Quiz 3 - Cardio Physio, ECG, Acid/Base, O2/CO2, Chemical Reactions Flashcards
(121 cards)
1
Q
Epicardium
A
Outermost layer of heart, contiguous with visceral pericardium, simple squamous mesothelium that secretes fluid, supported by loose CT, contains coronary vessels, nerves, fat, ectodermal origin, contains keratins
2
Q
Myocardium
A
Cardiac muscle, thicker in ventricles
3
Q
Endocardium
A
Loose CT with smooth muscle cells, purkinje fibers, mesodermal origin, produces clotting proteins, contains vimentins
4
Q
Mesothelium
A
Mesodermal origin, single cell layer protects body cavities and organs. Does not involve transportation of blood. Pleural (lungs), pericardial (heart), peritoneal (abdominal organs)
5
Q
Atrium muscle
A
Thin epicardium, roughly equal myocardium and endocardium.
6
Q
Ventricle muscle
A
Tiny endocardium, thick myocardium, thicker epicardium than atrium (mostly adipose)
7
Q
Conduction system of the heart
A
Sinoatrial Node > Atrioventricular Node > Bundle of His > Left and right bundle branches > Purkinje fibers Nodes are modified cardiac muscle, bundle and fibers are conducting muscle fibers
8
Q
Purkinje Fibers
A
Myofibers but larger than contractile muscle fibers, pale staining fibers, lack intercalated discs, don’t contract but conduct, contain lots of glycogen, mitochondria
9
Q
Atrial Natriuretic Peptide
A
Synthesized by atrial myocytes, responds to high BP, acts to lower BP, Stimulates Na+ loss from blood into urine, relaxes vascular smooth muscle, prevents water retention hormones
10
Q
Hypertrophy
A
Cells get bigger
11
Q
Hyperplasia
A
Cells increase in number
12
Q
Vasa Vasorum
A
Blood vessels that feed walls of large blood vessels
13
Q
Tunica Intima
A
Innermost, thinnest layer, CT
14
Q
Internal elastic lamina
A
Dense, elastic membrane that separates Tunica intima from tunica media
15
Q
Tunica media
A
Thickest layer, contains smooth muscle, elastic fibers, connective tissue
16
Q
External elastic lamina
A
Dense elastic membraane that separates Tunica Media from Tunica adventitia
17
Q
Tunica adventitia
A
Connective tissue, nutrient vessels (vasa vasorum), autonomic nerves (nervi vasorum)
18
Q
Aorta structure
A
Most of the wall is tunica media, smooth muscle cells synthesize elastic fibers to smooth out pressure pulses
19
Q
Vernhoff stain
A
Stains elastic fibers
20
Q
Azan stain
A
Stains collagen fibers
21
Q
Muscular Artery
A
Thick, highly layered tunica media, regulates blood pressure
22
Q
Elastic artery
A
Aorta, pulmonary artery, branches, carry blood to smaller arteries, tunica media has lots of elastic fibers, expand and recoil with systole and diastole
23
Q
Small arteries
A
Contain up to 5-6 layers of smooth muscle,
24
Q
Arterioles
A
25
Precapillary sphincters
Surround arterioles allow blood into capillary beds
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Thermoregulation
High capillary flow = more heat dissipation, reduced flow = high conservation
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Nitric Oxide
Released by vascular endothelial cells. Causes smooth muscle to relax, vasodilation
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Endothelins
Released by vascular endothelial cells. Causes smooth muscle to contract, vasoconstriction
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Continuous capillaries
Most common type. Endothelial cells linked by tight junctions
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Fenestrated capillaries
Contain openings in endothelium that facilitate exchange. Found in kidney glomerulus, choroid plexus
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Sinusoids
Have larger openings for greater exchange. Blood cells can squeeze through. Found in liver, bone marrow
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Pericyte
Periendothelial cells. Critical for blood-brain barrier, small vessel hemostasis, contraction, phagocytosis, repair and regeneration
33
Transcytosis
Movement of big proteins, etc. through capillaries via vesicles
34
Venule and Muscular venule
Smallest of veins, major site of vascular permeability, particularly sensitive to histamine, small but less defined "roundness" than arterioles
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Medium vein
Contain semilunar valves, have thicker Tunica Adventitia, small tunica media and tiny tunica intima
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Large vein
Have thicker Tunica Adventitia, small tunica media and tiny tunica intima
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Angiogenesis
Blood vessel formation, driven by multiple factors including Vascular Endothelial Growth Factors
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Age and arteries
Elastic lamellae become fragmented and discontinuous, making vessels stiff
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Arteriosclerosis
Hardening of arteries because of age, calcium salt deposits, thickening of TI
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Myocardial Infarction
Blockage of Coronary artery kills cardiac muscle cells, scar tissue replaces it, blood leaks into epicardium
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Electrocardiography
Records electrical activity of heart
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Diastole
relaxation of heart chambers which fill with blood
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Systole
Contraction of heart chambers
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Ventricular filling
mid to late ventricular diastole
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S1 heart sound
Lub, closure of AV valves at beginning of ventricular systole
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S2 heart sound
Dub, closure of semilunar valves at beginning of ventricular diastole
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Pacemaker cells
SA node, AV node, Bundle of His, Bundle branches, Purkinje fibers, have intrinsic rhythmnicity
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Working myocardial cells
Most of heart cells
49
Normal Activation Sequence
SA node \> Atria \> AV node \> His \> Bundle \> Purkinje \> Ventricles
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Fast-response Action Potential - Plateau phase prolonged by Ca2+
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Slow-Response Action Potential - in Pacemaker cells, slowly depolarize in Phase 4 to automatically trigger AP
52
Excitation-Contraction Coupling in Cardiac Muscle
Action potential travels along sarcolemma (plasma membrane) and into T tubules, causing Ca2+ to enter cells. Ca2+ triggers opeining of Ca2+ release channels in sarcoplasm. Ca2+ binds to tropomyosin, allowing myosin fibers to bind to actin and trigger contraction. "Ca2+-induced Ca2+ release"
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Cardiac Output
= Stroke Volume X Heart Rate
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Stroke Volume
= End Diastolic Volume - End Systolic Volume
Usually about 70-80 mL
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Total Peripheral Resistance
Sum of the resistance of all peripheral vasculature in the circulatory system
56
Blood Pressure
= Cardiac Output X Total Peripheral Resistance
57
Baroreceptor Reflex
Responds to change in arterial pressure by increasing or decreasing heart rate as needed
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Bainbridge Reflex
Responds to changes in blood volume. Increases heart rate when there is increased arterial presure.
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Normal Sinus Rhythm
When the SA node is acting as the pacemaker.
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Normal Heart Rate
60-100 beats/min.
Tachycardia - \>100 beats/min.
Bradycardia - \<60 beats/min.
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Electrocardiogram
Machine to measure heart's electrical potential.
Lead - electrical potential difference between two electrodes
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P Wave
Atrial depolarization
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PR Interval
Atrioventricular conduction. (0.12-0.2 sec)
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QRS Complex
Ventricular Depolariation 0.06-0.1 sec
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ST Segment
Index of ventricular AP plateau 0.14-0.16 sec
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QT Interval
Ventricular Action Potential 0.3-0.4 sec
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R-R Interval
Interval between ventricular beats, varies with heart rate, used to calculate HR
68
T Wave
Ventricular Repolarization
69
ECG Abnormalities with MI
ST elevation
T wave inversion
Exaggerated Q waves
ST depression
70
Dipole Orientation
If the + end of dipole approaches + electrode, signal up
If + end of dipole approaches - electrode, signal down
If electro
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ECG time scale
Each large box is equivalent to 0.5 mV and 0.2 seconds.
Each small box is equivalent to 0.1 mV and 0.04 seconds.
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HR in beats per minute on ECG
=60/R-R interval
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Lead 1
- electrode on RA, + electrode on LA
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Lead 2
- electrode on RA, + electrode on LL
Most closely paralells average dipole during QRS wave.
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Lead 3
- electrode on LA, + electrode on LL
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Einthoven's Law
Lead I + Lead III = Lead II
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Dipole calculation
Amplitude of a lead = (+) deflection + (-) deflection
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Augmented Vector Right
Perpendicular to lead III
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Augmented Vector Left
Perpendicular to Lead II
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Augmented Vector Feet
Perpendicular to lead I
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Atrial Fibrillation
No clear P waves, absence of isoelectric baseline
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Second Degree AV block
Type 1 and 2. Dropping QRS wave. More frequent in Type 2
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Third Degree (Complete) AV block
Dropped QRS wave, needs pacemaker immediately
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Ventricular Tachycardia
Deep inverted Rs repeating
85
Long QT syndrome
QT interval elongated, can lead to ventricular tachyarrythmias, can be congenital, aquired from medications, or from hypokalemia
86
Torsade de Pointes
ECG turns into big squiggly lines around baseline, twisting of ventricle muscle
87
Physiological pH
7.4
88
Bronsted-Lowry Acids/Bases
Acids donate protons, Bases accept protons
89
Strong Acids/Bases
Completely Dissociate in solution. Ex.) HCl, NaOh
90
Weak Acids
Donate relatively few of their H+/OH- ions. Ex.) H2S, NH3
91
Reason for pH regulation
Proteins, ions, muscle contraction, etc. all rely on specific pH range.
92
Carbonic Anhydrase
Converts CO2 to carbonic acid to dissolve it into the blood
93
Ways to control H+ ion concentration in the serum
Lungs: remove CO2
Kidneys: Removes H+, Retains HCO3-
Buffering: Resists pH change (does not remove H+ ions)
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Volatile Acid
Can be released in gas form. CO2/Carbonic acid
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Nonvolatile Acid
Acids that are not released in the blood. Lactic acid, etc.
96
Acidemia
High concentration of H+. Acidosis decribes conditions leading to acidemia
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Alkalemia
Low H+ concentration in blood. Alkalosis is term for conditions leading to alkalemia.
98
pH regulation in Lungs
Increase in pH from 7.4-7.0 results in 4-5X increase in alveolar ventilation. Raised pH causes respiratory depression.
Lungs only deal with volatile acid
99
pH regulation in Kidneys
Slow acting
Kidneys can excrete or retain acids (H+ or NH4+)
Kidneys can excrete or retain HCO3- or generate it from Glutamine
100
pH regulation in Buffers
Bicarbonate: in extracellular fluid
Phosphate: in intracellular fluid
101
Henderson-Hasselbach Equation
pH = pKa + log [A-]/[HA]
Buffers are most effective when pH = pKa
102
Intracellular pH regulation
Low IC pH: Na+ gradient pushes H+ out and HCO3- in
High IC pH: Cl- gradient pushes HCO3- out and OH- out
H2PO4- buffer
103
Respiratory Acidosis/Alkalosis
Hyper/Hypoventilation causes Alkal/acidosis
Involves lungs and volatile acids (CO2)
104
Metabolic Acidosis/Alkalosis
Disturbances in HCO3 because of Kidney function or other systems.
Abnormal loss or retention of HCO3
105
Mixed Acid-Base Disorder
Acid-base disorders are rarely just one thing. Respiratory acidosis can exist at the same time as metabolic alkalosis
106
^G Free Energy
Released or consumed by a chemical reaction to perform work
107
Free Energy Equation
^G = ^H - T^S
^H = enthalpy (heat) change
T = Temperature
^S = Entropy (disorder)
(+)^G decreases entropy
(-)^G increases entropy
108
Anabolism
(+)^G
Going "Up" from precursor molecules to macromolecules
109
Catabolism
(-)^G
From energy containing macromolecules to their end products with the release of energy
110
5 main types of chemical reactions
1. Making and breaking carbon bonds
2. Molecular Rearrangements
3. Free Radical Reactions
4. Group Transfers
5. REDOX reactions
111
Condensation Reactions
Make carbon bonds, water is major byproduct
112
Carboxylation/Decarboxylation
Addition/Removal of Carboxyl Group (CO2)
113
Molecular Rearrangements
Change in shape of a single structure
Ex.) cAMP --\> AMP
114
Free Radical Reactions
Molecule containing an unpaired electron, highly reactive
Ex.) Dopamine can become a superoxide radical in right conditions.
Ex.) Vitamin E functions as antioxidant to neutralize free radicals by donating an electron, then rearranging its molecules to reduce charge
115
Group Transfers
Adding or removing a functional group
Phosphorylation -- Kinase
Ubiquitination -- Ubiquitin Ligase
Acetylation -- Acetyltransferase
Methylation -- Methyltransferase
Hydroxylation -- Hydroxylase
116
How does ATP function?
Transfers Phosphate group.
Higher concentrations of ATP relative to ADP cause a greater release of energy.
Energy released usually by transfer rather than hydrolysis
117
Protein Kinase A
Phosphate transfer drives signal transduction
118
REDOX Reactions
Involve a Reduction and an Oxidation
Reduction: Load molecules with electrons (+)^G
Oxidation: Remove electrons from a molecule (-)^G
119
Carbon Oxidation state
Reduced Carbons energy rich
Long saturated carbon chains
120
Beta Oxidation
Conversion of long lipid chains into Acetyl-CoA for use in citric acid cycle and electron transport chain
121
NAD+
Major carrier of electrons for REDOX transfer of electrons
