Anatomy Study Guide Updated
Compare and contrast endocrine vs endocrine glands. Use examples.
Exocrine glands-
Secrete their products into DUCTS that carry the secretions into the body cavities, into the lumen of an organ, or to the outer surface of the body
NONE ARE HORMONES
Examples include-
Sudoriferous (sweat) glands
Sebaceous (oil) glands
Mucous glands
Digestive glands
Endocrine glands-
Secrete their HORMONES directly into the INTERSTITIAL FLUID that surrounds them
From the interstitial fluid, hormones diffuse into the bloodstream through blood CAPILLARIES and are carried to TARGET CELLS *receptor specific throughout the body
Examples include-
Pituitary gland
Thyroid gland/parathyroid gland
Adrenal gland
Pineal gland
Hormone-secreting cells can be found in the hypothalamus, thymus, skin, pancreas, gonads, stomach, liver, heart…
Discuss hormone function and activity.
Receptors *protein receptors are hormone-specific receptors like enzymes
Continually being synthesized and broken down
Maybe down-regulated in the presence of high concentrations of hormone→# of target cell receptors to decrease **up-regulated is the opposite process
Types of hormones
Circulating hormones- carried through the bloodstream to act on DISTANT target cells (through interstitial fluid+bloodstream)
Local hormones- act LOCALLY on neighboring cells or on the same cell that secreted them WITHOUT entering the bloodstream (just interstitial fluid)
Paracrine (neighboring cell) /autocrine (same cell)
Lipid soluble hormones- *diffuses easily through the lipid bilayer
Bind to receptors WITHIN nucleus or mitochondria of target cells
In CAPILLARIES, the hormone is carried through the blood with a TRANSPORT PROTEIN (moves not very easily in the blood)
Transport protein then releases the hormone into the interstitium
Water soluble hormones
Bind to receptors on the EXTERIOR surface of a target cell
Move through the blood quickly WITHOUT transporting proteins (easily)
Outline and discuss the mechanisms of hormone action.
How/why it responds to hormones-
Hormones concentration in the blood itself
The number of hormone receptors on a target cell
Influences from other hormones
Synergistic effect→ ex: estrogen and prolactin work together to achieve the same goal
Antagonistic effect→ ex: insulin and glucagon work opposite of one another
Hormone secretion is regulated by-
Signals from the nervous system
Chemical changes in blood
Other hormones
Discuss negative and positive feedback for the control of hormone secretions. Use an example.
Negative feedback- responding to a disruption/stimulus (example)
Stimulus: disruption in homeostasis by decreasing…
Controlled condition: decreasing glucocorticoid levels in the blood
Receptors: neurosecretory cells in the hypothalamus provide input
Input: increased corticotropin-releasing hormones (CRH) and decreased cortisol to the …
Control center: corticotrophs in the anterior pituitary provide output
Output: increased adrenocorticotropic hormone (ACTC) to
Effectors: cells of zona fasciculata in the adrenal cortex which secrete glucocorticoids
Response: increased glucocorticoid levels in the blood
Return to homeostasis: when the response brings glucocorticoid level in the blood back to normal the “loop” turns off
Positive feedback- disrupting homeostasis
Ex: childbirth: hormone oxytocin stimulates contraction of the uterus to in turn stimulate more oxytocin release
Make a flow chart for all classes of hormones.
Discuss the function of the hypothalamus. Outline and discuss all regulatory hormones.
Hypothalamus: secretes releasing and inhibiting hormones that control the release of hormones by the pituitary gland
Hormones reach the pituitary gland via the hypophyseal portal system (blood vessels that connect the hypothalamus and anterior pituitary gland)
Anterior pituitary hormones- 7 regulatory hormones of the hypothalamus
Posterior pituitary hormones- 2 hormones of the hypothalamus
Hypophyseal portal system
*anterior pituitary Superior hypophyseal artery picks up hormones in the hypothalamus through capillary beds through capillary plexus and takes hormones in the blood through the body *hypophyseal portal vein
*posterior pituitary inferior hypophyseal artery into the capillary plexus of infundibular processes and picks up all hormones being stored in neurohypophysis and carries them throughout the body (in the blood)
Outline and discuss the hormones of the pituitary. (details here)
Hormones (anterior pituitary) make and secretes + glandular *adenohypophysis
Growth hormone (GH) is secreted by somatotropic cells
Stimulates secretion: growth hormone-releasing hormone (GHRH)
Inhibits secretion: growth hormone inhibiting hormone (GHIH)
Thyroid-stimulating hormone (TSH) is secreted by thyrotropic cells
Stimulates secretion: thyrotropin-releasing hormone (TRH)
Inhibits secretion: growth hormone inhibiting hormone (GHIH)
Follicle-stimulating hormone (FSH) is secreted by gonadotropic cells
Stimulates secretion: gonadotropin-releasing hormone (GnRH)
Luteinizing hormone (LH) is secreted by gonadotropic cells
Stimulates secretion: gonadotropin-releasing hormone (GnRH)
Prolactin (PRL) is secreted by prolactin cells
Stimulates secretion: prolactin-releasing hormone (PRH)
Inhibits secretion: prolactin-inhibiting hormone (PIH), which is dopamine
Adrenocorticotropic hormone (ACTH) is secreted by corticotropic cells
Stimulates secretion: corticotropin-releasing hormone
Melanocyte-stimulating hormone (MSH) is secreted by corticotropic cells
Stimulates secretion: corticotropin-releasing hormone
Inhibits secretion: dopamine
**fetal development pars intermedia (very small or absent in adulthood)
Hormones (posterior pituitary) secretes and stores + not glandular *neurohypophysis
Oxytocin (OT)
Stimulates contraction of smooth muscle cells of the uterus during childbirth; stimulates contraction of myoepithelial cells in mammary glands to cause milk ejection
Antidiuretic hormone (ADH)
Conserves body water by decreasing urine volume; decreases water loss through perspiration; raises blood pressure by constricting arterioles
Outline and discuss the adrenal glands. Identify all layers/regions and what they do.
Adrenal gland: secretes DHEA, a hormone that makes men masculine during puberty but is insignificant for females until menopause when there is no more estrogen
Adrenal medulla- norepinephrine and epinephrine are secreted from chromaffin cells
Hormones increase heart rate, and blood pressure, and mobilize/utilize glucose for energy
Adrenal cortex-
3 regions
Zona glomerulosa- secretes aldosterone to maintain homeostasis between sodium and potassium
Aldosterone- RAA pathway
Mineralocorticoids (class)
Zona fasciculata- cortisol, anti-inflammatory and makes glucose
Glucocorticoids
Zona reticularis- sex hormones
Androgens
Outline and discuss the stress response. **sympathetic division of the autonomic nervous system
Eustress is helpful, everyday stress that prepares us to meet good challenges *good stress
Distress is any type of harmful stress that may become damaging
1st stage of stress- sympathetic nervous system
2nd stage of stress- resistance reaction
This stage lasts much longer and if overused can cause exhaustion
Identify and discuss the endocrine disorders discussed in class.
Suprarenal gland disorders:
Cushing’s syndrome- hypersecretion of the suprarenal cortex
Addison’s disease- hyposecretion of glucocorticoids and aldosterone
Pheochromocytoma- benign tumors that cause hypersecretion of epinephrine and norepinephrine
Pancreatic disorders:
Type 1 diabetes- autoimmune disorder in which the body destroys its beta cells in the pancreatic islet cells creating an insufficient amount of insulin
Symptoms include: high levels of sugar in urine/blood, dehydration, and constant thirst
Type 2 diabetes- adult onset, caused by obesity, poor diet, and lack of exercise causing beta cells to ignore the stimulus to make insulin
Can be fixed by weight loss, exercise, and a better diet
Gestational diabetes- *females when they are pregnant
Can be diagnosed with a simple glucose test when high levels of sugar show up in urine
This disease causes babies to be born big and increase the chances of a c-section or other procedure
Thyroid disorders:
Hypothyroid- (underactive thyroid) weight gain, stores glucose, and slow metabolism
Hyperthyroid (overactive thyroid) weight loss, super fast metabolism
Goiter- enlarged thyroid gland
Hashimoto syndrome- autoimmune disease, hypothyroid
Affects women more than men
Parathyroid disorders:
Hypoparathyroidism- too much potassium, causes dropping of the face
Outline and discuss the functions and properties of blood.
Blood plasma (55%)
Consists of water (91.5%), proteins (7%), and other solutes (1.5%)
Red blood cells (45%) *erythrocyte
The number of RBCs and platelets remains rather steady while that of WBCs varies depending on invading pathogens and other foreign antigens
Contain hemoglobin that is used to carry oxygen to all cells and to carry some carbon dioxide to the lungs
Buffy coat is composed of white blood cells and platelets
Cellular components (formed elements) of blood include red blood cells, white blood cells, and platelets *thrombocyte
White blood cells *leukocyte
Functions of blood
Blood transports oxygen, carbon dioxide, nutrients, hormones, heat, and waste products
Blood regulates the homeostasis of all body fluids, pH, body temperature, and water content of cells
Blood protects against excessive loss by clotting and uses white blood cells to protect against infections
Outline and discuss the composition of blood.
Blood plasma (55%)
Consists of water (91.5%), proteins (7%), and other solutes (1.5%)
Blood plasma proteins (7%)
Albumins (54%) smallest and most numerous plasma protein
Globulins (38%) large protein
Fibrinogen (7%) large protein
Other solutes (1.5%)
Electrolytes- help maintain osmotic pressure and play essential roles in cell functions
Nutrients- essential roles in cell functions, growth, and development
Gasses- oxygen (important in cellular functions), nitrogen (no known function), carbon dioxide (involved in the regulation of blood pH)
Enzymes- catalyze chemical reactions
Hormones- regulate metabolism, growth, and development
Vitamins- cofactors for enzymatic reactions
Waste products- breakdown products of protein metabolism that are carried by the blood to organs of excretion
Red blood cells (45%) *erythrocyte
The number of RBCs and platelets remains rather steady while that of WBCs varies depending on invading pathogens and other foreign antigens
Contain hemoglobin that is used to carry oxygen to all cells and to carry some carbon dioxide to the lungs
Each hemoglobin molecule constraints an iron ion which allows each molecule to bind to four oxygen molecules
Hemoglobin is involved in regulating blood flow and BP via the release of NO
Nitric oxide (NO) causes vasodilation, which improves blood flow and enhances oxygen delivery
No nucleus or other organelles *biconcave discs- this allows them to carry O2 better
RBCs contain carbonic anhydrase, which catalyzes the conversion of carbon dioxide and water to carbonic acid
Carbonic acid transports about 70% of the carbon dioxide in plasma
Live for only 120 days
Dead cells are removed from circulation by the spleen and liver
Breakdown products from the RBCs are recycled and reused
Erythropoiesis (production of RBCs) begins in the red bone marrow
Erythropoietin, a hormone secreted by the kidneys in response to lowered oxygen concentration (hypoxia) stimulates the differentiation of hematopoietic stem cells into erythrocytes
Reticulocytes (immature RBCs) enter the circulation and mature in 1 to 2 days
Stimulus→controlled condition→receptors→input→control center→output→ effectors→response *return to homeostasis when o2 delivery to kidneys increases to normal
Buffy coat is composed of white blood cells and platelets
Cellular components (formed elements) of blood include red blood cells, white blood cells, and platelets *thrombocyte
White blood cells *leukocyte
Contain a nucleus and organelles, but NO HEMOGLOBIN
May live for several months or years- the main function is to combat invading microbes
During an invasion, many WBCs can leave the bloodstream and collect at sites of invasion
This is called emigration
An elevation in the white blood count indicates an infection or inflammation
A low white blood cell count may develop due to several causes
A differential white blood cell count will help to determine if a problem exists
Classified as granular and agranular
Granular- containing vesicles that appear when the cells are stained
Granular leukocytes: neutrophils, eosinophils, basophils
Agranular- containing no granules
Agranular leukocytes: lymphocytes, monocytes
(most abundant to least: Never Let Monkeys Eat Bananas
Neutrophils (60-70%)
Lymphocytes (20-25%)
Able to live for years, while most other blood cells live for hours, days, or weeks
Monocytes (3-8%)
Eosinophils (2-4%)
Basophils (0.5-1%)
Outline and discuss the formation of blood cells.
Hematopoiesis- formation of blood cells
Pluripotent stem cells differentiate into each of the different types of blood cells
Outline and discuss the epidemiology of sickle cell anemia.
People with this disorder have an abnormal kind of hemoglobin
RBC is sickle or crescent-shaped
Sickled RBCs break down prematurely (5-7 days)
Sickle cells do not move easily through blood vessels preventing O2 transport
People with sickle cell anemia are not allowed to do high-impact activities ex. sports due to this risk
Symptoms include- shortness of breath, fatigue paleness, and delayed growth in children
Positive- builds resistance to malaria
Because sickled cells last 5-7 days, we get rid of the third stage of malaria
Outline and discuss the different types of white blood cells and what they do.
Classified as granular and agranular
Granular- containing vesicles that appear when the cells are stained
Granular leukocytes: neutrophils, eosinophils, basophils
Agranular- containing no granules
Agranular leukocytes: lymphocytes, monocytes
(most abundant to least: Never Let Monkeys Eat Bananas
Neutrophils (60-70%)
The high count may indicate: bacterial infection, burns, stress, inflammation
The low count may indicate: radiation exposure, drug toxicity, vitamin b12 deficiency, systemic lupus erythematosus
Lymphocytes (20-25%)
The high count may indicate: viral infections, some leukemias, infectious mononucleosis
The low count may indicate: prolonged illness, HIV infection, immunosuppression, treatment with cortisol
Able to live for years, while most other blood cells live for hours, days, or weeks
Monocytes (3-8%)
The high count may indicate: viral or fungal infections, tuberculosis, some leukemias, or other chronic diseases
The low count may indicate: bone marrow suppression, treatment with cortisol
Eosinophils (2-4%)
The high count may indicate: allergic reactions, parasitic infections, autoimmune diseases
The low count may indicate: drug toxicity, stress, acute allergic reactions
Basophils (0.5-1%)
The high count may indicate: allergic reactions, leukemias, cancers, hypothyroidism
The low count may indicate: pregnancy ovulation, stress, hypothyroidism
** LAB MANUAL
Outline and discuss the steps in hemostasis.
Hemostasis- is a sequence of responses that stop bleeding
Process involves-
Vascular spasm
Platelet plug formation
Blood clotting (coagulation)
Blood clotting involves several clotting (coagulation) factors
Blood clotting can be activated in one of two ways-
Extrinsic pathway
Intrinsic pathway
Both pathways lead to the formation of prothrombinase and, from there, the common pathway continues
Outline and discuss the steps in clot formation. Be sure to discuss all three pathways including all clotting factors.
Steps in clot formation
(Hemostasis) Process involves-
Vascular spasm
Platelet plug formation
Platelet adhesion → platelet release reaction → platelet aggregation
Blood clotting (coagulation)
Blood clotting cascade
Once the clot forms, it tightens to pull the edges of the damaged vessel together
Vitamin K is needed for normal clot formation because it is used in the synthesis of 4 clotting factors
Small, unwanted clots are dissolved by plasmin, an enzyme that is part of the fibrinolytic system
Clotting (coagulation) factors
I Fibrinogen: source- liver
Pathways of activation → common
II Prothrombin: source- liver
Pathways of activation → common
III Tissue factor (thromboplastin): damaged tissues and activated platelets
Pathways of activation → extrinsic
IV Calcium ions: diet, bones, and platelets
Pathways of activation → all
V Proaccelerin, labile factor or accelerator globulin: liver and platelets
Pathways of activation → extrinsic and intrinsic
VII Blood serum prothrombin conversion accelerator (SPCA): liver
Pathways of activation → extrinsic
VIII Antihemophilic factors (AHF): liver
Pathways of activation → intrinsic
IX Plasma thromboplastin component (PTC): liver
Pathways of activation → intrinsic
X Stuart factor: liver
Pathways of activation → extrinsic and intrinsic
XI Blood plasma thromboplastin antecedent (PTA): liver
Pathways of activation → intrinsic
XII Hageman factor: liver
Pathways of activation → intrinsic
XIII Fibrin-stabilizing factor (FSF): liver and platelets
Pathways of activation → common
Outline and discuss the plasma proteins found in the blood.
Blood plasma (55%)
Consists of water (91.5%), proteins (7%), and other solutes (1.5%)
Blood plasma proteins (7%) *MOST are produced by the liver
Albumins (54%) smallest and most numerous plasma protein
Help maintain osmotic pressure *important factor in the exchange of fluids across blood capillary walls
Globulins (38%) large proteins (plasmocytes produce immunoglobulins)
Immunoglobulins help attack viruses and bacteria *alpha and beta globulins transport iron, lipids, and fat-soluble vitamins
Fibrinogen (7%) large protein
Plays an essential role in blood clotting
Discuss blood groups and blood types.
Blood is characterized into different blood groups based on the presence or absence of agglutinogens on the surface of RBCs
24 blood groups and more than 100 antigens
Blood types vary among different populations
Classification is based on antigens labeled A, B, or AB, with O being no antigens
85% of the population is Rh positive
Blood plasma usually contains antibodies that react with A or B antigens
An individual will not have agglutinins against his or her blood type *hemolytic disease
Type A
An antigen
Anti-B antibody
Compatible donor blood types: A, O
Type B
B antigen
Anti-A antibody
Compatible donor blood types: B, O
Type AB
Both A and B antigens
Anti-A antibody
Compatible donor blood types: A, B, AB, O
*Universal recipient
Type O
Neither A nor B antigen
Both anti-A and anti-B antibodies
Compatible donor blood types: O
*Universal donor
Discuss the hemolytic disease of newborns.
At birth small amounts of fetal blood leak into the maternal circulation
If the baby is Rh+ and the mother is Rh-, she will develop antibodies to the Rh factor
During her next pregnancy with an Rh+ baby, when she transfers antibodies to the fetus, the transferred anti-Rh antibodies will attack some of the fetal’ RBCs causing clotting and hemolysis
Outline and discuss the different components of the pericardium and any possible infections that can occur.
The heart is enclosed and held in place by the pericardium (heart wall)
Consists of an outer fibrous pericardium and an inner serous pericardium
The serous pericardium has 2 layers-
The Visceral- (epicardium) adheres to the surface of the heart
Parietal-fused to the fibrous pericardium
The visceral and parietal layers are separated by the serous cavity, a fluid-filled space
This fluid reduces friction between the layers of the serous pericardium as the heart moves
Infection: Pericarditis- inflammation of the pericardium; chest pain and pericardial friction rub
The wall of the heart (pericardium) has 3 layers
Epicardium (visceral pericardium) *outer layer
Myocardium- cardiac muscle; responsible for pumping action of the heart (contracts to help move blood throughout the heart); thickest layer
Cardiac muscle is involuntary, arranged in bundles that swirl diagonally around the heart *striated + intercalated discs
Infection: myocarditis- inflammation of the myocardium; may cause fatigue, chest pain, irregular heartbeat *severe cases lead to cardiac failure and death
Endocardium- the innermost layer of the heart
Has a slip and slide texture→ water=blood plasma, produces a friction-free environment for formed elements to move through without any damage
Infection: endocarditis- inflammation of endocardium; may cause fever, heart murmurs, irregular heartbeat, fatigue
Trace blood flow through the heart and identify all the blood vessels, valves, and chambers it passes through. (systemic and pulmonary circulations)
Right atrium- pushes deoxygenated blood through the tricuspid valve →
Right ventricle- pushes deoxygenated blood through the pulmonary valve →
Pulmonary trunk- where deoxygenated blood moves out through the left and right pulmonary arteries →
Left and right lungs- in the pulmonary capillaries, blood loses CO2 and gains O2 **blood is now oxygenated →
The oxygenated blood moves through the left and right pulmonary veins →
Left atrium- oxygenated blood is then pushed through the bicuspid valve →
Left ventricle- pushes oxygenated blood through the aortic valve →
Aorta and systemic arteries- where the oxygenated blood is →
Systemic capillaries- where blood loses O2 and gains CO2 *because O2 is being absorbed
The deoxygenated blood moves through the superior vena cava, inferior vena cava, ad coronary sinus back into the right atrium
Outline and discuss the conduction system through the heart (5 steps).
Cardiac cells are self-excitable (autorhythmic)- repeatedly generate spontaneous pulses that trigger heart contractions *these cells form the conduction system
5 steps of the conduction system
**SA node, AV node, AV bundle, right and left bundle branches, Purkinje fibers
SA node in the wall atrium is activated and atrial activations begin
Time=0
SA node cells repeatedly depolarize to threshold spontaneously→ pacemaker potential
When the pacemaker potential reaches the threshold, it triggers an action potential that propagates both atria
Stimulus spreads across the atrial surfaces and reaches the AV node
Elapsed time: 50 msec
The AV node is located at the interatrial septum
There is a 100 msec delay at the AV node; atrial contraction occurs
Elapsed time=: 150 msec
Both atria are fully depolarized
AV valves open (atrioventricular)
SL valves close (semilunar)
The impulse travels along the interventricular septum within the atrioventricular bundle and the bundle branches into the right and left bundle branches to the Purkinje fibers via the moderator band, to the papillary muscles of the right ventricle
Elapsed time: 175 msec
Impulse is distributed by Purkinje fibers and relayed throughout the ventricular myocardium- atrial contraction is completed, and ventricular contraction begins
Both ventricles are fully depolarized
AV valves closed
SL valves opened
Time elapsed: 225 msec
**Hormones can modify the heart rate and force of contraction but they do not set the fundamental rhythm for the heart (medulla oblongata)
Discuss an EKG tracing and identify all the waves and complexes.
Action potential in a (ventricular) contractile fiber:
AP initiated by the SA node travels along the conduction system and spreads out to excite the “working” atrial and ventricular fibers (contractile fibers)
An AP in a contractile fiber is characterized by a rapid depolarization
Steps/patterns shown on EKG:
(1) Rapid depolarization- due to Na+ inflow when collage-gated fast Na+ channels open (contractile fibers are brought to threshold)
(2) Plateau (maintained depolarization)- due to Ca2+ inflow when voltage-gated slow Ca2+ channels open and the K+ outflow when some voltage-gated slow K+ channels open
*Ca2+ inflow balances out K+ outflow
Allows a sustaining of longer contraction cycling of the heart muscle
Allowing time for blood to move its respective parts
*Prevents tetanus in cardiac muscle fibers
(3) Repolarization (return to resting membrane potential)- due to closing of Ca2+ channels and K+ outflow when additional voltage K+ channels open
Refractory period- occurs during the plateau phase and parts of repolarization
There cannot be another AP coming to stimulate another depolarization phase until this construction is complete
Important in preventing tetanus and arrhythmias
Electrocardiogram (EKG):
Measures electrical conduction through the heart
P wave- small upward deflection on ECG that represents atrial depolarization
PQ interval- from the start of the P wave to the beginning of the QRS complex, the time required for the AP to travel through the atria, AV node, and remaining fibers of the conduction system
QRS complex- represents rapid ventricular depolarization
ST segment- from the end of the QRS complex to the start of the T wave that represents a time when the ventricular fibers are depolarized during the plateau phase of the AP
T wave- represents ventricular repolarization (ventricles relaxing) occurs more slowly than depolarization (wave is smaller and wider than QRS complex)
QT interval- from the start of the QRS complex to the end of the T wave
Contraction of ECG waves with atrial and ventricular systole
*depolarization causes contraction and depolarization causes relaxation of cardiac muscle fibers
Depolarization of atrial contractile fibers produces P wave
Atrial systole (contraction) after the P wave begins
Atrial diastole (relaxation) is masked by QRS complex
Depolarization of ventricular contractile fibers produces QRS complex
Ventricular systole (contraction) shortly after QRS complex begins
Repolarization of ventricular contractile fiber produces T wave
Ventricular diastole (relaxation) shortly after the T wave begins
One cardiac cycle consists of the contraction )systole) and relaxation (diastole) of both atria, rapidly followed by the systole and diastole of both ventricles
During atrial systole (contraction)
Electrical events of EKG-
Atrial depolarization (marked by P wave) causes atrial systole
The onset of ventricular depolarization with the onset of QRS complex
Pressure change
As the atria contract, pressure is exerted on the blood within, forcing the blood through the open AV valves into the ventricles
Aortic pressure is slightly decreasing (think: because atria are contracting, not the ventricles thus, BP is low)
Left ventricular pressure is low (small hump before ventricular systole)
Left atrial pressure is low (small hump_ because the distance is not very far (only pushing blood into ventricles right below it)
Volume changes
Volume in the ventricle increases (being filled with blood)
The end of each atrial systole is also the end of each ventricular diastole (relaxation)
This blood volume is called end-diastolic volume (EDV)
Heart sounds- Auscultation: s4, but can’t hear it with a stethoscope
Mechanical event- atrial systole (contraction) and ventricle diastole (relaxation)
During ventricular systole (contraction)
Electrical events of EKG
Ventricular depolarization causes ventricular systole, marked by QRS complex
T wave in ECG marks onset of ventricular repolarization
Pressure change
As ventricular systole (contraction) begins, pressure rises inside the ventricles and pushes up against the AV valves, forcing them to shut
Isovolumetric contraction- period of about (0.5 secs) when both semilunar and AV valves are closed
During this interval, cardiac muscle fibers are contracting and exerting force but are not shortening (yet)
All four valves are closed- ventricular volume remains the same
Continued contraction of the ventricles causes pressure inside the chambers to rise sharply
When left ventricular pressure surpasses aortic pressure at 80mmHg the aortic semilunar valve opens and the ventricular ejection begins (pressure continues to rise to 120mmHg)
Volume changes
The blood volume in ventricles decreases (ventricle is ejecting blood)
End systolic volume- volume remaining in each ventricle at the end of systole
Stroke volume- volume ejected per beat from each ventricle
SV= end diastolic volume (-) end systolic volume
At rest: SV is about 130 mL-60mL=70mL
Heart sounds- auscultation: heart 1st sound (s1), a club sound
This sound is caused by blood turbulence associated with the closure of AV valves soon after ventricular contraction begins
Mechanical event: isovolumetric contraction and ventricular ejection
During ventricular diastole (relaxation):
Electrical events of EKG
Ventricular repolarization causes ventricular diastole, as marked by the end of the tZ wave in the EKG
Pressure change
As the ventricles relax, the pressure within the chambers falls, and blood in the aorta and pulmonary trunk begins to flow backward toward the region of lower pressure in the ventricles
Back-flowing blood catches in the valve cusps and closes the semilunar valves
Aortic valves close
The rebound the blood from the closed cusps of the aortic valve produces the dicrotic wave on the aortic pressure curve
Following the aortic pressure decreases
Volume changes
After the SL valves close, there is a brief period (isovolumetric relaxation) when ventricular blood volume does not change because all 4 valves are closed
Pressure falls quickly as ventricles relax
When ventricular pressure drops below atrial pressure, the AV valves open and blood rushes rapidly into the ventricles
Another P wave signals the start of another cardiac cycle
The blood volume in the ventricle increases because the AV valve is open and blood is flows in
Heart sounds- auscultation:
Hear the 2nd sound, s2, a dubb sound
Sound is caused by blood turbulence associated with the closure of SL valves
Mechanical event
Isovolumetric relaxation and ventricular filling
Cardiac output:
The volume of blood ejected from the heart (ejected from the left or right ventricle into the aorta or pulmonary trunk each minute)
Stroke volume=amount of blood pumped out of the ventricle in one beat
(mL/beat) x (heart rate)= about 75 beats per minute
In a typical man: SV is mL/beat and heart rate is about 75 beats per minute
CO= 70 x 75= 5250 mL/min= 5ish liters a minute
Regulation of stroke volume
Preload
The degree of stretch on the heart before it contracts
The volume of the blood in ventricles at the end of diastole (just before contraction is about to begin)
A greater stretch (preload) on cardiac muscle before contraction increases the force of contraction
The more the heart fills with blood during diastole, the greater the force of contraction during systole
Preload is increased in:
Hypervolemia: increased BV
Regurgitation of cardiac valves
Heart failure
Contractility
The forcefulness of contraction of individual ventricular muscle fibers
The ability which the heart can contract
Affects stroke volume
Get older, the compliance of the heart reduces, and it is harder for the heart to contract
Afterload
The pressure that must be exceeded before rejection of blood from the ventricles can occur
The resistance the left ventricle must overcome to circulate blood
Resistance may be: the length of blood vessels or the diameter of the lumen of blood vessels
Increased in:
Hypertension (high BP)
The heart is working overtime to produce more pressure
The delicate aorta can rupture (aneurysm)
Vasoconstriction (smaller lumen, increased BP)
Factors that regulate heart rate:
Autonomic nervous system
The sympathetic nervous system increases the heart rate
The parasympathetic nervous system decreases the heart rate
Hormones
Adrenaline (epinephrine and norepinephrine) increases heart rate
Ions
Increase Ca2+ ions, increase contractility, increases heart rate
Na+ ions need to be exactly regulated- if the flow of Na is disrupted the heart beats irregularly
Age
The older we get, the harder our heart has to work to pump
Kids: have faster heart rates because their metabolism is faster
Gender
Females have higher heart rates because of estrogen and progesterone
Physical fitness
Better shape= lower heart rate *heart is much more efficient
Temperature
Increase body temperature increases heart rate
Nervous system control of the heart
Input to cardiovascular center in the medulla oblongata
From higher brain centers: cerebral cortex, limbic system, and hypothalamus
From sensory receptors
Proprioceptors- monitor body position/movement
Chemoreceptors- monitor blood chemistry
Baroreceptors- monitor blood pressure
Output to heart
Through cardiac accelerator nerves (sympathetic)
Increased rate of spontaneous depolarization in SA and AV nodes
Increases heart rate and contractility of atria and ventricles (SV)
Through Vagus (X) nerves (parasympathetic)
Decreased rate of spontaneous depolarization in SA and AV nodes
Decreases heart rate
Factors that increase cardiac output
Increased end-diastolic volume (stretches the heart( → increased preload → within limits, cardiac muscle fibers will contract more forcefully with stretching → increased stroke volume → increased cardiac output
Increased contractility→ increase stroke volume→ increased cardiac output
Decreased arterial BP during relaxation decreased afterload→ increases stroke volume→ increased cardiac output
Nervous system: cardiovascular centers in the medulla oblongata receive input from the cerebral cortex, limbic system, hypothalamus, proprioceptors, chemoreceptors, and baroreceptors → increased sympathetic stimulation and decreases parasympathetic stimulation → increased heart rate → increased cardiac output
Chemicals: catecholamine or thyroid hormones in the blood; moderate increase in extracellular Ca2+ → increased heart rate → increases cardiac output
Other factors: infants and elderly; females; low physical fitness; increased body temperature → increased heart rate → increased cardiac output
Discuss layers of blood vessels
Arteries and arterioles
*Carry blood away from the heart to the tissues
The walls of the arteries are ELASTIC, allowing them to absorb the PRESSURE created by ventricles of the heart as they pump blood into the arteries
PRESSURE RESERVOIRS
*high pressure within them
Because of the smooth muscle in the tunica media (the thickest layer in arteries), arteries can regulate their diameter
Layers of arteries
Tunica intima (endothelium)- the innermost layer of the artery
Basement membrane- between endothelium/ tunica intima and internal elastic membrane
Internal elastic membrane- swiss cheese looking membrane that surrounds the tunica media on the medial to the lumen
Tunica media (smooth muscle)- middle layer; the thickest layer of the arteries; surrounded by elastic membranes (more elastic tissue and less smooth muscle tissue)
External elastic membrane- swiss cheese looking membrane that surrounds the tunica media lateral to the lumen
Tunica Externa- the outermost layer of the artery
Veins and venules
Venules are small vessels that are formed by the union of several capillaries
Venules drain blood from capillaries into veins
VOLUME RESERVOIR
*low pressure within
Layers of veins
Tunica intima (endothelium)- the innermost layer of the vein; adjacent to the lumen
Compared to arteries this is thinner in veins
Basement membrane- between endothelium/tunica intima and tunica media
Tunica media (smooth muscle)- middle layer; smooth muscle and elastic fibers (more smooth muscle less elastic)
Compared to arteries this is thinner in veins
Tunica Externa- the outermost layer of the vein; adjacent to surrounding tissue
Compared to arteries this is thicker in veins
Does not have elastic membranes within it
Histologically very different
Vein contain VALVES
Capillaries
Capillaries are microscopic vessels that usually connect arterioles and venules
Layers of capillaries
Capillary walls are composed of a single layer of cells and a basement membrane
Because their walls are so thin, capillaries permit the exchange of nutrients and wastes between blood and tissue cells
*Think of popped blood vessels (those are capillaries) that exploded due to high pressure -strap bar
Discuss types of arteries and veins.
Types of arteries
Elastic arteries (conducting arteries)
Large diameter
More elastic fibers, less smooth muscle
Function as PRESSURE RESERVOIRS
Muscular arteries (distributing arteries)
Medium diameter
More smooth muscle, few elastic fibers
Distribute blood to various parts of the blood
Anastomoses- the union of the two branches of 2 or more arteries supplying the same region of the body **alternate route (backroads think traffic)
Arteries that do not form these are called “end arteries”
If an end artery is blocked, blood cannot get to that region and tissues can die
Types of veins
Postcapillary venules
Pass blood into muscular venules; permit exchange of nutrients and wastes between blood and interstitial fluid function in white blood cell emigration
Muscular venules
Pass blood into a vein; act as reservoirs for accumulating large volumes of blood (along with postcapillary venules)
Veins
Return blood to the heart, facilitated by valves in limb veins
Varicose and spider veins
Formed when venous valves become weak or damaged
Veins are dilated and twisted in appearance
Dilated venules close to the skin, especially in the lower limb of the face
They appear red, blue, or purple, resembling a spider web
Outline and discuss capillary types and locations.
Types of capillaries
Continuous capillaries
Formed by endothelial cells
Consist of a basement membrane, pinocytic vesicle, nucleus of endothelial cell, lumen, and intercellular cleft
Fenestrated capillaries
Consists of a fenestration, intercellular cleft, lumen, pinocytic vesicle, basement membrane, and nucleus of endothelial cell
Sinusoid capillaries
Consists of an incomplete basement membrane, lumen, nucleus of endothelial cell, and intercellular cleft
Discuss blood flow through capillaries.
Blood flow into the capillaries is controlled by smooth muscle tissue located at the arterial end of a capillary called a precapillary sphincter (which may close or open the capillary, by contracting or relaxing)
The precapillary sphincter responds to the demands of the cells the capillary supplies
When contractions of oxygen and nutrients in these cells are low, the precapillary sphincter relaxes,, and blood flow increases; the precapillary sphincter contracts again when cellular requirements have been met
Discuss the blood distribution in the body.
At rest, the largest portion of the blood is in the systemic veins and venules, which are considered “blood reservoirs”
Systemic veins and venules- 64%
Systemic capillaries- 7%
Systemic arteries and arterioles- 13%
Heart- 7%
Pulmonary vessels- 9%
Discuss capillary exchange.
Substances across capillary walls by:
Diffusion
Substances such as oxygen, carbon dioxide, g;glucose, amino acids, and some hormones cross capillary walls via simple diffusion
Transcytosis
Large, lipid-insoluble molecules (like insulin) cross capillary walls in vesicles via transcytosis
Bulk flow
Bulk flow is a passive process in which large numbers of ions, molecules, or particles in a fluid move together in the same direction
Occurs from an area of HIGH PRESSURE to an area of LOW PRESSURE, and it continues as long as a pressure difference exists
Bulk flow is more important for the regulation of the relative volumes of blood and interstitial fluid
Filtration and reabsorption
Filtration is pressure- the driven movement of fluid and solutes from blood capillaries into the interstitial fluid
Blood hydrostatic pressure (BHP) and interstitial fluid osmotic pressure (IFOP) promote filtration
Reabsorption is the pressure-driven movement of fluid and solutes from the interstitial fluid into blood capillaries
Interstitial fluid hydrostatic pressure (IFHP) and blood colloid osmotic pressure (BCOP) promote reabsorption
Outline and discuss the dynamics of capillary exchange, with a formula.
Arterial end: *positive
Blood hydrostatic pressure (BHP)= 35mmHg
Blood colloid osmotic pressure (BCOP)= 26mmHg
**NPF=(35+1)-(26+0)=10mmHg
NET FILTRATION
Venous end: *negative
Blood hydrostatic pressure (BHP)= 16mmHg (*lower on venous side)
Blood colloid osmotic pressure (BCOP)= 26mmHg (same on both sides)
**NFP= (16+1)-(26+0)=-9
NET REABSORPTION
In between (Arterial side and venous side) CONSTANT VALUES
Interstitial fluid osmotic pressure (IFOP)= 1mmHg
Interstitial fluid hydrostatic pressure (IFHP)=0mmHg
Under normal conditions, the volume of fluid and solutes reabsorbed is almost as large as the volume filtered → NFP=(BHP + IFOP) - (BCOP + IFHP)
*Starling’s Law of the Capillaries
Discuss vascular resistance.
R is the opposition to blood flow due to friction between blood and the walls of blood vessels
The higher the R, the smaller the blow flow
R depends on:
Size of the blood vessel lumen
Blood viscosity *polycythemia
Total blood vessel length (*obese people have very long blood vessels)
Outline venous return.
Venous return- the volume of blood flowing back to the heart through the systemic veins, occurs due to the pressure generated by contractions of the heart’s left ventricle
Venous return is assisted by:
Valves
Respiratory pumps
Skeletal muscle pumps *primary way
During exercise,, blood moves faster through the body
Ex. in a still leg the valves within this pump close
Discuss the relationship between the blood velocity and cross-sectional area of BVs.
Blow flow is the volume of blood that flows through tissue in a given period
Blood flow is inversely related to the cross-sectional area of blood vessels
*surface area versus blood flow
Things to remember- BP
BP is highest at the aorta and continues to decrease
At the capillaries,, BP is the lowest (thin vessels can not handle a lot of pressure)
In the veins and venules,, BP starts to raise again but not nearly as high as before
Things to remember- surface area
Within the aorta, arteries, and arterioles the surface area is at its lowest, but slowly increasing
Within the capillaries,, the surface area reaches its peak (greatest distance within the body)
In venules, veins, and venae cavae the surface area initially plummets, but then slowly starts to raise again as blood moves back to the heart
Outline and discuss factors that affect and control Blood pressure.
Cardiac output
Increased heart rate and contractility- increases BP
Systemic vascular resistance
Increases BP- vasoconstriction
Decreases BP- vasodilation
Blood volume
Blood volume increase- increases BP
Blood volume decrease- decreases BP
*Green side of the chart
Increased blood volume, vasoconstriction, and activations of skeletal muscle pumps and respiratory pumps
Causes: Increased venous return
Decreased parasympathetic impulses and increased sympathetic impulses and hormones from the suprarenal medulla
Causes: Increased heart rate (HR)
Increased venous return and increased sympathetic impulses and hormones from the suprarenal medulla
Causes: Increased stroke volume (SV)
Increased heart rate and increased stroke volume
Causes: Increased cardiac output (CO)
Increased cardiac output
Causes: Increased mean arterial pressure (MAP)
*Blue side of the chart
Increased number of RBCs (polycythemia)
Causes: Increased blood viscosity
Increased body size, as in obesity
Causes: Increased total blood vessel length
Increased blood viscosity, increased total blood vessel length, and decreased blood vessel radius (vasoconstriction)
Causes: Increased systemic vascular resistance (SVR)
Increased systemic vascular resistance (SVR)
Causes: Increased mean arterial pressure (MAP)
Compare and contrast endocrine vs endocrine glands. Use examples.
Exocrine glands-
Secrete their products into DUCTS that carry the secretions into the body cavities, into the lumen of an organ, or to the outer surface of the body
NONE ARE HORMONES
Examples include-
Sudoriferous (sweat) glands
Sebaceous (oil) glands
Mucous glands
Digestive glands
Endocrine glands-
Secrete their HORMONES directly into the INTERSTITIAL FLUID that surrounds them
From the interstitial fluid, hormones diffuse into the bloodstream through blood CAPILLARIES and are carried to TARGET CELLS *receptor specific throughout the body
Examples include-
Pituitary gland
Thyroid gland/parathyroid gland
Adrenal gland
Pineal gland
Hormone-secreting cells can be found in the hypothalamus, thymus, skin, pancreas, gonads, stomach, liver, heart…
Discuss hormone function and activity.
Receptors *protein receptors are hormone-specific receptors like enzymes
Continually being synthesized and broken down
Maybe down-regulated in the presence of high concentrations of hormone→# of target cell receptors to decrease **up-regulated is the opposite process
Types of hormones
Circulating hormones- carried through the bloodstream to act on DISTANT target cells (through interstitial fluid+bloodstream)
Local hormones- act LOCALLY on neighboring cells or on the same cell that secreted them WITHOUT entering the bloodstream (just interstitial fluid)
Paracrine (neighboring cell) /autocrine (same cell)
Lipid soluble hormones- *diffuses easily through the lipid bilayer
Bind to receptors WITHIN nucleus or mitochondria of target cells
In CAPILLARIES, the hormone is carried through the blood with a TRANSPORT PROTEIN (moves not very easily in the blood)
Transport protein then releases the hormone into the interstitium
Water soluble hormones
Bind to receptors on the EXTERIOR surface of a target cell
Move through the blood quickly WITHOUT transporting proteins (easily)
Outline and discuss the mechanisms of hormone action.
How/why it responds to hormones-
Hormones concentration in the blood itself
The number of hormone receptors on a target cell
Influences from other hormones
Synergistic effect→ ex: estrogen and prolactin work together to achieve the same goal
Antagonistic effect→ ex: insulin and glucagon work opposite of one another
Hormone secretion is regulated by-
Signals from the nervous system
Chemical changes in blood
Other hormones
Discuss negative and positive feedback for the control of hormone secretions. Use an example.
Negative feedback- responding to a disruption/stimulus (example)
Stimulus: disruption in homeostasis by decreasing…
Controlled condition: decreasing glucocorticoid levels in the blood
Receptors: neurosecretory cells in the hypothalamus provide input
Input: increased corticotropin-releasing hormones (CRH) and decreased cortisol to the …
Control center: corticotrophs in the anterior pituitary provide output
Output: increased adrenocorticotropic hormone (ACTC) to
Effectors: cells of zona fasciculata in the adrenal cortex which secrete glucocorticoids
Response: increased glucocorticoid levels in the blood
Return to homeostasis: when the response brings glucocorticoid level in the blood back to normal the “loop” turns off
Positive feedback- disrupting homeostasis
Ex: childbirth: hormone oxytocin stimulates contraction of the uterus to in turn stimulate more oxytocin release
Make a flow chart for all classes of hormones.
Discuss the function of the hypothalamus. Outline and discuss all regulatory hormones.
Hypothalamus: secretes releasing and inhibiting hormones that control the release of hormones by the pituitary gland
Hormones reach the pituitary gland via the hypophyseal portal system (blood vessels that connect the hypothalamus and anterior pituitary gland)
Anterior pituitary hormones- 7 regulatory hormones of the hypothalamus
Posterior pituitary hormones- 2 hormones of the hypothalamus
Hypophyseal portal system
*anterior pituitary Superior hypophyseal artery picks up hormones in the hypothalamus through capillary beds through capillary plexus and takes hormones in the blood through the body *hypophyseal portal vein
*posterior pituitary inferior hypophyseal artery into the capillary plexus of infundibular processes and picks up all hormones being stored in neurohypophysis and carries them throughout the body (in the blood)
Outline and discuss the hormones of the pituitary. (details here)
Hormones (anterior pituitary) make and secretes + glandular *adenohypophysis
Growth hormone (GH) is secreted by somatotropic cells
Stimulates secretion: growth hormone-releasing hormone (GHRH)
Inhibits secretion: growth hormone inhibiting hormone (GHIH)
Thyroid-stimulating hormone (TSH) is secreted by thyrotropic cells
Stimulates secretion: thyrotropin-releasing hormone (TRH)
Inhibits secretion: growth hormone inhibiting hormone (GHIH)
Follicle-stimulating hormone (FSH) is secreted by gonadotropic cells
Stimulates secretion: gonadotropin-releasing hormone (GnRH)
Luteinizing hormone (LH) is secreted by gonadotropic cells
Stimulates secretion: gonadotropin-releasing hormone (GnRH)
Prolactin (PRL) is secreted by prolactin cells
Stimulates secretion: prolactin-releasing hormone (PRH)
Inhibits secretion: prolactin-inhibiting hormone (PIH), which is dopamine
Adrenocorticotropic hormone (ACTH) is secreted by corticotropic cells
Stimulates secretion: corticotropin-releasing hormone
Melanocyte-stimulating hormone (MSH) is secreted by corticotropic cells
Stimulates secretion: corticotropin-releasing hormone
Inhibits secretion: dopamine
**fetal development pars intermedia (very small or absent in adulthood)
Hormones (posterior pituitary) secretes and stores + not glandular *neurohypophysis
Oxytocin (OT)
Stimulates contraction of smooth muscle cells of the uterus during childbirth; stimulates contraction of myoepithelial cells in mammary glands to cause milk ejection
Antidiuretic hormone (ADH)
Conserves body water by decreasing urine volume; decreases water loss through perspiration; raises blood pressure by constricting arterioles
Outline and discuss the adrenal glands. Identify all layers/regions and what they do.
Adrenal gland: secretes DHEA, a hormone that makes men masculine during puberty but is insignificant for females until menopause when there is no more estrogen
Adrenal medulla- norepinephrine and epinephrine are secreted from chromaffin cells
Hormones increase heart rate, and blood pressure, and mobilize/utilize glucose for energy
Adrenal cortex-
3 regions
Zona glomerulosa- secretes aldosterone to maintain homeostasis between sodium and potassium
Aldosterone- RAA pathway
Mineralocorticoids (class)
Zona fasciculata- cortisol, anti-inflammatory and makes glucose
Glucocorticoids
Zona reticularis- sex hormones
Androgens
Outline and discuss the stress response. **sympathetic division of the autonomic nervous system
Eustress is helpful, everyday stress that prepares us to meet good challenges *good stress
Distress is any type of harmful stress that may become damaging
1st stage of stress- sympathetic nervous system
2nd stage of stress- resistance reaction
This stage lasts much longer and if overused can cause exhaustion
Identify and discuss the endocrine disorders discussed in class.
Suprarenal gland disorders:
Cushing’s syndrome- hypersecretion of the suprarenal cortex
Addison’s disease- hyposecretion of glucocorticoids and aldosterone
Pheochromocytoma- benign tumors that cause hypersecretion of epinephrine and norepinephrine
Pancreatic disorders:
Type 1 diabetes- autoimmune disorder in which the body destroys its beta cells in the pancreatic islet cells creating an insufficient amount of insulin
Symptoms include: high levels of sugar in urine/blood, dehydration, and constant thirst
Type 2 diabetes- adult onset, caused by obesity, poor diet, and lack of exercise causing beta cells to ignore the stimulus to make insulin
Can be fixed by weight loss, exercise, and a better diet
Gestational diabetes- *females when they are pregnant
Can be diagnosed with a simple glucose test when high levels of sugar show up in urine
This disease causes babies to be born big and increase the chances of a c-section or other procedure
Thyroid disorders:
Hypothyroid- (underactive thyroid) weight gain, stores glucose, and slow metabolism
Hyperthyroid (overactive thyroid) weight loss, super fast metabolism
Goiter- enlarged thyroid gland
Hashimoto syndrome- autoimmune disease, hypothyroid
Affects women more than men
Parathyroid disorders:
Hypoparathyroidism- too much potassium, causes dropping of the face
Outline and discuss the functions and properties of blood.
Blood plasma (55%)
Consists of water (91.5%), proteins (7%), and other solutes (1.5%)
Red blood cells (45%) *erythrocyte
The number of RBCs and platelets remains rather steady while that of WBCs varies depending on invading pathogens and other foreign antigens
Contain hemoglobin that is used to carry oxygen to all cells and to carry some carbon dioxide to the lungs
Buffy coat is composed of white blood cells and platelets
Cellular components (formed elements) of blood include red blood cells, white blood cells, and platelets *thrombocyte
White blood cells *leukocyte
Functions of blood
Blood transports oxygen, carbon dioxide, nutrients, hormones, heat, and waste products
Blood regulates the homeostasis of all body fluids, pH, body temperature, and water content of cells
Blood protects against excessive loss by clotting and uses white blood cells to protect against infections
Outline and discuss the composition of blood.
Blood plasma (55%)
Consists of water (91.5%), proteins (7%), and other solutes (1.5%)
Blood plasma proteins (7%)
Albumins (54%) smallest and most numerous plasma protein
Globulins (38%) large protein
Fibrinogen (7%) large protein
Other solutes (1.5%)
Electrolytes- help maintain osmotic pressure and play essential roles in cell functions
Nutrients- essential roles in cell functions, growth, and development
Gasses- oxygen (important in cellular functions), nitrogen (no known function), carbon dioxide (involved in the regulation of blood pH)
Enzymes- catalyze chemical reactions
Hormones- regulate metabolism, growth, and development
Vitamins- cofactors for enzymatic reactions
Waste products- breakdown products of protein metabolism that are carried by the blood to organs of excretion
Red blood cells (45%) *erythrocyte
The number of RBCs and platelets remains rather steady while that of WBCs varies depending on invading pathogens and other foreign antigens
Contain hemoglobin that is used to carry oxygen to all cells and to carry some carbon dioxide to the lungs
Each hemoglobin molecule constraints an iron ion which allows each molecule to bind to four oxygen molecules
Hemoglobin is involved in regulating blood flow and BP via the release of NO
Nitric oxide (NO) causes vasodilation, which improves blood flow and enhances oxygen delivery
No nucleus or other organelles *biconcave discs- this allows them to carry O2 better
RBCs contain carbonic anhydrase, which catalyzes the conversion of carbon dioxide and water to carbonic acid
Carbonic acid transports about 70% of the carbon dioxide in plasma
Live for only 120 days
Dead cells are removed from circulation by the spleen and liver
Breakdown products from the RBCs are recycled and reused
Erythropoiesis (production of RBCs) begins in the red bone marrow
Erythropoietin, a hormone secreted by the kidneys in response to lowered oxygen concentration (hypoxia) stimulates the differentiation of hematopoietic stem cells into erythrocytes
Reticulocytes (immature RBCs) enter the circulation and mature in 1 to 2 days
Stimulus→controlled condition→receptors→input→control center→output→ effectors→response *return to homeostasis when o2 delivery to kidneys increases to normal
Buffy coat is composed of white blood cells and platelets
Cellular components (formed elements) of blood include red blood cells, white blood cells, and platelets *thrombocyte
White blood cells *leukocyte
Contain a nucleus and organelles, but NO HEMOGLOBIN
May live for several months or years- the main function is to combat invading microbes
During an invasion, many WBCs can leave the bloodstream and collect at sites of invasion
This is called emigration
An elevation in the white blood count indicates an infection or inflammation
A low white blood cell count may develop due to several causes
A differential white blood cell count will help to determine if a problem exists
Classified as granular and agranular
Granular- containing vesicles that appear when the cells are stained
Granular leukocytes: neutrophils, eosinophils, basophils
Agranular- containing no granules
Agranular leukocytes: lymphocytes, monocytes
(most abundant to least: Never Let Monkeys Eat Bananas
Neutrophils (60-70%)
Lymphocytes (20-25%)
Able to live for years, while most other blood cells live for hours, days, or weeks
Monocytes (3-8%)
Eosinophils (2-4%)
Basophils (0.5-1%)
Outline and discuss the formation of blood cells.
Hematopoiesis- formation of blood cells
Pluripotent stem cells differentiate into each of the different types of blood cells
Outline and discuss the epidemiology of sickle cell anemia.
People with this disorder have an abnormal kind of hemoglobin
RBC is sickle or crescent-shaped
Sickled RBCs break down prematurely (5-7 days)
Sickle cells do not move easily through blood vessels preventing O2 transport
People with sickle cell anemia are not allowed to do high-impact activities ex. sports due to this risk
Symptoms include- shortness of breath, fatigue paleness, and delayed growth in children
Positive- builds resistance to malaria
Because sickled cells last 5-7 days, we get rid of the third stage of malaria
Outline and discuss the different types of white blood cells and what they do.
Classified as granular and agranular
Granular- containing vesicles that appear when the cells are stained
Granular leukocytes: neutrophils, eosinophils, basophils
Agranular- containing no granules
Agranular leukocytes: lymphocytes, monocytes
(most abundant to least: Never Let Monkeys Eat Bananas
Neutrophils (60-70%)
The high count may indicate: bacterial infection, burns, stress, inflammation
The low count may indicate: radiation exposure, drug toxicity, vitamin b12 deficiency, systemic lupus erythematosus
Lymphocytes (20-25%)
The high count may indicate: viral infections, some leukemias, infectious mononucleosis
The low count may indicate: prolonged illness, HIV infection, immunosuppression, treatment with cortisol
Able to live for years, while most other blood cells live for hours, days, or weeks
Monocytes (3-8%)
The high count may indicate: viral or fungal infections, tuberculosis, some leukemias, or other chronic diseases
The low count may indicate: bone marrow suppression, treatment with cortisol
Eosinophils (2-4%)
The high count may indicate: allergic reactions, parasitic infections, autoimmune diseases
The low count may indicate: drug toxicity, stress, acute allergic reactions
Basophils (0.5-1%)
The high count may indicate: allergic reactions, leukemias, cancers, hypothyroidism
The low count may indicate: pregnancy ovulation, stress, hypothyroidism
** LAB MANUAL
Outline and discuss the steps in hemostasis.
Hemostasis- is a sequence of responses that stop bleeding
Process involves-
Vascular spasm
Platelet plug formation
Blood clotting (coagulation)
Blood clotting involves several clotting (coagulation) factors
Blood clotting can be activated in one of two ways-
Extrinsic pathway
Intrinsic pathway
Both pathways lead to the formation of prothrombinase and, from there, the common pathway continues
Outline and discuss the steps in clot formation. Be sure to discuss all three pathways including all clotting factors.
Steps in clot formation
(Hemostasis) Process involves-
Vascular spasm
Platelet plug formation
Platelet adhesion → platelet release reaction → platelet aggregation
Blood clotting (coagulation)
Blood clotting cascade
Once the clot forms, it tightens to pull the edges of the damaged vessel together
Vitamin K is needed for normal clot formation because it is used in the synthesis of 4 clotting factors
Small, unwanted clots are dissolved by plasmin, an enzyme that is part of the fibrinolytic system
Clotting (coagulation) factors
I Fibrinogen: source- liver
Pathways of activation → common
II Prothrombin: source- liver
Pathways of activation → common
III Tissue factor (thromboplastin): damaged tissues and activated platelets
Pathways of activation → extrinsic
IV Calcium ions: diet, bones, and platelets
Pathways of activation → all
V Proaccelerin, labile factor or accelerator globulin: liver and platelets
Pathways of activation → extrinsic and intrinsic
VII Blood serum prothrombin conversion accelerator (SPCA): liver
Pathways of activation → extrinsic
VIII Antihemophilic factors (AHF): liver
Pathways of activation → intrinsic
IX Plasma thromboplastin component (PTC): liver
Pathways of activation → intrinsic
X Stuart factor: liver
Pathways of activation → extrinsic and intrinsic
XI Blood plasma thromboplastin antecedent (PTA): liver
Pathways of activation → intrinsic
XII Hageman factor: liver
Pathways of activation → intrinsic
XIII Fibrin-stabilizing factor (FSF): liver and platelets
Pathways of activation → common
Outline and discuss the plasma proteins found in the blood.
Blood plasma (55%)
Consists of water (91.5%), proteins (7%), and other solutes (1.5%)
Blood plasma proteins (7%) *MOST are produced by the liver
Albumins (54%) smallest and most numerous plasma protein
Help maintain osmotic pressure *important factor in the exchange of fluids across blood capillary walls
Globulins (38%) large proteins (plasmocytes produce immunoglobulins)
Immunoglobulins help attack viruses and bacteria *alpha and beta globulins transport iron, lipids, and fat-soluble vitamins
Fibrinogen (7%) large protein
Plays an essential role in blood clotting
Discuss blood groups and blood types.
Blood is characterized into different blood groups based on the presence or absence of agglutinogens on the surface of RBCs
24 blood groups and more than 100 antigens
Blood types vary among different populations
Classification is based on antigens labeled A, B, or AB, with O being no antigens
85% of the population is Rh positive
Blood plasma usually contains antibodies that react with A or B antigens
An individual will not have agglutinins against his or her blood type *hemolytic disease
Type A
An antigen
Anti-B antibody
Compatible donor blood types: A, O
Type B
B antigen
Anti-A antibody
Compatible donor blood types: B, O
Type AB
Both A and B antigens
Anti-A antibody
Compatible donor blood types: A, B, AB, O
*Universal recipient
Type O
Neither A nor B antigen
Both anti-A and anti-B antibodies
Compatible donor blood types: O
*Universal donor
Discuss the hemolytic disease of newborns.
At birth small amounts of fetal blood leak into the maternal circulation
If the baby is Rh+ and the mother is Rh-, she will develop antibodies to the Rh factor
During her next pregnancy with an Rh+ baby, when she transfers antibodies to the fetus, the transferred anti-Rh antibodies will attack some of the fetal’ RBCs causing clotting and hemolysis
Outline and discuss the different components of the pericardium and any possible infections that can occur.
The heart is enclosed and held in place by the pericardium (heart wall)
Consists of an outer fibrous pericardium and an inner serous pericardium
The serous pericardium has 2 layers-
The Visceral- (epicardium) adheres to the surface of the heart
Parietal-fused to the fibrous pericardium
The visceral and parietal layers are separated by the serous cavity, a fluid-filled space
This fluid reduces friction between the layers of the serous pericardium as the heart moves
Infection: Pericarditis- inflammation of the pericardium; chest pain and pericardial friction rub
The wall of the heart (pericardium) has 3 layers
Epicardium (visceral pericardium) *outer layer
Myocardium- cardiac muscle; responsible for pumping action of the heart (contracts to help move blood throughout the heart); thickest layer
Cardiac muscle is involuntary, arranged in bundles that swirl diagonally around the heart *striated + intercalated discs
Infection: myocarditis- inflammation of the myocardium; may cause fatigue, chest pain, irregular heartbeat *severe cases lead to cardiac failure and death
Endocardium- the innermost layer of the heart
Has a slip and slide texture→ water=blood plasma, produces a friction-free environment for formed elements to move through without any damage
Infection: endocarditis- inflammation of endocardium; may cause fever, heart murmurs, irregular heartbeat, fatigue
Trace blood flow through the heart and identify all the blood vessels, valves, and chambers it passes through. (systemic and pulmonary circulations)
Right atrium- pushes deoxygenated blood through the tricuspid valve →
Right ventricle- pushes deoxygenated blood through the pulmonary valve →
Pulmonary trunk- where deoxygenated blood moves out through the left and right pulmonary arteries →
Left and right lungs- in the pulmonary capillaries, blood loses CO2 and gains O2 **blood is now oxygenated →
The oxygenated blood moves through the left and right pulmonary veins →
Left atrium- oxygenated blood is then pushed through the bicuspid valve →
Left ventricle- pushes oxygenated blood through the aortic valve →
Aorta and systemic arteries- where the oxygenated blood is →
Systemic capillaries- where blood loses O2 and gains CO2 *because O2 is being absorbed
The deoxygenated blood moves through the superior vena cava, inferior vena cava, ad coronary sinus back into the right atrium
Outline and discuss the conduction system through the heart (5 steps).
Cardiac cells are self-excitable (autorhythmic)- repeatedly generate spontaneous pulses that trigger heart contractions *these cells form the conduction system
5 steps of the conduction system
**SA node, AV node, AV bundle, right and left bundle branches, Purkinje fibers
SA node in the wall atrium is activated and atrial activations begin
Time=0
SA node cells repeatedly depolarize to threshold spontaneously→ pacemaker potential
When the pacemaker potential reaches the threshold, it triggers an action potential that propagates both atria
Stimulus spreads across the atrial surfaces and reaches the AV node
Elapsed time: 50 msec
The AV node is located at the interatrial septum
There is a 100 msec delay at the AV node; atrial contraction occurs
Elapsed time=: 150 msec
Both atria are fully depolarized
AV valves open (atrioventricular)
SL valves close (semilunar)
The impulse travels along the interventricular septum within the atrioventricular bundle and the bundle branches into the right and left bundle branches to the Purkinje fibers via the moderator band, to the papillary muscles of the right ventricle
Elapsed time: 175 msec
Impulse is distributed by Purkinje fibers and relayed throughout the ventricular myocardium- atrial contraction is completed, and ventricular contraction begins
Both ventricles are fully depolarized
AV valves closed
SL valves opened
Time elapsed: 225 msec
**Hormones can modify the heart rate and force of contraction but they do not set the fundamental rhythm for the heart (medulla oblongata)
Discuss an EKG tracing and identify all the waves and complexes.
Action potential in a (ventricular) contractile fiber:
AP initiated by the SA node travels along the conduction system and spreads out to excite the “working” atrial and ventricular fibers (contractile fibers)
An AP in a contractile fiber is characterized by a rapid depolarization
Steps/patterns shown on EKG:
(1) Rapid depolarization- due to Na+ inflow when collage-gated fast Na+ channels open (contractile fibers are brought to threshold)
(2) Plateau (maintained depolarization)- due to Ca2+ inflow when voltage-gated slow Ca2+ channels open and the K+ outflow when some voltage-gated slow K+ channels open
*Ca2+ inflow balances out K+ outflow
Allows a sustaining of longer contraction cycling of the heart muscle
Allowing time for blood to move its respective parts
*Prevents tetanus in cardiac muscle fibers
(3) Repolarization (return to resting membrane potential)- due to closing of Ca2+ channels and K+ outflow when additional voltage K+ channels open
Refractory period- occurs during the plateau phase and parts of repolarization
There cannot be another AP coming to stimulate another depolarization phase until this construction is complete
Important in preventing tetanus and arrhythmias
Electrocardiogram (EKG):
Measures electrical conduction through the heart
P wave- small upward deflection on ECG that represents atrial depolarization
PQ interval- from the start of the P wave to the beginning of the QRS complex, the time required for the AP to travel through the atria, AV node, and remaining fibers of the conduction system
QRS complex- represents rapid ventricular depolarization
ST segment- from the end of the QRS complex to the start of the T wave that represents a time when the ventricular fibers are depolarized during the plateau phase of the AP
T wave- represents ventricular repolarization (ventricles relaxing) occurs more slowly than depolarization (wave is smaller and wider than QRS complex)
QT interval- from the start of the QRS complex to the end of the T wave
Contraction of ECG waves with atrial and ventricular systole
*depolarization causes contraction and depolarization causes relaxation of cardiac muscle fibers
Depolarization of atrial contractile fibers produces P wave
Atrial systole (contraction) after the P wave begins
Atrial diastole (relaxation) is masked by QRS complex
Depolarization of ventricular contractile fibers produces QRS complex
Ventricular systole (contraction) shortly after QRS complex begins
Repolarization of ventricular contractile fiber produces T wave
Ventricular diastole (relaxation) shortly after the T wave begins
One cardiac cycle consists of the contraction )systole) and relaxation (diastole) of both atria, rapidly followed by the systole and diastole of both ventricles
During atrial systole (contraction)
Electrical events of EKG-
Atrial depolarization (marked by P wave) causes atrial systole
The onset of ventricular depolarization with the onset of QRS complex
Pressure change
As the atria contract, pressure is exerted on the blood within, forcing the blood through the open AV valves into the ventricles
Aortic pressure is slightly decreasing (think: because atria are contracting, not the ventricles thus, BP is low)
Left ventricular pressure is low (small hump before ventricular systole)
Left atrial pressure is low (small hump_ because the distance is not very far (only pushing blood into ventricles right below it)
Volume changes
Volume in the ventricle increases (being filled with blood)
The end of each atrial systole is also the end of each ventricular diastole (relaxation)
This blood volume is called end-diastolic volume (EDV)
Heart sounds- Auscultation: s4, but can’t hear it with a stethoscope
Mechanical event- atrial systole (contraction) and ventricle diastole (relaxation)
During ventricular systole (contraction)
Electrical events of EKG
Ventricular depolarization causes ventricular systole, marked by QRS complex
T wave in ECG marks onset of ventricular repolarization
Pressure change
As ventricular systole (contraction) begins, pressure rises inside the ventricles and pushes up against the AV valves, forcing them to shut
Isovolumetric contraction- period of about (0.5 secs) when both semilunar and AV valves are closed
During this interval, cardiac muscle fibers are contracting and exerting force but are not shortening (yet)
All four valves are closed- ventricular volume remains the same
Continued contraction of the ventricles causes pressure inside the chambers to rise sharply
When left ventricular pressure surpasses aortic pressure at 80mmHg the aortic semilunar valve opens and the ventricular ejection begins (pressure continues to rise to 120mmHg)
Volume changes
The blood volume in ventricles decreases (ventricle is ejecting blood)
End systolic volume- volume remaining in each ventricle at the end of systole
Stroke volume- volume ejected per beat from each ventricle
SV= end diastolic volume (-) end systolic volume
At rest: SV is about 130 mL-60mL=70mL
Heart sounds- auscultation: heart 1st sound (s1), a club sound
This sound is caused by blood turbulence associated with the closure of AV valves soon after ventricular contraction begins
Mechanical event: isovolumetric contraction and ventricular ejection
During ventricular diastole (relaxation):
Electrical events of EKG
Ventricular repolarization causes ventricular diastole, as marked by the end of the tZ wave in the EKG
Pressure change
As the ventricles relax, the pressure within the chambers falls, and blood in the aorta and pulmonary trunk begins to flow backward toward the region of lower pressure in the ventricles
Back-flowing blood catches in the valve cusps and closes the semilunar valves
Aortic valves close
The rebound the blood from the closed cusps of the aortic valve produces the dicrotic wave on the aortic pressure curve
Following the aortic pressure decreases
Volume changes
After the SL valves close, there is a brief period (isovolumetric relaxation) when ventricular blood volume does not change because all 4 valves are closed
Pressure falls quickly as ventricles relax
When ventricular pressure drops below atrial pressure, the AV valves open and blood rushes rapidly into the ventricles
Another P wave signals the start of another cardiac cycle
The blood volume in the ventricle increases because the AV valve is open and blood is flows in
Heart sounds- auscultation:
Hear the 2nd sound, s2, a dubb sound
Sound is caused by blood turbulence associated with the closure of SL valves
Mechanical event
Isovolumetric relaxation and ventricular filling
Cardiac output:
The volume of blood ejected from the heart (ejected from the left or right ventricle into the aorta or pulmonary trunk each minute)
Stroke volume=amount of blood pumped out of the ventricle in one beat
(mL/beat) x (heart rate)= about 75 beats per minute
In a typical man: SV is mL/beat and heart rate is about 75 beats per minute
CO= 70 x 75= 5250 mL/min= 5ish liters a minute
Regulation of stroke volume
Preload
The degree of stretch on the heart before it contracts
The volume of the blood in ventricles at the end of diastole (just before contraction is about to begin)
A greater stretch (preload) on cardiac muscle before contraction increases the force of contraction
The more the heart fills with blood during diastole, the greater the force of contraction during systole
Preload is increased in:
Hypervolemia: increased BV
Regurgitation of cardiac valves
Heart failure
Contractility
The forcefulness of contraction of individual ventricular muscle fibers
The ability which the heart can contract
Affects stroke volume
Get older, the compliance of the heart reduces, and it is harder for the heart to contract
Afterload
The pressure that must be exceeded before rejection of blood from the ventricles can occur
The resistance the left ventricle must overcome to circulate blood
Resistance may be: the length of blood vessels or the diameter of the lumen of blood vessels
Increased in:
Hypertension (high BP)
The heart is working overtime to produce more pressure
The delicate aorta can rupture (aneurysm)
Vasoconstriction (smaller lumen, increased BP)
Factors that regulate heart rate:
Autonomic nervous system
The sympathetic nervous system increases the heart rate
The parasympathetic nervous system decreases the heart rate
Hormones
Adrenaline (epinephrine and norepinephrine) increases heart rate
Ions
Increase Ca2+ ions, increase contractility, increases heart rate
Na+ ions need to be exactly regulated- if the flow of Na is disrupted the heart beats irregularly
Age
The older we get, the harder our heart has to work to pump
Kids: have faster heart rates because their metabolism is faster
Gender
Females have higher heart rates because of estrogen and progesterone
Physical fitness
Better shape= lower heart rate *heart is much more efficient
Temperature
Increase body temperature increases heart rate
Nervous system control of the heart
Input to cardiovascular center in the medulla oblongata
From higher brain centers: cerebral cortex, limbic system, and hypothalamus
From sensory receptors
Proprioceptors- monitor body position/movement
Chemoreceptors- monitor blood chemistry
Baroreceptors- monitor blood pressure
Output to heart
Through cardiac accelerator nerves (sympathetic)
Increased rate of spontaneous depolarization in SA and AV nodes
Increases heart rate and contractility of atria and ventricles (SV)
Through Vagus (X) nerves (parasympathetic)
Decreased rate of spontaneous depolarization in SA and AV nodes
Decreases heart rate
Factors that increase cardiac output
Increased end-diastolic volume (stretches the heart( → increased preload → within limits, cardiac muscle fibers will contract more forcefully with stretching → increased stroke volume → increased cardiac output
Increased contractility→ increase stroke volume→ increased cardiac output
Decreased arterial BP during relaxation decreased afterload→ increases stroke volume→ increased cardiac output
Nervous system: cardiovascular centers in the medulla oblongata receive input from the cerebral cortex, limbic system, hypothalamus, proprioceptors, chemoreceptors, and baroreceptors → increased sympathetic stimulation and decreases parasympathetic stimulation → increased heart rate → increased cardiac output
Chemicals: catecholamine or thyroid hormones in the blood; moderate increase in extracellular Ca2+ → increased heart rate → increases cardiac output
Other factors: infants and elderly; females; low physical fitness; increased body temperature → increased heart rate → increased cardiac output
Discuss layers of blood vessels
Arteries and arterioles
*Carry blood away from the heart to the tissues
The walls of the arteries are ELASTIC, allowing them to absorb the PRESSURE created by ventricles of the heart as they pump blood into the arteries
PRESSURE RESERVOIRS
*high pressure within them
Because of the smooth muscle in the tunica media (the thickest layer in arteries), arteries can regulate their diameter
Layers of arteries
Tunica intima (endothelium)- the innermost layer of the artery
Basement membrane- between endothelium/ tunica intima and internal elastic membrane
Internal elastic membrane- swiss cheese looking membrane that surrounds the tunica media on the medial to the lumen
Tunica media (smooth muscle)- middle layer; the thickest layer of the arteries; surrounded by elastic membranes (more elastic tissue and less smooth muscle tissue)
External elastic membrane- swiss cheese looking membrane that surrounds the tunica media lateral to the lumen
Tunica Externa- the outermost layer of the artery
Veins and venules
Venules are small vessels that are formed by the union of several capillaries
Venules drain blood from capillaries into veins
VOLUME RESERVOIR
*low pressure within
Layers of veins
Tunica intima (endothelium)- the innermost layer of the vein; adjacent to the lumen
Compared to arteries this is thinner in veins
Basement membrane- between endothelium/tunica intima and tunica media
Tunica media (smooth muscle)- middle layer; smooth muscle and elastic fibers (more smooth muscle less elastic)
Compared to arteries this is thinner in veins
Tunica Externa- the outermost layer of the vein; adjacent to surrounding tissue
Compared to arteries this is thicker in veins
Does not have elastic membranes within it
Histologically very different
Vein contain VALVES
Capillaries
Capillaries are microscopic vessels that usually connect arterioles and venules
Layers of capillaries
Capillary walls are composed of a single layer of cells and a basement membrane
Because their walls are so thin, capillaries permit the exchange of nutrients and wastes between blood and tissue cells
*Think of popped blood vessels (those are capillaries) that exploded due to high pressure -strap bar
Discuss types of arteries and veins.
Types of arteries
Elastic arteries (conducting arteries)
Large diameter
More elastic fibers, less smooth muscle
Function as PRESSURE RESERVOIRS
Muscular arteries (distributing arteries)
Medium diameter
More smooth muscle, few elastic fibers
Distribute blood to various parts of the blood
Anastomoses- the union of the two branches of 2 or more arteries supplying the same region of the body **alternate route (backroads think traffic)
Arteries that do not form these are called “end arteries”
If an end artery is blocked, blood cannot get to that region and tissues can die
Types of veins
Postcapillary venules
Pass blood into muscular venules; permit exchange of nutrients and wastes between blood and interstitial fluid function in white blood cell emigration
Muscular venules
Pass blood into a vein; act as reservoirs for accumulating large volumes of blood (along with postcapillary venules)
Veins
Return blood to the heart, facilitated by valves in limb veins
Varicose and spider veins
Formed when venous valves become weak or damaged
Veins are dilated and twisted in appearance
Dilated venules close to the skin, especially in the lower limb of the face
They appear red, blue, or purple, resembling a spider web
Outline and discuss capillary types and locations.
Types of capillaries
Continuous capillaries
Formed by endothelial cells
Consist of a basement membrane, pinocytic vesicle, nucleus of endothelial cell, lumen, and intercellular cleft
Fenestrated capillaries
Consists of a fenestration, intercellular cleft, lumen, pinocytic vesicle, basement membrane, and nucleus of endothelial cell
Sinusoid capillaries
Consists of an incomplete basement membrane, lumen, nucleus of endothelial cell, and intercellular cleft
Discuss blood flow through capillaries.
Blood flow into the capillaries is controlled by smooth muscle tissue located at the arterial end of a capillary called a precapillary sphincter (which may close or open the capillary, by contracting or relaxing)
The precapillary sphincter responds to the demands of the cells the capillary supplies
When contractions of oxygen and nutrients in these cells are low, the precapillary sphincter relaxes,, and blood flow increases; the precapillary sphincter contracts again when cellular requirements have been met
Discuss the blood distribution in the body.
At rest, the largest portion of the blood is in the systemic veins and venules, which are considered “blood reservoirs”
Systemic veins and venules- 64%
Systemic capillaries- 7%
Systemic arteries and arterioles- 13%
Heart- 7%
Pulmonary vessels- 9%
Discuss capillary exchange.
Substances across capillary walls by:
Diffusion
Substances such as oxygen, carbon dioxide, g;glucose, amino acids, and some hormones cross capillary walls via simple diffusion
Transcytosis
Large, lipid-insoluble molecules (like insulin) cross capillary walls in vesicles via transcytosis
Bulk flow
Bulk flow is a passive process in which large numbers of ions, molecules, or particles in a fluid move together in the same direction
Occurs from an area of HIGH PRESSURE to an area of LOW PRESSURE, and it continues as long as a pressure difference exists
Bulk flow is more important for the regulation of the relative volumes of blood and interstitial fluid
Filtration and reabsorption
Filtration is pressure- the driven movement of fluid and solutes from blood capillaries into the interstitial fluid
Blood hydrostatic pressure (BHP) and interstitial fluid osmotic pressure (IFOP) promote filtration
Reabsorption is the pressure-driven movement of fluid and solutes from the interstitial fluid into blood capillaries
Interstitial fluid hydrostatic pressure (IFHP) and blood colloid osmotic pressure (BCOP) promote reabsorption
Outline and discuss the dynamics of capillary exchange, with a formula.
Arterial end: *positive
Blood hydrostatic pressure (BHP)= 35mmHg
Blood colloid osmotic pressure (BCOP)= 26mmHg
**NPF=(35+1)-(26+0)=10mmHg
NET FILTRATION
Venous end: *negative
Blood hydrostatic pressure (BHP)= 16mmHg (*lower on venous side)
Blood colloid osmotic pressure (BCOP)= 26mmHg (same on both sides)
**NFP= (16+1)-(26+0)=-9
NET REABSORPTION
In between (Arterial side and venous side) CONSTANT VALUES
Interstitial fluid osmotic pressure (IFOP)= 1mmHg
Interstitial fluid hydrostatic pressure (IFHP)=0mmHg
Under normal conditions, the volume of fluid and solutes reabsorbed is almost as large as the volume filtered → NFP=(BHP + IFOP) - (BCOP + IFHP)
*Starling’s Law of the Capillaries
Discuss vascular resistance.
R is the opposition to blood flow due to friction between blood and the walls of blood vessels
The higher the R, the smaller the blow flow
R depends on:
Size of the blood vessel lumen
Blood viscosity *polycythemia
Total blood vessel length (*obese people have very long blood vessels)
Outline venous return.
Venous return- the volume of blood flowing back to the heart through the systemic veins, occurs due to the pressure generated by contractions of the heart’s left ventricle
Venous return is assisted by:
Valves
Respiratory pumps
Skeletal muscle pumps *primary way
During exercise,, blood moves faster through the body
Ex. in a still leg the valves within this pump close
Discuss the relationship between the blood velocity and cross-sectional area of BVs.
Blow flow is the volume of blood that flows through tissue in a given period
Blood flow is inversely related to the cross-sectional area of blood vessels
*surface area versus blood flow
Things to remember- BP
BP is highest at the aorta and continues to decrease
At the capillaries,, BP is the lowest (thin vessels can not handle a lot of pressure)
In the veins and venules,, BP starts to raise again but not nearly as high as before
Things to remember- surface area
Within the aorta, arteries, and arterioles the surface area is at its lowest, but slowly increasing
Within the capillaries,, the surface area reaches its peak (greatest distance within the body)
In venules, veins, and venae cavae the surface area initially plummets, but then slowly starts to raise again as blood moves back to the heart
Outline and discuss factors that affect and control Blood pressure.
Cardiac output
Increased heart rate and contractility- increases BP
Systemic vascular resistance
Increases BP- vasoconstriction
Decreases BP- vasodilation
Blood volume
Blood volume increase- increases BP
Blood volume decrease- decreases BP
*Green side of the chart
Increased blood volume, vasoconstriction, and activations of skeletal muscle pumps and respiratory pumps
Causes: Increased venous return
Decreased parasympathetic impulses and increased sympathetic impulses and hormones from the suprarenal medulla
Causes: Increased heart rate (HR)
Increased venous return and increased sympathetic impulses and hormones from the suprarenal medulla
Causes: Increased stroke volume (SV)
Increased heart rate and increased stroke volume
Causes: Increased cardiac output (CO)
Increased cardiac output
Causes: Increased mean arterial pressure (MAP)
*Blue side of the chart
Increased number of RBCs (polycythemia)
Causes: Increased blood viscosity
Increased body size, as in obesity
Causes: Increased total blood vessel length
Increased blood viscosity, increased total blood vessel length, and decreased blood vessel radius (vasoconstriction)
Causes: Increased systemic vascular resistance (SVR)
Increased systemic vascular resistance (SVR)
Causes: Increased mean arterial pressure (MAP)