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Anatomy Final
Anatomy Final
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195 Terms
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Physical location
within thoracic cavity
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mediastinum=
region between pulmonary cavities
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heart size
approximately the size of closed fist
* varies with age, height, weight, gender
* important to consider for treatment
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Pericardium
surrounds heart, protection, roots, great vessels
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Fibrous pericardium-
made of dense and loose CT, fairly non-pliable
anchors heart, prevents overdistension, protects against blunt force
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Serous pericardium (2 layers)
parietal layer- outer/ fused to fibrous pericardium
Visceral layer- inner/ aka epicardium, covers heart
* pericardial fluid between layers
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Visceral pericardium
superficial, thin, smooth layer
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Myocardium
middle, very thick, composed of cardiac myocytes (contractility)
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endocardium
deep, somewhat thin, simple squamous epithelium over CT layer
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4 chambered heart
2 superior chamber: right atrium and left atrium
2 inferior chambers: right ventricle, left ventricle
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4 heart chambers separated by
interatrial septum and interventricular septum
* separation of O2 Rich and O2 poor Blood
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heart valves
allow one-way blood flow and prevent black flow of blood
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Cusps/leaflets
flaps that make up valves
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Atrioventricular valves (AV Valves)
Tricuspid valve (Right) 3 cusps
Bicuspid valve (left) 2 cusps
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Chordae tendineae
connects AV Valves to papillary muscle within heart
prevents inversion of valves during ventricular contraction
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Coronary arteries
originate from aorta, supply O2 rich blood to heart tissue
Left coronary artery, right coronary artery- both exit aorta
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Left coronary artery
Left anterior descending a.
Left marginal a.
circumflex a.
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Right coronary artery
right marginal a
Posterior descending a.
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cardiac veins
Drain O2 poor blood from heart tissue
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Major veins
Great cardiac vein- Left side
Middle cardiac vein- posterior
Small cardiac vein- Right side
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coronary sinus
collects O2 poor blood from above and empties into R atrium
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Coronary blockage
cholesterol and fatty deposits (plaques)
infarction
* necrosis due to insufficient blood flow
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Myocardial infarction (heart attack)
Necrosis of myocardium due to one or more coronary blockage
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Widowmaker
blockage of left anterior descending artery
* supplies the L ventricle
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Characteristics of Cardiac Muscle
Branched and networked
Joined by intercalated discs
High levels of communication between cardiac myocytes
Allows for coordinated contraction of cardiac muscle tissue
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Cardiac syncytium
Arrangement of cardiac myocytes to form an interconnected mass
* when one cell becomes excited, all cells become excited and heart can contract as one unit
* “all or none principle”
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Two syncytia
atrial syncytium- coordinated contraction of both atria
Ventricular syncytium- coordinated contraction of both ventricles
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blood components
Plasma (55-65%)
Formed elements (35- 45%)
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Formed elements of blood
Erythrocytes (RBC)
Leukocytes (WBC)
Thrombocyte (platelets)
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functions of blood
Transport
PH balance
Extracellular fluid volume
Body temperature regulation
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blood transport
Gases
Nutrients
Regulatory molecules
* hormones
* enzymes
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plasma
Mostly water
Colloid
Plama proteins in suspension
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colloid
liquid that contains suspended substances
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Plasmsa protiens in suspension
Albumin
Globulins
Fibrinogen
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Albumin
regulates water balance between tissues and blood and osmotic pressure
Transport of hormones (T3 and T4) and other molecules
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Globulins
Transport of hormones (E2, CORT) and other molecules
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Fibrinogen
Clotting
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serum
Let blood clot, then centrifuge sample
Liquid fraction= serum
Does not contain clotting factors
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Plasma
Blood is collected with anticoagulant (no clotting), and is centriguged
* liquid fraction= plasma
* contains clotting factors
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RBC: Erythocytes
O2 transport
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White blood cells. leukocytes
Involved with immune function
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Platelet/ thrombocytes
Cell fragments
Necesary for clot formation
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Granulocytes
Neutrophils
Eosinophils
Basophils
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Agranulocytes
Lymphocytes
Monocytes
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WBC chemotaxis
Movement of WBC between circulation and tissueC
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Chemotaxis in response to:
Toxins
Chemicals released form damaged/ infected tissue
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WBC chemotaxis inflammation
vasodialation (histamines)
Increased capillary permeability
Neutrophil and macropphage accumulation
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Neutrophils
Most common (60-70%)
Multi-lobed nuclei
First responders to infections
Phagocytize bacteria, antigen A antibody complexes, and other foreign bodies
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Eosinophils
less common (2-4%)
Defense against parasites
Attach to parasite and release chemicals to kill it
* no phogocytosis
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Regulation of inflammatory response
Aggregate in tissues during allerfic reaction
Destroy inflammatory chemicals, prevent spread of allergic inflammation
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Basophils
Rare (0.5-1%)
Proliferate during allergic reaction
* release heparin
* Release histamines
* Vasodilation, itching, swelling
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Lymphocytes
Fairly common (20-25%)
B Lymphocytes
* differentiate into plasma cells or memory cells
T cells
* cytotoxic T cells: destroy tumor and Virus-infected cells
* Helper T cells: activate B cells and cytotoxic cells
Natural killer cells: destroy tummor and virus- infected cells
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Monocytes
Less common (3-8%)
When leave circulation→ macrophages
* phagocytize bacteria, debris, etc.
* stimulate chemotaxis of other cells
* \
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RBC primary function
oxygen and carbon dioxide transport
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Hemoglobin
Protien with four subunits
* each subunit= global (polypeptide) bound to heme
* Heme: red pigment molecule, contains one fe atom
Oxygen binds to heme, at fe center
How many 02 can each hemoglobin molecule carry?
Also transports CO2, attaches to global, not Fe
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Hemoglobin Major types:
Embyonic hemoglobin, fetal hemoglobin, adult hemoglobin
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Embryonic hemoglobin
3 week to 3 months of pregnancy
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Fetal hemoglobin
3 months until birth
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Adult hemeglobin
Takes about 2 years to fully transition from fetal to adult hemoglobin
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sickle cell disease
abnormality of hemoglobin gene
Irregular RBC shape
Cells block blood flow or break
Reduced oxygen delivery to tissues
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sickle cell carriers:
some protection from plasmodium parasites (malaria)
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Anemia
Hemoglobin deficiency
Blood loss: chronic bleeding, menstruation
Iron deficiency
Vitamin B12 and folate deficiency
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Sickle cell anemia
Reduced O2 delivery due to sickling of RBCs
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Polycythemia
Excess RBC
Hypoxia: Compensatory polycythemia- low O2 content due to high altitude
Polycythemia Vera: Rare blood disorder, overproduction of blood cells especially RBCs (thickening of blood, poor blood flow)
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Hematopoiesis
blood cell production
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Fetal hematopoiesis
occurs in yolk sac, liver, thymus, spleen, lymph nodes, and red marrow
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Post natal/ adult hematopoiesis
occurs mostly in red marrow
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hemocytoblasts
stem cell origin of all formed elements
blood cell production
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Hemocytoblast division→
one daughter cell reamins as hemocytoblast, other daughter becomes either:
myeloid stem cell: Develop into RBCs, platelets, and most WBCs
Lymphoid stem cell: develop into lymphocytes (another WBC)
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Hemostasis
Stoppage of bleeding
1. vascular spasm
2. platelet plug formation
3. coagulation
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Vascular spasm
immediate temporary constricution of blood vessel
Damage to vessels activates reflexes
stops blood flow
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platelet plug formation
Accumulation of platelts to seal breaks in vessel
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Platelet adhesion
VWF helps platelets bind to damaged vessel platelet activation
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Platelet release reaction
Release of ADP and thromboxanes by activated platelets
→ leads to additional platelet activation
positive feedback loop!
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Platelet aggregation
Platelet shape change, fibrinogen bridges platelets forming plug
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coagulation
formation of a clot
Network of fibrin, traps blood cells, platelets, and fluid
Clot formation depends on clotting factors ( protiens in plasma)
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coagulation- Activation of clotting factors:
extrinsic pathway- initiated by chemicals outside the blood
Intrinsic pathway- intiated by chemicals within the blood
Conversion of fibrinogen (from platelet plug!) to fibrin
* fibrin makes up clot
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blood type based on which antigen on surface of RBCs
Antibodies associated with each blood group!
ABO blood group
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If you have type A bllod you:
Have antigen A on RBCs
produce anti-B antibody
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If blood is not compatible in transfusion…
if you got type B blood (with Antigen B and Anti-A antibody), the anti-A antibodies would bind with your Antigen A== Bad Reaction
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Antigen + antibody reaction= agglutination (clumping)
Rapid hemolysis, coagulation, shock, renal failure, death
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Rh blood group
first studied in rhesus monkeys
Based on antigen D on RBCs
Genetically determine
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Rh antigen develop in Rh negative person is exposed to Rh positive blood
through transfusion
Blood crossing placenta from mother to fetus
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Respiratory system function
Respiration
* ventilation
* external respiration (O2 enters and CO2 leaves through lungs)
* Gas transport
* Internal respiration- gas exchange in tissues
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Regulation of Ph
changing CO2 levels
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Production of chemical mediatiors
angiotensin-converting enzyme (ACE), Bp regulation
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Upper respiratory tract
External nose
Nasal cavity
Pharynx
Larynx
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Lower respiratory tract
Trachea
Bronchi and Bronchioles
Lungs
Alveoli
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Upper respiratory infection
usually symptoms above the neck (coughing, sneezing, sore throat, etc.) and less serious
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Lower respiratory infections
bronchitis, pneumonia, etc. usually last longer and are more serious
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conducting zone
where air movements occure
Nose to bronchioles
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Respiratory zone
site of gas exchange
alveoli
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Air movement (nasal cavity)
Turbinates force air into slow steady pattern to contract surface area with epithelium
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clean air (nasal cavity)
pseaudostratified cilitated columnar epithelium w/ goblet cells
\-mucous production
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olfactory epithelium
scent detection
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Pharynx
common opening for digestive and respiratory system
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nasopharynx
connects to nasal cavity
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oropharynx
connects to oral cavity
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laryngopharynx
route food/drink to esophagus, and air to larynx
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larynx
rigid and strong
* 9 cartilages connected by muscle and ligaments
* biggest is thryroid catrilage
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