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Transcript
LEUKOCYTES (White blood cells)
all fight infection

BASOPHILS
– MAST CELL
EOSINOPHILS
 NEUTROPHILS
 MONOCYTES

– MACROPHAGES

LYMPHOCYTES
– B CELLS
– T CELLS
BASOPHILS

Basophils – only about
0.5% of all leukocytes
– Granules secrete
histamines (vasodilation;
more WBCs can get to the
infection site)
– Antihistamines interfere
with the function of
basophils.
– Mast Cell: a basophil that
leaves the blood vessel
and enters the tissues.
Eosinophils

Eosinophils –
compose 1-4% of all
WBCs
– Play roles in:
 Ending allergic
reactions, parasitic
infections
 During these conditions
they increase in
numbers
Neutrophils
Neutrophils – most
numerous WBC
 First to respond to
infection

– Phagocytize and destroy
bacteria
– Also destroy bacterial
toxins in body fluids
– Nucleus – has two to six
lobes
Monocytes




Comprise about 5% of all WBC’s.
Like neutrophils, they phagocytize
(eat) bacteria, old cells, and
foreign bodies. They have more
types of lysosome enzymes than
neutrophils so they are better at
killing difficult pathogens.
They also use antibodies for
opsonization.
When they leave the
bloodstream and enter the
tissues, they are called
MACROPHAGES.
Lymphocytes

20–45% of WBCs
– The most important cells of the
immune system
– There are two types of
lymphocytes; one type is
effective in fighting infectious
organisms like body cells
infected with viruses
– Both types of lymphocytes act
against a specific foreign
molecule (antigen)
Lymphocytes
Two main classes of lymphocyte

–
–
B cells – Originate in the bone marrow,
mature into plasma cells. A mature
plasma cell fights infection by
producing antibodies
T cells – Originate in the thymus gland.
They attack foreign cells directly (including
organ transplants!). They can also kill
viruses.
Lymphocytes
B cells – mature into plasma cells
Plasma cells secrete antibodies; the
plasma cell’s antibodies are what
kills the attacking cell.
Antibodies attack in two ways:



–
–
They attach to bacteria and pop the cell
membrane
They attach to encapsulated bacteria to
help neutrophils and macrophages to
phagocytize them.
T-cell Lymphocytes

T cells are the cells that attack
organ transplants!



Immunosuppression drugs are designed to
inhibit the action of T cells.
T cells are attacked by the HIV (AIDS)
virus.
The thymus gland secrets certain
hormones which can cause T cells to
become immunocompetent (makes the
cells mature and start to work)
T Cells
There are several types of T cells. The main types are
 Cytotoxic (Killer) T cells
– Go out and directly kill bacteria or infected host cells
 Helper T cells
– Release chemicals called “cytokines” to call in more
white blood cells of all types to join in the war. They
also present the macrophage’s antigen to a plasma
cell, which causes the plasma cell to produce
antibodies against that particular bacteria.
 Suppressor T cells
– Stop the immune process when it is over, and also "tell" some
plasma cells to "remember" how to destroy that specific
pathogen. Those plasma B-cells are then called Memory B-Cells.
They can react to the same pathogen faster, the next time it
invades because Memory B-cells already have the proper
antibodies stored up for that pathogen.
Capsule
Pops
the cell
Virus
Opsonization
Bacteria
Bacteria
Antibodies
Plasma
Cell
Pops the cell
Cytokines
Phagocytosis
STOP
Presentation
Neutrophil
Macrophage
(Monocyte
in bloodstream)
B-Cell
Helper
T-Cell
Killer
T-Cell
Lymphocytes
Suppressor
T-Cell
Platelets

Cell fragments
– Break off from
megakaryocytes

Function in clotting of
blood
Platelets
Megakaryocyte
RBC Development


A mature RBC is called an
ERYTHROCYTE, which circulates in the
blood.
If the body makes too few erythrocytes
it can lead to one form of ANEMIA.
ERYTHROBLASTS

These mature into
RETICULOCYTES, a
RBC with bits of
nucleus material,
which later dissolves
to make room for
more Hgb. It is now
called an
ERYTHROCYTE.
Anemia


Characteristic sign of anemia: see
reticulocytes in the blood (immature red
blood cells).
Remnants of the nucleus are still in the
cell.
Disorders of RBCs
Polycythemia
 Anemia

–
–
–
–
–
–
Too few RBC’s
Iron deficiency
Hemorrhagic anemia (person lost blood)
Pernicious anemia (lack of vitamin B12 or intrinsic factor)
Excess RBC destruction (immune disorder or infection)
Hemoglobin abnormalities
 Thalassemia
 Sickle cell disease
 Megaloblastic anemia (pernicious anemia)
More Causes of Anemia
Hemorrhagic anemia: loss of blood
 Pernicious anemia: lack of vitamin B12 or
intrinsic factor, which is needed to make
the hemoglobin in a RBC
 Excess RBC destruction (from an
autoimmune disease, infection, etc)
 Genetic defect in Hemoglobin (deforms
the cell)

Thalassemia
A form of anemia where the RBCs have abnormal
hemoglobin that deforms the cells
TEAR DROP
TARGET CELLS
SPHEROCYTE
Sickle Cell Disease

Present in African Americans more than
in other groups, and is always
characterized by sickled erythrocytes.
Megaloblastic Anemia
(Large RBCs: Note that the lymphocyte is the
same size as the huge RBCs)
Hematocrit





A quick screening test for anemia is the
hematocrit.
A drop of blood is drawn up a small glass
capillary tube and the tube is centrifuged to
pack the red blood cells at the bottom with the
plasma on top.
Hematocrit measures the percentage of blood
volume that consists of erythrocytes.
The hematocrit is the ratio of packed red blood
cells to total blood volume.
Normal is about 45% (46% for men and 38%
for women.)
Disorders of WBCs

Disorders of leukocytes
– Leukemia – too few mature WBC’s (may see
increase in immature forms); a form of cancer
– Classified as lymphoblastic (too many
immature lymphocytes) or myeloblastic (too
many immature neutrophils)
Disorders of Platelets
– Thrombocytopenia
 Abnormally low
concentration of platelets
 Blood does not clot
properly
HEMOPHILIA
A hereditary disease of males, where they are
unable to clot properly because they are missing
some clotting factors.
 When they get even a slight bump or bruise
they have to have an intravenous infusion of
clotting factors or they will bleed to death.
 This is probably the disease that was in the
genes of Henry VIII, which caused all of his
male children to become weak and die in
infancy.

Blood Clots

Thrombus
– A clot in a vessel

Embolism
– a thrombus that broke away and
travels in the blood stream.
– It usually lodges in a smaller blood
vessel and blocks circulation distal
to that point.
BLOOD TYPING





These proteins are called antigens (something
that causes an allergic reaction). There are two
types of blood antigens: Type A and Type B.
A person with Type A antigens on their blood
cells have Type A blood.
A person with Type B antigens have Type B
blood.
A person with both types has type AB blood.
A person with neither antigen has type O blood.
RH FACTOR

The reason this is so important is that if
an Rh- mother has an Rh+ fetus in her
womb (from an Rh+ father), her
antibodies will attack the red blood cells of
the fetus because her body detects the Rh
protein on the baby’s red blood cells and
thinks they are foreign objects. This is
called Hemolytic Disease of the Newborn
(HDN).
IMMUNE SYSTEM
INFLAMMATORY REACTION: When you get
stuck by a thorn or have an infected cut, the
body goes through a series of events called an
inflammatory reaction.
 Four outward signs:

–
–
–
–
Redness (erythema or rubor)
Heat (calor)
Swelling (edema)
Pain (dolor)
ADAPTIVE IMMUNITY

Two types of Adaptive Immunity
– ACTIVE immunity
 Naturally Acquired
 Artificially Acquired
You can also think
of it this way
– PASSIVE immunity
 Naturally Acquired
 Artificially Acquired
ALLERGIES

From a hypersensitivity to substances such
as pollen or animal hair that would not
ordinarily cause a reaction. There are two
types of allergic responses:
Immediate
Delayed
AUTOIMMUNE DISEASE

A hereditary problem where the body
thinks its own tissues are foreign bodies,
and it constantly tries to kill off its own
tissues.
Tunica intima
Endothelium
Subendothelium
Tunica media
Smooth muscles
Elastic fibers
Tunica adventitia
Vasa vasorum
Types of Blood Vessels

Arteries – carry blood away from the heart
– It does not matter if it is oxygenated or deoxy
blood. If it is leaving the heart, it is an artery.

Capillaries – smallest blood vessels
– The site of exchange of molecules between
blood and tissue fluid

Veins – carry blood toward the heart
It does not matter if it is oxygenated or deoxy blood.
If it is entering the heart, it is a vein.
Arteries





ARTERIES carry
blood away from the
heart.
Arteries have a smaller
lumen than veins of
similar size.
Arterial walls are
thicker than venous
walls.
Arteries have more
elastin than veins.
Arteries have no
valves because the
blood pressure in
arteries is high enough
that there is no
backflow of blood.
ARTERIOLES
These are microscopic; they are the
smallest type of artery.
 Large ones look like muscular arteries.
 Small ones only have two layers:
endothelium and tunica media.
 One of the characteristics of an arteriole is
that when it contracts, the lumen closes
completely.



A sac-like outpouching of an
artery
– Can rupture at any time;
in aorta or brain can
cause death within a few
seconds.
– Symptoms: Swelling or
throbbing (asymptomatic
in brain)
Some common locations for
aneurysms include:
– Aorta
– Brain
– Leg
– Intestine (mesenteric
artery aneurysm)
– Splenic artery
aneurysm (can form
during pregnancy)
Aneurysm
Aneurysm

Causes of an aneurysm:
– Defect in part of the artery wall
– High blood pressure (abdominal aortic
aneurysms)
– Congenital (present at birth)
Usually not detected except by an
angiogram or ultrasound.
 Treatment: surgical repair

Some clinically significant
arteries
Femoral artery: easy to find pulse, but
susceptible to injury.
 Circle of Willis: loop of arteries around
pituitary and optic chiasma. Common area
for stroke to cause blindness.

Types of Capillaries
CONTINUOUS CAPILLARIES
 FENESTRATED CAPILLARIES
 DISCONTINUOUS CAPILLARIES

PRE-CAPILLARY SPHINCTER
A small muscle in front of each capillary, controls
the flow of blood to individual capillaries.
 ARTERIOLES direct the blood flow to the
specific tissue. PRE-CAPILLARY SPHINCTERS
direct the blood flow to specific cells.
 If one cell is starving, the capillary next to it will
open. The sphincter opens and closes
depending on the needs of individual cells.

Veins

Veins take blood TO the heart. Two types:
– Venuole: from the capillary to the vein
– Vein: takes blood to the heart.
 Thinner walls (less pressure here)
 Larger lumen (blood moves more slowly)
 Skeletal muscle pushes on the vein to move the
blood uphill.
 Need valves in veins
Valves in Veins
How does blood get uphill back to the heart?
Veins need valves.
 Veins are the only BLOOD vessels that have
valves (although LYMPH vessels also have
valves).
 Valves in veins allow blood to move in only one
direction. What pushes the blood? The muscles
of the body constrict, squeezing the vessels.
This is a type of blood pump.

Clinically Significant Veins
Greater Saphenous vein: used for
coronary bypass; most likely becomes
varicose.
 Facial vein: “Danger triangle” infection
spreads to meninges in brain.
 Renal vein: oxygen poor, and
contains the lowest concentration of
nitrogen waste.

Veins that are rich in
oxygen and nutrients



Umbilical vein
Hepatic Portal vein
Pulmonary vein
Varicose Veins
The valves become incompetent:
 They can’t close all the way because too
much fluid has built up in them and the
lumen has stretched too wide.
 They might be asymptomatic or they may
be painful (phlebitis).

Edema
If the veins are varicose for a long time,
plasma may leak out into the tissues,
causing edema.
 Edema means swelling anywhere in the
body (including from an injury or from
hanging your legs down too long like
when on an airplane), but it frequently
occurs from incompetent veins in the legs.
There are two types of edema:

– Pitting
– Non-pitting
PHLEBITIS
Inflammation of a vein
 Usually in the legs.
 When phlebitis is associated with the
formation of blood clots (thrombosis),
usually in the deep veins of the legs, the
condition is called Deep Vein
Thrombophlebitis (DVT).

DEEP VEIN
THROMBOPHLEBITIS
Signs and Symptoms
 Redness (erythema) and warmth with a
temperature elevation of a degree or more
above the baseline
 Pain or burning along the length of the
vein
 Swelling (edema)
 Vein being hard, and cordlike
 Need ER if all symptoms are present

Spider Veins
Small superficial veins become varicose
and do not function properly.
 Cause an unsightly appearance but are
not dangerous.
 Injections of alcohol or saline into the vein
will sclerose them (scar them shut).
 A laser can also be used to do the same.
 After treatment, macrophages will
eventually phagocytize them and they will
disappear.

Tissue Necrosis
Necrosis = dead
 Caused by infection, toxins, or trauma
 Almost always detrimental and can be
fatal

Peripheral Vascular Disease
(PVD)


Refers to the obstruction of large arteries, frequently in
the lower extremity. Usually caused from
atherosclerosis (fatty plaques).
Symptoms
– Claudication: pain, weakness, numbness, or
cramping in muscles due to decreased blood flow
– Sores, wounds, or ulcers that heal slowly or not at
all
– Change in color (blueness or paleness) or
temperature (coolness) when compared to the other
limb
– Diminished hair and nail growth on affected limb and
digits (shiny, hairless skin)
Lymph System
The lymph system retrieves excess tissue fluid
(plasma that leaks out of the blood vessels) and
filters it and cleans it and returns it to the blood.
 This plasma is now called lymphatic fluid. It is sent
through the lymph nodes throughout the body.
 There are hundreds of lymph nodes in the body,
occurring in clusters.
 Each lymph node filters the lymph fluid to get rid of
bacteria and viruses, and returns the fluid back into the
blood.

How does lymph move?
All of the following mechanisms help move
lymph through the lymphatic vessels
 Body movements during exercise
 Contraction of skeletal muscles
 Contractions of smooth muscle in the wall
of the lymph vessels.
Network of lymph vessels

Lymph vessels drain into the right thoracic
duct near the clavicle.
Lymph Node
Figure 20.4a
GIANT LYMPH NODES
Considered as lymph organs
 1. TONSILS and ADENOIDS
 2. THYMUS
 3. PAYER’S PATCHES
 4. APPENDIX
 5. SPLEEN
Lymph Disorders





Hodgkin’s Disease: cancer of lymph node; does NOT
feel tender
Lymphangitis: inflammation of lymph vessels, usually
from infection
Mononucleosis: Epstein-Barr virus attacks Blymphocytes; characterized by inflammation of lymph
vessels (lymphangitis).
Edema: accumulation of fluid in connective tissue
Bubo: infected node with trapped pathogens that are
not destroyed
Layers of tissues around the heart:
PERICARDIUM
1) Parietal pericardium
2) Pericardial cavity
3) Visceral pericardium
HEART
1) Epicardium (same as
visceral pericardium)
2) Myocardium
3) Endocardium
Parietal
pericardium
Visceral
pericardium
PERICARDITIS
Inflamed outer layer of heart.
 Fluid accumulates in pericardial cavity, putting
pressure on heart  improper beat
 Pericarditis can be caused by damage to the
blood vessels  blood leaks into pericardial
cavity  pressure  improper beat.
 Pericarditis can lead to pericardial friction rub,
adhesions, and additional excess fluid in the
pericardial cavity.

PERICARDITIS




CARDIAC TAPENADE: In severe cases of
pericarditis, or if there is a stab wound to the
heart wall that causes fluid to exude into the
pericardial cavity.
The excess fluid compresses the heart and
diminishes the heart’s ability to pump.
Don’t get this confused with arrhythmia that is
caused from a problem with the SA or AV node.
The irregular heart beat from cardiac tapenade is
caused from fluid entering the pericardial cavity
and putting pressure on the heart.
Treatment is to stick a needle in the cavity and
drain the fluid.
ENDOCARDITIS
More serious:
 Bacteria enter bloodstream (dental
procedures, IV drug abuse, catheter) 
damage to lining and valves  blood
clots.
 Those who already have damaged heart
valves need prophylactic antibiotics.
 Don’t get endocarditis (bacterial
infection) mixed up with pericarditis,
which can lead to cardiac tapenade.

Blood Flow
When the ventricles relax, the PULMONARY
SEMILUNAR VALVE closes to prevent blood
from going from the pulmonary artery
back into the right ventricle.
 Do the semilunar valves have a chordae
tendonae?
 No; the blood is not being forced back (with a
contraction), it just falls back with gravity, so
there’s not as much pressure.

• Therefore, the left ventricle is the chamber
which is responsible for generating the largest
pressure upon contraction.
SVC
IVC
RA
RV
Tricuspid valve
Pulmonary
artery
Pulmonary
vein
LA
LV
Pulmonary
semilunar valve
Bicuspid valve (Mitral)
Aorta
• The blood then goes past the AORTIC
SEMILUNAR VALVE, into the AORTA, and back
to the body.
The semilunar
valves are
located
between the
ventricles and
the great
arteries.
IVC
SVC
RA
RV
Tricuspid valve
Pulmonary
artery
Pulmonary
vein
LA
LV
Pulmonary
semilunar valve
Bicuspid valve (Mitral)
Aorta
Aortic semilunar valve
Body
SUMMARY OF BLOOD FLOW

Deoxy blood  sup/inf vena cava  R
atrium  tricuspid valve  R ventricle 
pulmonary semilunar valve  pulmonary
artery  lungs  pulmonary veins  Left
atrium  mitral (bicuspid) valve  Left
ventricle  aortic semilunar valve  aorta
 rest of body.
Mitral Valve Stenosis
• If there is stenosis (blockage) of the mitral valve, where will
the blood back up into?
• Answer: the pulmonary circulation.
SVC
IVC
RA
RV
Tricuspid valve
Lungs
Pulmonary
artery
Pulmonary
vein
LA
LV
Pulmonary
semilunar valve
Bicuspid valve (Mitral)
Aorta
Aortic semilunar valve
Body
HEART BEATS
The pressure of blood against blood vessel walls
is called blood pressure.
 Blood pressure is recorded systole over diastole.
Normal resting blood pressure is said to be
120/80. When blood pressure is too high, it is
called HYPERTENSION.
 The sound your heart makes when it is beating
is the sound of the blood hitting the valves after
they are closed.
 The heart normally beats at a rate of 60-80
beats per minute. A faster (tachycardia) or
slower (bradycardia) heart rate is an indication
of a problem.

HEART BEATS

SYSTOLE:
– Ventricles contract
– Atria relax

DIASTOLE:
– Ventricles relax
– Atria contract
Valve Problems

HEART MURMUR
– If the valve leaks, it doesn’t close all the
way
– “Lub-squirt”
– Most murmurs are benign; fairly
common, esp. in babies and some
adults.
Valve Problems


PROLAPSED VALVE is more serious.
Mitral valve is most likely to prolapse because it pumped
the hardest. See how much thicker the left ventricle is?
Mitral Valve Prolapse is the most common heart valve
disorder. Might need artificial valve.
What controls the heart beat?
There is a small region in the right atrium
= SA NODE (Sino-atrium node) =
pacemaker of the heart. Its job is to speed
up or slow down the heart rate as needed.
 SA node sends an electrical signal (action
potential) to the AV NODE (atrio-ventricular
node)  atrium contraction  then the
signal pauses while the signal is
transmitted to both ventricles (atria are
now relaxing)  sends the action potential
to all parts of the heart so it can contract.

Conducting System
Heart Beats

The heart does not need a nerve to stimulate it to
contract; rather, specialized heart cells can
spontaneously start an action potential that spreads to
depolarize the rest of the cardiac muscle cells. These are
the specialized cells:
– A. SA node
– B. AV node
– C. Bundle of His (AV bundle)
– D. left and right bundle branches
– E. Purkinje fibers
Heart Beats

This is the order in which these specialized cells function:

First the Sinoatrial (SA) node starts an action potential which causes the
atria to depolarize.
This depolarization will then reach the AV node at the bottom portion of
the right atrium and there is a delay here because these cells are so small
in diameter.
Another delay in the transmission of the depolarization at the bundle of
His (AV bundle) because these special heart cells travel through the
atrioventricular septum which is non-conductive fibrous connective tissue.
The Bundle of His slows down the electrical pathway to give the atria a
chance to finish contacting.
Next, the depolarizing event travels through the left and right bundle
branches, found in the interventricular septum, to finally arrive at the
Purkinje fibers in the lateral walls of the myocardium of the ventricles.




Problems
ARRHYTHMIA
 Problem with the SA or AV node 
improper heart beat.
 Treatment is medicines or a pacemaker.

Ventricular Fibrillation
FIBRILLATION is when the heart beat is
not really present…it just vibrates.
 A heart in fibrillation does not contract
rhythmically; it just quivers without
pumping blood.
 The ventricles are unable to pump blood
efficiently due to rapid, random contraction
of cardiac muscle fibers.
 The muscle doesn’t contract as a unit.
Treatment is defibrillate with electric shock
 closes down heart  maybe it will
restart.

Coronary Vessels
1)
Right coronary artery
The left one is too short to be counted
2) Circumflex artery
3) Anterior Interventricular artery
4) Posterior Interventricular artery

The coronary sinus is a collection of veins joined
together to form a large vessel that collects blood from
the myocardium of the heart and delivers it into the right
atrium.
THE HEART NEEDS ITS OWN
BLOOD/O2
If one of the four coronary arteries becomes
clogged, ISCHEMIA (lack of oxygen) to part of
the heart muscle will result.
 This is a painful condition, and the pain of it is
called ANGINA (heart pain).
 If nothing is done immediately to increase the
blood flow, the myocardial tissue can die; this
condition is called a HEART ATTACK.

Coronary Bypass
People who have an angina attack can take
nitroglycerine as a tablet under the tongue
that dissolves quickly.
 This medicine will dilate the blood vessels.

Coronary Bypass

When a person has their first angina
attack, the doctor will order an
ANGIOGRAM to look for a
narrowing in an artery, especially in
one of the coronary arteries.
Coronary Bypass
If a coronary artery is found to have
a severe blockage, they can do a
CORONARY BYPASS.
 In this procedure, the doctor takes
another blood vessel graft (from the
greater saphenous vein in the thigh)
and sews it in around the blockage.
 For double or triple bypasses, that’s
how many vessels are affected.

TERMS
ANGINA: heart pain, usually caused from
not enough oxygen to the myocardium
(ischemia)
 ISCHEMIA: lack of blood/oxygen
 MYOCARDIAL INFARCTION: heart
attack from blood clot in coronary artery,
causing ischemia, which causes angina

HEART ATTACK

Not enough blood to the heart’s myocardium
layer  MILD ISCHEMIA  severe pain:
ANGINA (angina pectoris)
– Treatment is nitroglycerine to open arteries
Complete blockage  not enough O2 to that
area = SEVERE ISCHEMIA  that part of
heart muscle dies = MYOCARDIAL
INFARCTION.
 Heart muscle never regenerates. If a large area
dies, person will die.

Heart Medicines
t-PA (dissolves blood clots)
 Beta-blockers (slows heart rate)
 Aspirin (prevents blood clots)
 Nitroglycerine (dilates coronary arteries)

Causes of High Blood
Pressure

ARTERIOSCLEROSIS (hardening of the arteries):
caused by a build-up of calcium deposits in the artery
wall; artery cannot expand with blood surges. Tends to
be hereditary.
The blood vessel becomes hard like a rock; it
can’t expand or contract, causes increase in
blood pressure.
 Diet and exercise don’t help this much. Both
arteriosclerosis and atherosclerosis cause high
blood pressure.

Causes of High Blood
Pressure

ATHEROSCLEROSIS (a build-up of fat in
the arteries): caused from eating fatty
food  narrowing of artery  Spasm
shut or blood clot.
EMBOLISM
When fat builds up in a lump in one place,
it is called a PLAQUE. It causes the
lumen to narrow, restricting blood flow.
 If this fatty plaque breaks off and travels
in the bloodstream, it is now called an
EMBOLISM. An embolism can also be
made of blood instead of fat.

How a thrombus becomes
embolism
If a platelet catches on a piece of this fat, it can
start a blood clot (thrombus).
 If a piece of the clot (thrombus) breaks off
and enters the circulation, it is now called
an embolism, it can lodge in a smaller blood
vessel and block the oxygen to all the tissue
past that point, and the tissue dies.

Blockage of blood vessel
If the embolism lodges in the coronary
arteries  myocardial infarct (Heart
attack).
 If the embolism lodges in an artery in the
brain  stroke
 If the embolism lodges in the lungs 
pulmonary embolism

ANGIOGRAM

An ANGIOGRAM is a procedure to inject
dye into the arteries and x-ray to see if
there is narrowing (sclerosis) of a vessel.
This can be done anywhere in the body
that is of interest, but frequently it is done
to check the coronary arteries.
ANGIOGRAM

If an artery is too narrow, an
ANGIOPLASTY can be performed to
open it up. This involves sticking a balloon
into the artery and inflating it, causing the
vessel to enlarge a little to increase blood
flow. This can be done anywhere in the
body, but is frequently done in coronary
arteries.
CORONARY BYPASS
For a coronary artery that has become
extremely narrow from plaques, you can do a
CORONARY BYPASS.
 People who exercise have the same number of
heart attacks as those who don’t, but they tend
to survive them.

VENTRICULAR FIBRILLATION

Even a small clot can be a problem. If it
happens to enter the interior of the heart
and lodge in the wall of the atrium, it can
block the conduction of the signal of the
AV node  VENTRICULAR
FIBRILLATION.
ANEURYSM
High blood pressure is due to high pressure of
blood against the walls of the blood vessels; the
blood vessels compensate by developing a
thicker wall.
 The vessels can no longer expand during
systole, so the vessel gets thicker and thicker,
and the blood pressure goes up more.
 If the blood pressure gets too high, an
ANEURYSM can form, which is a weakening in
the wall of the blood vessel, causing it to expand
like a balloon.

Coronary artery disease terms

Coronary artery disease
– Atherosclerosis – fatty deposits
– Angina pectoris – chest pain
– Myocardial infarction – blocked coronary artery
– Silent ischemia – lack of blood flow that
happens to not cause any pain or other
symptoms; leads to an unexpected heart
attack.
– Stroke – ruptured blood vessel in the brain.
Also called Cerebral Vascular Accident (CVA)
Other Heart Conditions

Congestive Heart failure
– Progressive weakening of the heart
– Blood backs up into lungs (may cough up
blood)
– Cannot meet the body’s demands for
oxygenated blood

Hypertrophic cardiomyopathy
– Congenital condition where the walls of the
left ventricle are so thick that the lumen is too
small to hold much blood.
Disorders of Conduction

Ventricular fibrillation
– Rapid, random firing of electrical impulses in
the ventricles of the AV node

Atrial fibrillation
– Rapid, random firing of electrical impulses of
the SA node
Most Common Heart Problems
ATHEROSCLEROSIS
 VENTRICULAR FIBRILLATION
 Congestive heart failure
 Hypertrophic cardiomyopathy

FORAMEN OVALE



The lung tissue needs some oxygenated blood, but only
a little. Therefore, there is an opening from the right to
the left atrium called the FORAMEN OVALE which
shunts blood from the right to the left side of the heart
to bypass the lungs.
There is a foramen ovale in the skull and another one in
the heart. The foramen ovale in the heart normally
closes shortly after birth, and is then called the FOSSA
OVALIS.
A ‘blue baby” has low oxygen levels in the blood that
may be due to failure of the foramen ovale to close at
birth: Patent foramen ovale.
DUCTUS ARTERIOSIS

Another shunt: between the pulmonary artery
and the aortic arch so that most of the blood
bypasses the immature lungs Therefore, there
are two shunts to take blood away from the
lungs.

If the electrical signals from the atria
were conducted directly into the
ventricles across the AV septum, the
ventricles would start to contract at
the top (base). Then the blood would
be squeezed downward and trapped at
the bottom of the ventricle.

The apex to base contraction squeezes
blood toward the arterial opening at
the base of the heart.

The AV node also delays the
transmission of action potentials
slightly, allowing the atria to complete
their contraction before the ventricles
begin their contraction. This AV
nodal delay is accomplished by the
naturally slow conduction through the
AV node cells. (Why are they slow
conductors? Small diameter cells,
fewer channels)
Fibers within the heart


Specialized Fibers
– are the fibers that can spontaneously
initiate an AP all by themselves!
– The AP will spread to all other fibers via
gap junctions
– AKA “leading cells”
– But they are also muscle, so they do
contract, albeit feebly!
– They are not nerves!!!!
Contractile Fibers
– These maintain their RMP forever, unless
brought to threshold by some other cell
– They cannot generate an AP by themselves
– AKA “following cells”
– But they do have gap junctions, so once
they’re triggered, they will help spread the
AP to neighbors.
Pathway of Heartbeat





Begins in the sinoatrial (S-A)
node
Internodal pathway to
atrioventricular (A-V) node
Impulse delayed in A-V node
(allows atria to contract
before ventricles)
A-V bundle takes impulse
into ventricles
Left and right bundles of
Purkinje fibers take impulses
to all parts of ventricles
KEY
Red = specialized cells;
all else = contractile cells
How can these Specialized fibers
spontaneously “fire?”



Can’t hold stable resting
membrane potential
Potentials drift (gradual
depolarization)
During this time, they have a
gradually increasing perm to Na+
and less leaky to K+ (more “+”
inside causes cell to depolarize,
remember?). Only specialized
fibers of the heart can depolarize
on their own.

This is what gives the heart it’s
rhythm.
Na+
Specialized fibers of
conductive system

These rhythms can
ALSO be modified by
the ANS

Neurotransmitters can cause
faster or slower rise to
threshold by altering ion
permeability.
Acetylcholine (ACh) slows the
heart rate (parasympathetic
division of ANS)
Norepinephrine (NE) speeds up
the heart rate (sympathetic
division of ANS)


K+ efflux
Sympathetic and Parasympathetic
Sympathetic – speeds heart rate by  Ca++ & Na+
channel influx and  K+ permeability/efflux
(increases sodium and calcium permeability)
 Parasympathetic – slows rate by  K+ efflux & 
Ca++ influx (decreases sodium and calcium
permeability)


Which neurotransmitter will cause your heart to
pound rapidly?
– Norepinephrine
Blood Flow (L/min)

Blood flow is the quantity of

Overall flow in the circulation
of an adult is 5 liters/min
which is the cardiac output.

HR = heart rate

SV = stroke volume

CO= HR X SV

70 b/min x 70 ml/beat
=4900ml/min
blood that passes a given
point in the circulation in a
given period of time.
108
Ventricular Ejection Volume =
Stroke Volume




Stroke Volume (SV)
– amount ejected, ~ 70 ml
End Diastolic Volume (EDV)
SV/EDV= ejection fraction,
– at rest ~ 60%
– during vigorous exercise as
high as 90%
– diseased heart < 50%
End-systolic volume: amount
left in heart (50ml)
Cardiac Output (CO)
Amount ejected by a ventricle in
1 minute
 CO = HR x SV
 Resting values, 4- 6 L/min
 Vigorous exercise, 21 L/min
 Cardiac reserve: difference
between maximum and resting CO

If resting CO = 6 L/min and after exercise
increases to 21 L/min, what is the cardiac reserve?
CR = 21 – 6
CR = 15 L/min
Volumes and Fraction
End diastolic volume
= 120 ml
End systolic volume
= 50 ml
Ejection volume (stroke volume) = 70 ml
Ejection fraction = 70ml/120ml = 58%
(normally 60%)
• If heart rate (HR) is 70 beats/minute, what is
cardiac output?
• Cardiac output = HR * stroke volume
= 70/min. * 70 ml
= 4900ml/min.
•
•
•
•
Questions
• If EDV = 120 ml and ESV = 50 ml:
• What is the SV?
• 120-50 = 70 ml
• What is the EF?
• 70/120 = 58%
• What is the CO if HR is 70 bpm?
• 70/bpm * 70 ml = 4900ml/min.
Ohm’s Law: Q=P/R

Flow (Q) through a blood vessel which is the same thing
as saying Cardiac Output (CO). It is usually 5.
 The pressure difference (P) is normally 100.
 Resistance (R) of the vessel needs to be calculated.
 Therefore, applying Ohm’s Law (Q=P/R) to a normal
person, we get this:
5 = 100/R
Solving for R:
R = 100/5
R = 20 PRU
 That means that the normal amount of resistance in the
blood vessels is 20 PRU (peripheral resistance units).
 Overall, the values for a normal person are:
5 = 100/20
Factors Affecting CO



Blood viscosity (decreases CO)
Total vessel length (longer decreases CO)
Vessel diameter (larger increases CO)
Regulation of Blood Flow

Vasodilators
increase blood
flow

Vasoconstrictors
decrease blood
flow
Vasomotor control: Sympathetic Innervation
of Blood Vessels

Sympathetic nerve fibers
innervate all vessels except
capillaries and precapillary
sphincters (precapillary sphincters
follow local control)

Innervation of small arteries and
arterioles allow sympathetic nerves
to increase vascular resistance.

Large veins and the heart are also
Figure 18-2; Guyton and Hall
sympathetically innervated.
116
Baroreceptors respond to changes in
arterial pressure.

As blood pressure increases the number of impulses from carotid
sinus increases which results in:
1) inhibition of vasoconstricton (so the blood vessels
dilate, which lowers blood pressure)
2) activation of the vagal center (lowers blood pressure)
As blood pressure decreases the number of impulses from
carotid sinus decreases which results in:
1) Increased sympathetic activity (which causes blood vessels to constrict)
2) vasoconstricton (which raises blood pressure)
117
Drugs Affecting CO



Atropine- blocks parasympathetic
system (increase in sympathetic
responses)
Pilocarpine- drug that causes
skeletal muscle neurons to
release ACH, which decreases
heart rate.
Propranalol- blocks sympathetic
effect of heart. This causes
decreased heart rate and force
of contraction, and lowers blood
pressure.
Drugs Affecting CO (2)

Digoxin (shorter ½ life)
or Digitoxin- come from
group of drugs derived
from digitalis. Digitalis
derived from foxglove
plant. Slows heart rate
but increases force of
contraction. Is only
drug with this effect on
heart.
– Disadvantage of using digitalis
is that it’s extremely toxic.
The optimal dose is very close
to lethal dose- stops heart
Causes of Edema


Excessive accumulation of tissue
fluid.
Edema may result from:
– High arterial blood pressure.
– Venous obstruction.
– Leakage of plasma proteins
into interstitial fluid.
– Valve problems
– Cardiac failure
– Decreased plasma protein.
– Obstruction of lymphatic
drainage.
– Elephantiasis
120
Control of Hormones Release: Three Mechanisms
Figure 25.2a-c
The Pituitary Gland
Secretes nine major hormones
 Attached to the hypothalamus by the
infundibulum
 Two basic divisions of the pituitary gland

– Adenohypophysis (anterior lobe)
– Neurohypophysis (posterior lobe)
The Adenhypophysis
 Growth hormone (GH)
– Causes the body to grow
 Prolactin (PRL)
– Stimulates lactation (milk production) in females
– Produces desire to cry
– Decreased in adolescent males so it decreases
desire to cry
 Thyroid Stimulating Hormone (TSH)
– Causes the thyroid gland to release thyroid hormone
The Adenhypophysis




Adrenocorticotropic hormone (ACTH)
– Acts on adrenal cortex to stimulate the release of cortisol
– Helps people cope with stress
Melanocyte-stimulating hormone (MSH)
– Darkens skin pigmentation
– Increases during pregnancy
– Also has effects on appetite and sexual arousal
Follicle-stimulating hormone (FSH)
– Present in males and females, affects both
– Stimulates maturation of sex cells
Luteinizing hormone (LH)
– Induces ovulation
Study Tip to remember the hormones
secreted by the pituitary gland

“Melons grow and produce through late fall” stands for the
hormones made in the anterior pituitary.

Melanocyte stimulating hormone (MSH)
Growth Hormone (GH)
Adrenal corticotropic Hormone (ACTH)
Prolactin (stimulates the production of breast milk)
Thyroid stimulating hormone (TSH)
Luteinizing Hormone (LH)
Follicle stimulating Hormone (FSH)






125
The Neurohypophysis
This is a continuation of the brain; cell bodies
of special neurons in the hypothalamus have
axons which go to the neurohypophysis and
synapse on capillaries there. Instead of
releasing neurotransmitter, they release
hormones.
 Oxytocin

– Childbirth contractions

Antidiuretic hormone (ADH)
– Signals kidneys to increase water reabsorption
Figure 25.6
Hypothalamus Regulation

The hypothalamus produces hormones which
affect the pituitary, for example:

Thyroid Stimulating Hormone Releasing Hormone (TSHRH)
– Causes adenohypophysis to secrete TSH
– TSH affects thyroid gland to secrete TH
Thyroid Stimulating Hormone Inhibiting Hormone (TSHIH)
– Causes adenohypophysis to stop secreting TSH so
thyroid gland stops secreting thyroid hormone
The hypothalamus affects the adenohypophysis, and
that’s about it.


Pituitary Disorders

Gigantism and Acromegaly
– Hypersecretion of GH in children
– Gigantism is overall growth
– Acromegaly is enlarged hands and feet

Pituitary dwarfism
– Hyposecretion of GH
– Proportions are normal, overall size is small

Diabetes insipidus
– Not enough ADH (anti-diuretic hormone; a diuretic
takes out excess fluid from the body)
The Thyroid Gland

Thyroid hormone (TH)
–
–
–
–

Acts on most cells of the body
Increases metabolic rate
Controlled by humeral (blood) elements
Iodine is needed to make TH
Calcitonin
– Lowers blood calcium levels in children
– Slows osteoclasts to allow for bone deposition
(Vitamin D is synthesized and secreted by bone cells)
Thyroid Hormone





The major stimulus for the release of thyroid hormone is
humeral (blood elements tell the body it needs more
thyroid hormone).
Thyroid hormone is partly made of iodine. Iodine is
essential for the formation of thyroxin. If a person
doesn’t eat enough iodine, they can’t make thyroid
hormone.
The hypothalamus responds by putting out more TSHRH.
The pituitary will respond by releasing TSH.
But the thyroid can’t respond by releasing TH if it does
not have the iodine to make the hormone, so it the size
of the follicle grows  gland grows  GOITER.
Problems with Thyroid

Goiter
– Too little iodine in the diet

Hyperthyroidism (Graves’ Disease)
– Caused by autoimmune disorder
– Leads to nervousness, weight loss, sweating,
and rapid heart rate

Hypothyroidism
– Decreases metabolism, causes obesity
Hypothyroidism

Hashimodo’s Thyroiditis
– Antibodies attack and destroy thyroid tissue
– Low metabolic rate and weight gain are
common symptoms

Cretinism – hypothyroidism in children
– Short, disproportionate body, thick tongue
and mental retardation
Parathyroid Glands

Parathyroid hormone (PTH)
 Increases blood concentration of Ca2+
 Tells osteoclasts to release calcium from bone
 Tells kidneys to decrease secretion of calcium
 Activates vitamin D which increases calcium uptake by
intestines
 Does NOT metabolize calcium
THYMUS GLAND

Hormones produced by this organ
stimulate the production of T cells.
The Adrenal Glands
Located on the superior surface of the
kidneys
 Two endocrine glands in one

– Adrenal cortex – bulk of the adrenal gland
– Adrenal medulla – a knot of nervous tissue
within the gland
The Adrenal Cortex





Secretes a variety of hormones; All are steroids
CORTISONE  reduces inflammation
CORTISOL helps the body deal with stressful situations like
fasting, anxiety, trauma, and infection. It keeps the blood protein
and glucose levels high enough to support the brain’s activities
and affects the metabolic rate. When the brain perceives a
stressful situation, the hypothalamus tells the pituitary to secrete
ACTH, which travels to the adrenal gland and signals it to release
cortisol to most of the cells of the body.
ALDOSTERONE increases blood volume during hemorrhage or
drop in blood pressure. It causes kidney to reabsorb more
sodium; water follows with it, so the blood volume increases.
SEX HORMONES for the opposite sex: Males produce estrogen
here, and females produce testosterone.
The Adrenal Medulla

Secretes catecholamines:
ADRENALIN (AKA epinephrine “above the kidney”;
Greek).
This is the neurotransmitter for the sympathetic
nervous system.
The adrenal medulla also has sympathetic neurons
which synapse on it, so when you are spooked, the
neurons fire and stimulates the adrenal medulla to
release more epinephrine to increase the effects of
the sympathetic nervous system.
Adrenal Gland Disorders

Cushing’s syndrome
– hypersecretion of cortisol
– Round “moon” face and “buffalo hump”

Addison’s disease
– Hyposecretion of cortisol
– Low blood pressure results
– Also get hyperpigmentation
The Pineal Gland

Pinealocytes secrete melatonin
– A hormone that regulates circadian rhythms
(sense of daytime and night; it regulates
sleep cycle)
Endocrine Hormones
of the Pancreas

Glucagon
 Signals liver to break down glycogen into glucose
 Raises blood sugar

Insulin
 Signals most body cells to take up glucose from
the blood
 Promotes storage of glucose as glycogen in liver
 Lowers blood sugar
Diabetes

DIABETES INSIPIDUS
– pituitary gland does not secrete antidiuretic hormone, or the
kidney does not respond to the hormone.

DIABETES MELLITUS
– hereditary lack of insulin secretion in the pancreas, or resistance
to insulin by the body’s cells.
 Type I diabetes (insulin dependent, develops in children)
– Destruction of pancreatic islets by autoimmune disorders.
– Need insulin injections daily throughout life.
 Type II diabetes (not insulin dependent, develops in adults)
– Consequence of obesity: cells are less sensitive to insulin.
– Initially treated with diet and exercise.
– Oral medicines or injected insulin may be needed.
The Gonads

Ovaries
– Secrete progesterone
 Prepares uterus for pregnancy
– Secrete estrogen
 Female secondary characteristics
 Stores enough for several months

Testes
– Secrete androgens (e.g. testosterone)
 Promotes the formation of sperm
 Maintains secondary sex characteristics
 Testes are the primary sex organs in the male, NOT the
penis
This is what happens in the body:
Hypothalamus (the boss) makes
TSH-RH (thyroid stimulating hormone
releasing hormone)
 Pituitary (the manager) makes TSH
(thyroid stimulating hormone)
 Thyroid gland (the worker) makes TH
(thyroid hormone)

143
Thyroid Hormone


The hypothalamus releases its hormone (TSH-RH) to the
pituitary, telling the pituitary to release its hormone
(TSH), which tells the thyroid gland to release thyroid
hormone (TH).
When thyroid hormone is released, it will circulate
throughout the body, causing an increase in metabolism
in all of those cells. Some of the TH will bind to
receptors in the hypothalamus, and then the
hypothalamus knows there is enough TH, and it will stop
releasing TSH-RH. Until the receptors in the
hypothalamus are bound with the resulting thyroid
hormone, the hypothalamus is not satisfied that there is
enough thyroid hormone present.
144
What if the hypothalamus released its signal and the
thyroid released too much hormone?
The hypothalamus will stop secreting its
releasing hormone. This is a negative
feedback signal.
 When very few TH receptors are bound
on the hypothalamus, it will keep releasing
its hormone. When its thyroid receptors
are saturated, will stop.

145
What if a gland disobeys the negative feedback?




Example: Thyroid gland is impaired by a tumor.
A thyroid tumor might cause it to over-secrete or under-secrete TH.
Under-secreting thyroid tumor: what happens to the other
hormone levels? Start with the problem area (in this case, the
thyroid is the place with the tumor), and then evaluate the other
glands. (Start with the problem area, the thyroid gland)
– TH will be low (hypothyroidism)
– TSH-RH will be high, since only a few hypothalamus
receptors are bound
– TSH levels will be high.
Over-secreting thyroid tumor:
– TH will be high (hyperthyroidism)
– TSH-RH will be low
– TSH levels will be low. This combination tells you the source
of the problem is the thyroid.
146
Another Example: Pituitary tumor



Under-secreting pituitary tumor (Start with the problem
area, the pituitary)
– TSH is low
– TH is low (hypothyroidism)
– TSH-RH is high
Over-secreting pituitary tumor
– TSH is high
– TH is high (hyperthyroidism)
– TSH-RH is low
NOTE: If the problem is the TSH, we don’t bother injecting TSH, we
just give the hormone that is lacking: Thyroid hormone.
147
Example: Hypothalamic Tumor
 Under-secreting hypothalamic tumor
(Start with the problem area, the
hypothalamus)
– TSH-RH is low
– TSH is low
– TH is low (hypothyroidism)
 Over-secreting hypothalamic tumor
– TSH-RH is high
– TSH is high
– TH is high (hyperthyroidism)
148
Other Hormone Cycles

The adrenal cortex has the same cycle as
thyroid hormone; it needs ACTH-RH
(adrenocorticotropic releasing hormone),
ACTH, CH (cortisol hormone).
149
Hormone Levels
Know what would happen to the three
hormone levels (TSH-RH, TSH, TH) in the
following conditions:
 Antibodies attacking thyroid gland,
destroying the gland
 Antibodies binding to the TSH receptor,
stimulating it
 Graves’ Disease
 Hashimoto’s Thyroiditis

150
Regulation of Blood Glucose Levels




When blood glucose is high, the pancreas secretes insulin, which
tells the cells to take in the sugar from the bloodstream. If the blood
sugar levels remain high, the excess sugar is taken to the liver and
converted to glycogen for storage.
When blood glucose is low, the pancreas secretes glucagon, which
tells the liver to take the glycogen and break it back down into
glucose and release it into the bloodstream.
Gluconeogenesis is when the liver takes fatty acids (leftover from
fat metabolism) and joins them to amino acids (from broken down
proteins), and makes new glucose molecules that you did not get
from eating glucose. These new glucose molecules are then
released into the bloodstream to elevate blood glucose levels.
Summary:
– When blood glucose is high, insulin lowers blood glucose levels.
– When blood glucose is low, glucagon causes glycogen breakdown and
gluconeogenesis to raise blood glucose levels.
151
Hyperthyroidism
(Most commonly caused by Graves Disease)
Signs include thinness, eyes that stick out
like a bug (exophthalmoses).
 Graves Disease is a person who has
antibodies that bind to thyroid gland,
tricks it into making excess TH, while
TSH-RH and TSH levels are
decreased. You can also get
hyperthyroidism from over-secreting
thyroid tumors.

152
Disorders of the thyroid-- hyperthyroidism
•Graves disease
•Tumor (of the hypothalamus, pituitary, or thyroid)
Hypothalamus _
TRH
+
Pituitary
Figure 76-8 Patient with exophthalmic
hyperthyroidism. Note protrusion of the eyes and
retraction of the superior eyelids. The basal
metabolic rate was +40. (Courtesy Dr. Leonard
Posey.)
_
Abs
Draw the disrupted pathways!
TSH
+
+
Thyroid
T3, T4
153
Hypothyroidism
This can be caused by
 Hashimoto’s thyroiditis
 Iodine deficiency
 Tumor
154
Cretinism (diminished mental ability)

This term describes babies whose
MOTHER had the lack of iodine. Baby now
cannot get iodine, and the baby will have
reduced growth and intellectual ability.
Once it is born and gets a healthy diet, it
still won’t go back to normal because TH
is necessary for proper myelination and
synaptic formation.
155
Congenital Hypothyroidism
Congenital hypothyroidism is the term
for a baby whose thyroid gland is not
working correctly (not secreting enough
TH). The problem is only with baby, not
with the mom.
 Congenital hypothyroidism and cretin
babies have similar symptoms. Child will
stay tiny because GH does not work
without TH.

156
Hashimoto’s thyroiditis
Hashimoto’s thyroiditis is an autoimmune disorder,
where antibodies attack and destroy the thyroid gland,
and TH goes down while TSH-RH and TSH are
elevated. The healthy remaining thyroid tissue will
enlarge.
 Myxedema is non-pitting edema. Touch it, feels solid,
and does not leave a fingerprint when you push on it. It
is a common symptom in Hashimoto’s thyroiditis. A few
people (4%) with Graves’ Disease get myxedema also.
 People with Hashimoto’s thyroiditis have depressed
mental and emotional activity, may have psychosis, not
in touch with reality, detached. They gain weight easily,
are tired and sleep a lot.
157

The Adrenal Glands
Located on the superior surface of the kidneys
Two endocrine glands in one (different embryological origin)


– ADRENAL MEDULLA – a knot of sympathetic nervous
tissue
 Secretes catecholamines (mostly epinephrine)
– Active in “fight, flight, and fright” response
– ADRENAL CORTEX – bulk of the adrenal gland
 Secretes aldosterone (salt and water balance for blood
pressure)
 Secretes androgens and estrogens (sex hormones)
 Secretes cortisol (anti-stress and anti-inflammation
hormone)
158
Adrenal Medulla
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The adrenal medulla releases catecholamines (epinephrine and
norepinephrine).
These catecholamines are released when the sympathetic nervous system is
activated (“fight or flight”).
When you run from a predator, is that when you want insulin to take glucose from
blood? No, you want to keep it there so the brain can get the glucose. The brain
needs to think of a way to escape, and thinking burns glucose.
Therefore, epinephrine is antagonistic to insulin
Cells that don’t get the glucose during fight or flight break down fatty acids to get
their ATP. These fatty acids will be taken to the liver for gluconeogenesis to elevate
the depleted blood glucose levels. Glycogen will also be broken down to glucose to
elevate the depleted blood glucose levels.
Epinephrine has the same effect as the sympathetic nervous system:
– Heart rate and force increases.
– Digestion slows
– respiratory passages open (bronchiole dilation)
– BP goes up (from vasoconstriction in less-needed organs).
159
Adrenal Cortex

Secretes a variety of hormones- all are steroids (steroids are
made from cholesterol) and are grouped into three main
categories:
– Mineralocorticoids
 Aldosterone -Sodium/water reabsorbed
– Androgens and Estrogens
 Male sex hormones (Androgens)
 Female sex hormones (estrogen)
– Glucocorticoids
 Cortisol – secreted in response to ACTH from the
pituitary gland. Cortisol stimulates fat and protein
catabolism to use for gluconeogenesis.
160
Adrenal Cortex Hormones
Aldosterone
 Testosterone and Estrogen
 Cortisol

161
Aldosterone
Aldosterone (a mineralocorticoid) targets the
cells of kidney, increases the amount of salt and
water that is reabsorbed, and that increases blood
volume, which elevates blood pressure.
162
How Low BP is Raised

When baroreceptors detect low blood pressure, the
kidney releases an enzyme called renin, which cuts
Angiotensinogen into angiotensin-1 (A1), which travels
through blood to the pulmonary capillary bed, where
cells have angiotensin converting enzyme that cuts A1
into A2 (the active form).
– Any word that ends in –ogen means it is a longer, inactive
protein, called a zymogen.
– To become activated, they need to be cut by an enzyme into a
smaller segment.

These high levels of A2 stimulates the adrenal cortex
to make more aldosterone, and also stimulates the
hypothalamus to release ADH.

This will raise the blood pressure.
163
Prednisone,
cortisone, cortisol,
and aldosterone
are all similar in
structure. One can
be used to make
the others.
If ACTH is demanding
more cortisol, but the
body cannot make
enough, it may start
making androgens
instead.
164
Androgens
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Androgens are called male sex hormones because they cause male
secondary sexual characteristics to develop, such as facial hair and
low voice.
The main androgen secreted by the adrenal gland is called DHEA.
DHEA can be converted into testosterone or estrogen.
A large amount of testosterone is made in the testes in males.
A small amount of testosterone is made in adrenal cortex in males
and females.
If the adrenal cortex hyper-secretes testosterone and other
androgens, it won’t impact a male, because the testes make more
than that already.
However, in females, hypersecretion causes masculinization (such
as facial hair and low voice).
165
Estrogen

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Estrogens are one of the female sex hormones because they cause
female secondary sexual characteristics to develop, such as breasts.
A large amount of estrogen is made in the ovaries in females.
A small amount of estrogen is made in adrenal cortex in males and
females.
The androgen, DHEA, can be converted into estrogen.
If the adrenal cortex hypersecretes estrogen, it won’t impact a
female’s sex characteristics, because the ovaries make more than
that already.
However, in males, hypersecretion causes feminization (such as
breast development).
166
Cortisol: Hormonal Mechanism
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ACTH-RH is released by the hypothalamus.
ACTH is released by pituitary.
Cortisol (also called corticotropic hormone or CT).
Cortisol affects almost all cells in body.
Note: When ACTH plus cholesterol is present, you can
take cortisol and turn it into aldosterone if you need to.
– It does not do this unless the blood pressure is too low, because
aldosterone is under a humeral mechanism (turned on by high
blood levels of potassium or A2).
167
Glucocorticoids (cortisol)
Glucocorticoids (GC) are a class of steroid hormones that
bind to the glucocorticoid receptor (GR), which is
present in almost every cell in the body.
 The name glucocorticoid (glucose + cortex + steroid)
derives from their role in the regulation of the
metabolism of glucose, their synthesis in the adrenal
cortex, and their steroidal structure. They suppress the
immune system (they are anti-inflammatory).
 Cortisol (also known as hydrocortisone) is one of the
most important glucocorticoids.
 Others are prednisone, prednisolone, dexamethasone,
and triamcinolone, which are also commonly used
medicines for anti-inflammation.

168
Effects of Increased
Glucocorticoids
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Cortisol is called an anti-stress hormone because it does several
things:
Stimulates protein and fat catabolism (breakdown)
– The breakdown products are then taken to the liver for
gluconeogenesis in the liver
Inhibits glucose uptake by the body but not the brain
It elevates blood glucose (diabetogenic effect)
It inhibits non essential functions like reproduction and growth
It suppresses the immune response
– That means it is an anti-inflammatory agent
It is prescribed as a medicine to suppress inflammation and the
immune system.
169
Cortisol



Cortisol (also known as corticosterol and also
known as hydrocortisone)
The hypothalamus releases ACTH-RH, pituitary releases
ACTH, adrenal gland releases cortisol. The adrenal gland
also can release androgens.
When there is an intense need to make cortisol in
response to stress, and if the body cannot keep
up with the demand for cortisol, excess ACTH
might be shunted into the androgen production
pathway, so that androgens are secreted instead
of cortisol. Excess androgens do not affect males,
but females might develop more masculine
features.
170
Prednisone


If a person has a lot of cortisol or prednisone in their
body, blood sugar levels rise too much, and sugar spills
out in the urine. They have symptoms of diabetes,
although that is not their disease. You have some
cortisol in you now to help maintain normally
elevated blood glucose levels between meals, and
glucocorticoids stimulate smooth muscle in the
vasculature to maintain BP.
In high doses only, prednisone may be given for
asthma because it suppresses smooth muscle
from constricting, and bronchioles cannot close up.
What would you predict their natural prednisone
hormone levels to be, without the inhaler? high
171
ADDISON’S DISEASE
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Also called Primary Adrenal Insufficiency and hypoadrenalism;
mainly see effects in the hands, fingers, and gums.
Addison’s disease may be caused by anything that disturbs the
production of adrenal hormones (for some reason, Tuberculosis
attacks the adrenal glands as well as the lungs, and can cause
hypoadrenalism).
In Addison’s disease, the adrenal cortex does not respond to
pituitary orders. Cortisol levels are low, but pituitary ACTH
and hypothalamus ACTH-RH hormones are high.
Symptoms of Addison’s disease are decreased glucose
levels, a drop in blood pressure from water and salt
imbalance, and darkening of the skin.
172
CUSHING’S DISEASE

Excess ACTH caused only by a pituitary
tumor. Patient has excess cortisol, high
blood pressure, high blood glucose, and too
much aldosterone is produced. More salt and
water is reabsorbed by the kidney, so the blood
volume increases. In this disorder, the
hypothalamus (ACTH-RH) levels are low,
the other hormone levels (ACTH, cortisol,
androgens, and aldosterone) are high.
173
Symptoms of Cushing’s Disease and Cushing’s
Syndrome
Fat
deposition around waist, scapula (buffalo hump),
and “moon” shaped face. There is muscle loss and
weakness (cortisol tells muscles to break down), thin skin
with striae, (High levels of cortisol leads to destruction of
collagen, get thin and striae on skin), hyperglycemia,
immune suppression. Excessive amounts of adrenal
stimulation causes release of male steroids, causing male
secondary characteristics, but only in females. Adult
onset disease in females causes masculinization,
including facial hair, thicker jaw and skull.
174
GROWTH HORMONE
(SOMATOTROPIN)
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GH needs TH to be present. GH stimulates all cells to
increase protein synthesis, fat utilization, and
gluconeogenesis.
Gigantism is the result of excess GH during pre-puberty
and acromegaly is the result of excess GH after growth
plates closed.
The genetic determination of a person’s height has
multiple genes involved, so parents might be tall and
have smaller children. There are no rules to predict it. A
child may also be small due to a defect in the placenta,
blocking nutrients during development.
175
PARATHYROID GLANDS
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There are several of these glands, embedded in the
thyroid gland on the posterior surface.
The parathyroid glands are the ones that are the most
responsible for maintaining blood calcium levels.
They accomplish this by releasing parathyroid
hormone, which stimulates osteoclasts to chew away
bone, releasing the bone’s calcium into the
bloodstream.
176
PARATHYROID GLANDS
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The antagonist of parathyroid hormone is
calcitonin, which is produced in the thyroid gland, and
stimulates osteoblasts to take calcium from the blood
and deposit it in bone.
Parathyroid levels are released by a humeral
mechanism.
If blood calcium levels are low, parathyroid hormone is
released.
If blood calcium levels are high, parathyroid levels are
low.
NOTE: Parathyroid glands are do not actually metabolize
(use up) calcium.
177
PARATHYROID GLANDS
There are three ways that the
parathyroid gland raises blood
calcium levels
 Stimulates osteoclasts to move bone
calcium into the bloodstream
 Stimulates the intestines to absorb more
calcium from diet
 Stimulates the kidneys to stop excreting
calcium

178
Other Endocrine Glands
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Many of the glands we talked about have no other function than to
make hormones. But almost all organs are endocrine glands in
addition to their other functions.
Heart pumps blood and produces hormones
GI tract digests food and produces hormones.
Liver makes enzymes, produces hormones, is involved in calcium
metabolism
Kidney: excretes wastes, makes hormones, is involved in calcium
metabolism and RBC production
Dermis Involved in calcium metabolism, vitamin D synthesis
– Epithelial glands that have ducts are NOT endocrine glands

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Lungs oxygenates and produces hormones.
Bones synthesize and secrete Vitamin D.
Placenta oxygenates and produces hormones.
The only thing that does NOT make hormones are epithelial glands
that have ducts (hormone glands are by definition without ducts).