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CVR Midterm > Midterm > Flashcards

Midterm Flashcards

1
Q

3 things which determine inotropic state

A
  1. Ca2+ in the cytosol
  2. Number of functional myocytes
  3. Coronary artery supply

Inotropic state is NOT affected by preload and afterload

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2
Q

3 things which control stroke volume

A
  1. Preload
  2. Afterload
  3. Inotropic state
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3
Q

What are connexons?

A

Transmembrane protein complexes which provide electrical communication, nutrients, metabolites, and water between cells. Large in diameter.

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4
Q

Ventricular AP timing and characteristics

A

Lasts 250-300ms. Resting potential around -90. Amplitude is 110-120 to a peak of +20-30. Fast upstroke and slow decline due to Ca2+. Ca2+ comes from Ca channels and SR. 1/3 of time in AP and 2/3 of time in rest. Phases are 0, 1, 2, 3, 4

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5
Q

Pacemaker SA node AP timing and characteristics

A

Pacemaker for the heart. No resting potential because always moving. Reaches threshold around -35 and then fires spontaneously. Phases are 0, 3, 4

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6
Q

Extracellular fluid ion concentrations

A

Na+: 135-145mM
K+: 3.5-5mM
Ca2+: 2-2.6mM
Cl-: 98-106

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7
Q

Intracellular fluid ion concentrations

A

Na+: 10-15mM
K+: 140mM
Ca2+: 50nM
Cl-: 10mM

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8
Q

What is E(K)?

A

-95mV

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9
Q

What happens when no ATP like in an MI?

A

Potential becomes 0

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10
Q

Features of the AV node

A

Only electrical connection of the atria and ventricles

Propagation very slow (AV nodal delay)

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11
Q

L-type Ca2+ channels

A

In all cardiac cells. Contribute to plateau of AP and gradual upstroke of SA and AV node

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12
Q

Voltage gated Na+ channels

A

In contractile cells of atria and ventricles and Purkinje cells. Cause rapid upstroke of AP.

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13
Q

T-type Ca2+ channels

A

In SA and AV node (maybe in all cardiac). Transient channels which open at more negative values than L-type. Contributes to pacemaker activity.

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14
Q

Inward rectifier K+ channels

A

In most cardiac cells. Maintains relatively high K+ permeability at rest. Current higher at rest than when at more positive values.

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15
Q

Transient outward K+ channels

A

In contractile cells. Contribute to Phase 1 of AP (to the repolarization)

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16
Q

Delayed rectifier K+ channels

A

In most cardiac cells. Responsible for repolarization of AP

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17
Q

ACh activated K+ channels

A

In SA, AV nodes and atria. Contributes to parasympathetic stimulation

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18
Q

ATP sensitive K+ channels

A

In most cardiac cells. Increases K+ permeability when ATP is low.

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19
Q

Pacemaker channels

A

In SA, AV nodes and Purkinje systems. Allows both Na and K+ to cross membrane. Contributes to pacemaker activity.

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20
Q

Duration of AP vs. contraction in ventricular myocytes

A

Roughly same duration

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21
Q

Fast response vs slow response APs

A

o Fast response action potentials
• APs of the contractile (atrial and ventricular) cells of the heart
• Ventricular APs are longer than atrial APs
• Purkinje fiber APs similar to ventricular muscle, but few contractile proteins
o Slow response action potentials
• APs of the SA and AV node
• Both SA and AV node potentials show pacemaker activity and relatively slow upstroke

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22
Q

Ion channels in ventricular AP

A 
Phase 0: 
-Voltage gated Na+ cause depolarization
-Inward rectifier K+ channels active
 Phase 1: 
-Na+ channel inactivation
-Activation of L-type Ca2+ channels
Phase 2 (small currents): 
-Na+/Ca2+ exchanger active (3 Na+ for 1 Ca2+ causing inward current)
-L-type Ca2+ active keeping a plateau
-Delayed rectifier K+ channels active
Phase 3:
-L-type Ca2+ channel inactivation and deactivation
-Delayed rectifier K+ channels active
-Inward rectifier channels active
Phase 4: 
-Inward rectifier channels most active
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23
Q

Removal of Ca2+ at end of AP

A

• Contraction ends shortly after AP ends as a result of low Ca2+ concentration around the contractile proteins
• Ca2+ channels in surface membrane close
• Ca2+ influx is stopped from extracellular fluid and from the SR
• SR Ca2+ pump partially sequesters Ca2+ into SR
• Na+/Ca2+ exchanger moves Ca2+ back into extracellular fluid
o 1 Ca2+ out exchanged for 3 Na+ ions in

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24
Q

Sympathetic heart activity

A

o Positive chronotropic effect: increased heart rate
o Positive inotropic effect: increased force contraction of atria and ventricles
o Increased AP conduction velocity through AV node (shortens AV nodal delay)
o Enhanced SR pump activity due to phosphorylation of phospholamban which is part of the pump
o Decreased myofilament sensitivity to Ca2+ due to TnI phosphorylation
o Altered gating of SR Ca2+ release channel (ryanodine receptor) leading to enhanced SR release of Ca2+
o Shortened AP duration
o Shortened contraction duration

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25
Q

Channels which are opened by phosphorylation when beta andrenergic receptors in heart stimulated by E, NE, or drugs

A
  • L-type Ca2+ channels
  • Pacemaker channels
  • Delayed rectifier K+ channels
  • cAMP dependent Cl- channels (ICl,cAMP)
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26
Q

Fibrous skeleton of the heart

A
  • 4 fibrous rings of dense irregular CT
  • Provide attachment sites for valve leaflets and myocardium
  • Electrical insulator
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27
Q

3 layers of heart wall

A
  1. Epicardium: mesothelial cells, small amount of CT, vessels/nerves/fat
  2. Myocardium: cardiac muscle
  3. Endocardium: endothelium, fibroelastic CT (Purkinje fibers)
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28
Q

Vessel wall layers

A
  1. Tunica intima (closest to lumen)
  2. Tunica media
  3. Tunica adventitia (usually CT)
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29
Q

Components of the tunica intima

A

Endothelial cells with basal lamina, loose CT, internal elastic lamina in arteries

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30
Q

Components of the tunica media

A

Smooth muscle (which make ECM), collagen, reticular fibers, PG. In arteries: elastic fibers in lamella and external elastic lamina

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31
Q

Components of the tunica adventitia

A

Fibroblasts, collagenous CT, elastic fibers, vasa vasorum (vessels of the vessel), nervi vascularis. Largest veins: longitudinal smooth muscle

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32
Q

Elastic artery features

A
  • Thick tunica intima
  • Thick tunica media with prominent elastic laminae
  • Tunica adventitia with vasa vasorum and nervi vascularis
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33
Q

Muscular artery features

A

-Thinner tunica intima
-Prominent internal elastic lamina
-Thick media
External elastic lamina

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34
Q

Arteriole features

A
  • No more than 2 smooth muscle layers thick
  • No elastic lamina visible
  • Very thin tunica intima
  • Thin tunica adventitia
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35
Q

Capillary features

A
  • Lumen 8-12 micrometers in diameter
  • Wall simple endothelial tube 1 layer thick
  • May have tunica media comprised of pericyte
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36
Q

What is a pericyte?

A
  • CT cell similar to mesenchymal
  • Surrounds capillary endothelium within basal lamina providing physical stability
  • Contractile ability
  • Physical and chemical signaling
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37
Q

Types of capillaries

A
  1. Continuous (solid wall w/out spaces, tight junctions; muscle, fat, nervous system)
  2. Fenestrated without diaphragms (has holes; GI, endocrine, kidney)
  3. Fenestrated with diaphragms (molecular sieves; GI, endocrine, kidney)
  4. Sinusoid discontinuous (spaces between endothelial cells, incomplete basal lamina; liver, marrow, spleen)
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38
Q

Control of blood through capillaries

A

Can be shunted with metarterioles with pre capillary sphincters

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39
Q

Veins vs arteries

A
  1. Larger lumen
  2. Thinner walls with less smooth muscle
  3. May be irregularly shaped, collapsed
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40
Q

Postcapillary venules

A
  • Receive blood from capillaries
  • Site of action for histamine and serotonin
  • Site of extravasation of WBCs
  • Lumen 10-15 micrometers
  • Wall simple endothelial tube (intima)
  • May have pericyte tunica media
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41
Q

Venule features

A
  • Lumen up to 100 micrometers diameter

- Wall very thin with no smooth muscle

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42
Q

Small/Medium vein features

A
  • Luminal diameter up to 10mm
  • Tunica media has smooth muscle, elastic and collagen fibers
  • Tunica adventitia thicker than media, network of collagen and elastic fibers
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43
Q

Large vein features

A
  • Tunica intima endothelium and sub endothelial CT with internal elastic lamina
  • Tunica media circumferential smooth muscle, collagen, fibroblasts
  • Adventitia thickest tunic with collagen, elastic fibers, fibroblasts, bundles of longitudinal smooth muscle
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44
Q

Lymphatic capillary features

A
  • Blind ended (don’t leave)
  • Simple endothelial tubes
  • Anchoring filaments (contain elastic fibers)
  • Discontinuous basal lamina
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45
Q

Large lymphatic vessels

A
  • Like veins but less organized
  • Indistinct tunics
  • Circular and longitudinal smooth muscle
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46
Q

Endothelial cells

A
  • Anchored to basal lamina via hemidesmosomes
  • Contain Weibel-Palade bodies
  • Maintain selectively permeable barrier
  • Regulation of cell growth
  • Regulation of immune response
  • Maintains ECM
  • Activates Angiotension I to Angiotension II
  • Modifies lipoproteins
  • Modulates blood flow, vascular resistance
  • Barrier between platelets and sub endothelial tissue
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47
Q

What are Weibel-Palade bodies?

A
  • Contain von Willebrand factor which plays a role in blood coagulation
  • Deficiency results in Willebrand disease
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48
Q

Aneurysm

A

Weakening in vessel wall usually related to tunica media and defect in collagen

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49
Q

Varicose veins

A
  • Dilated veins

- Alteration in vessel wall and valvular incompetence in veins

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50
Q

Transplanted heart

A
  • Denervated organ

- no ANS innervation to modulate and coordinate organ w environment

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51
Q

Atherosclerosis

A
  • Disorder of arterial wall char. by accumulation of cholesterol esters in cells derived from monocyte-macrophage lineage, smooth muscle cell proliferation, fibrosis
  • Lesion in vessel featuring plaques in tunica intima
  • Plaque contains fibrous CT, macrophages, smooth muscle, foam cells, lymphocytes, cellular debris
  • May lead to MI, stroke, gangrene
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52
Q

CV development

A
  • 1st major system to function in embryo (3rd wk and functions at 4th wk)
  • Derived from splanchnic mesoderm and paraxial and lateral mesoderm
  • Position cranial then future thoracic cavity
  • Shaped as a tube
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53
Q

Folding of embryo

A
  • Heart begins in cranial region then during folding swings down to lie in thorax (area will develop into esophagus)
  • Aorta posterior to foregut
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54
Q

Embryonic to adult structures:

  1. Truncus arteriosus
  2. Bulbus cordis
  3. Ventricle
  4. Atrium
  5. Sinus venosus
A
  1. Aorta and pulmonary trunk
  2. Smooth left and right ventricles
  3. Trabeculated carnae of left and right ventricles
  4. Trabeculated (pectinate muscles) of left and right atria
  5. Smooth part of right atrium and coronary sinus
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55
Q

Endocardial cushions

A
  • 4 cushions: 2 lateral, anterior, posterior
  • Formed from neural crest cells and mesenchymal tissue
  • Opposing cushions form right and left AV canals
  • More central parts form mitral and tricuspid valves
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56
Q

Septum primum, septum secundum, foramen primum, foramen secundum, foramen ovale

A
  • Septum primum: crescent shaped membrane which grows down from roof of atria and divides them leaving a foramen primum to allow blood to flow from right to left atria
  • While foramen primum gets smaller apoptosis causes holes in the septum primum forming the foramen secundum
  • Septum secundum: Grows down like curtain overlapping foramen secundum forming the foramen ovale
  • Inferior vena cava points right into foramen ovale and superior vena cava points into right ventricle
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57
Q

Interventricular septum development

A

-Appears in the floor of common ventricle and grows upward toward endocardial cushions closing the inter ventricular foramen (becomes membranous portion of septum)

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58
Q

Separation of aorta and pulmonary trunk from truncus arteriosus
-What are the ridges called which are made by the endocardial cushions?

A

-Endocardial cushions grow towards each other like a spiral staircase through conotruncal ridges so when done pulmonary trunk communicates with RV and aorta with LV

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59
Q

Prenatal bypasses of the liver and lungs

A
  • Ductus venosus: connects umbilical vein with inferior vena cava bypassing lungs
  • Foramen ovale: connects RA to LA to bypass lungs
  • Ductus arteriosus: connects left pulmonary artery with aortic arch
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60
Q

Changes after birth:

  1. Ductus venosus
  2. Foramen ovale
  3. Ductus arteriosus
  4. Umbilical arteries/vein
A
  1. Ligamentum venosus to connect to liver
  2. Fossa ovalis due to BP increase in LA
  3. Ligamentum arteriosus due to increase in oxygen and decrease in circulating prostaglandins
  4. Constrict (save for GI block)
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61
Q

Atrial septal defects: Patent foramen ovale, ostium primum, ostium secundum

A
  • PFO: 2:1 female to male prevalence, allow interatrial shunting of blood
  • Ostium primum defects close to tricuspid valve
  • Ostium secundum defects farther away from tricuspid valve
62
Q

Ventricular septal defects

A
  • Mostly isolated, mix ventricular blood

- Usually occur in membranous portion of septum

63
Q

Tetralogy of fallot

A 
-Ventricular septal defect
Early cyanosis (blue baby)
-Most common cause of cyanosis
-Pulmonary stenosis, ventricular septal defect, overriding aorta, hypertrophied RV (due to other defects listed)
64
Q

Transposition of great vessels

A
  • Right to left shunting in ventricles causing cyanosis
  • Aorta rises from RV, pulmonary trunk from LV
  • ASD, VSD, patent ductus arteriosus
65
Q

Persistant truncus arteriosus

A
  • Right to left shunting in ventricles causing cyanosis
  • Partial development of AV septum
  • ALWAYS membranous VSD
66
Q

Mediastinum

A
  • Thick midline partition
  • Anterior-posterior direction from sternum to thoracic vertebrae
  • Superior-inferior direction from superior thoracic aperture to diaphragm
67
Q

Parts of the sternum

A
  • Manubrium (like the knot of a tie)
  • Body of the sternum
  • Xiphoid process (tip of the tie)
68
Q

Diaphragm

A

Left lobe higher than right because of the liver

69
Q

Arterial supply to the breast

A
  • Lateral thoracic artery (from axillary)
  • Internal thoracic artery
  • Intercostal arteries
70
Q

What is the clavipectoral fascia?

A

Surrounds the pectoralis minor, separates from pectoralis major

71
Q

Where are the intercostal vein, artery, and nerve located? Where should you do a thoracocentesis?

A
  • At the inferior border of the the superior rib in the costal groove.
  • Insert needle into superior border of the inferior rib
72
Q

Intercostal muscles (function and 3 types)

A
  • Maintain tone in intercostal space
    1. External intercostal muscles: superficial, do not attach to sternum, replaced by aponeurosis called external intercostal membrane
    2. Internal intercostal muscles: intermediate, also replaced by aponeurosis called internal intercostal membrane, most active during expiration to move ribs downward
    3. Innermost intercostal muscles: deepest, most active during expiration as well
73
Q

Blood supply and veins of the thoracic wall

A
  • Posterior intercostal arteries: originate from aorta
  • Anterior intercostal arteries: originate from internal thoracic cavity
  • Posterior intercostal veins drain into azygous system
  • Anterior intercostal veins drain into internal thoracic veins
74
Q

Layers of thoracic wall from superficial to deep

A 
o	Skin
o	Superficial fascia
o	External intercostal muscle between ribs
o	Internal intercostal muscle
o	Intercostal artery, vein, and nerve
•	At the inferior border of the superior rib in the costal groove (space)
•	Will be seen on the posterior thoracic wall
o	Innermost intercostal muscle
o	Endothoracic fascia
o	Parietal pleura
o	Pleural cavity
o	Visceral pleura
o	Lung
75
Q

Phrenic nerves

A

o Adherent to the pericardium

o Pass just anterior to the root of the lung on their course to innervate the diaphragm

76
Q

Sources of energy for cardiac muscle

A
  • Glucose, fatty acids, ketone bodies
  • Normal conditions: glucose, FA
  • Starvation: FA, ketone bodies (cause acidosis)
  • Glycogenolysis, glycolysis, fatty acid oxidation, hydrolysis of phosphocreatine
77
Q

Heart energy reserves

A

-Short term fixes, not substantial
-Glycogen (stored glucose)
-Phosphocreatine: high energy bond CK
CK + ATP –> Creatine-phosphate + ADP

78
Q

Ischemia consequences

A
  • Lactate end product of glycolysis under anaerobic conditions
  • During ischemia lactic acid lowers pH and leads to lactic acidosis
  • Angina from nociceptors (pain receptors) triggered by H+
79
Q

Angina pectoris

A
  • Reversible myocardial ischemia
  • Imbalance between supply and demand
  • Commonly caused by narrowing of coronary arteries (by atherosclerosis or spasm)
80
Q

Myocardial infarction

A
  • Ischemia persists long enough to cause severe damage (necrosis) to heart muscle
  • Blood clot forms at site of narrowing and obstructs vessel
81
Q

Major 6 risk factors for coronary heart disease

A
  1. Diabetes
  2. Smoking
  3. Family history of premature coronary heart disease
  4. High serum triglycerides
  5. High serum cholesterol
82
Q

Plasma lipoproteins

A
  • Synthesized in the intestine, liver
  • Mixed group of lipid-protein (apoprotein) complexes
  • Solubilize fats for transportation in blood
  • Carry fats to and from tissues
  • Include VLDL, LDL, HDL
83
Q

Chylomicrons

A
  • Formed in the intestine
  • Transport triacylglycerol, cholesterol, and fat-soluble vitamins from food
  • Fatty acids are taken up by adipose and other tissue
  • Chylomicron remnants are formed that deliver cholesterol to the liver and may play a role in atherogenesis
84
Q

Chylomicron pathway

A

Intestine–> Chylomicron–> Periphery–> Chylomicron remnant–> Liver or Arterial wall

85
Q

VLDL/LDL

A

-Synthesized in liver from FA and cholesterol
-Fatty acids taken up by adipose tissues
-Converted to LDLs
-LDLs deliver cholesterol to peripheral tissues and back to liver
Liver–> VLDL –> Periphery–> VLDL remnant–> Liver or Arterial wall or LDL–> Liver

86
Q

HDL

A

-Synthesized by liver, intestines
-Pick up cholesterol from periphery and deliver it to liver
-Reverse cholesterol trafficking (taking cholesterol from LDL)
-Fights atherosclerosis
HDL–> Periphery–> Cholesterol-rich HDL–> Liver

87
Q

Risk of CHD and lipoproteins

A
  • LDL, VLDL remnants, chylomicron remnants increase risk
  • apo A have decreased risk (HDL), apo E and especially apo B increased risk
  • Breakdown components have higher risk than complete
88
Q

Normal cholesterol values

A

TC: 120-200
HDL-cholesterol: >40
Triglycerides: <100

89
Q

Friedwald formula

A 
VLDL = Triglycerides/5
TC = VLDL + HDL + LDL
90
Q

Atherosclerosis steps

A
  1. Endothelial cells bind LDL
  2. LDL enters intima (if oxidized more easily enters and entrapped)
  3. Injured endothelial cells initiate monocyte migration and macrophage formation
  4. PDGF, other growth factors stimulate migration of smooth muscle cells into intima
  5. Macrophages, smooth muscle cells accumulate LDLs forming foam cells
  6. Thickened intima with roughened surface of vessel lumen becomes plaque
91
Q

How are monounsaturated, omega-3, and omega-6 fatty acids good?

A
  • Monounsaturated fatty acids: decrease TG, increases LDL and VLDL remnant clearance
  • Omega 3: Decrease TG, decrease VLDL triglyceride synthesis
  • Omega-6: Lower LDL, enhance clearance of VLDL remnant and LDL
  • 2/3 of fat intake should be mono or polyunsaturated
92
Q

Meds for cholesterol

A
  • Statins: inhibit cholesterol synthesis and stimulate liver uptake of LDL
  • Ezetimibe and fibrate: lower absorption of cholesterol
  • Colestipol: increases bile salts to increase LDL uptake by liver
93
Q

Isoenzyme measurement in MI

A
  • Arise from different genes so may identify site of tissue damage
  • Separate using electrophoresis
94
Q

Creatine Kinase in MI

A

Creatine + ATP –> Creatine-phosphate + ADP

  • Dimer with 2 types of subunits (which can be phosphorylated simultaneously; 3 combos)
  • CK1: BB in brain
  • CK2: MB in myocardium
  • CK3: MM in muscle
  • Elevation of CK2 specific to monocyte necrosis
  • Can detect reinfarction because levels should fall after a day
95
Q

LDH in MI

A

Lactate + NAD+ –> Pyruvate + NADH

  • Tetramer containing 2 kinds of subunits (5 combos)
  • LDH1: HHHH in myocardium (more) and RBC
  • LDH2: HHHM in myocardium and RBC (more)
  • LDH3: HHMM in brain, kidney
  • LDH4: HMMM no specific site
  • LDH5: MMMM in liver, skeletal muscle
  • High ratio of LDH1 to LDH2 suggests MI
  • Can be done 30min-1hr after MI
96
Q

Troponin subunits in MI

A
  • cTn-T2 increases within 4 hours of MI but can check right away
  • Levels remain high for 14 days
  • Highly sensitive and specific
  • Detects smaller MIs than other tests
  • Cannot detect reinfarction for 2 weeks
  • Elevated Tn-I also can indicate MI or adverse outcomes of angina
97
Q

Therapeutic agents for MI

A
  • Inactive plasminogen in blood can dissolve blood clot if activated by t-PA or streptokinase
  • Need high doses because removed from circulation fast
98
Q

ATP in cross-bridging cycle

A
  • ATP binding causes myosin to dissociate from actin-myosin complex
  • When hydrolyzed myosin head returns to cocked formation (resting state)
99
Q

Differences in arrangement between cardiac and skeletal muscle

A
  • More sparse SR
  • T-tubules at Z line
  • Bigger T-tubules
  • Dyads instead of triads
100
Q

Differences in E-C coupling between cardiac and skeletal muscle

A
  • Calcium-induced calcium release (so Ca2+ from outside and from SR)
  • DHPR is Ca2+ channel
  • Cannot contract without extracellular Ca2+
  • L-type Ca2+ channels major regulator
101
Q

Ca2+ entry and removal mechanisms in cardiac cells

A 
Entry:
-DHPR (extracellular)
-RyR (SR)
Exit:
-SR ATPase
-Surface ATPase
-Surface Na/Ca exchanger
-Mitochondrial uniporter
102
Q

Length-tension relationship in cardiac muscle

A

Resting cardiac muscle length is below optimal length

103
Q

Frank-Starling’s law

A
  • Increased stretching of myocardial fibers results in stronger contraction
  • Due to increase in tension
104
Q

Things which alter contractility in myocytes

A
  • Sympathetic stimulation increases contractility at same length
  • Heart failure decreases contractility at same length
105
Q

What do beta blockers do?

A

Decrease CO through blocking sympathetic andrenergic tone

106
Q

SA node AP

A

-Slower than ventricular AP
Phase 0:
-T-type Ca2+ channels open
-L-type Ca2+ channels a little later
-No Na+ channels
Phase 4:
-Nonspecific pacemaker channels open when potential goes down
-Inward rectifier channels resist depolarization
-T-type Ca2+ channels pull up the potential

107
Q

AP in MI

A
  • Less ATP
  • Less negative voltage
  • Na+ inactivation gates close
  • Decreased AP conduction
  • Fibrous tissue from MI in the way and doesn’t conduct AP so it has to go around it
108
Q

Smooth muscle APs

A
  • Many don’t require nervous input to generate AP
  • Varicosities (wide synapses)
  • alpha and beta receptors distributed over entire cell
  • Response global, graded, global
109
Q

2 mechanisms exchanging heat between core and surface

A
  1. Circulation (forced convection): primary mode but need to counter different metabolic rates in body, deal with different levels of heat production based on situation, and overcome insulating properties of fat
  2. Conduction: minimal amount
110
Q

Basic requirement for maintaining core temp

A

Heat production must equal heat loss

111
Q

2 compartment (core-periphery) model of thermo-regulatory system

A
  • All heat exchanges take place at the skin
  • Heat transfer from core to skin through circulation (result of convection and conduction) due to temp gradient

Core:
-Brain, viscera, skeletal muscle
-Site of heat production
-Contains internal temp sensors and neural regulatory mechanisms
-Core temp is what is regulated
Periphery:
-Skin, subcutaneous fat
-Site of heat exchange with the environment
-Temp sensors
-Periphery temp not regulated or constant

112
Q

3 mechanisms for the body to regulate core temp

A
  1. Vary metabolic heat production: increases in muscular tone, shivering, activity but difficult to reduce
  2. Vary heat transfer between surface and environment
  3. Vary rate of heat transfer between core and surface
113
Q

Mechanisms to exchange heat with environment

A
  1. Conduction
  2. Convection
  3. Radiation
  4. Evaporation (always losing heat to environment)
114
Q

Mechanisms of heat exchange within the body

A
  1. Convection (molecule to molecule heat transfer where one molecule flows past the other) Primary mode
  2. Conduction (molecule to molecule heat transfer when molecules collide)
115
Q

Changes in cold, hot environments

A

Cold:
-Can only reduce Ts by decreasing blood flow to skin
-Close AV shunts (reduce Ts and decrease heat loss from skin)
-Counter-current exchange (conserves core heat while supplying extremities)
-Shivering (increase metabolic activity)
Hot:
-Evaporation to lose heat, eccrine glands secrete sweat, (innervation sympathetic and cholinergic)
-Vasodilation, shunts open

116
Q

Thermoregulatory control

A
  • Thermoreceptors detect temp
  • Info transmitted to CNS integrating network in hypothalamus and preoptic area
  • Set point compared to signal
  • Production of error signals
  • Transmission of error signals to effector mechanisms controlling shivering, sweating, vasomotor action
117
Q

Hypothalamic set-point

A
  • Preferred temp
  • Can be increased by calcium, dehydration, exercise, pyrogens
  • Can be decreased by decreased serum Na+, other
118
Q

Thermoreceptors

A
  • Located in hypothalamus, skin, other locations
  • Neurons or naked nerve endings whose firing rate changes with temp
  • Separate cold and warm sensors
119
Q

Integration of core/skin temp info

A
  • Skin temp can modify thermoregulatory response (usually much larger changes in Ts than Tc required for given thermoregulatory response)
  • Sweating, shivering, and vasomotor responses controlled by core temp
  • Rapid changes in skin and core temp produce larger thermoregulatory response
120
Q

Fever

A
  • Phagocytic cells release pyrogens which raise hypothalamic set point causing fever
  • Body responds as if cold
  • Part of the integrated homeostatic response to pathogenic agents, NOT temp regulation disorder
121
Q

Common heat illnesses

A
  • Heat exhaustion: extreme fatigue, skin pale, clammy skin, water/salt depletion
  • Heat syncope: fainting from high temp due to low arterial pressure from poor venous return after vasodilation
  • Heat stroke: breakdown of CNS functioning when core temp at 4-43C, no sweating, increased metabolic rate
  • Anesthetic (malignant) hypothermia: rare condition caused by anesthesia, sudden rapid rise in body temp and tachycardia, high metabolic rate, could be caused by Ca2+ gates locking open with continuous release
122
Q

Blood flow equation

A

Q = (P1-P2)/R

123
Q

Linear velocity equation

A

V(l) = Q/A

124
Q

MAP equations using resistance, output

A

MAP = CO (TPR)
When venous pressure must be accounted for:
MAP-Pv = CO (TPR)

125
Q

Cardiac output equation

A

CO = HR (SV)

126
Q

Poiseuille’s law (Resistance and radius relationship)

A

R = k/r^4

127
Q

Diffusion equation

A

Js = Ds (A) ([S1]-[S2])/x

128
Q

Net force (filtration and reabsorption)

A

net force = (Pc-Pi) - sigma (pi(c)-pi(i))
pi = oncotic pressures
sigma = permeability of capillary wall from 0-1

129
Q

Resistance in series, parallel equations

A

Series: Rtot = R1 + R2 + R3….
Parallel: 1/Rtot = 1/R1 + 1/R2 + 1/R..

130
Q

Compliance equation

A

C = delta V/ delta P

131
Q

MAP equations using pressures

A 
MAP = Pd + (Ps - Pd) / 3
MAP = (2Pd + Ps) /3
132
Q

Left ventricular flow equation

A

Qlv = V(O2) / ([O2]ao - [O2]mv)

133
Q

Pulmonary flow equation

A

Qpul = V(O2) / ([O2]pv - [O2]pa)

134
Q

Hydrostatic pressure equation

A

Phyd = (rho)(g)(h) which is .75mmHg per 1cm blood

135
Q

Differences between smooth muscle and skeletal

A
  • Calponin and Caldesmon (instead of troponin and tropomyosin)
  • Dense bodies (instead of z-lines)
  • Dense areas (for mechanical coupling)
  • No T-tubules bc slow contraction
  • Myosin splits ATP slower
136
Q

Tonic vs phasic contraction

A
  • Tonic: maintain continuous level of contraction (blood vessels, lungs, sphincters)
  • Phasic: contract rhythmically or intermittently (uterus, GI, urinary)
137
Q

Calcium sources in smooth muscle

A
  • Graded contraction based on cytoplasmic Ca2+
    1. Voltage-gated Ca2+ channels
    2. Ligand-gated receptor gated stretch activated Ca2+ channels 3. SR Ca2+ from RyR receptor
138
Q

What does Ca2+ bind to in smooth muscle? Then what?

A
  • Calmodulin
  • Ca2+-Calmodulin complex activates MLCK
  • MLCK hydrolyzes ATP to phosphorylate inactive MLC
  • “Switch” is the phosphorylation of the MLC
  • Continues as long as ATP available and MLC is phosphorylated
139
Q

Relaxation of smooth muscle

A
  • Nitric oxide and epinephrine can cause relaxation

- Even if Ca2+ present can have relaxation occur

140
Q

Slow wave vs pacemaker potentials in smooth muscle

A
  • Pacemaker: spontaneous due to cationic current
  • Slow wave: spontaneous due to hyper polarizing and depolarizing swings
  • Not all smooth muscle cells generate APs (not always required for contraction)
141
Q

Types of coupling in smooth muscle

A
  1. E-C coupling with twitch, summation
  2. E-C coupling with AP bursts at wave crests
  3. E-C coupling with no AP
  4. Pharmacomechanical coupling: no changes in Vm, due to drugs and hormones
142
Q

Single unit vs multi-unit smooth muscle

A
  • Single unit: act as cardiac muscle (any cell can initiate contraction)
  • Multiunit: act as skeletal muscle (neural regulation important)
143
Q

Receptors and responses in smooth muscle

A
  • Beta2: increases cAMP, causes dilation of bronchial SM, decreases GI activity
  • Alpha1: IP3, constricts sphincters, vasoconstricts arterioles
  • Alpha2: decreases cAMP, peripheral vasoconstriction

-ACh: contracts pupil, vasodilates blood vessels, constriction of bronchial, increases GI motility, contraction of bladder wall

144
Q

Ganglia used by GVE fibers in the CNS

A
  • Lateral (paravertebral): paired structures alongside vertebral column (sympathetic trunk)
  • Collateral (prevertebral): anterior to vertebral column in abdomen
  • Terminal: only in parasympathetic, near walls of target organs
145
Q

Components of a reflex arc

A
  1. Receptor
  2. Afferent pathway
  3. Integrating center
  4. Efferent pathway
  5. Effector organs
146
Q

What are the exceptions to SNS using andrenergic nerves?

A

-Some blood vessels and sweat glands use ACh

147
Q

What is increased when volume and baroreceptors decrease firing?

A
  • Long term adjustments
  • ADH causing increased water reabsorption
  • Increased aldosterone and renin which increase blood volume
148
Q

In severe hemorrhage what happens to IS?

A

It drops in direct response and steady state response (doesn’t follow flow chart rules)

149
Q

What happens to SV in exercise?

A

In steady state it drops due to the muscle pump

150
Q

If ATP significantly reduced in cardiac muscle what happens?

A

SR Ca2+ pump will not work and gradient of Ca2+ will be reduced between SR and myoplasm and between myoplasm and cytoplasm

151
Q

What is true of receptor potentials?

A

They are like EPSPs and IPSPs where they specially and temporally summate (graded)

152
Q

GI tract receptor responses

A
  • Alpha1: Contraction
  • Alpha2: Contraction
  • Beta2: Relaxation
  • M3: Contraction

CVR Midterm (1 decks)

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