A&P II Unit 1 Exam

Peripheral NS

13 pairs of nerves that carry info back and forth from body to CNS

Somatic sensory

sensory from skin, skeletal muscles, bones, joints

Somatic motor

motor to skeletal muscles

Autonomic motor

motor to smooth muscles, heart muscle, glands

Effector organs (somatic motor)

skeletal muscles

Control (somatic motor)

voluntary movement

\# neurons from CNS to effector organ (somatic motor)

1

NT released to effector organ (somatic motor)

acetylcholine (ach) - always excitatory

Amount of myelin (somatic motor)

lots

* usually type a fibers (wide diameter, lots of myelin)

Effector organs (autonomic motor)

heart, smooth muscle, glands

Control (autonomic motor)

involuntary movement

\# neurons from CNS to effector organs (autonomic motor)

series of 2

* ach or NE released
* excitatory or inhibitory

NT released to effector organ (autonomic motor)

acetylcholine (ach)

* cholinergic axons

norepinephrine (ne)

* epinephrinergic axons, adernergic axons

Amount of myelin (autonomic motor)

little to 0 myelin

* type b - medium diameter, some myelin
* type c - 0 myelin, smallest diameter

Sympathetic NS

sympathetic info carried via branches spinal nerves T1-L2

Location of sympathetic ganglia

* close to spinal cord
* on either side of spinal cord “sympathetic chain ganglia”
* front of spinal cord “collateral ganglia”

Sympathetic fibers

usually release NE to effector organ (few release Ach)

Sympathetic nerve distribution

all over body

* smooth muscles, glands in head
* in eye - change shape of lens + diameter of pupil
* lacrimal + salivary glands
* viscera
* smooth muscle + glands in skin (sweat glands, arrector pili muscles)
* circular smooth muscle in vessels (arteries + veins)

Cx of sympathetic nerves

decrease diameter of vessel

Sympathetic NS function

* circular smooth muscle moving materials thru (beta)
* forming sphincters (cx - alpha)
* blood vessels to digestive, urinary, reproductive restricts (decrease blood flow)
* circular smooth muscle cx (alpha)
* blood vessels to skeletal muscles, heart, brain (increase blood flow - beta)
* arrector pili muscles cx (alpha - smooth muscle)

The fight or flight system

sympathetic NS

Fight or flight body conditions

* pupils dialate
* decrease saliva secretion (alpha)
* increase heart rate (beta)
* bronchi dialate (beta - circular smooth muscle relax)
* digestive, urinary, reproductive inhibited
* decrease secretion digestive enzymes, sexual fluids (alpha)

Norepinephrine + Epinephrine alpha receptors

NE binding to receptors

* smooth muscle cx
* glands decrease secretion

Norepinephrine + Epinephrine beta receptors

NE binding to receptors

* smooth muscle relax
* heart muscle: increase heart rate

Parasympathetic NS

“craniosacral”

* info carried via 4 cranial nerves (III oculomotor, VII facial, IX glossopharyngeal, X vagus)

Parasympathetic ganglia location

in/near effector organs “terminal ganglia”

NT released by parasympathetic NS

always ach

Distribution of parasympathetic fibers

* smooth muscle + glands in head (smooth muscle in eye, lacrimal, salivary glands)
* has no effect b/c they receive no parasympathetic stimulation
* distributed all over

NO parasympathetic nerve fibers to

* smooth muscles + glands in skin
* circular smooth muscle in any vessels (arteries, veins; except to arteries to genitals - arousal)

Parasympathetic NS function

* “resting + digesting”, “feeding + breeding”
* stimulate activity for survival
* increase activity of digestive, urinary, reproductive
* pupils constrict
* decrease heart rate

Parasympathetic NS nicotine receptors

on all post-ganglionic neurons

* ach binding, always excitatory

Parasympathetic NS muscarinic receptors

found on all effector organs that receive parasympathetic nerve supply (heart, smooth muscle, glands)

* ach binding, excitatory or inhibitory

Autonomic innervation of effector organs

dual innervation + single innervation

Dual innervation (autonomic)

* organs receive both sympathetic + parasympathetic nerve supply
* act antagonistically - one stimulates, other inhibits
* smooth muscle, glands in head
* viscera

Single innervation (autonomic)

* some organs receive only sympathetic nerve supply
* circular smooth muscles in vessels, arrector pili muscles, sweat glands DON’T receive any parasympathetic nerve supply
* controlled by increase/decrease sympathetic stimulation ONLY
* does NOT give as much control as dual innervation

Control of autonomic NS

hypothalamus has most direct control

Mimetics (agonists) + autonomic NS

* mimic/stimulate system by increase release or inhibit breakdown of NT or bind to + stimulate NT receptors

Types of mimetics

sympathomimetics + parasympathomimetics

Sympathomimetics

mimic/stimulate sympathetic NS by increase release or inhibit breakdown of NE or stimulate NE receptors

Parasympathomimetics

mimic/stimulate parasympathetic NS by increase ach at sympatic cleft, stimulates ach receptors

Blockers (antagonists, lytics) + autonomic NS

* block/inhibit system by decrease amount NT at synaptic cleft (decrease release or increase breakdown of NT) OR bind to NT receptors + block them

Sympathetic blockers

decrease amount NE at synaptic cleft or block NE receptors

Parasympathetic blockers

decrease amount ach at synaptic cleft or block ach receptors

RBCs

no nucleus, carry O2

WBCs

immunity

pH of blood

7\.35-7.45

Function of blood

* transport O2, nutrients, wastes, hormones
* regulate body temp

Blood compostition

* plasma - 55% blood vol
* formed elements (blood cells + platelets) - 45% blood vol

Plasma

* 91% water
* 7% proteins (albumin, globulins, fibrinogen)
* 2% other solutes (nutrients, gasses, hormones, ect)

Albumin

* most abundant plasma protein
* maintain blood vol
* draws H2O into blood

Globulins

* plasma protein
* transport (vitamins, minerals, hormones)
* clotting factors
* antibodies: “immunoglobins”

Fibrinogen

clotting factor plasma protein

Formed elements

erythrocytes (RBC) + leukocytes (WBC)

Granular leukocytes (granulocytes)

* neutrophils, basophils, eosinophils
* visibly stained granules

Agranular leukocytes (agranulocytes)

* lymphocytes, monocytes
* no visibly staining granules

Formation of formed elements

* all originate in red bone marrow
* all develop from blood stem cell - each type develops in response to specific hormones that triggers blood stem cell to develop into specific formed elements

Erythrocytes

* biconcave discs
* no nucleus
* can’t divide/repair
* no organelles
* can only make ATP anaerobically (w/o O2)

“Bags of hemoglobin”

erythrocytes

* each RBC has around 280 million hemoglobin cells

\# RBC

* 4.5-6 million RBC/mm^3 blood

Hematocrit

% total blood vol

* women: 37-47% - due to periods each month + men have more testosterone, increase RBC formation
* men: 42-52%

RBC function

carry O2

* hemoglobin

Hemoglobin

4 hemes, 4 globins

* each heme has iron molecule, each iron bonds to O2
* globin = proteins

Production RBCs

* all originate in red bone marrow
* need iron to make hemoglobin
* need amino acids to make globin
* need vit. B12 + fulic acid for cell division
* produced in response to erythroprotein from kidneys (maintain normal RBC production)

Lifespan RBC

110 (women) - 120 (men) days

Breakdown of RBCs

broken down in liver, spleen, bone marrow

Hemoglobin + breakdown RBCs

* hemes (iron): recycles + reused


* bilirubin: not H2O soluble, transported to liver bound to albunin
* globin (amino acid): reused by body

Anemia

RBC disorder

* decrease O2 carry capacity in blood due to decrease RBC, decrease Hb, abnormal Hb

Symptoms of anemia

pale, cold, fatigue, short breath

Iron deficiency anemia

* decrease Hb
* most common
* Tx: greens + iron supplements

Folic acid deficiency anemia

* decrease RBCs b/c folic acid needed for cell division
* large, fragile RBCs - rupture easily
* Hb can be released into plasma - damage kidneys
* “megablastic anemia”

Pernicious anemia

* B12 deficiency, decrease RBCs b/c B12 needed for cell division
* large, fragile cells
* to absorb B12, need intrinsic factor = produced by stomach
* Tx: B12 supplement, B12 injections

Hemorrhage anemia

excess blood loss

* Tx: stop bleeding, blood transfusion, fluid replacement

Sickle cells anemia

* genetic disorder
* more common in africans, mediterranians
* mutations in beta globin - if decrease O2, hemoglobin changes shape, Hb stacks into rigid rods, changing shape of cell
* Tx: O2 therapy, pain meds, blood transfusions, meds to dialate vessels, meds to increase production fetal hemoglobin

Erythrocytosis

* excess RBCs
* hematocrit may reach 80%
* blood gets thick, viscious, harder to pump thru vessels

Primary erythrocytosis

abnormality in bone marrow increase RBC production

Secondary erythrocytosis

increase EPO b/c decrease O2 in blood or EPO injections

ABO blood typing

determined by type of antigen on surface of RBCs

Antigen on surface of A blood

a antigen

Antibodies in plasma of A blood

anti-b antibody

Antigen on surface of B blood

b antigen

Antibody in plasma of type B blood

anti-a antibody

Antigen on surface of AB blood

AB antigen

Antibody in plasma of type AB blood

0 antibodies

Antigen on surface type 0 blood

0 antigens

Antibody in plasma of type 0 blood

anti-a and anti-b antibodies

Antibodies in plasma

develop antibodies to any antigen not present on RBC surface

Anti-a antibody

clumps any RBC with type a antigen

Anti-b antibody

clumps any RBC with type b antigen

Transfusions

antigens on donor blood do not react with antibodies in recipient plasma

Transfusion Ex: What can the recipient receive?

\
Recipient: type a blood, a antigens, anti-b antibody

\
Mom: type a blood

Dad: type b blood, b antigens

Sister: type ab blood, a + b antigens

Type 0, 0 antigens

* mom: yes
* dad: no - b/c recipient antibodies clump b antigen blood received
* sister: no - b/c recipient’s antibodies clump b antigens on RBC
* Type 0 - yes
* DONOR ANTIGEN + RECIPIENT ANITBODY MUST BE COMPATIBLE

Universal donor

type 0

* no antigens to react with any antibodies in recipient’s plasma

Universal recipient

type ab

* 0 antibodies to react with donor antigens

Rh factor

another antigen that may or may not be on surface of RBC

* if Rh factor present - Rh+
* if Rh factor not present - Rh-
* if Rh- is exposed to Rh+ blood, they will produce anti-Rh antibodies, clumps any Rh+ blood

1st exposure b/t Rh+ and Rh- blood

1st exposure of Rh - to Rh+ blood, anti Rh antibody production slow + low #, no reaction

Subsequent exposures b/t Rh+ and Rh- blood

Rh- person has some anti-Rh antibodies present from 1st exposure to Rh+ blood, + Rh antibodies produced faster, increased #s

Hemolytic disease of newborn (erythroblastosis fetalis)

Tx + prevention:

* intrauterine blood transfusion w Rh- blood for fetus
* bili lights for jaundice
* rhogam (Rh immunoglobin)
* antibodies that bind to any Rh+ fetal blood in mom’s bloodstream
* antibodies block Rh factor on fetal RBCs, mom’s immune system never “sees” Rh factor on fetal RBCs and it doesn’t make anti-Rh antibodies

Leukocytes

all can undergo chemotaxis, diapedesis, ameboid movement

Chemotaxis

follow chem trail to site of injury/infection

Diapedesis

squeeze thru vessel wall and go into tissues

Ameboid movement

crawl thru tissues