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ENDOCRINE SYSTEM • 2pancreatic juice secretion

PAGE 1750/ p. 1420 Kidney (juxtaglomerular cells)- erythropoietin renin (hormones


produced)
ENDOCRINE SYSTEM- The endocrine system works with
the nervous system to maintain internal homeostasis and to • Increases red blood cell production
integrate the body’s response to the external environment • Stimulates increase in blood pressure and vascular
volume
• The activities and functions are closely related that it
refers to them as neuroendocrine system Ovaries- estrogen, progesterone (hormones produced)

KEY TERMS • Promotes secondary sex characteristics, prepares


female body for pregnancy
Anterior pituitary: lobe of the pituitary gland that produces
stimulating hormones as well as growth hormone, prolactin and Pancreas- insulin, glucagon, somastostatin (hormones
melanocyte stimulating hormone produced)

Diurnal rhythm: response of the hypothalamus and then the • Regulation of glucose, fat metabolism (islet of
pituitary and adrenals to wakefulness, sleeping and light Langerhans)
exposure
Parathyroid glands- parathyroid hormone (hormones produced)
Glands: organized groups of specialized cells that secrete
• Increases serum calcium levels
hormone or chemical messengers directly into the bloodstream
to communicate within the body Pineal gland- melatonin (hormones produced)
Hormones: chemical messengers working within the endocrine • Affects secretion of hypothalamic hormones,
system to communicate within the body particularly gonadotropin-releasing hormone
Hypothalamic-pituitary axis: interconnection of the Placenta- estrogen, progesterone (hormones produced)
hypothalamus and pituitary gland to regulate levels of certain
endocrine hormones through a complex series of feedback • Maintain fetal growth and development, prepares the
systems body for delivery

Hypothalamus: “master gland of the neuroendocrine system; Stomach- gastrin (hormones produced)
regulates both nervous and endocrine responses to internal and
external stimuli • Stimulates stomach acid production

Negative feedback system: control system in which increasing Testes- testosterone (hormones produced)
levels of a hormone lead to decreased lebels of releasing and • Stimulates secondary sex characteristics in males
stimulating hormones, leading to decreased hormone levels,
which stimulates release of releasing and stimulating Thyroid- thyroid hormone, calcitonin (hormones produced)
hormones; allows tight control of the endocrine system
• Stimulates basal metabolic rate (how the body uses
Neuroendocrine system: the combination of the nervous and energy)
endocrine systems, which work closely together to maintain • Decreases serum calcium levels
regulatory control and homeostasis in the body
HORMONES
Pituitary gland: gland found in the sella turcica of the brain;
produces hormones, endorphins and enkephalins and stores two • Chemicals that are produced in the body that meet
hypothalamic hormones specific criteria
• Produced in very small amounts
Posterior pituitary: lobe of the pituitary that receives • Secreted directly in to the bloodstream
antidiuretic hormone and oxytocin via nerve axons from the • Travel through the blood to specific receptor sites
hypothalamus and stores them to be released when stimulated throughout the body
by the hypothalamus • Act to increase or decrease the normal metabolic
Releasing hormone or factors: chemicals released by the processes of cells when they react with their specific
hypothalamus into the anterior pituitary to stimulate the release receptor sites
of anterior pituitary hormones • Are immediately broken down
• Some hormones react with specific receptor sites on a
GLANDS cell membrane to stimulate the nucleotide cyclic
adenosine monophosphate (cyclic AMP) within the
Adrenal cortex- cortisol aldosterone (hormones produced)
cell to cause an effect
• Increases glucose levels, suppresses inflammatory and
Key points:
immune reactions
• The endocrine system and the nervous system regulate
Intestine- secretin, cholestocytokinin (hormones produced)
body functions and maintain homeostasis largely with
the help of hormones, which are chemicals produced
within the body. Hormones increase or decrease PITUITARY GLAND
cellular activity
• The endocrine system regulates growth and • Located in the skull in the bony Sella turcica under a
development, reproduction, energy use in the body layer of dura mater.
and electrolyte balance • Divided into three lobes:
• Hormones can react with receptors on the cell • Anterior lobe
membrane to cause an immediate effect on a cell by • A posterior lobe
altering systems near the cell membrane, or they may • Intermediate lobe
enter the cell and react with receptor sites on
ANTERIOR PITUITARY- produces six major hormones
messenger RNA, which then enters the nucleus and
alters cell function. ✓ GH
✓ Adrenocorticotropic hormone (ACTH)
HYPOTHALAMUS
✓ Follicle-stimulating hormone (FSH)
• Coordinating center for the nervous and endocrine ✓ Luteinizing hormone (LH)
responses to internal and external stimuli ✓ PRL
• Monitors the body’s homeostasis by analyzing input ✓ Thyroid stimulating hormone (TSH/thyrotropin)
from the periphery and the CNS and coordinating • These hormones are essential for the regulation of
responses through autonomic, endocrine and nervous growth reproduction and some metabolic processes
systems • The anterior pituitary hormones are released in a
• Responsible for regulating a number of body rhythmic manner called diurnal rhythm
functions, including body temperature, thirst, hunger, • Diurnal rhythm occurs when the hypothalamus begins
water retention, blood pressure, respiration, secretion of corticotropin-releasing factor (CRF) in
reproduction, and emotional reactions the evening, peaking at about midnight; adrenocortical
• Maintains internal homeostasis by sensing blood peak response is between 6 and 9 am; levels fall during
chemistries and by stimulating or suppressing the day until evening, when the low level is picked up
endocrine, autonomic and CNS activity. by the hypothalamus and CRF secretion begins again
• Known as the master switchboard of the • produces melanocyte-stimulating hormone (MSH)
neuroendocrine system and various lipotropins.
• Produces: GHRH, TRH, GnRH, CRH, PRH, ADH, • MSH plays an important role in animals that use skin
oxytocin color changes as an adaptive mechanism.
• The hypothalamus is connected to the pituitary gland GROWTH HORMONE ANTAGONISTS
by two networks:
• A vascular capillary network carries the hypothalamic- Gigantism: response to excess kevels of growth hormone
releasing factors directly into the anterior pituitary before the epiphyseal plates close; heights of 7 to 8 feet are not
• A neurological network delivers two other hypothalamic uncommon
hormones—Antidiuretic hormone (ADH) and
Acromegaly: thickening of bony surfaces in response to excess
oxytocin—to the posterior pituitary to be stored
growth hormone after the epiphyseal plates have closed
Other controls
Pegvisomant is a GH receptor antagonist
• Glucose levels
• it binds to the GH receptor but does not activate or
• Calcium levels
stimulate IGF-1 secretion
• Renal blood flow
• approved by the FDA for the treatment of acromegaly
• Local GI stimuli
• administered SC
• Potassium levels
• based on serum IGF-1 levels, the dose is titrated at 4–
• Other local stimuli
6-week intervals
HYPOTHALAMIC RELEASIC FACTORS STOMASTOTIN- it inhibits the release of GH, glucagon,
• Growth hormone releasing hormone (GHRH) insulin, and gastrin has limited therapeutic usefulness
• Thyrotropin releasing hormone (TRH) OCTEOTIDE- reduced symptoms caused by a variety of
• Gonadotrophin releasing hormone (GnRH) hormone-secreting tumors
• Corticotropin releasing hormone (CRH)
• Prolactin releasing hormone (PRH) • acromegaly; the carcinoid syndrome; gastrinoma;
glucagonoma; nesidioblastosis
Key Points: • the watery diarrhea, hypokalemia and achlorhydria
(WDHA) syndrome; and diabetic diarrhea
• The hypothalamus produces stimulating and inhibiting
factors that travel to the anterior pituitary through a POSTERIOR PITUITARY HORMONES
capillary system to stimulate the release of pituitary
hormones or block the production of certain pituitary • stores two hormones that are produced by the
hormones when levels of target hormones get too high hypothalamus and deposited in the posterior lobe via
the nerve axons where they are produced.
• antidiuretic hormone (ADH), also known as hypothalamus secretes releasing factors to cause the
vasopressin and oxytocin anterior pituitary to release stimulating hormones,
• oxytocin stimulates milk ejection or let down in which act with specific endocrine glands to cause the
lactating women release of hormone
• ADH is directly released in response to increased • GH and PRL are released by the anterior pituitary and
plasma osmolarity or decreased blood volume. directly influence cell activity. These hormones are
• Osmoreceptors stimulate the release of ADH regulated by the release of the hypothalamic-
• ADH acts in the kidneys to increase retention of water inhibiting factors somatostatin and PIF in response to
in order to decrease the osmolarity of the blood the levels of the pituitary hormones GH and PRL
volume.
CHAPTER 35: HYPOTHALAMIC AND
ADH DISORDERS PITUITARY AGENTS

• diabetes insipidus (DI): results from insufficient Key Terms:


secretion of ADH
• syndrome of inappropriate antidiuretic hormone Acromegaly: thickening of bony surfaces in response to excess
growth hormone after the epiphyseal plates have closed
(SIADH) occurs with excessive secretion of ADH
Diabetes insipidus: condition resulting from a lack of
VASOPRESSIN AND DESMOPRESSIN- treatments of
antidiuretic hormone, which results in the production of
choice for antidiuretic replacement therapy in central diabetes
copious amounts of glucose-free urine
A. vasopressin (synthetic vasopressin)
Dwarfism: small stature, resulting from lack of growth
Diabetes insipidus- vasodilatory shock, effective in some cases hormone in children
of esophageal variceal bleeding and colonic diverticular
bleeding Gigantism: response to excess levels of growth hormone before
the epiphyseal plates close; heights of 7 to 8 are not uncommon
B. desmopressin
Hypopituitarism: lack of adequate function of the pituitary;
diabetes insipidus- nocturnal enuresis, hemophilia A, von reflected in many endocrine disorders
willebrand’s disease (Vwd) (Type 1)
DRUGS AFFECTING HYPOTHALAMIC HORMONES
INTERMEDIATE LOBE
AGONISTS
• produces endorphins and enkephalins, which are
released in response to severe pain or stress and • Goserelin
occupy specific endorphin receptor sites in the • Histrelin
brainstem to block the perception of pain.
leuprolide
Key points:
• Nafarelin
The pituitary gland has three lobes: • Tesamorelin

• the anterior lobe produces stimulating hormones in ANTAGONISTS


response to hypothalamic stimulation
• Cetrorelix
• the posterior lobe stores ADH and oxytocin, which are
• Degarelix
two hormones produced by the hypothalamus
• Ganirelix
• the intermediate lobe produces endorphins and
enkephalins to modulate pain perception DRUGS AFFECTING ANTERIOR PITUITARY
HORMONES
HYPOTHALAMIC-PITUITARY AXIS

• uses series of negative feedback system works muck GROWTH HORMONE AGONISTS
like the law of supply and demand in business • somatropin
• when the hypothalamus senses a need for a particular • Somatropin rDNA origin
hormone such as thyroid hormone where it secretes the
releasing hormone or factor TRH directly into the GROWTH HORMONE ANTAGONISTS
anterior pituitary.
• The anterior pituitary secretes TSH which stimulates • bromocriptine mesylate
thyroid gland to produce thyroid hormone. • Lanreotide
• When the hypothalamus senses the rising levels of • Octeotide acetate
thyroid hormone, It stops secreting TRH, resulting in • Pegvisomant
decreased TSH production DRUGS AFFECTING OTHER ANTERIOR PITUITARY
Key points: HORMONES

• The hypothalamus and pituitary operate by a series of • Chorionic gonadotropin


negative feedback mechanisms called the HPA. The • Chorionic gonadotropin alpha
• Cosyntropin reach a low in the late evening, with the lowest levels
• Pasireotide around midnight
• Thyrotropin alpha
GLUCOCORTICOIDS
DRUGS AFFECTING POSTRIOR PITUITARY
• Enter target cells and bind to cytoplasmic receptors,
HORMONES
initiating many complex reactions that are responsible
• Conivaptan for anti-inflammatory and immunosuppressive effects
• Desmopressin • Indicated for the short-term treatment of many
• Tolvaptan inflammatory disorders, to relieve discomfort and to
give the body a chance to heal from the effects of
DRUGS AFFECTING HYPOTHALAMIC HORMONES inflammation
• Adverse effects: fluid retention, congestive heart
Stimulate the release of hormones failure, increased appetite, weight gain, fragile skin,
loss of hair, weakness, muscle atrophy, increased
• Growth hormone-releasing hormone (GHRH)
susceptibility to infections, development of cancers
• Thyrotropin-releasing hormone (TRH)
• Adverse effects on children: risk for growth
• Gonadotropin-releasing hormone (GnRH)
retardation associated with suppression of the
• Corticotropin-releasing hormone (CRH)
hypothalamic pituitary system
• Prolactin releasing hormone (PRH)
MINERALCORTICOIDS
Inhibit the release of hormone
• Increase sodium reabsorption in the renal tubules and
• Stomastotin
increase potassium and hydrogen excretion, leading to
• Prolactin-inhibiting factor (PIF) water and sodium retention
Hypothalamic releasing hormones • Indicated in combination with a glucocorticoid, for
replacement therapy in primary and secondary adrenal
• Goserelin (zoladex) (synthetic GnRH) insufficiency, treatment of salt-wasting adrenogenital
• Histrelin (Vantas) (antineoplastic agent) syndrome
• Leuprolide (Lupron) • Adverse effects: increased fluid volume seen with
• Nafarelin (synarel) sodium and water retention, headache, edema,
• Tesamorelin (Egrifta) hypertension, CHF, arrythmias, weakness,
hypokalemia
Antagonists that block the effects of hypothalamic-releasing
hormones CHAPTER 37: THYROID AND PARATHYROID
AGENTS
• Cetrorelix (cetrotide) (GnRH antagonist and fertility
drug) HYPOTHYDOIDISM
• Degarelix (Firmagon) (Blocks GnRH and is used as
an antineoplastic agents) • Absence of thyroid gland
• Ganirelix acetate (antagon) (blocks GnRH) • Lack of sufficient iodine in the diet to produce the
needed level of thyroid hormone
CHAPTER 36: ADRENOCORTICAL AGENTS • Lack of sufficient functioning thyroid tissue due to
humor or autoimmune disorders
(P. 1836/ p. 1478) • Lack of TSH due to pituitary diseases
ADRENAL GLANDS • Lack of TRH related to a tumor or disorder of the
hypothalamus
• adrenal medulla: inner layer of the adrenal gland:
sympathetic ganglia, releases norepinephrine and CRETINISM: lack of thyroid hormone in the infant; if
epinephrin into circulation in response to sympathetic untreated, leads to mental retardation
stimulation MYXEDEMA: severe lack of thyroid hormone In adults
• adrenal cortex: layer of the adrenal gland; produces
glucocorticoids and mineralocorticoids in response to Treatment:
ACTH stimulation; also responds to sympathetic
• Levothyroxine (levoxyl, Synthroid, tirosint, unithroid,
stimulation
unithroid direct), a man-made version of the thyroid
DIURNAL RHYTHM hormone thyroxine (T4). It acts just like the hormone
your thyroid gland normally makes. The right dose can
• Secretion of CRH, ACTH and cortisol are high in the make you feel a lot better
morning in day-oriented people those who have
regular cycle of wakefulness during the day and sleep HYPERTHYROIDISM
during the night. In such individuals, the peak levels
• Excess levels of thyroid hormone
of cortisol usually come between 6 and 8 am. The
levels then fall off slowly (with periodic spurts) and • Graves’ disease is thought to be an autoimmune
problem
• Treatments: surgical removal of the gland or portions • Polydipsia: increased thirst, seen in diabetes when loss
of the gland; treatment with radiation to destroy parts of fluid and increased tonicity of the blood lead to
or all of the gland; or drug treatment to block the hypothalamic thirst center to make the patient feel
production of thyroxine in the thyroid gland or to thirsty
destroy parts or all of the gland • Ketosis: breakdown of fats for energy, resulting in an
increase in ketones to be excreted from the body
ANTITHYROID AGENTS
DIABETES RELATED DISORDERS
• Thioamides
• propylthiouracil, • Atherosclerosis: heart attacks and strokes
• methimazole • Retinopathy: loss of vision
• iodine solutions • Neuropathies: motor and sensory changes in the feet
and legs and progressive changes in other nerves
PAGET’S DISEASE- of bone interferes with your body’s • Nephropathy: renal dysfunction
normal recycling process, in which new bone tissue gradually
replaces old bone tissue. Over time, the disease can cause KETOACIDOSIS
affected bones to become fragile and misshapen. PAGET’S
DISEASE of bone most commonly occurs in the pelvis, skull, • Fruity breath as the ketones builds up in the system
spine and legs and are excreted through the lungs
• Dehydration as fluid and important electrolytes are
ANTIHYPERCALCEMIC AGENTS lost through the kidneys
• Slow, deep respirations as the body tries to rid itself of
• BISPOSPHONATES- patient must stay upright for
high acid levels
at least 30 minutes after taking the drug on an empty
• Loss of orientation and coma
stomach
• CALCITONINS Diabetic ketoacidosis- is a serious complication of diabetes that
occurs when your body produces high levels of blood acids
BISPOHSPONATES- are a class of drugs that prevent the loss
called ketones. The condition develops when your body can’t
of bone density, used to treat osteoporosis and similar diseases.
produce enough insulin
They are the most commonly prescribed drugs used to treat
osteoporosis. Ketoacidosis vs nonketotic hyperosmolar syndrome
Side effects for all the bisphosphonates • Although both conditions can occur at ant age,
diabetic ketoacidosis typically develops in younger
• Alendronate, ibandronate, risedronate and zoledronic
patients, less than 45 years, who have little or no
acid
endogenous insulin production, whereas HHS usually
• Bone, joint or muscle pain, nausea, difficult
occurs in much older non-insulin-dependent patients
swallowing, heartburn, irritation of the esophagus
( who are often greater than 60 years old)
(tube connecting the throat to the stomach) and
gastric ulcer HYPOGLYCEMIA
CALCITONIN- is a hormone that is produced in humans by • Blood sugar level below 40 mg/dl, occurs in a number
the parafollicular cells (commonly known as c-cells) of the of clinical situations, including starvation and when
thyroid gland treatment of hyperglycemia with insulin or oral agents
lowers the blood sugar too far
• Is involved in helping to regulate levels of calcium
• Sympathetic response to lower blood sugar
and phosphate in the blood, opposing the action of
parathyroid hormone

CHAPTER 38: ANTIDIABETIC AGENTS THE TYPE OF INSULIN INCLUDE:

DIABETES MELLITUS • Rapid-acting


• Short-acting
• Most common of all metabolic disorders • Intermediate-acting
• Affects many end organs and causes numerous clinical • Long-acting
complications • Pre-mixed
• Treatment is aimed at tightly regulating the blood
sugar level through the use of insulin or insulin SULFONYLUREAS
stimulating drugs
• Bind to potassium channels on pancreatic beta cells to
HYPERGLYCEMIA increase insulin secretion
• May improve insulin binding to insulin receptors and
• Glycosuria: presence of glucose in the urine increase the number of insulin receptors
• Polyphagia: increased hunger, sign of diabetes when • Increase the effect of ADH on renal cells
cells cannot use glucose for energy and feel that they
• Effective only in patients who have functioning beta
are starving, causing hunger
cells
NONSULFONYLUREAS CHAPTER 43: DRUGS AFFECTING BLOOD
PRESSURE
• Acarbose
• Metformin
• Miglitol
• Pioglitazone CATEGORIES RATING THE SEVERITY OF
• Repaglinide HYPERTENSION
• Rosiglitazone BP RANGE CATEGORY
• Nateglinide
Systolic pressure Diastolic pressure
CHAPTER 42: INTRODUCTION TO THE
CARDIOVASCULAR SYSTEM
<130 mmHg <85 mmHg Normal blood
CARDIAC CYCLE pressure

Diastole: resting phase of the heard; blood is returned to the 130-139 85-89 High normal
heart during this phase blood pressure

Systole: contracting phase of the heart; blood is pumped out of 140-159 90-99 Stage 1 (mild)
the heart during this phase hypertension
160-179 100-109 Stage 2
Cardiac cycle: a period of cardiac muscle relaxation followed (moderate)
by a period of contraction in the heart hypertension
180-209 110-119 Stage 3 (severe)
Deoxygenated blood: right atrium through tricuspid valve to hypertension
the lungs
>210 >120 Stage 4 (very
Oxygenated blood: through the pulmonary veins to the left severe)
atrium through the mitral valve to the left ventricle, through the hypertension
aortic valve to the aorta ANTIHYPERTENSION

Membrane potential: refers to the difference in charge • Diuretics


between the inside and outside of a neuron, which is created • beta blockers
due to the unequal distribution of ions on both side of the cell • alpha and beta blockers
• alpha adrenergic blockers
Action potential: refers to the electrical signaling that occurs • alpha1 blockers
within neurons
• alpha2 agonists
MECHANICAL ACTIVITY
ANGIOTENSIN-CONVERTING ENZYME INHIBITORS
Sarcomere: functional unit of a muscle cell, composed of actin (ACE)
and myosin molecules arranged in layers to give the unit a
• prevent angiotensin-converting enzymes from
striped or striated appearance
converting angiotensin I to angiotensin II, a powerful
Actin: thin filament that makes up a sarcomere or muscle unit vasoconstrictor and stimulator of aldosterone release,
leading to a decrease in blood pressure and in
Myosin: thin filament with projections that makes up a aldosterone secretion with a resultant slight increase in
sarcomere or muscle unit serum potassium and a loss of serum sodium and fluid
• indicated for the treatment of hypertension, alone or in
Troponin: chemical in heart muscle that prevents actin and
combination with other drugs
myosin from reacting, leading to muscle relaxation, inactivated
by calcium during muscle stimulation to allow actin and myosin
to react, causing muscle contraction

Hydrostatic pressure (HP): driving force of heart ends to push


fluid out of capillary ANGIOTENSIN II RECEPTOR BLOCKERS (ARB)

Oncotic pressure (OP): pressure exerted by plasma proteins • selectively bind with angiotensin II receptor sites in
ends to pull fluid into capillary vascular smooth muscle and in the adrenal gland to
block vasoconstriction and the release of aldosterone
Filtration pressure: net force on fluid, determined by the • indicated to be used alone or in combination therapy
balance between HP and OP for the treatment of hypertension

CALCIUM CHANNEL BLOCKERS

• inhibit the movement of calcium ions across the


membranes of myocardial and arterial muscle cells,
altering the action potential and blocking muscle cell
contraction; depressing myocardial contractility,
slowing cardiac impulse formation in the conductive diuretics alone or who have poor response to digoxin,
tissues, and relaxing and dilating arteries, causing a diuretics and vasodilators
fall in blood pressure and a decrease in venous return
• indicated for treatment of hypertension and angina CHAPTER 45: ANTIARRHYTHMIC AGENTS

VASODILATORS Membrane potential: refers to the difference in charge


between the inside and outside of a neuron, which is created
• act directly on vascular smooth muscle to cause due to the unequal distribution of ions on both sides of the cell
muscle relaxation, leading to vasodilation and drop in
blood pressure Action potential: refers to the electrical signaling that occurs
• indicated for the treatment of severe hypertension that within neurons
has not responded to other therapy
CARDIAC ARRHYMIAS
ANTIHYPOTENSIVE AGENTS
Tachycardia- more than 100 heart bpm
• sympathetic adrenergic agonists Bradycardia- less than 60 heart bpm
• midodrine
Premature atrial contraction (PACs)- Caused by an ectopic
CHAPTER 44: CARDIOTONIC AGENTS focus in the atria stimulating an atrial response

Premature ventricular contractions (PVCs)- an ectopic


focus in the ventricles stimulating the cells and causing an early
Congestive heart failure: a condition in which the heart contraction
muscle fails to adequately pump blood around the
cardiovascular system leading to a backup or congestion of Heart blocks- blocks conduction of an impulse
blood in the system
CAUSES OF CARDIAC ARRHYTHMIAS
Pulmonary edema: severe left-sided congestive heart failure
with backup of blood into the lungs, leading to loss of fluid into • electrolyte disturbances
the lung tissue • decreases in the oxygen delivered to the cells
• structural damage
Inotropic agents, or inotropes: are medicines that change the • acidosis or the accumulation of waste products
force of your heart’s contractions. There are 2 kinds of
inotropes. Positive inotropes strengthen the force of the ANTIARRHYTHMIC DRUGS
heartbeat. Negative inotropes weaken the force of the heartbeat
Antiarrhythmics- drugs that can affect the action potential of
Chronotropic effects (from chrono- time, and tropos- a turn) are cardiac cells and are used to treat arrhythmias and return normal
those that change the heart rate rate and rhythm

Digitalis glycosides exert a positive inotropic effect, i.e. an Proarrhythmic- tending to cause arrhythmias; many of the
increase in myocardial contractility associated with a drugs used to treat arrhythmias have been found to generate
prolongation of relaxation period, and glycosides lower the arrhythmias
heart rate (negative chronotropic), impede stimulus conduction
Cardiac arrhythmia suppression trial (CAST)- a large research
(negative dromotropic) and promote myocardial excitability
study, basis for current indication for antiarrhythmics- used for
CARDIAC GLYCOSIDES short term to treat life threatening ventricular arrhythmias, not
long term.
• increase intracellular calcium and allow more calcium
to enter myocardial cells during depolarization, NORMAL SINUS RHYTHM
causing the following effects
• increased force of myocardial contraction
• increased cardiac output and renal perfusion
• slowed heart rate by slowing the rate of cellular
repolarization
• decreased conduction velocity through the AV node

PHOSPHODIESTERASE INHIBITORS

• block the enzyme phosphodiesterase leading to an


increase in myocardial cell cAMP, which increases
calcium levels in the cell causing a stronger
contraction and prolonged effects of sympathetic
stimulation, leading to vasodilation, increased
oxygen consumption and arrhythmias
• indicated for the short-term treatment of CHF in
patients who are not responding to digoxin or
SINUS TACHYCARDIA

SINUS BRADYCARDIA

NITRATES

• caused direct relaxation of smooth muscle with a


resultant decrease in venous return and decrease in
PREMATURE ATRIAL CONTRACTION arterial pressure, which reduces cardiac workload and
decreases myocardial oxygen consumption
• indicated for the prevention and treatment of attacks
of angina pectoris
• adverse effects are related to the vasodilation and
decrease in blood flow that occurs

BETA BLOCKERS
PREMATURE VENTRICULAR CONTRACTION • competitively block beta-adrenergic receptors in the
heart and juxtaglomerular apparatus, decreasing the
influence of the sympathetic nervous system on these
tissues and thereby decreasing the excitability of the
heart, cardiac output, and cardiac oxygen
compensation, and lowering blood pressure
• indicated for the long-term management of angina
3RD DEGREE HEART BLOCK pectoris caused by atherosclerosis
• adverse effects are related to their blockade of the
sympathetic nervous system

CALCIUM CHANNEL BLOCKERS

• inhibit the movement of calcium ions across the


membranes of myocardial and arterial muscle cells,
CHAPTER 46: ANTIANGINAL AGENTS altering the action potential and blocking muscle cell
contraction
CORONARY ARTERY DISEASE • indicated for the treatment of prinzmetal’s angina,
chronic angina, effort-associated angina, and
Atheromas: fatty tumors in the intima of the vessels
hypertension
Atherosclerosis: narrowing of the arteries caused by build up of • adverse effects are related to their effects on cardiac
atheromas, swelling and acculation of platelets; leads to a loss output and on smooth muscle
of elasticity and responsiveness to normal stimuli
CHAPTER 47: LIPID LOWERING AGENTS
Angina pectoris: “suffocation of the chest”; pain caused by the
imbalance between oxygen being supplied to the heart and CORONARY ARTERY DISEASE RISK FACTORS
muscle and demand for oxygen by the heart muscle
Unmodifiable risk factors
Myocardial infarction: end result of vessel blockage in the
heart, leads to ischemia and then necrosis of the area cut off • genetic predispositions, age, gender
from the blood supply; can heal, replacing the dead cells with modifiable risk factors
scar tissue
• gout, cigarette smoking, sedentary lifestyle, high
Prinzmetal’s angina: drop in blood flow through the coronary stress levels, hypertension, obesity, diabetes,
arteries caused by a vasospasm in the artery, not by bacterial infections
atherosclerosis
METABOLISM OF FATS • the most common adverse effect associated with
these drugs reflect their effects on the GI system
Bile acids: cholesterol-containing acids found in the bile, which
act like detergents to break up fats in the small intestine OTHER DRUGS USED TO AFFECT LIPID LEVELS
Cholesterol: necessary component of human cells and the Clofibrate- inhibits liver synthesis of LDL and cholesterol,
formation of steroid hormones; produced in the body and found lowers serum lipids, and has an antiplatelet effect
in dietary fats
Fenofibrate- inhibits triglyceride synthesis in the liver, resulting
Chylomicron: carrier for lipids in the blood stream, consists of in the reduction of LDLs; increases uric acid secretion; and may
proteins and lipids, cholesterol and so forth stimulate triglyceride breakdown
Low density lipoproteins (LDL): tightly packed fats that are Gemfibrozil- inhibits peripheral breakdown of lipids, reduces
thought to contribute to the development of CAD when triglyceride production and LDL production, and increases
remnants left over from the LDL are processed in the arterial HDL concentrations
lining
Vitamin niacin- inhibits the release of free fatty acids rom
High density lipoproteins (HDL): loosely packed chylomicron adipose tissue, increases the rate of triglyceride removal from
containing fats, able to absorb fats and fat remnants in the plasma, and generally reduces LDL and triglyceride levels and
periphery; thought to have a protective effect, decreasing increases HDL levels
development of CAD
CHAPTER 48: DRUGS AFFECTING BLOOD
HMG CoA reductase: enzyme that regulates the last step in COAGULATION
cellular cholesterol synthesis

Factor XI/ plasma thromboplastin antecedent: is the zymogen


form of factor XLa, one of the enzymes of the coagulation
cascade

Partial thromboplastin Time (PTT): a blood test that measures


BILE ACID SEQUESTRANTS the time it takes your blood to clot. A PPT test can be used to
check for bleeding problems. Blood clotting factors are needed
• bind with bile acids in the intestine to form a complex for blood to clot (coagulation)
that is excreted in the feces
• used to reduce serum cholesterol in patients with • The reference range of the aPTT is 30-40 seconds. The
primary hypercholesterolemia (with high LDLs) as an reference range of the PTT is 60-70 seconds. In
adjunct to diet and exercise patients receiving anticoagulant therapy, the reference
• adverse effects include: direct GI irritation, including range is 1.5-2.5 times the control value in seconds
nausea, and constipation that may progress to fecal Prothrombin time: test measures how quickly your blood clots.
impaction Sometimes called a PT or pro time test, a prothrombin time test
HMG CoA REDUCTASE INHIBITORS uses a sample of your blood. Prothrombin is a protein produced
by your liver. It is one of many factors in your blood that help
• block the formation of cellular cholesterol, leading to it to clot appropriately.
a decrease in serum cholesterol and a decrease in
serum LDLs, with a slight increase or no change in • Most of the time, results are given as what is called
the levels of HDLs INR (international normalized ratio). If you are not
• indicated as adjuncts with diet and exercise for the taking blood thinning medicines, such as warfarin, the
treatment of elevated cholesterol and LDL levels in normal range for your PT results is: 11 to 13.5
patients unresponsive to dietary restrictions alone; to seconds
slow the progression of CAD in patients with ANTIPLATELET DRUGS
document CAD; to prevent first MI in patients who
are at risk for MI development • Inhibit platelet adhesion and aggregation by blocking
receptor sites on the platelet membrane, preventing
platelet-platelet interaction or the interaction of • Tranexamic acid
platelets with other clotting chemicals • Aprotinin
• Used to decrease the risk of fatal MI, to prevent • Diamino arginine vasopressin
reinfarction after MI, to prevent thromboembolic
stroke, and to maintain the patency of grafts CHAPTER 49: DRUGS USED TO TREAT ANEMIAS
• Most common adverse effects seen with these drugs is
bleeding BLOOD

Antiplatelets include Plasma: the liquid part of blood

• ASA: aka acetylsalicylic acid (aspirin, asaphen, Erythrocytes: RBC


entrophen, novasen) clopidogrel (Plavix) Erythropoiesis: RBC production
• Prasugrel (effient)
• Ticagrelor (brilinta) Anemia: decrease in the number of RBCs

ANTICOAGULANTS • Megaloblastic anemia: bone marrow contains large


number of large immature RBCs
• Interfere with the normal cascade of events involved • Iron deficiency anemia: low amounts of iron available
in the clotting process in the blood
• Used to treat thromboembolic disorders such as atrial • Pernicious anemia: gastric mucosa cannot produce
fibrillation, MI, pulmonary embolus, and evolving intrinsic factor and vitamin B12 cannot be absorbed
stroke, and to prevent the formation of thrombi in such
disorders LARGE, STRUGCTURALLY ABNORMAL,
• Most commonly encountered adverse effect is IMMATURE RBC
bleeding
• Oral-warfarin
• Parenteral- heparin: low molecular weight heparins

THROMBOLYTIC AGENTS

• Work by activating plasminogen to plasmin, which in


turn breaks down fibrin threads in a clot to dissolve a
formed clot
• Indicated for the treatment of acute MI; to treat
pulmonary emboli and ischemic stroke; and to open
clotted IV catheters
• Most common adverse effect is bleeding

The most commonly used clot-busting drugs aka Thrombolytic ERYTHROPOIETIN


agents include
• Act like natural glycoprotein erythropoietin to
• Eminase (anistreplase) stimulate the production of RBC in the bone marrow
• Retavase (reteplase) • Indicated for the treatment of anemia associated with
• Streptase (streptokinase, kabikinase) renal failure or for patients on dialysis; to decrease the
• T-PA (class of durgs that include activase) need for blood transfusions in surgical patients, for the
• TNKase (Tenecteplase) treatment of anemia associated with AIDS treatment,
• Abbokinase, kinlytic (rokinase) and for the treatment of anemia associated with cancer
chemotherapy
BLEEDING DISORDERS

• Hemophilia
• Liver disease
• Bone marrow disorders

DRUGS USED TO CONTROL BLEEDING

• Antihemophilic agents
• Systemic hemostatic agents
• Topical hemostatic agents

Substances- hemostatic agents

• Aminocaproic
• Antifibrinolytic agents IRON DEFICIENCY ANEMIAS
• Estrogens, conjugated (USP)
• Hemostatics • Menstruating women who lose RBCs monthly
• Pregnant and nursing women who have increased • Produced by C (parafollicular) cells
demands for iron
• Rapidly growing adolescents, especially those who do
not have nutritious diet
• Persons with GI bleeding; even individuals with slow
bleeding associated with NSAIDs may develop this
disorder

IRON PREPARATIONS

• Elevate the serum iron concentration


• Indicated for the treatment of iron deficiency anemias,
may also be used for adjunctive therapy in patients
receiving epoetin alfa
• Most common adverse effects associated with oral
iron are related to direct GI irritation

Megaloblastic anemia treatments PARATHYROID GLANDS


• Folic acid derivatives • Tiny masses on the posterior of the thyroid
• Vitamin B12

ENDOCRINE AND CIRCULATORY SYSTEM

• Found at the base of the throat


• Consists of two lobes and a connecting isthmus
• Produces two hormones
• Thyroid hormone
• calcitonin

THYROID HORMONE

• Major metabolic hormone • Secrete parathyroid hormone


• Composed of 2 active iodine-containing hormones • Stimulate osterclasts to remove calcium from bone
• Thyroxine (T4)- secreted by thyroid follicles • Stimulate the kidneys and intestine to absorb more
• Triiodothyronine (T3)- conversion of T4 at calcium
target tissues • Raise calcium levels in the blood

ADRENAL GLANDS
CALCITONIN • Two glands
• Cortex- outer glandular region in three layers
• Decreases blood by calcium levels by causing its
• Medulla- inner neural tissue region
• Sits on top of the kidneys

HORMONES OF THE ADRENAL CORTEX

Mineralocorticoids (mainly aldosterone)

• Produced in outer adrenal cortex


• Regulate mineral content in blood, water and
electrolyte balance
• Target organ is the kidney
deposition on bone • Production stimulated by renin and aldosterone
• Antagonistic to parathyroid hormone
• Production inhibited by atrial natriuretic peptide • The islets of the pancreas produce hormones
- Insulin: allows glucose to cross plasma membranes
into cells from beta cells
- Glucagon: allows glucose to enter the blood from
alpha cells
- These hormones are antagonists that maintain blood
sugar homeostasis

Glucocorticoids (including cortisone and cortisol)

• Produced in the middle layer of the adrenal cortex


• Promote normal cell metabolism
• Help resist long-term stressors
• Released in response to increased blood levels of ACTH

Sex hormones

- Produced in the inner layer of the adrenal cortex


- Androgens (male) and some estrogen (female)

HORMONES OF THE ADRENAL MEDULLA

• Produces 2 similar hormones (catecholamines)


- Epinephrine
- Norepinephrine
• These hormones prepare the body to deal with short
term stress

ROLES OF THE HYPOTHALAMUS AND ADRENAL


GLANDS IN THE STRESS RESPONSE

Short term stress response (catecholamines) EPI/NOREPI PANCREATIC HORMONES AND BLOOD SUGAR

1) Increased HR PINEAL GLAND


2) Increased BP
3) Liver converts glycogen to glucose and releases • Fond on the 3rd ventricle of the brain
glucose to blood • Secretes melatonin
4) Dilation of bronchioles - Helps establish the body’s wake and sleep cycles
5) Changes in blood flow patterns, leading to increased - May have other as yet unsubstantiated functions
alertness and decreased digestive and kidney activity THYMUS
6) Increased metabolic rate
• Located posterior to the sternum
Long term stress response (Mineralocorticoids)
• Largest in infants and children
1) Retention of sodium and water by kidneys • Produces thymosin
2) Increased blood vol and BP - Matures some types of WBC
- Important in developing the immune system

HORMONES OF THE OVARIES

Estrogen- produced by graafian follicles/ placenta


Glucocorticoids

1) Proteins and fats converted to glucose or broken down


for energy
2) Increased blood sugar
3) Suppression of immune system

PANCREATIC ISLETS

• The pancreas is a mixed gland


- Stimulates the development of secondary female
characteristics
- Matures female reproductive organs
- Helps prepare the uterus to receive a fertilized
egg
- Helps maintain pregnancy
- Prepares the beast to produce milk

Progesterone- produced by the corpus luteum

- Acts with estrogen to bring about the menstrual


cycle
- Helps in the implantation of an embryo in the
uterus

HORMONES OF THE TESTES

- Interstitial cells of tester are hormone producing - Classified as a connective tissue


- Produce several androgens - Living cells- formed elements
- Testosterone is the most important androgen - Non living matrix- plasma
✓ Responsible for adult male secondary sex
characteristics PHYSICAL CHARACTERISTICS OF BLOOD
✓ Promotes growth and maturation of male
- Color range:
reproductive system
✓ Oxygen- rich blood is scarlet red
✓ Required for sperm cell production
✓ Oxygen poor blood is dull reed
OTHER HORMONE-PRODUCING TISSUES AND - pH must remain between 7.35-7.45
ORGANS - blood temperature is slightly higher than body
temperature
- Parts of the small intestine
- Parts of the stomach BLOOD PLASMA
- Kidneys
- composed of approximately 90% water
- Heart
- includes many dissolved substances
- Many other areas have scattered endocrine cells
✓ nutrients
ENDOCRINE FUNCTION OF THE PLACENTA ✓ salts (metal ions)
✓ respiratory gases
- Produces hormone that maintain the pregnancy ✓ hormones
- Some hormones play a part in the delivery of the baby ✓ proteins
✓ waste products

PLASMA PROTEINS

Albumin: regulates osmotic pressure

Clotting proteins- help to stem blood loss when a blood vessel


is injured

Antibodies- help protect the body from antigens

FORMED ELEMENTS

Erythrocytes: RBC

- Produces HCG in addition to estrogen, progesterone Leukocytes: WBC


and other hormones Platelets: cell fragments
DEVELOPMENTAL ASPECTS OF THE ENDOCRINE ERYTHROCYETS (RBC)
SYSTEM
- the main function is to carry oxygen
- Most endocrine organs operate smoothly until old age - outnumber WBC 1000:1
✓ Menopause is brought about by lack of efficiency
of the ovaries anatomy of circulating erythrocytes:
✓ Problems associated with reduced estrogen are
common - biconcave disks
✓ Growth hormone production declines with age - essentially bags of hemoglobin
✓ Many endocrine glands decrease output with age - anucleate (no nucleus)
- contain very few organelles
BLOOD- the only fluid tissue in the human body
HEMOGLOBIN - blood cell formation
- occurs in red bone marrow
- iron-containing protein - all blood cells are derived form a common stem cell
- binds strongly, but reversibly, to oxygen (hemocytoblast)
- each hemoglobin molecule has four oxygen binding - hemocytoblast differentiation
sites ✓ lymphoid stem cell produced lymphocytes
- each erythrocyte has 250 mil hemoglobin molecules ✓ myeloid stem cell produced other formed
LEUKOCYTES (WBC) elements

- crucial in the body’s defense against diseases FATE OF ERYTHROCYTES


- these are complete cells, with a nucleus and organelles
• unable to divide, grow, or synthesize proteins
- able to move into and out of blood vessels (diapedesis)
• wear out in 100 to 1200 days
- can move by ameboid motion
• when worn out, are eliminated by phagocytes in the
- can respond to chemicals release by damaged tissues
spleen or liver
LEUKOCYTE LEVELS IN THE BLOOD • lost cells are replaced by division of hemocytoblasts

- normal levels are between 4000 and 11,000 cells/ml CONTROL OF ERYTHROCYTE PRODUCTION

abnormal leukocyte levels: - rate is controlled by a hormone (erythropoietin)


- kidneys produce most erythropoietin as a response to
leukocytosis: above 11,000 leukocytes/ml reduced oxygen levels in the blood
- indicates an infection - homeostasis is maintained by negative feedback from
blood oxygen levels
leukopenia: abnormally low leukocyte level

- commonly caused by certain drugs

TYPES OF LEUKOCYTES

Granulocytes: granules in their cytoplasm can be stained

- include neutrophils, eosinophils and basophils

agranulocytes: lack visible cytoplasmic granules

- include lymphocytes and monocytes

GRANULOCYTES

neutrophils: multilobed nucleus with fine granules HEMOSTASIS


- act as phagocytes at active sites of infection - stoppage of blood flow
eosinophils: large brick red cytoplasmic granules - result of a break in a blood vessel
- hemostasis involves three phases
- found in response to allergies and parasitic worms ✓ platelet plug formation
✓ vascular spasms
basophils: have histamine containing granules ✓ coagulation
- initiate inflammation PLATELET PLUG FORMATION
AGRANULOCYTES - collagen fibers are exposed by a break in a blood
Lymphocytes: nucleus fills most of the cell vessel
- platelet become “sticky” and cling to fibers
- play an important role in the immune response - anchored platelets release chemical to attract more
platelets
monocytes: largest of the WBC - platelets pile up to form a platelet plug
- function as macrophages VASCULAR SPASMS
- important in fighting chronic infection
- anchored platelets release serotonin
PLATELETS - serotonin causes blood vessel muscles to spasm
- derived from ruptured multinucleate cells - spasms narrow the blood vessel, decreasing blood loss
(megakaryocytes) COAGULATION
- needed for the clotting process
- normal platelet count= 300, 000/mm3 - injured tissues release thromboplastin

HEMATOPOIESES
- PF3 (a phospholipid) interacts with thromboplastin, - Most Americans are Rh+
blood protein clotting factors, and calcium ions to - Problems can occur in mixing Rh+ blood into a body
trigger a clotting cascade with Rh- blood
- Prothrombin activator converts prothrombin to
thrombin (an enzyme) Rh DANGERS DURING PREGNANCY
- Thrombin joins fibrinogen proteins into hair-like - Danger is only when the mother is Rh- and the father
fibrin is Rh+ and the child inherits the Rh+ factor
- Fibrin forms a meshwork (the basis for a clot) - The mismatch of an Rh- mother carrying an Rh+ baby
BLOOD CLOTTING can cause problems for the unborn child
- The first pregnancy usually proceeds without
- Blood usually clots within 3-6 min problems
- The clot remains as endothelium regenerates - the immune system is sensitized after the first
- The clot is broken down after tissue repair pregnancy
- in a second pregnancy, the mother’s immune system
UNDESIRABLE CLOTTING produces antibodies to attack the Rh+ blood
Thrombus: a clot in an unbroken blood vessel (hemolytic disease of the newborn)

- Can be deadly in areas like the heart BLOOD TYPING

Embolus: a thrombus that breaks away and floats freely in the - blood samples are mixed with anti-A and anti-B serum
bloodstream - coagulation or no coagulation leads to determining
blood type
- Can later clog vessels in critical areas such as the brain - typing for ABO and Rh factors is done in the same
manner
BLEEDING DISORDERS
cross matching: testing for agglutination of donor RBCs by the
Thrombocytopenia: platelet deficiency
recipient’s serum and vice versa
- Even normal movements can cause bleeding form
DEVELOPMENTAL ASPECTS OF BLOOD
small blood vessels that require platelets for clotting
- fetal hemoglobin differs from hemoglobin produced
Hemophilia: hereditary bleeding disorder
after birth
- Normal clotting factors are missing
Sites of blood cell formation:
BLOOD GROUPS AND TRANSFUSIONS

- Large losses of blood have serious consequences


- Loss of 15-30% causes weakness
- Loss of over 30% causes shock which can be fatal
- Transfusions are the only way to replace blood quickly
- Transfused blood must be of the same blood group

HUMAN BLOOD GROUPS

- Blood contains genetically determined proteins


- A foreign protein (antigen) may be attacked by the
immune system
- Blood is “types” by using antibodies that will cause
- the fetal liver and spleen are early sites of blood cell
blood with certain proteins to clump (agglutination)
formation
- There are over 30 common RBC antigen
- bone marrow takes over hematopoiesis by the seventh
- The most vigorous transfusion reactions are caused by
month
ABO and Rh blood group antigens
HbA: refers to adult hemoglobin which a α2β2 tetramer
ABO blood groups
HbF: refers to fetal hemoglobin, which is an α2γ2 tetramer that
- Based on the presence or absence of two antigens
can bind to oxygen with greater affinity than HbA.
- Type a
- Type b - HbF has a higher affinity for oxygen than HbA
- The lack of these antigens is called type O
- The presence of both A and B is called type AB
- The presence of either A or B is called types A and B
THE CARDIOVASCULAR SYSTEM
respectively
- A closed system of the heart and blood vessels
Rh blood groups
- The heart pumps blood
- Named because of the presence or absence of one of - Blood vessels allow blood to circulate to all parts of
eight Rh antigens (agglutinogen D) the body
- The function of the cardiovascular system is to deliver
oxygen and nutrients and to remove CO2 and other
waste products

THE HEART

Location:

- Thorax between the lungs


- Pointed apex directed towards left hip
- About the size of your fist

THE HEART: VALVES

- Allow blood to flow in only one direction


THE HEART: COVERINGS - Four valves
Pericardium: a double serous membrane - Valves open as blood is pumped through
- Help in place by chordae tendineae (heart strings)
Visceral pericardium: next to heart - Close to prevent backflow
Parietal pericardium: outside layer Atrioventricular valves- between atria and ventricles
- Serous fluid fills the space between the layers of - Bicuspid valve (left) and tricuspid valve (right)
pericardium
Semilunar valves- between ventricle and artery
THE HEART: HEART WALL
- Pulmonary semilunar valve
Three layers: - Aortic semilunar valve
1) Epicardium- outside layer OPERATION OF HEART VALVES
- This layer is the parietal pericardium
- Connective tissue layer
2) Myocardium- middle layer
- Mostly cardiac muscle
3) Endocardium- inner layer
- Endothelium

THE HEART: CHAMBERS

- Right and left side act as separate pumps

four chambers:

1) Atria- receiving chambers


- Right and left atrium
2) Ventricles- discharging chambers
- Right and left ventricle

THE HEART: ASSOCIATED GREAT VESSELS

Aorta: leaves left ventricle

Pulmonary arteries: leaver right ventricle

Vena cava: enters right atrium

Pulmonary veins (four): enter left atrium

CORONARY CIRCULATION
- Blood in the heart chambers does not nourish the THE HEART: CARDIAC OUTPUT
myocardium
- The heart has its own nourishing circulatory system Cardiac output (CO)- amount of blood pumped by each side of
- Coronary arteries the heart in one minute
- Cardiac veins - CO= (heart rate (HR)) x (stroke volume (SV))
- Blood empties into the right atrium via the coronary
sinus Stroke volume: volume of blood pumped by each ventricle in
one contraction

THE HEART: REGULATION OF HEART RATE


THE HEART: CONDUCTION SYSTEN
- Stroke volume usually remains relatively constant
- Intrinsic conduction system (nodal systems) - Starling’s law of the heart- the more that the cardiac
- Heart muscle cells contract, without nerve impulses, muscle is stretched, the stronger the contraction
in a regular continuous way - Changing heart rate is the most common way to
- Special tissue sets the pace change cardiac output
- Sinoatrial node: pacemaker
- Atrioventricular node Increased heart rate
- Atrioventricular bundle - Exercise
- Bundle branches - Decreased blood volume
- Purkinje fibers 1) Sympathetic nervous system
HEART CONTRACTIONS - Crisis
- Low blood pressure
- Contraction is initiated by the sinoatrial node 2) Hormones
- Sequential stimulation occurs at other autorhythmic - Epinephrine
cells - Thyroxine

DECREASED HEART RATE

- Parasympathetic nervous system


- High blood pressure or blood volume
- Decreased venous return

BLOOD VESSELS: THE VASCULAR SYSTEM

- Taking blood to the tissues and back


- Arteries
- Arterioles
- Capillaries
- Venules
THE HEART: CARDIAC CYLE - Veins

- Atria contract simultaneously


- Atria relax, then ventricles contract
- Systole= contraction
- Diastole= relaxation

Cardiac cycle: events of one complete heart beat

Mid to late diastole: blood flows into ventricles

Ventricular systole- blood pressure builds before ventricle


contracts, pushing out blood

Early diastole: atria finish re-filling, ventricular pressure is low


THE VASCULAR SYSTEM

BLOOD VESSELS: ANATOMY PULSE

Three layers (tunics)

- Tunic intima (endothelium)


- Tunic media (smooth muscle): controlled by
sympathetic nervous system
- Tunic externa: mostly fibrous connective tissue

DIFFERENCE BETWEEN BLOOD VESSEL TYPES

BLOOD PRESSURE
MOVEMENT OF BLOOD TRHOUGH VESSELS

MEASURING ARTERIAL BLOOD PRESSURE

CAPILLARY BEDS
BLOOD PRESSURE: EFFECTS OF FACTORS
VARIATIONS IN BLOOD PRESSURE

CAPILLARY EXCHANGE

CAPILLARY EXCHANGE: MECHANISMS

DEVELOPMENTAL ASPECTS OF THE


CARDIOVASCULAR SYSTEM

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