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Tuesday Week 3 Flashcards

1
Q

What is in plasma?

A

albumins, globulins, fibrinogen, and electrolytes, organic nutrients and wastes

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2
Q

what is hematocrit?

A

percentage of formed elements in the blood

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3
Q

Which cells don’t come from the myeloid stem cell?

A

Lymphocytes. The rest come from the myeloid stem cell

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4
Q

What cell becomes platelets

A

magkaryocyte

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5
Q

what is the lifespan of an RBC

A

120 days

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6
Q

Explain erythropoiesis to the reticulocyte stage

A

day 1: Myeloid stem cells destined to become RBCs differentiate into pro erythroblasts
Day 2: now we are basophilic erythroblasts, which actively synthesize hemoglobin.
Day 3: now we are polychromatophilic erythroblasts and the nucleus is shrinking
Day 4: Normoblast ejects nucleus to become
Day 5: reticulocyte which enters blood stream

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7
Q

explain the life events of an RBC starting at reticulocyte and ending in complete recycle of components.

A

pages 632 and 633

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8
Q

Which WBCs can phaygocytize?

A

Neutrophils, eosinophils & monocytes can undergo phagocytosis

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9
Q

Which WBC’s are granulocytes?

A

neutrophils, basophils and eosinophils (monocytes and lymphocytes aren’t)

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10
Q

What are the three stages of clotting response?

A

Vascular phase, platelet phase and coagulation phase

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11
Q

Describe the vascular phase of clotting

A

This is the initial 30 minutes; the endothelial cells contract and begin releasing factors and hormones. ENDOTHELINS are a hormone that stimulate smooth muscle contraction and promote vascular spasm. The spasm prevents blood loss from the open vessel. Also, the endothelial plasma membranes become sticky.

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12
Q

Describe the platelet phase of clotting

A

This begins with the attachment of platelets to sticky endothelial surfaces, the basement membrane, and to each other. The activated platelets go on to release other chemicals, including platelet factors and calcium ions.

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13
Q

Describe the extrinsic route to the common pathway of clotting.

A

This starts when damaged epithelial cells or tissues release TISSUE FACTOR. Tissue factor combines with calcium insane another clotting factor to form an enzyme complex in order to activate FACTOR X to start the common pathway.

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14
Q

Describe the intrinsic pathway to the common pathway.

A

This begins with the activation of proenzymes exposed to collagen fibers at the injury site. We need PF-3 (released by platelets). After a series of reactions, factors combine to form an enzyme complex capable of activating FACTOR X to start the common pathway of clotting.

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15
Q

Describe the common pathway of clotting, starting with activated FACTOR X.

A

Activated FACTOR X activates a complex called prothrombin activator. Prothrombin activator convert prothrombin to thrombin. Thrombin then completes the clotting process by converting fibrinogen to fibrin. Fibrin makes a mesh network to trap more cells, making a clot!!

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16
Q

Describe three nutritionally based blood disorders

A

Iron deficiency can lead to microcytic RBC’s because not enough functional hb is produced.
Vitamin B12- problems with stem cell division leads to pernicious anemia (macrocytic)
Calcium and Vit K deficiency can lead to clotting problems

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17
Q

Describe three congenital blood disorders

A

Sickle cell anemia -arises in a mutation for a gene coding for Hb
Hemophilia: reduced production of a single clotting factor
Thalassemias: inherited blood disorder, mutation for gene coding for protein subunits of Hb.

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18
Q

Describe three kinds of blood infections

A

Bacteremia: bacteria circulate in blood, but don’t multiply there. (Viremia for viruses)
Sepsisemia: pathogens are present and multiplying in the blood and spreading throughout the body.

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19
Q

What are two kinds of leukemia?

A

Myeloid leukemia: abnormal granulocytes

Lymphoid leukemia: lymphocytes and their stem cells are affected

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20
Q

Describe the layers of the arterial wall.

A

There is an inner layer, known as the tunica intima: this has the endothelial lining and underlying layer of connective tissue with elastic fibers.

There is a middle layer known as the tunica media , which is basically concentric sheets of smooth muscle tissue.

There is an outer layer called tunica external, which is a connective tissue sheath.

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21
Q

How do veinous walls differ from arterial walls?

A
  1. They are usually flattened or collapsed, with thinner walls and larger lumens.
  2. Their tunica intima lacks the internal elastic membrane
  3. Their tunica media also lack elastic fibers and are much thinner.
  4. Their tunica external have smooth muscle cells.
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22
Q

How do blood vessels change with distance from the heart?

A

They get progressively smaller.

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23
Q

What are the “classes” of veins, biggest to smallest?

A

Large veins (all three layers), medium veins (all three layers), venules (no tunica media), and capillaries.

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24
Q

What is different about capillaries?

A

They are the only blood vessels whose walls permit exchange between blood and interstitial fluids.

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25
What are the "classes of arteries, biggest to smallest?
Elastic arteries (very resilient), muscular artery (thick tunica media), arterioles (poorly defined tunica externa), and capillaries.
26
Describe the two kinds of capillaries
Continuous and fenestrated. Continuous permits passage of water, small solutes, etc across, but permeability is still restricted by tight junctions. Fenestrated contain pores that penetrate the endothelial lining, which allow solutes as big as peptides to cross into and out of the interstitial fluid.
27
What are sinusoids?
These are similar to menstruated capillaries, except they are flattened and irregularly shaped. basement membranes are absent, and theses are found in the bone marrow, liver, spleen and endocrine glands.
28
Describe capillary beds
There is a pre capillary arteriole with pre capillary sprinters to control blood flow. The thorough fare has continuous blood flow across the bed.
29
What are the two controllers of vasomotion?
sympathetic innervation and cardiovascular centers of the medulla oblongata
30
Blood pressure in venules and medium sized veins is so low that it can't overcome gravity on its own. What helps?
Valves and skeletal muscle contraction.
31
At any given time, where is most of your blood?
In your venous system. 64%
32
If hemorrhaging occurs, what can the the MO do?
Its vasomotor center stimulates sympathetic nerves to constrict the veins. this helps maintain the volume within the arterial system to near normals despite significant blood loss.
33
Describe how blood vessels form
Through vasculogenesis and angiogenesis. At about 4 weeks gestation, hemangioblasts form little blood islands. The ones in the center differentiate into hematopoietic stem cells, but the ones in the periphery become angioblases, which become blood vessels.
34
describe the heart wall
There is a pericardium with a visceral layer (epicardium) and a parietal layer (dense and fibrous). The heart has a myocardial layer and an inner endocardial layer. The endocardial layer has an endothelium and areolar tissue.
35
What are myocardial bundles
These are parallel muscle patterns that wrap around the heart in the configuration need to squeeze the blood the appropriate direction.
36
What is the biggest way cardiac muscle tissue is different than skeletal muscle tissue.
Cardiac muscle has intercalated discs. Entwined plasma membranes with gap junctions and desmosomes. On the sarcomeres, they run along the z lines.
37
What is pericarditis?
``` An infection of the pericardium. Heart attack-like pain Fever Coughing Friction rub heard by stethoscope ```
38
Where do we find the trabeculae carnae? The pectinate muscle?
Trabeculae carnae: ventricles | Pectinate: atria
39
Why would the patent foramen ovale be a problem in adulthood?
40% of stroke sufferers, particularly young ones, have patent foramen ovale.
40
Which valves are closed during ventricular relaxation?
the semilunar valves
41
Which valves are closed during ventricular contraction?
The AV valves
42
What is the cardiac skeleton?
Fibrous network of dense connective tissue Stabilizes valves and muscle Electrically isolates the ventricular myocardium from the atrial myocardium.
43
A full cardiac cycle includes which actions?
A full cycle of systole and diastole
44
How long is the average cardiac cycle, and what is conventionally at the beginning?
800mSec, begins with atrial systole
45
Give the seven steps of the cardiac cycle in order
1. cycle begins (all relaxed, ventricles partly filled) 2. atrial systole 3. atrial diastole 4. early ventricular systole (isovolumetric contraction) 5. late ventricular systole (ventricular ejection) 6. early ventricular diastole (isovolumetric relaxation, AV valves still closed) 7. late ventricular diastole (passive filling)
46
Lub dup. What is happening at each?
``` Lub= AV valves closing Dup= semilunar valves closing ```
47
Give the 5 electrical events happening at the conducting system of the heart
1. An action potential at the senatorial node (SA) 2. Stimulus spreads across atrial surface by cell to cell contact within the internodal pathways. 3. Stimulus delays for 100mSec at the AV node. (atrial contraction occurs) 4. Impulse travels along inter ventricular septum (AV bundle, bundle branches) to the Purkinje fibers, and to the papillary muscles via the moderator band. This initiates ventricular contraction. 5. The impulse is distributed by Purkinje fibers and relayed throughout the ventricular myocardium and ventricular contraction completes
48
How is a cardiac muscle action potential different than a skeletal muscle action potential?
In cardiac, the action potential is prolonged because calcium ions continue to enter the cell for an extended period. The refractory period continues until relaxation is well under way. Tetany can't occur.
49
What happens at the plateau of a cardiac action potential?
The potential remains near 0mV. Two opposing factors are involved. At +30mV, the voltage gated sodium channels close and the cell begins actively pumping sodium out. At the same time, voltage gated calcium channels open. These are fairly slow though.
50
How does the cardiac membrane repolarize?
slow calcium channels begin closing and slow potassium channels begin opening. Potassium exits the cell.
51
With out regulation, how would the pacemaker cells fire?
SA node: 80-100 bpm AV node: 40-60 bpm This is one reason we need nervous and hormonal regulation.
52
How do acetylcholine and norepinephrine affect cardiac action potentials?
ACh opens chemically gated K+ channels --> this slows the rate of spontaneous depolarization (hyper polarization of membrane). This is parasympathetic stimulation. Norepinephrine binds Beta 1 receptors, opening ion channels that increase the rate of depolarization and shorten the period of repolarization. This increases the heart rate by sympathetic stimulation.
53
Describe sympathetic innervation of the heart
Arrives in posganglionic fibers within the cardiac nerves. They innervate the nodes, the conducting system, and the atrial and ventricular myocardium.
54
Describe parasympathetic innervation of the heart
Arrives in the vagus nerve and synapses with ganglion cells in the cardiac plexus. Postganglionic fibers innervate the SA node, AV node, and atrial musculature.
55
Describe the cardiac centers of the MO
These contain the cardioinhibitory center, which controls the parasympathetic neurons to slow the heart rate. The cardioacceleratory center controls the sympathetic neurons that increase the heart rate.
56
What is the equation for cardiac output?
CO=Stroke volume X heart rate
57
What is ESV?
Some blood remains in the ventricle at the end of ventricular systole. Thus, stroke volume (SV)= EDV-ESV
58
What is EDV?
This is all the blood in the ventricle at the end of atrial systole and end of ventricle diastole.
59
What factors affect venous return to heart?
Muscle activity, blood volume, rate of flow
60
What factors effect EDV?
Filling time and venous return
61
What is preload?
The amount of myocardial stretching. This is affected by EDV. Higher EDV makes a higher preload.
62
What is contractility?
the amount of force produced during a contraction at a given amount of preload. Sympathetic stimulation increases contractility. Greater contractility makes for a smaller ESV.
63
What is afterload?
This is the amount of tension the ventricle must overcommit force open the semilunar valve and eject blood. The higher the after load, the the larger the ESV, and the lower the CO
64
What are two drugs that reduce contractility of the heart?
beta blockers and calcium channel blockers
65
What is normal cardiac output range during heavy exercise? What is heart failure? What is average resting output?
18-30 L/min 3 L/min or less 6 L/min
66
What happens at the P wave?
Depolarization of the atria - atria are contracting, pumping blood into the ventricles.
67
What happens at the QRS complex?
Depolarization of the ventricles- contraction begins right after the peak of the R wave.
68
What happens at the PR interval?
transit time for the electrical signal to travel from the sinus node to the ventricles.
69
What happens at the QT interval?
one round of electrical depolarization and repolarization of the ventricles
70
What happens at the T wave?
This is where the ventricle repolarizes
71
What does foramen ovale do for a fetus? Ductus arteriosus?
Foramen ovale is an interatrial opening to allow blood to pass from the right to the left atrium in lieu of going to the pulmonary circuit. Ductus arteriosus is a connection for the right ventricle to send blood out to the systemic circuit instead of the pulmonary circuit.
72
What is a ventricular septal defect?
The bad septum causes the more powerful left ventricle to push blood into the right ventricle and pulmonary circuit, This mixes the oxygenated and deoxygenated blood.
73
Discuss the patent foramen ovale and patent ductus arteriosus.
Mixes oxygenated and deoxygenated blood Left ventricle has to work harder to get enough blood to the systemic circuit Cyanosis
74
What happens in tetralogy of Fallot
1. patent ductus arteriosus 2. pulmonary stenosis 3. ventricular septal defect 4. enlarged right ventricle
75
What atrioventricular septal defect?
both the atria and ventricles are incompletely separated. common in Down's Syndrome babies
76
What does total peripheral resistance depend on?
1. diameter and length of vessels 2. turbulence (can be result of plaque) 3. Viscosity (dehydration)
77
Blood flow depends on what two factors?
total peripheral resistance and arterial pressure
78
what is the pressure gradient? What alters it?
The difference in pressure from one end of the vessel to the other. The cardiovascular center (cardio acceleratory, cardio inhibitory, and vasomotor centers) can alter the gradient
79
Which three processes are at play during capillary exchange?
Diffusion, filtration, and osmosis
80
What drives the filtration aspect of capillary exchange?
Capillary hydrostatic pressure. it causes liquid and small solutes to be pushed out of the capillary.
81
What is blood colloid osmotic pressure?
BCOP is what draws water back into the capillary due to solute concentration in the capillary. causes water reabsorption
82
What is net filtration?
CHP-BCOP
83
Describe autoregulation versus central regulation of cardiovascular changes in blood pressure or chemistry
Autoregulation is changes in pattern of blood flow within capillary beds as pre capillary sprinters close and ope in response to chemical changes. Central regulation involves both neural and endocrine responses. The cardiovascular centers can use sympathetic stimulation to return homeostasis. Or for more long term regulation, an endocrine response can increase blood pressure.
84
Where do we find baroreceptors?
carotid sinuses, aortic sinuses, in the walls of the ascending aorta and the right atrium
85
What is the baroreceptor reflex?
increasing blood pressure stimulates baroreceptors which stimulate cardioinhibitory centers and inhibit cardioacceleratory centers and vasomotor centers. This results in decreased cardiac output and vasodilation to decrease blood pressure.
86
What happens when baroreceptors are inhibited, due to low blood pressure?
The vasomotor center gets stimulated and the cardioacceleratory center gets stimulated and the cardioinhibitory center gets inhibited. This causes vasoconstriction and increased cardiac output to increase blood pressure.
87
Describe the endocrine responses to low blood pressure and low blood volume
Sort term: sympathetic activation and release of adrenal hormones E and NE to increase cardiac output and peripheral vasoconstriction. Long term: Kidney releases RENIN, which activates ANGIOTENSIN I, which gets converted in the lung capillaries to ANGIOTENSIN II by ACE. ANGIOTENSIN II causes widespread vasoconstriction, causes the release of ADH, the release of Aldosterone, and causes thirst, all of which increase blood pressure. The kidney can also release EPO to make more RBC's
88
Describe the endocrine response to high blood pressure
The heart releases Atrial Natriuretic peptides (ANP) which increase sodium and water loss in urine, reduce thirst, and inhibit ADH, aldosterone, E, and NE release. It also causes peripheral vasodilation. All of this decreases blood pressure.
89
Where do we find chemoreceptors that monitor blood chemistry?
In the carotid bodies, aortic bodies, ventrolateral surfaces of the medulla oblongata
90
How does the body respond to chemoreception indicating increasing CO2 levels (and corresponding decrease in pH and O2)in the blood?
Chemoreceptors stimulate the cardioacceleratory center and inhibit the cardioinhibitory center and stimulate the vasomotor center. This causes increased cardiac output and blood pressure and vasoconstriction. They also stimulate respiratory centers in the medulla oblongata. This increases the respiratory rate to breathe off the excess CO2.
91
What is the respiratory pump?
: Each inhalation creates negative pressure, pulling blood into the venae cavae
92
Describe circulatory shock and how the body deals with it
This is a blood loss of over 35%. Progressive shock is the initial stage that sets in motion a series of positive feedback loops that accelerate tissue damage. If no intervention happens, then MAP falls below 50mmHg and damage soon becomes irreversible and results in death.
93
What is arteriosclerosis?
Thickening of the arterial walls, can result in CAD, stroke, blockage of coronary artery, resulting in ischemia.
94
What is atherosclerosis?
This is lipid deposits on the tunica media of arteries. it is the most common type of arteriosclerosis.

A & P Lab (8 decks)

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