Biology 13A – Test 3 Lecture Notes
Chapter 10 – Senses
A. Sense Reception and Perception
a. Types of Receptors – chemoreceptors, pain receptors, thermoreceptors,
mechanoreceptors, photoreceptors
b. Receptors send signals to the brain to allow for sensation to be perceived.
i. Sensory adaptation – when stimuli are ignored from repeated exposure.
B. General Senses
a. Touch and Pressure (Fig. 10.1)
i. Free nerve endings – extend just a bit into epidermis of skin. Very sensitive and
responds to itching and pain
ii. Tactile corpuscles – knobs of nerves high in the dermis. Sensitive to light
touches.
iii. Lamellated corpuscles – nerve surrounded by heavy connective tissue. Deep in
dermis. Responds to heavy pressure.
b. Temperature
i. Warm and cold receptors detect temperatures near body temperature. If very hot
or very cold, pain receptors are triggered instead.
ii. Warm and cold receptors adapt very quickly (less than one minute) upon
repeated stimulation.
c. Pain
i. Pain receptors consist of free nerve endings. Sensory adaptation is very poor (you
keep feeling pain when stimulated)
ii. Nerve fibers conduct impulses from pain receptors (Fig. 10.3)
1. Acute – myelinated. Gives sharp pain sensation.
2. Chronic – unmyelinated. Gives dull, aching sensation.
iii. Pain is suppressed by neurotransmitters that act on the brain. Enkephalins,
serotonin, and endorphins are examples.
C. Smell and Taste
a. Olfactory (Fig. 10.4)
i. The olfactory organ contains receptors and the bulb.
ii. Receptors – are chemoreceptors that have exposed cilia in the nasal cavity. These
cilia contain proteins that bind to chemicals in the air. There are hundreds of
different proteins that can combine to make thousands of different odors. Each
receptor contains one type of protein.
iii. Bulb – picks up signals for receptors and sends to the brain.
b. Taste (Fig. 10.5)
i. The tongue, throat, and roof of mouth contain taste buds
ii. Each bud contains about 100 taste cells that can detect at least 5 types of tastes:
sweet, sour, bitter, salty, umami, and maybe others (metallic, alkaline)
iii. Don’t believe tongue maps!
D. Hearing and Equilibrium
a. Structure of the Ear (Fig. 10.6)
i. Outer Ear – collects sound and transmits it to the middle ear. It terminates at the
eardrum.
ii. Middle Ear – vibration from the eardrum moves the auditory ossicles (three
earbones) which transmits vibrations to the inner ear
iii. Auditory Tube – maintains pressure behind the eardrum
iv. Inner Ear – detects sound and involved in equilibrium (Fig. 10.8)
1. The labyrinth is the main organ of chambers and tubes
a. The semicircular canals control equilibrium
b. The cochlea controls hearing
b. Hearing (Fig. 10.9)
i. Sound enters the outer ear and transmitted through the middle ear and inner ear.
ii. Sound circles through the cochlea and triggers hair cells. The hair cells at
different lengths of the cochlea respond to different frequencies and are hooked
up to nerve cells that lead to the brain.
c. Equilibrium
i. Static equilibrium senses position (Fig. 10.11)
1. Maculae are structures containing hair cells projecting into gelatin.
2. When the head changes position, the gelatin moves and bends the hair
cells.
ii. Dynamic equilibrium senses movement (Fig. 10.12, 13))
1. Ampullae are structures containing hair cells projecting into gelatin.
2. Head movement forces liquid in the semicircular canals move and push
against gelatin. This bends hair cells.
E. Sight
a. Structure of the eye. Light passes through cornea  lens  retina (Fig. 10.17)
i. Smooth muscles control the iris which dilate or constricts. This controls the size
of the pupil and how much light passes through. Autonomic nerves involved
(Fig. 10.20)
ii. Ciliary muscles control the lens and change its shape to focus the light on retina
(Fig. 10.19)
iii. Retina is multilayered. Contains photoreceptors and optic nerves. (Fig. 10.21)
b. Vision
i. The lens focuses light onto the retina.
ii. When light hits the retina, the sharpest vision is produced from the fovea
centralis. The optic disc has no receptors and is a blind spot. (Fig. 10.23)
iii. Photoreceptors are rods and cones (Fig. 10.25)
1. Rods – are suited to dim light and cannot perceive colors. Contains
rhodopsin which is broken down by light and triggers nerve
transmission. Bright light breaks them all down and decreases sensitivity.
2. Cones – are suited to bright light and produce sharp colorful images. The
fovea centralis consists only of cones. Cones contain red, blue, or green
pigments.
Chapter 11 – Hormones
A. The Endocrine System
a. Endocrine cells produce hormones as signaling molecules. (Fig. 11.1b)
b. Location of some of the endocrine glands (Fig. 11.2)
c. Hormone signaling systems
i. Intracellular receptor signaling (steroidal) – signal diffuses into cell and bind
receptor that transports it to target. (Fig. 11.3)
ii. Membrane receptor signaling (nonsteroidal) – uses a receptor on membrane to
relay signal. (Fig. 11.4)
d. Regulation of hormone secretions is by negative feedback loops (Fig. 11.5)
B. Controlling Glands (Fig. 11.7, 8)
a. Hypothalamus – master controller. Sends releasing hormones or inhibiting hormones to
pituitary.
b. Pituitary – sends signals to turn on other glands or to inhibit hypothalamus.
i. Anterior – produces hormones
1. Growth hormone (GH)
2. Prolactin (PRL) for milk production
3. Thyroid-stimulating hormone (TSH)
4. Adrenocorticotropic hormone (ACTH) for adrenal function
5. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) for
ovary and testes function
ii. Posterior – releases hormones sent from hypothalamus
1. Antidiuretic hormone (ADH) slows urine production
2. Oxytocin (OT) involved in childbirth and lactation
C. Some Pituitary Responding Glands
a. Thyroid – under voicebox (Fig. 11.10)
i. Functions: regulates metabolism by controlling oxygen consumption during
cellular respiration
ii. TRHTSHT3 and T4 (Fig. 11.9)
iii. T3 (triiodothyronine) and T4 (thyroxine) require iodine for production.
1. Hypothyroidism (too little hormone) – slows metabolism
2. Hyperthyroidism (too much) – increase metabolism. Graves Disease is
an example.
3. Goiter can be formed from too little iodine causing hypothyroidism.
b. Adrenal – on top of kidneys (Fig. 11.13)
i. Functions: response to stress (Fig. 11.18)
ii. Adrenal medulla (center) responds to short-term stress. Hooked up to nerves for
fast response. Epinephrine and norepinephrine increases heart rate, metabolism,
glucose release.
iii. Adrenal cortex (outside) responds to long-term stress. ACTH 
corticosteroids.(Fig. 11.14)
1. Aldosterone – mineral and fluid balance. Effects blood pressure
2. Cortisol – increases breakdown of proteins and fats leading to increase
glucose.
D. Pancreas: regulates blood glucose (Fig. 11.15, 17)
a. Not controlled by pituitary
b. After a meal: Insulin  uptake of glucose into tissues and makes liver store as glycogen.
c. Before a meal: Glucogon  makes liver breakdown glycogen into glucose and release
into blood.
d. Diabetes: lack of insulin or inability to respond
i. Type 1 – autoimmune. Body attacks pancreas so that insulin is not produced
ii. Type 2 – may be due to insulin deficiency or irresponsive receptors. More
common and associated with overweight.
Chapter 12 – Blood
A. Components of Blood (Fig. 12.1)
a. Cells (Fig. 12.4)
i.
Red blood cells (erythrocytes) carry oxygen
1. Live for 120 days and have no nucleus or mitochondria.
2. Erythropoeitin signals red bone marrow to produce them. This is a
negative feedback loop (Fig. 12.3). B vitamins and folic acid are also
required.
3. Anemia is too few functional red blood cells. Sickle-cell anemia gives
deformed red blood cells because hemoglobin is misshapen.
4. RBCs are eventually destroyed in the liver. This breaks down
hemoglobin into bilirubin and releases it through bile into the small
intestine (Fig. 12.5). Jaundice is poor release of bilirubin into bile, so it
goes back into the blood stream and makes you yellow.
ii.
White blood cells (leukocytes) are involved in immunity.
1. Lymphocytes are T and B cells used in adaptive immunity.
2. Monocytes will become macrophages that phagocytose foreign and
unwanted cells.
3. Granulocytes have granules and release chemicals or are phagocytic.
4. Disorders
1. Leukocytosis – elevated numbers due to response to an infection
or other condition.
2. Leukopenia – lowered numbers due to immunocompromised
condition such as infection by HIV.
3. Leukemia – cancer of white blood cells. Any of the types can
divide too much and spread cancer cells throughout body.
iii.
Platelets (thrombocytes) are involved in blood clotting
1. Thrombopoietin signals red bone marrow to produce them.
b. Plasma (Tab. 12.2)
i.
Water
ii.
Proteins
1. Albumin – solute “filler”. Helps maintain solute concentration and
osmotic balance.
2. Globulin – act as transport proteins for lipids and antibodies for the
immune system.
3. Fibrinogen – functions in blood clotting
iii.
Nutrients and wastes – dissolved components that need to be transported to and
from tissues
iv.
Electrolytes – ions for pH and solute balance.
B. Blood Clotting (Hemostasis)
a. Vasospasm – breakage of a vessel will promote this. Smooth muscles constrict and cutoff
blood loss.
b. Platelet Plug Formation – platelets stick to torn vessels by binding to exposed collagen at
the break. This forms a temporary plug. (Fig. 12.13)
c. Blood Coagulation
i.
Fibrin forms threads that trap cells producing a clot (Fig. 12.14)
ii.
Tissue damage promotes production of prothrombin activator. This turns
prothrombin into thrombin. Thrombin turns fibrinogen into fibrin (Fig. 12.16).
Hemophilia is a disorder where one of the clotting proteins is missing.
iii.
Cells invade the clot and help seal the vessels and promote healing. The clot
will eventually dissolve by the enzyme plasminogen. Plasminogen is a
treatment for heart attacks.
iv.
Thrombus is an inappropriate clot. Atherosclerosis (fat build up in arteries) can
cause this (Fig. 12.15)
C. Blood Groups
a. ABO Group
i.
ii.
iii.
iv.
Four blood types A, B, AB, O.
A=carbohydrate A, B=carbohydrate B, AB=both, O=none (Fig. 12.17)
Rejection occurs when the patient makes an antibody against the foreign
carbohydrate. E.g. A is rejected by a B patient. (Tab. 12.3)
Blood typing is done by using antibodies and checking for clumping (Fig.
12.18)
b. Rh Group
i.
Rh+ means Rh protein is made. Rh- means not made.
ii.
Rejection occurs when Rh- person makes antibody against Rh+ blood.
iii.
Pregnant mothers that Rh- could reject a child that is Rh+ (only on second
birth). Treatment is anti-Rh antibodies during births. (Fig. 12.19)
Chapter 13 – Cardiovascular System
A. Circuits (Fig. 13.1)
a. Pulmonary – takes blood between the lungs and the heart. Lungs oxygenate the blood.
b. Systemic – takes blood between tissues and the heart. Tissues take up oxygen from blood.
c. Arteries take blood away from heart, veins take blood to the heart.
B. Heart
a. Structure
i. Pericardium surrounds heart and allows movement (Fig. 13.2)
ii. Heart wall contains cardiac muscle and is very thick
iii. Chambers (Fig. 13.5)
1. Upper chambers are left and right atria
2. Lower chambers are left and right ventricles
3. Blood enters each atria and exit ventricle on same side
iv. Valves (Fig. 13.6, 7)
1. Tricuspid and bicuspid valves (AV valves) separate the right and left
atria and ventricles, respectively.
2. Pulmonary and aortic (semilunar valves) valve separate the right and left
ventricles and arteries.
v. Coronary arteries supply blood to heart and cardiac veins take away blood. Heart
attacks occur when these are blocked (Fig. 13.9)
b. Cardiac Cycle
i. Systole – contraction, diastole – relaxation.
ii. When atria contract, ventricles relax and vice-versa.
iii. Valves open and close to allow blood to move and to prevent backflow. “Lubbdupp” sound is AV valves closing and pulmonary/aortic valves closing. (Fig.
13.10).
iv. Conduction
1. The sinoatrial (SA) node is the main pacemaker that sends signals to the
AV node.
2. The atrioventricular (AV) node sends signals down muscle fibers
3. Muscle fibers activate cardiac muscles in wavelike fashion. (Fig. 13.11)
v. Electrocardiogram (ECG) detects electrical changes in cardiac muscle. A specific
pattern indicates a normally functioning heart (Fig. 13.14). Damaged fibers or
other problems can give a different pattern. Defibrillation may be repaired by an
electric shock, shutting down the SA node.
vi. Regulation
1. Autonomic control by the baroreceptor reflex (Fig. 13.16)
2. Temperature and ions, especially calcium and potassium, can affect heart
rate.
C. Vessels
a. Types (Fig. 13.17)
i. Arteries and arterioles
1. Carry blood away from heart.
2. They have thick layers of smooth muscle and lack valves. They can
vasodilate and constrict.
3. They experience high blood pressure.
ii. Veins and venules
1. Carry blood toward the heart.
2. They have thin layers of smooth muscle and have valves to prevent
backflow Fig. 13.23).
3. They experience low blood pressure.
iii. Capillaries are very permeable and consist of single layer of endothelial cells.
1. Exchange at capillaries (Fig. 13.21)
a. Arterial side – blood pressure > osmotic pressure  net out
b. Venous side – blood pressure < osmotic pressure  net in.
b. Blood Pressure (Fig. 13.24)
i. Blood pressure highest in arteries right outside of the heart.
ii. Velocity highest in largest vessels.
iii. Measured by a cuff that cuts off main artery
Chapter 14 – Lymphatic System
A. Lymphatic Pathways
a. Overview
i. The lymphatic system is a circulatory system that connects with the
cardiovascular system (Fig. 14.1)
ii. Functions in transport of liquids and fats from tissues and in immunity (Fig.
14.2).
b. Structure (Fig. 14.4)
i. Capillaries draw in fluids from tissues
ii. Vessels transport fluids to lymphatic trunk
iii. The lymphatic trunk drains into two collecting ducts that drain into the
cardiovascular system at the subclavian veins.
iv. Lymph is the fluid in the lymphatic system
1. Formed from tissue fluid after filtration from blood capillaries.
2. Has lower tonicity from filtration, so there is osmotic pressure pushing it
into lymphatic capillaries.
3. Blockage of vessels causes edema, swelling, because fluid does not
escape tissues. Elephantiasis is a severe case from a worm infection.
v. Nodes are lymph glands located along large vessels of the lymphatic system.
(Fig. 14.6)
1. Nodules are the functional unit of the node. They contain white blood
cells.
2. Function in filtration and immunity.
3. Blood vessels and nerves feed into nodes.
c. Organs
i. Thymus
1. Large in infants and children and shrinks until adulthood. T cells mature
here.
2. Located behind the sternum (Fig. 14.9)
ii. Spleen
1. Red pulp filters blood and removes old red blood cells.
2. White pulp contains lymphocytes.
3. Located on the left of the stomach (Fig. 14.9, 14.10)
B. Innate Immunity
a. Barriers
i. Skin – dead cells forming a protective barrier
ii. Mucous membranes – lining of digestive, urinary, and respiratory systems
1. Secretions: enzymes, acid etc. to kill pathogens
2. Mucus: traps organisms and is moved to the stomach or out the nose.
Moved by ciliary action.
b. White blood cells
i. Phagocytes eat pathogens
ii. Natural Killer Cells kill our own cells that are infected
c. Inflammatory Response – defends injuries from infection (discussed in chapter 6)
i. Histamine is produce by damaged cells. This relaxes capillaries allowing greater
blood flow. This invites white blood cells and platelets. Swelling occurs.
d. Fever – raising of body temperature
i. Reduces growth rate of pathogen
ii. Stimulates phagocytes.
iii. Stimulates interferon, proteins that prepare other body cells against attack by
pathogens
C. Adaptive Immunity
a. Overview
i. Three steps: recognize, destroy, remember
ii. Two systems: humoral (B-cell mediated) and cell-mediated (T-cell mediated).
Lymphocytes are made in red bone marrow and stored in lymph nodes. (Fig.
14.11)
iii. Antigen: a foreign molecule that is part of the pathogen and that the immune
system recognizes. Usually a carbohydrate or protein.
iv. Antibodies
1. Produced by B-cells and recognize specific antigens.
2. Each B-cell makes one kind of antibody. Every newly formed B-cell will
make a different kind (out of 100 million types). This gives the immune
system the ability to recognize almost any antigen.
3. Antigen binding site can bind to antigen
4. Functions: tags cells for destruction, tells other cells what kind of antigen
to look for, and stimulates other white blood cells.
v. T-cell receptors – produced by T-cells. Same as an antibody but remains attached
to T-cells.
b. Humoral Immunity
i. First a naïve B-cell binds an antigen.
ii. Next, clonal selection of B-cell – makes more of itself and differentiates into
(Fig. 14.14):
1. Plasma B-cells – makes and releases antibodies.
2. Memory B-cells – stored in case of attack later.
c. Cell-mediated Immunity
i. Activation involves binding and clonal selection.
ii. Cell types:
1. Cytotoxic T-cells kill infected cells or pathogens directly
2. Helper T-cells help stimulate more cells
3. Memory T-cells function like memory B-cells.
d. Vaccination (Fig. 14.16)
i. Tricks the immune system into an immune response. This makes it easier to fight
an infection on secondary response.
ii. Mothers’ milk contains antibodies to help baby fight infections. This is passive
immunity and does not stimulate an immune response.
e. Immune Dysfunction
i. Overactive:
1. Allergies: an immune response against a harmless antigen. Histamine is
often involved.
2. Transplant rejection: foreign tissues are rejected because they contain
nonself antigens.
3. Autoimmune diseases: when the immune system attacks own body. E.g.
multiple sclerosis (neural), rheumatism (joints), Lupus (DNA).
ii. Underactive: bubble-boy David Vetter was missing B cells and T cells (Fig.
14A).
D. HIV and AIDS
a. HIV (Human immunodeficiency virus)
i. Retrovirus that attacks CD4 Helper T cells.
ii. Life cycle involves insertion of the virus into the host cell’s DNA.
b. AIDS epidemiology
i. 33 million infected, 25 million dead. Transmission by bodily fluids only.
ii. Stages of disease
1. Acute phase – initial infection launches immune response. Flu-like
symptoms that pass in a few weeks.
2. Asymptomatic phase – prophage produces very little viral particles
3. AIDS – immune system depressed. High viral titer. Opportunistic
infections usually causes death.
c. Avoiding the immune response
i. Latent infection (asymptomatic phase)- very little or no RNA and protein made.
ii. High mutation rate- reverse transcriptase is very error-prone.
iii. Immune suppression- infects the immune system itself.
d. Therapies (show movie again)
i. Many drugs (AZT, protease inhibitors) block specific parts of the HIV life cycle.
ii. Cocktails (combination of drugs) work the best
iii. Vaccine – problem of developing because of high mutation rate of HIV.