For physiology-Palomar College
Gas exchange between blood cells and capillaries
Refractory period
Involved in killing foreign objects and pathogens as well as maintaining a healthy body
Process of developing new blood vessels
Cells that produce antibodies
Cells that will immediately destroy a pathogen (neutrophils, macrophages, Natural Killer (NK) cells).
Cells that eliminate a target through pinocytosis
Cells that are highly specific highly effective
Basophils
Adaptive
Innate
Shutting of aortic and pulmonary valves
Ventricles contracting
Shutting of tricuspid and mitral valves
Atrium contracting
ANS
CNS
Defect in Uropophyrinogen III Decarboxylase
Defect in Coproporphyrinogen III (CP-III)
Defect in Ferrochelatase
Defect in 5 ALA conversion to Porphobilinogen caused by lead
A single gene defect in Beta Globin chain
Absent production of a particular chain
Complete absence of Beta Chains
Malaria
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What happens when you work out
Development of new blood
Prevention of capillaries from being over leaky
Pericytes and smooth muscle receive low oxygen
Hypoxia Reductible Factor (HRF) which produces VEGF and FGF
New blood production
High blood pressure
Hypoxia Inducible Factor (HIF) which produces VEGF and FGF
Artery's, arteriole, vein
Venule, veins, artery's
Arteriole, venule, capillary
Capillary, vein, venule
Allows vessel to expand and snap back into shape, helps in propelling blood forward
Provides structural integrity
Innervated by the ANS and helps with constriction or relaxation
Because its elastic
Gas exchange by hemeglobin
Circulation
To keep organs functioning
Immunity
Porphyrin ring containing Fe (iron)
Oxygen
Heme
Alpha and beta chains
Aid in the immune response
Cause nutritional deficiency
Its cell membrane pinches off to form platelets
Cause spontaneous clotting
AV delay
Atrial depolarization
Ventricular depolarization
Ventricular re-polarization
Complete heart block
Atrial fibrillation
Ventricle fibrillation
Amlodipine
Hydrochlorothiazide
Lisinopril
Metoprolol
Amlodipine
Metoprolol
Hydrochlorothiazide
Lisinopril
Hydrochlorothiazide
Lisinopril
Amlodipine
Metoprolol
Decrease the volume of blood pressure
Lower systemic vascular resistance
Effect B1 receptors
Stop stimulation of aldosterone
Work in kidneys to prevent reclaiming ions- decrease the volume of blood pressure
Prevent an enzyme that converts angiotension I to angiotension II
Lower systemic vascular resistance
Affect B1 receptors
Anaphylactic
Dehydration
Neurogenic
Cardiogenic
Dehydration
Shock
Orthostatic hypotension
Anaphylaxis
Atpase
DHP receptor
CICR
Option 4
P Wave
T wave
QRS
PR
Lisinopril
Dobutamine (Beta 1 agonist) and norepinephrine (alpha 1 agonist)
Neurogenic
Anaphylactic
Voltage-gated Ca2+ channels
Calcium-Induced Calcium Rlease (CICR)
Mechanically-Gated Ca2+ Channels
Ca2+-ATPase
Phosphate
Ca
Triponon
Triptomyosin
The maximal pressure experience in a vessel during the peak of ventricular contraction
The residual pressure remaining in the vessel during ventricular relaxation
SBP >139 or DBP >89
SBP > 100 DBP >80
SBP >120 DBP > 40
SBP >130 DBP >60
SBP >200 or DBP >100
SBP >220 or DBP > 180
SBP >100 or DBP > 130
SBP > 250 or DBP >200
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Porphobilinogen, multiple steps, coproporphyrinogen III, protoporohobinlin III, Protophophyrin IX, Fe2, Ferrochelatase, Heme
Coproporphyrinogen III, multiple steps, Porphobilinogen, Protophophyrin III, Protophyrin IX, Fe2, Ferrochelatase, heme
Porphobilinogen, multiple steps, Protophophyrin III, Protophyrin IX, Coproporphyrinogen III, fe2, Ferrochelatase, Heme
Lead, porphobilinogen, multiple steps, coproporphyrinogen III, protoporohobinlin III, Protophophyrin IX, Fe2, Ferrochelatase, Heme
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Fibrin monomer, fibrin polymer, I (fibrinogen), II(prothrombin), IIa( thrombin), X-Xa+V, VII, IX-IXa, XI-XIa, XII-XIIa, XIII-XIIIa, Stable fibrin blood clot
XII-XIIa, XI-XIa, IX-IXa, VII, X- Xa +V, II(prothrombin), IIa (thrombin), I (fibrinogen), Fibrin monomer, fibrin polymer, XIII-XIIIa, Stable fibrin blood clot
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B lymphocytes
T lymphocytes
Plasma cells
CD8
Adaptive
Innate
Monocytes
Lymphocytes
CD4
CD8
B lymphocytes
Plasma Cells
Branch off bundle branches and dive into the muscle tissue
Diverts AP to left and right bundle branches
Travel down atrium to pacemaker cells
Delay the AP
Purkinje
AV
SAN
HIS
Adaptive immune system- they kill pathogens
Innate immune system- flood infection to eliminate pathogens by exocytosing enzymes (dead="pus")
Innate immune system- eliminate targets through pinocytosis and destroys them by merging vesicles containing proteolytic enzymes
Something to do with enzymes and killing foreign invaders
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Residual pressure in vessel during relaxation
Residual pressure in a vessel during contraction
Maximum pressure at peek of ventricular contraction
Maximum pressure at peek of atrial contraction
Angiotensin Converting Enzyme Inhibitors, B Receptor Blockers( B-Blockers), Calcium Channel Blockers, Diuretics
Beta 1, Beta 2, Alpha 1, Alpha 2 Blockers
Quit smoking, quit eating fatty foods, work out more, and less alcohol consumption
Multi unit
Visceral
Tonic
Phasic
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ALA Synthase, ferrochelatase, and glycine
Succinyl-CoA, Glycine and ALA Synthase
Succinyl-CoA, ALA Synthase, and porphobilinogen
Glycine, Succinyl-CoA, and Coprophophyrigen III
Bad heme production
Thalassemia
Porphyrias
Sickle cell anemia
The mitochondria
Plasma cells
Red blood cells
By antigens
Helper T cells, facilitate immune responce
Cytotoxic T cells, directly kill infection
Produce antibodies
Pinocytosis
CD8
CD4
Neutrophils
Macrophages
Pericytes
Smooth muscle
Fiberous tissue
Starling forces
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