback

Adenohypophysis

ACTH, TSH, GH, prolactin, LH, FSH, and prolactin

Posterior pituitary

Neural control

Neurohypophysis

ADH and oxytocin

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  • Adenohypophysis, or anterior pituitary, releases adrenocorticotropic hormone and is controlled by negative feedback.
    • Serum cortisol inhibits the release of ACTH from the anterior pituitary.
  • Stimuli that may trigger antidiuretic hormone (ADH) release from the posterior pituitary:
    • histamine
    • positive-pressure ventilation
    • pain
    • stress
    • hypoxia
  • The facial bone that houses the pituitary gland is the sphenoid.
  • The basilar artery supplies the vertebral arteries
  • Ligamentum flavum is immediately posterior to the epidural space.

Circle of Willis

Cerebral collateral blood flow

Great radicular artery

Major source of blood supply to lower spinal cord

3rd and 4th choroid plexuses

Cerebrospinal fluid formation

Arachnoid villi

Cerebrospinal fluid reabsorption

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Cranial Nerve

Function

Composition

I

Olfactory

Smell

Sensory

II

Optic

Vision

Sensory

III

Oculomotor

Eye muscles

Motor

IV

Trochlear

Superior oblique eye muscle

Motor

V

Trigeminal

Sensory from face and mouth; motor for chewing (mastication)

Both

VI

Abducens

Lateral rectus eye muscle

Motor

VII

Facial

Facial expression muscles; lacrimal and salivary glands

Both

VIII

Auditory

Equilibrium and hearing

Sensory

IX

Glossopharyngeal

Pharyngeal swallowing, posterior 1/3 tongue, and parotid salivary gland

Both

X

Vagus

Visceral organ sensations and parasympathetic motor regulation

Both

XI

Accessory (Spinal)

Head, neck, and shoulders muscles

Motor

XII

Hypoglossal

Tongue muscles

Motor

  • Cranial nerve III (oculomotor) controls the medial rectus muscle of the eye.

 

  • The glossopharyngeal cranial nerve is responsible for carotid body and carotid sinus afferents.

 

  • The mandibular nerve has motor and sensory innervation and is a branch of Cranial nerve V (Facial).

 

  • Spinal nerves
    • Afferent-sensory-enter dorsal (posterior) side
    • Efferent-motor-exit ventral (anterior) side

 

  • The xiphoid is the anatomic feature that resides in sensory dermatome T6.
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Musculoskeletal

Anatomy and Physiology

  • Skeletal muscle contains:
    • actin
    • myosin
    • troponin
  • Calcium combines with troponin in skeletal or cardiac muscle to initiate contraction.
    • The primary signaling chemical is acetylcholine, whose formation is catalyzed by choline acetyltransferase from acetyl coenzyme A and choline.
  • Acetylcholine is stored in vesicles that reside either in the active zone or away from the active zone in a reserve pool.

 

  • The process of acetylcholine mobilization and release utilizes calcium signaling; therefore, any impediment to that signaling can cause weakness. Examples:
    • Hypocalcemia and hypermagnesemia
    • Eaton-Lambert syndrome- antibodies against calcium channels
  • Acetylcholinesterase hydrolyzes acetylcholine into choline and acetic acid. Choline then reenters the presynaptic nerve terminal to be reused.
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Actin and Myosin

All skeletal muscles are composed of numerous fibers ranging from 10-80 micrometers in diameter.

  • The sarcolemma is the cell membrane of the muscle fiber. At each end of the muscle fiber is a tendon fiber, which collects to form the muscle tendons that insert into bones.
  • Sarcomere is the repeating unit or building block in striated muscles. The sarcomere is a part of the myofibril is from Z-line to Z-line.
  • Each muscle fiber contains several hundred myofibrils. Each myofibril is composed of about 1500 adjacent myosin filaments and 3000 actin filaments. These actin and myosin filaments are protein molecules that are responsible for muscle contraction.
  • Light bands only contain actin and are called I bands.
  • The dark bands are called A bands and only contain myosin.
  • Z disc passes across the myofibril and from myofibril to myofibril which connects them down the muscle fiber. The Z disc is made up of proteins that are filamentous.
  • The side-by-side relationship of actin and myosin is maintained by titin, which is a large protein molecule.
  • Muscle contraction steps:
    1. Action potential moves from the motor nerve to the muscle fiber endings.
    2. Here at the muscle fiber endings, large amounts of acetylcholine are secreted.
    3. The neurotransmitter, acetylcholine, opens channels to allow sodium ions to enter and initiate an action potential.
    4. The action potential depolarizes the muscle and causes a large release of calcium.
    5. The calcium ions are responsible for the actin and myosin attraction. These filaments slide alongside each other (contractile process).
    6. Then, the muscle contraction will cease once calcium ions are pumped into the sarcoplasmic reticulum.
  • Muscular movement is produced by the actin filaments (molecular tracks) and the myosin molecules (ATP-driven motors).
  • When the sarcomere is relaxed, the actin filament endings barely reach past the Z discs on each side. However, during contraction, the actin filaments are pulled in toward the myosin filaments to the max they can overlap. The muscle contraction is termed a sliding filament mechanism.
  • Skeletal muscles fibers contain cross-striated myofibrils.
  • Cardiac muscle is also cross-striated but the cardiomyocytes are positioned more irregularly and shorter.
  • Smooth muscle is similar to skeletal muscle in that that both contain actin and myosin filaments and contract. However, smooth muscle contracts over a large range compared to skeletal muscle and the actin and myosin filaments are not regularly organized into sarcomeres.
  • Normally, an actin filament binds quickly and intensely with myosin molecules. However, two components of the actin filament have an inhibitory effect on the binding/contraction of actin and myosin filaments. These proteins in the actin filament are tropomyosin and troponin.
    • If the tropomyosin-troponin complex is inhibited, the actin and myosin filaments can interact and cause a contraction.
    • Calcium causes a change in the troponin-tropomyosin complex and exposes the active sites.

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Endocrine

Anatomy and Physiology

  • The pancreatic duct and common bile duct unite to form the sphincter of Oddi, which empties into the duodenum.
    • The sphincter of Oddi is the muscular valve surrounding the common bile duct and pancreatic duct into the duodenum.
  • The sphincter of Oddi has three main functions:
    • regulation of bile flow into the duodenum
    • prevention of reflux into the bile or pancreatic duct
    • promotion of gallbladder filling in between digestive cycles
  • Insulin and glucagon are secreted by the islets of Langerhans.
    • Insulin is secreted by beta cells
    • glucagon is secreted by alpha cells
  • Insulin is produced in the beta cells of the pancreatic islets (of Langerhans), as you know.
    • Venous blood from the pancreatic islets drains into the hepatic portal vein, via the pancreatic vein, and then into the general circulation.
  • Adults normally secrete approximately 50 U of insulin each day from the beta cells of the islets of Langerhans in the pancreas.

 

  • Glycogen is a readily available source of glucose that does not contribute to intracellular osmolality.
    • Only the liver and muscle can store significant amounts of glycogen.
    • Insulin enhances glycogen synthesis.
  • Insulin has anabolic effects:  
    • promoting glycogenesis
    • increasing cholesterol synthesis
    • increasing protein synthesis
    • promoting glycolysis
    • promoting triglyceride storage
  • Insulin also has anticatabolic effects:
    • inhibiting glycogenolysis
    • inhibiting ketogenesis
    • inhibiting gluconeogenesis
  • Glucocorticoids, catecholamines, glucagon and thyroid hormone greatly enhance gluconeogenesis, whereas insulin inhibits it.

 

  • Somatostatin is produced by delta cells of the islet cells of the pancreas.
    • Somatostatin inhibits gastrointestinal motility and secretions including secretion of hydrochloric acid (HCl) by the stomach.
  • The islets cells include:
    • alpha cells
    • beta cells
    • delta cells
    • epsilon cells
    • pancreatic polypeptide (PP) cells
  • Each cell releases a specific hormone in response to signals.

ALPHA – GLUCAGON

BETA – INSULIN

DELTA – SOMATOSTATIN

EPSILON – GHRELIN (stimulates appetite, increases fat storage, and stimulates Growth hormone)

PP CELLS – PANCREATIC POLYPEPTIDE (decrease gastric acid secretion, gastric emptying, and upper intestinal motility)

Parathyroid

  • Parathyroid gland function and PTH secretion are inhibited by chronic and severe hypomagnesemia.

 

  • PTH secretion is also reduced with hypercalcemia. This can occur with:
    • Paget’s disease
    • malignancy
    • chronic immobility
  • Parathyroid hormone is the principal regulator of calcium homeostasis.
  • PTH increases serum calcium by:
    • promoting bone resorption
    • limiting renal excretion
    • enhancing GI absorption
  • The four parathyroid glands contain chief cells.
    • Chief cells secrete parathyroid hormone (PTH) and are located immediately behind the thyroid gland.
  • Parathormone regulates calcium and phosphate.
    • Hypocalcemia produces a rapid increase in PTH secretion from the parathyroid glands.
    • Hypocalcemia causes parathormone to increase serum calcium concentrations.
    • Hyperphosphatemia also stimulates parathormone secretion.
    • Hypomagnesemia inhibits parathormone secretion.
  • Parathyroid hormone controls extracellular calcium and phosphate levels by:
    • regulation of intestinal reabsorption
    • renal excretion
    • exchange between the extracellular fluid and bone
  • Release of PTH leads to increased calcium levels and a decrease in phosphate levels.
    • This is accomplished in two ways:
      • osteocytes initially
      • osteoclasts later
  • The thyroid hormones are:
    • triiodothyronine (T3)
    • thyroxine (T4)
    • calcitonin
    • thyroid-stimulating hormones
  • Osteoblasts deposit calcium by transporting calcium and phosphate into bone.
  • Osteoclasts release calcium from bone.
  • Secretion of parathyroid hormone results in increased calcium.
  • Calcitonin works inversely with PTH to lower serum calcium and increases calcium excretion.

Thyroid

Pituitary

  • Also known as the hypophysis
  • Master endocrine gland located in the center of the brain; more specifically, it is enclosed within a bone cavity of the sphenoid called the sella turcica.
  • The Pituitary stalk connects the pituitary to the hypothalamus

 

  • Hypothalamus helps to regulate the pituitary
    • Gathers signals related to pain, emotions, water, energy, etc. to help the pituitary
    • Hormones are also regulated by a negative-feedback loop
  • The pituitary has 2 parts:
    • Anterior lobe (adenohypophysis)
    • Posterior lobe (neurohypophysis)
  • Neuronal cells, called osmoreceptors, are excited by small increases in ECF osmolarity.
    • These cells send nerve signals to control their firing and secretion of ADH.  
  • Other stimuli that increase ADH secretion:
    • decreased arterial pressure
    • decreased blood volume
    • Nausea (potent stimulus for ADH release, which may increase to as much as 100 times normal after vomiting)
    • drugs such as nicotine and morphine 
  • Growth hormone is synthesized and secreted by cells in the anterior pituitary and is under dual control from the hypothalamus.
    • Growth hormone releasing hormone stimulates growth hormone release.
    • Growth hormone inhibiting hormone (somatostatin) is a powerful inhibitor of growth hormone release.
  • The posterior pituitary secretes antidiuretic hormone (ADH, vasopressin) and oxytocin.
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Adrenal Gland

  • Stimulation of the adrenal medulla results in release of the catecholamines- epinephrine (80%) and norepinephrine (20%).
    • Stimulation results from stress (anesthesia, surgery, hypoglycemia, etc.).
  • The adrenal medulla is innervated by preganglionic cholinergic fibers of the sympathetic nervous system. Therefore, acetylcholine would be the stimulus.

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Hepatic and Renal

HEPATIC

Anatomy and Physiology

  • The liver is a major reservoir of blood, holding up to 500 mL.
  • The hepatic artery provides 50% of the liver’s oxygen supply.
  • The hepatic portal vein receives 75% of the liver’s blood flow.
  • The hepatic portal vein is formed by the splenic and superior mesenteric veins.
  • Liver disease is best determined by the lab values PT and albumin.

 

  •  Functions:
    • Blood storage and filtration
    • Carbohydrate, fat, and protein metabolism
    • Bile secretion
    • Vitamin storage
    • Blood coagulation
    • Iron storage
    • Detoxification and excretion of drugs
  • Protein metabolism role:
    • Produces most proteins
    • Lipoprotein synthesis
    • Conversion of amino acids to carbohydrates and fatty acids for ATP
    • Produces urea to remove ammonia
  • The liver synthesizes many of the clotting factors necessary to form clots and prevent hemorrhage after trauma.

 

  • The following are NOT synthesized in the liver:
    • III (Tissue factor or thromboplastin) is from vascular wall and extravascular cell membranes.
    • IV (Calcium) is synthesized from diet.
    • VIII:vWF (Von Willebrand) is synthesized from endothelial cells.

RENAL

Anatomy and Physiology

The distal convoluted tubule comes into very close contact with the afferent glomerular arteriole, and the modified cells of each form the juxtaglomerular apparatus, a complex physiologic feedback control mechanism contributing in part to the precise control of intra- and extrarenal hemodynamics that is a hallmark feature of the normally functioning kidney.

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  • The kidney functions include:
    • waste filtration
    • endocrine and exocrine activities
    • immune and metabolic functions
    • maintenance of physiologic homeostasis
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  • Even though the kidneys are < 0.5% of total body weight, they receive 25% of the total cardiac output.
  • The kidneys are also responsible for tight electrolyte control.
  • Urine production occurs as water and solute pass through the glomerulus from the afferent arteriole.
  • Glomerular filtration rate (GFR) is the volume of fluid that is filtered from the renal glomerular capillaries per minute.
    • Flow to the glomerulus is effected by:
      • glomerular capillary pressure
      • glomerular oncotic pressure
  • Arterial tone coming to the kidney (afferent) and leaving the kidney (efferent) have direct effects on filtration pressure which alters glomerular flow.
  • An increase in afferent tone and/or a decrease in efferent tone will decrease filtration pressure and leads to a lower GFR.
  • A decrease in afferent tone and/or an increase in efferent tone increases the GFR because of increases glomerular flow.
  • Renal blood flow (RBF) and glomerular filtration is autoregulated and protects the glomerulus from excessive pressures.
  • There are two proposed mechanisms involved in autoregulation and both involve the afferent tone:
    • Myogenic reflex theory
      • Increase in systemic blood pressure causes the afferent arteriole to constrict reflexively.
    • Tubuloglomerular feedback
      • As RBF falls, there is a decrease in chloride that is delivered, specifically the juxtaglomerular apparatus. This induces afferent arteriole dilation. Due to this, glomerular flow and pressure then increase, and GFR returns to normal.
      • The efferent arteriole also plays a role in this mechanism. The decrease in chloride triggers a release of renin and formation of angiotensin II. This causes the efferent arteriole to constrict and increase glomerular pressure.

AUTOREGULATION OF URINE OUTPUT DOES NOT OCCUR… BUT THERE IS A LINEAR RELATIONSHIP BETWEEN A MEAN ARTERIAL PRESSURE OF 50 mm Hg AND URINE OUTPUT.

  • According to Barash, RBF autoregulation occurs between systolic blood pressures of 80-200 mm Hg.
  • Flow through the kidney
    • Blood via the afferent arteriole enters the glomerulus capillary tuft and interact with the Bowman’s capsule so that plasma waste products are filtered from the blood. The blood then exits Bowman’s capsule through the glomerular capillaries and merges with the efferent arteriole and peritubular capillaries.

NOTEWORTHY: VASA RECTA ARE THE PERITUBULAR CAPILLARIES THAT DIVE DEEP INTO THE MEDULLA TO RUN PARALLEL WITH THE LOOP OF HENLE. THE VASA RECTA ARE STRAIGHT ARTERIOLES THAT DESCEND INTO THE MEDULLA AND ASCEND INTO THE CORTEX AS STRAIGHT VENULES.

  • Urine flow
    • 20% of the plasma that enters the Bowman’s capsule is filtered through the capillary walls. The filtered plasma leaves Bowman’s capsule for the proximal convoluted tubule (PCT). PCT delivers the plasma/urine to the descending loop of Henle, travels through the ascending loop of Henle, and distal convoluted tubule (DCT). The final destination in the kidneys is the collecting ducts and then the urine makes its way to the ureters.
    • The medullary thick ascending limb of the loop of Henle has a high oxygen consumption because of metabolic activity. This portion of the nephron (inner stripe of the outer zone of the medulla) is most at risk during periods of hypotension.
  • The nephron is the functional unit of the kidney.
  • There are 2 types:
    • Cortical– short loops of Henle, superficial
    • Juxtamedullary– long loops of Henle, deep
  • Processes of the nephron:
    • Glomerular filtration
    • Tubular reabsorption
    • Tubular secretion
  • The kidneys correct hypoxia by stimulating red blood cell production.
  • Kidneys:
    • regulate extracellular fluid amount and composition
    • aid in blood pressure management
    • excretion of metabolic waste
    • have endocrine functions (erythropoietin, renin-angiotensin-aldosterone, and vitamin D)
  • Sodium contributes to 90% of the extracellular fluid osmolality.
  • Potassium is regulated by reabsorption and secretion in different parts of the kidneys, specifically the proximal tubule, Loop of Henle, distal tubule, and collecting tubule.
  • Bicarbonate is regulated in the same areas as potassium except the Loop of Henle.
  • Glomerular filtration rate will increase by:
    • Efferent arteriole constricts more than the afferent
    • Afferent arteriole dilates more than the efferent
  • Afferent arterioles play a major role in the autoregulation of renal blood flow. Blood is delivered via afferent arterioles and exits via efferent arterioles.
  • Atrial natriuretic factor is one of the most potent diuretics and is a renal hormone. It also decreases antidiuretic hormone secretion.
  • Aldosterone is a major regulator of extracellular potassium.
  • Renin is released from juxtaglomerular cells. The kidney’s response to a decreased glomerular filtration rate is renin.
  • Kidneys are regulated by sodium.
    • The expected response to hypernatremia is an increased rate of potassium secretion.
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Furosemide

Hydrochlorothiazide

Spironolactone

Acetazolamide

Mannitol

Ascending limb of Henle’s loop

Early distal tubule

Late distal tubule and collecting duct

Proximal tubule

Impermeable

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Loop of Henle

  • The loop of Henle lies within the medulla of the kidney.
  • It is a countercurrent multiplier.
  • It functions to increase the osmolality gradient in order to concentrate urine.
  • The primary function of the loop of Henle is to establish a hyperosmotic state.
  • As fluid flows through the loop of Henle and exits, water is impermeable in the inner stripe. The inner stripe is most vulnerable to ischemia.
  • Only 15% of filtered water is reabsorbed by the loop of Henle.

Proximal Convoluted Tubule

    • Proteins are reabsorbed from the proximal tubules by being engulfed from the tubular membrane.
    • Active, energy-dependent reabsorption.
    • It reabsorbs the majority of the fluid which is filtered (67%).
    • The main focus of the proximal tubule is sodium.
      • Glucose, amino acids, and other organic compounds are strongly coupled with sodium.

Distal Convoluted Tubule

  • Final corrections on the urine are made here.
  • The primary site of action for aldosterone is the distal tubule.
  • Aldosterone and antidiuretic hormone act on the late distal tubule of the nephron.
    • Antidiuretic hormone (ADH) acts on the late distal tubule and collecting ducts of the nephron.

Extra Cellular Fluid (ECF) Osmolality

  • Osmoregulators in the hypothalamus control the secretion of antidiuretic hormone (ADH).
    • Arterial baroreceptors are activated during hypotension
    • Atrial receptors are stimulated by decreased filling pressure.
  • Supraoptic and paraventricular nuclei of the hypothalamus are very sensitive to extracellular osmolality changes.
    • ECF increases, ADH is released from the posterior pituitary.
  • Other stimulators of ADH
    • carotid baroreceptor stretch (decrease blood volume)
    • pain
    • stress
    • hypoxia
  • Renin release from the afferent arterioles is caused by:
    • Hypotension
    • Decreased tubular concentration
    • Sympathetic stimulation
  • Renin then leads to angiotensin II production.
  • Angiotensin II promotes:
    • ADH release from the posterior pituitary
    • Sodium reabsorption in the PCT
    • Aldosterone release by the adrenal medulla
  • THE FOLLOWING OPPOSE RENIN/ANGIOTENSIN/ALDOSTERONE/ADH:
    • Atrial natriuretic peptide
    • Nitric oxide
    • Prostaglandins (phospholipase A2 and cyclooxygenase)
  • GFR 90-140 mL/min is considered normal renal function.
    • GFR below 60 mL/min indicates chronic kidney disease
    • GFR values less than 15 mL/min may require dialysis
  • The 2021 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine equation is the most accurate estimation of GFR when compared to the gold standard. 
  • SERUM CREATININE REMAINS THE MOST USED KIDNEY FILTRATION MARKER.
  • Fractional excretion of sodium (FENA) is a test that analyzes the kidneys’ ability to retain electrolytes using both blood and urine.
    • < 1% is normal
    • > 1 % implies acute tubular necrosis
  • During periods of stress or hypovolemia:
    • sympathetic nervous system is activated
    • norepinephrine is released
    • renin-angiotensin-aldosterone system is activated
    • ADH is released 
    • Increase in blood pressure and renal perfusion.
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Hematologic

Anatomy and Physiology

  • Erythropoietin is a hormone that comes primarily from the kidneys.
    • Released during hypoxia
    • Stimulates bone marrow to release red blood cells.
  • Hemoglobin is broken down in the liver into iron and porphyrin.
    • Porphyrin is converted to bilirubin.
  • Hematocrit effects
    • blood viscosity
    • oxygen-carrying capacity
  • Increase in hematocrit =  decrease in blood flow and increased oxygen-carrying capacity

 

Primary hemostasis

    • Vascular injury →
      • platelet activation 
        • stabilized by von Willebrand factor (vWF)
      • phospholipases A and C lead to thromboxane A2 and degranulation
      • adenosine diphosphate (ADP) alters glycoprotein IIb/IIIa
      • fibrinogen and platelets bind, resulting in a platelet plug.
  • TXA2 promotes platelet aggregation because it is a potent vasoconstrictor.

 

  • Platelet granules contain:
    • adenosine diphosphate (ADP)
    • TXA2
    • vWF
    • factor V
    • fibrinogen
    • fibronectin

Secondary hemostasis

    • Fibrin strengthens the clot
      • Can be formed either by the intrinsic or extrinsic pathways.
  • Intrinsic pathway
    • Occurs inside the blood vessel
      • platelet phospholipid (PF3) and factor XII
  • Extrinsic pathway
    • Tissue thromboplastin (factor III)
  • Factors III (tissue factor, thromboplastin), IV (calcium), and VII:vWF are the only clotting factors that are not synthesized in the liver.

PATHWAY

Extrinsic

Intrinsic

CLOTTING FACTORS

III and VII

XII, XI, IX, and VIII

LABORATORY TEST

PT/INR

PTT

DRUGS

Coumadin/Warfarin

Heparin

ANTIDOTE

Vitamin K

Protamine

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  • Vitamin K-dependent clotting factors:
    • II
    • VII
    • IX
    • X
  • Antithrombin III functions to eliminate the clotting factors AFTER the vessel injury is sealed with a clot
    • Gathers clotting factors XII, XI, X, IX, and II to inhibit further clot formation.
  • Antithrombin III deficiency can be seen during heparinization of open-heart surgery.
    • Heparin dose of 400 units/kg is administered through a central line to obtain an ACT value of 480 seconds.
    • If ACT is below 480 seconds after administration of 600 units/kg of heparin, heparin resistance is suspected and possibly antithrombin III deficiency.
    • 2 units of fresh frozen plasma will provide the clotting factors necessary for a desirable ACT value.

Nagelhout Nurse Anesthesia 7th edition, page 525

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Gastrointestinal

Anatomy and Physiology

Intestinal

  • The small intestine’s main objective:
    • absorb nutrients
    • aid in digestion.
  • The small intestine plays a major role in the immune system.
  • The large intestine’s primary goal:
    • store and expel waste.
    • the right colon helps to absorb water and sodium.

Parathyroid hormone acts on the intestine to absorb calcium.

  • Scleroderma leads to hypomotility of the lower esophagus and small intestine due to the progressive fibrosis of the GI tract.

Esophagus

The difference between the lower esophageal sphincter (LES) pressure and gastric pressure is “barrier pressure,” which is more important than the LES tone in the production of gastroesophageal reflux.

  • The adult esophagus extends from the cricopharyngeal sphincter at the level of the C6 vertebra to the gastroesophageal junction.
  • An inner circular layer surrounded by an outer longitudinal layer makes up the musculature. The upper third of the inner circular muscle is striated and the lower two-thirds are smooth.
  • The major physiological derangement in gastroesophageal reflux is a reduction in LES pressure.
  • The tunica muscularis is composed of two distinct layers of smooth muscle: an inner circular layer and an outer longitudinal layer. 
  • The autonomic innervation of the gastrointestinal tract functions through two distinct regions containing autonomic ganglia:
    • submucosal (Meissner’s) plexus
    • myenteric (Auerbach’s) plexus
  • Gastric pH in the fasted patient ranges from 1.6-2.2.

FACTORS THAT AFFECT LOWER ESOPHAGEAL SPHINCTER TONE

INCREASE TONE

NO CHANGE IN TONE

DECREASE TONE

DRUGS:

-Anticholinesterases

-Cholinergics

-Succinylcholine

-Antacids

-Metoclopramide

-Metoprolol

HORMONES/ NEUROTRANSMITTERS:

-Acetylcholine

-Alpha stimulation

-Gastrin

-Serotonin

-Histamine

-Pancreatic polypeptide

DRUGS:

-Histamine-2 antagonists

-Nondepolarizing muscle relaxants

-Propranolol

DRUGS:

-Inhaled anesthetics

-Opioids

-Anticholinergics

-Thiopental

-Propofol

-Beta agonists

-Ganglion blockers

-Tricyclic antidepressants

HORMONES:

-Secretin

-Glucagon

CONDITIONS/ OTHER:

-Cricoid pressure

-Obesity

-Hiatal hernia

-Pregnancy

GASTRIC NPO GUIDELINES

Clear liquids (water, fruit juices with no pulp, black coffee); breast milk

2 hours

Infant formula

4 hours

Nonhuman milk; light meal

6 hours

Solids; full meal (fatty or fried foods)

8 hours

  • Trendelenburg will help keep gastric contents in the oropharynx as opposed to being pulled down into the lungs.
  • Bile in the common bile duct and gall bladder is alkaline so that it can neutralize stomach acid before entering the small intestine.
  • Bicitra (sodium citrate) is an acid neutralizing buffer that raises gastric pH, which is advantageous should aspiration occur. Gastric pH in the fasted patient ranges from 1.6-2.2.
  • metoclopramide (GI pro kinetic) reduces aspiration risk by: 
    • increasing gastric motility
    • increasing lower esophageal sphincter tone
  • Anticholinergics, like scopolamine and glycopyrrolate, can inhibit the esophageal sphincter effects produced by metoclopramide.

ACID-BASE BALANCE

MEASURE

NORMAL

pH

7.35-7.45

PaCO2

35-45 mm Hg

HCO3

22-26 mEq/L

IMBALANCE

pH

PaCO2

HCO3

Respiratory acidosis

↓

↑ >45

↑ (compensatory)

Respiratory alkalosis

↑

↓ < 35

↓ (compensatory)

Metabolic acidosis

↓

↓ (compensatory)

↓ >26

Metabolic alkalosis

↑

↑ (compensatory)

↑ <22

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  • Metabolic ALKALosis can be a result of:
    • vomiting
    • laxative overuse
    • diuretic overuse
    • nasogastric suction
  • Ketoacidosis is a common cause of metabolic ACIDosis.
    • If the diabetic patient has insufficient insulin to block the mobilization and metabolism of free fatty acids, the metabolic byproducts are ketones.
    • Keytones cause metabolic acidosis with an increased unmeasured anion gap.
  • Common causes of metabolic ACIDosis:
    • ketoacidosis
    • lactic acidosis
    • renal failure
    • toxic dose of salicylates.
  • When the pH is decreased (acidosis) and its due to the bicarbonate level being low (acidosis), the lungs compensate by hyperventilating to decrease CO2.

Pancreatic (exocrine)

  • Pancreatic exocrine function:
    • continuous transductal secretion of 1.5-3 L of pancreatic juice
  • Main function of pancreatic fluid:
    • alter the pH of the contents from the duodenum
    • facilitate optimal activity of pancreatic enzyme.
  • 3 types of pancreatic enzymes:
    • amylose
    • trypsinogen
    • lipase
  • Pancreatic juice is secreted in to the duodenum of the small intestine by acinar cells.

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Immune

Anatomy and Physiology

  • Acquired immunity classification: 
    • Humoral
      • acquired
      • mediated by B lymphocytes
        • memory cells
        • plasma cells
    • Cell-mediated
      • acquired
      • mediated by T lymphocytes
        • T-helper (CD4)
        • T-suppressor (CD8)
        • T-cytotoxic/killer (CD8)
        • T-memory cells
  • Mature B lymphocyte plasma cells are the source of gamma globulins known as immunoglobulins.
    • IgG
    • IgA
    • IgM
    • IgD
    • IgE

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