RAT #5b Flashcards
Hypertension caused by drinking a large volume of water will trigger increased secretion of ________ leading to increased _____.
- ANP; vasoconstriction
- ANP; vasodilation
- ADH; vasoconstriction
- Aldosterone; vasodilation
- ADH; vasodilation
ANP; vasodilation
“ANP makes you pee”
At the site of blood vessel damage ______ promotes the conversion of plasminogen to _____.
- Thrombin; plasmin
- Fibrin; plasmin
- Plasmin; fibrin
- Plasmin; thrombin
- Thrombin; fibrin
Thrombin; plasmin
In patients with kidney failure who have abnormally low levels of plasma proteins, one would expect to see ______ due to _______.
- Hypotension; low peripheral resistance
- Myocardial infarction; hypotension
- Anemia; high plasma levels of EPO
- Systemic edema; low colloid pressure
- Hypertension; high stroke volume
Systemic edema; low colloid pressure
The most immediate reflex response to orthostatic hypotension is due to:
- Decrease stroke volume
- Decrease venous return
- Increase vasodilation
- Increase heart rate
- Decrease cardiac output
Increase heart rate
Living for weeks at high altitude causes the hematocrit to be _______ compared to normal; the hematocrit change is due to increased ________.
- Higher; EPO secretion from the kidney
- Higher; EPO secretion from the bone marrow
- Lower; renin secretion from the kidney
- Lower; renin secretion from the bone marrow
- Lower; thrombin secretion from the spleen
Higher; EPO secretion from the kidney
In a healthy person, saturation of cardiac troponin occurs:
- At rest
- Only during maximal exertion
- In every cardiac cycle
- Upon standing
- Upon waking up in the morning
Only during maximal exertion
Decreased calcium-calmodulin binding in smooth muscle cells results from:
- Increased levels of atrial natriuretic peptide at beta-adrenergic receptors
- Decreased levels of nitric oxide around blood vessels
- Increased levels of ANG 2 and ANG 2 receptors
- Increased levels of vasopressin at ADH receptors
- Increased levels of norepinephrine at beta-adrenergic receptors
Increased levels of norepinephrine at beta-adrenergic receptors
Decreased peripheral resistance can be caused by:
- Factors that decrease the hematocrit
- Increased myosin kinase activity in smooth muscle of peripheral blood vessels
- Growth of new capillaries associated with weight gain
- Decreased levels of histamine in the blood
- Arrival of EPI at alpha-adrenergic receptors
Factors that decrease the hematocrit
Excessive sweating during a marathon normally increases the secretion of _____ into the blood, leading to ____ diuresis and _____ blood vessels.
- ANP; decreased; constricted
- ADH; decreased; constricted
- ANG II; increased; no change in
- ADH; increased; dilates
- ANP; increased; dilates
ADH; decreased; constricted
Injury to a blood vessel exposes ______, this activating the agglutination of _______
- Thrombin; fibrin
- Smooth muscle; leukocytes
- Elastin; reticulocytes
- Collagen; erythrocytes
- Collagen; platelets
Collagen; platelets
Why is it necessary to maintain adequate mean arterial pressure to tissues?
Cells need a constant supply of oxygen which is why it is essential to maintain adequate blood pressure (MAP). This is especially true for tissues that cant be repaired like the heart and central nervous system.
Why do we need a circulatory system based on the concept of diffusion?
Because cellular life requires the exchange of matter between the external and internal environments; fuels move in as wastes move out, passing from the blood to the interstitial fluid and into the cells and vice versa
What is the pathway of a blood cell through the entire circulatory system?
Oxygen poor:
Vena Cave (superior/inferior), Right atrium, Tricuspid valve, Right ventricle, Pulmonary valve, pulmonary artery, pulmonary (arterioles, capillaries, venules, veins)
Oxygen rich
Left Atrium, Bicuspid valve, Left ventricle, Aortic valve, Aorta, Arteries (arterioles, capillaries, venules, veins) *repeat starting at superior vena cava
What is cardiac output?
The capacity of the heart to pump blood
- HR*SV
- Increased CO leads to increased MAP
- Decreased CO leads to decreased MAP
What is the difference between myocardial pumping cells and autorhythmic cells?
- 99% of the myocardial cells in the heart are called pumping or contractile cells - they do the work of pumping the blood.
- 1% of the myocardial cells are autorhythmic and conducting cells - these cells are referred to as “autorhythmic” because they are able to generate action potentials on their own.
- Autorhythmic and pumping cells are connected to each other by gap junctions, which allow AP’s to spread rapidly from one cell to the next.
- Autorhythmic cells are smaller and contain few contractile fibers - they dont contribute to the contractile force of the heart
Describe the pathway that action potentials follow through the heart, starting at the SA node
- Starts when an electrical impulse (AP) is generated by the SA node
- Electrical signal travels along conducting fibers in the walls of the atria (R atrium and L atrium) stimulating the atria to contract and pump blood into the ventricles
- Impulse also travels across the right atria through the atrioventricular node (AV) where it is delayed to let the ventricles relax and refill with blood
- Impulse travels along bundles of his, where the conducting pathways divide in two: forming right bundle branch and left bundle branch which lie in the interventricular septum
- From the bundle branches the impulse spreads into the inner wall of the ventricles (purkinje fibers)
- Finally, impulse travels up the outer walls of the ventricles towards the atria
What would be the effect of damage to connective tissue or pumping cells on heart rhythm
1
Describe ion movements in and out of an autorhythmic cell in the heart
- After hyperpolarization causes a sodium leak through channels causing a GP (aka pacemaker potential)
- Slow voltage gated calcium channels also open towards end in order to help bring the membrane to threshold - Rapid depolarization due to opening of voltage gated calcium channels (rapid influx of calcium)
- Very briefly depolarized from calcium entry
- Repolarization and after hyperpolarization due to opening of voltage gated potassium channels (repolarization) and closing of voltage gated calcium channels
Describe ion movements in and out of a myocardial pumping cell
- No graded depolarization, AP arrives directly through gap junctions so no GP needed
- Rapid depolarization due to opening of Voltage-gated sodium channels leading to Na+ entry
- Depolarization plateau due to opening of slow voltage gated calcium channels and closing of voltage gated sodium channels
- Repolarization due to closing of voltage gated calcium channels and opening of voltage gated potassium channels
Why is the refractory period of a myocardial pumping cell so long?
The refractory period prevents tetanus and keeps blood pumping by allowing the heart to relax
How does the autonomic nervous system affect cardiac output?
Pumping cells are only directly influenced by the sympathetic nervous system. In addition to the direct effects on the activity of pumping cells, sympathetic stimulation also increases stroke volume by causing an increase in venous return, meaning that peripheral vasoconstriction squeezes more blood into the heart-brain loop.
Note - CO = HR*SV so higher stroke volume = higher cardiac output
Describe how acetylcholine and EPI/NE influence heart rate based on their effect on ion channels
EPI/NE
3 main things happen:
1. Less hyperpolarization (less neg membrane potential)
2. Steeper rise to threshold (doesnt take as long)
3. More beats per minute
Summary:
When EPI and NE bind with receptors on autorhythmic cells they cause an increase is sodium leak - faster depolarizing. Also increase in permeability of calcium ions causes quicker depolarization resulting in an increased conduction velocity of AP’s through the heart
Describe an action potential of an autorhythmic cell in the heart after treatment with Ach or EPI/NE compared to “normal” rhythm.
Compared to normal heart rate treatment with EPI/NE would cause: less hyperpolarization, a steeper rise to threshold, and more beats per minute.
Compared to normal heart rate treatment with Ach would cause: more hyperpolarization, a slower rise to threshold, and fewer beats per minute.
Explain how EPI/NE increases stroke volume
Epinephrine/norepinephrine bind to beta adrenergic receptors on pumping cells causing an increase in stroke volume
Define starling’s law
Stroke volume increases in response to as increase in the volume of blood filling the heart
Define MAP and how to calculate it
MAP = Mean Arterial Pressure
-Average pressure in the arteries, generated by the heart
-Adequate MAP is necessary to deliver blood to within a cells length of every cell in the body
MAP = CO * TPR
CO = (HR+SV)
Describe the pressure changes that occur in the circulatory system from the aorta back to the vena cava
Pressure moves from highest to lowest as follows:
-Aorta -> arteries ->arterioles and metorterioles -> capillaries -> venules -> veins -> vena cava
Compare and contrast arterioles, arteries, capillaries, venules, and veins
- Capillaries - thinnest walled of all the blood vessels being composed of endothelial cells and lacking the smooth muscle, elastic and fibrous tissues of blood vessels.
- Arterioles - smooth muscle in their walls determines how much blood will enter a capillary bed
- Venules - site of exchange between blood and ISF
- Veins - have thinner walls with less elastic tissue than arteries, so they can expand easily when filled with blood. they also hold more than half of the blood in the circulatory system
Describe the variables that influence total peripheral resistance
Mainly influenced by a state of contraction of vascular smooth muscle
Explain the relationship between state of contraction of blood vessels and calcium levels in the cytosol
- More calcium in the cytosol = greater force of contraction
- Less calcium in the cytosol = more relaxation
List the factors that cause peripheral vasodilation
- increased concentration of bad stuff (co2, k+, and other organic acids)
- Decreased good stuff (oxygen, glucose)
- Sympathetic activation of beta-adrenergic receptors on blood vessels that supply skeletal muscle, liver, heart (bigger blood blast)
- Increased Atrial natriuretic peptide (ANP -makes u pee)
- Increased nitric oxide
- Increased histamine (too much can cause anaphylactic shock and constriction)
List the factors that cause peripheral vasoconstriction
- Sympathetic activation at alpha-adrenergic receptors
- Antidiuretic hormone
- Anglotensin II
Explain how lymphatic fluid is formed
1
Describe the effect that high MAP, histamine, disturbances to normal protein gradients, liver disease, and parasites have on the formation of lymphatic fluid
1
Describe a homeostasis loop for regulation of mean arterial pressure
Decreased MAP causes baroreceptors in the kidney, aortic arch and carotid artery to send error signals to the integrating center or CNS, the CNS causes effector tissues, vascular circular smooth muscle, SA node (autorhythmic cells), myocardial cells and the kidney to cause an increase in MAP
Describe the composition of blood with respect to the cellular elements and normal composition of plasma
1
Define hematocrit
Percentage of total blood volume that is occupied by packed red blood cells (ratio of red blood cells to plasma)
Explain why plasma osmolarity is regulated, and predict the effect of abnormally high or low osmolarity on the cellular elements of blood
1
Describe how the number of red blood cells is regulated by erythropoietin
Erythropoietin (EPO) is secreted by the kidney in response to low oxygen levels in the blood. EPO travels to receptors in the bone marrow and causes the synthesis of more red blood cells. When people spend more time at high altitudes their hematocrit increases because they are constantly exposed to hypoxic (low oxygen) conditions
Explain the common causes of jaundice in both neonates and adults
Hemoglobin is converted to a metabolite called bilirubin which is yellow in color and is excreted in the urine and feces. The spleen and liver are the main organs that produce bilirubin. Adults with liver disease very often appear yellow or jaundiced because they are not processing hemoglobin metabolites efficiently. This is also seen in newborns because their livers are still immature and they are switching from the fetal to adult form of hemoglobin and are producing large quantities of bilirubin.
Describe the clotting process starting with exposure of collagen to blood
Plug formation begins with platelet adhesion, when platelets adhere or stick to exposed collagen in the damaged area. The adhered platelets become activated, releasing cytokines into the area around the injury. These platelet factors reinforce local vasoconstriction and activate more platelets, which aggregate or stick to one another to form a loose platelet plug. Simultaneously, exposed collagen and tissue factor, initiate the third step, the formation of a fibrin protein mesh that stabilizes the platelet plug to form a clot. Fibrin is the end product of a series of enzymatic reactions known as the coagulation cascade. Eventually as the damaged vessel repairs itself, the clot retracts when fibrin is slowly dissolved by the enzyme plasmin.
Explain how Cox inhibitors and tissue plasminogen activators are used to reduce clotting
1
Explain how a clot forms in a blood vessel
- LDL - cholesterol accumulates between the endothelium and connective tissue and is oxidized
- Macrophages ingest cholesterol and become foam cells
- Smooth muscle cells, attracted by macrophage cytokines, begin to divide and take up cholesterol
- A lipid core accumulates beneath the endothelium
- Fibrous scar tissue forms to wall off the lipid core
- Smooth muscle cells divide and contribute to thickining o the intima
- Calcifications are deposited within the plaque
- Macrophages may release enzymes that dissolve collagen and convert stable plaques to unstable plaques
- Platelets that are exposed to collagen become activated and initiate a blood clot
Describe the process leading up to a myocardial infarction, starting with a blocked coronary artery and finishing with programmed cell death in myocardial pumping cells
1
Explain how each of the following are used to treat hypertension:
- diuretics
- calcium channel blockers
- beta blockers
- ACE inhibitors
- ANG II receptor blockers
Diuretics - diuretics make you have to pee and if blood volume increases, blood pressure increases, therefore if you take a diuretic you will be decreasing your blood volume thus decreasing blood pressure
Define inotropic agent and explain how they are used in cardiovascular medicine
1
How does Angiotensin II cause vasoconstriction
Decreased renal blood pressure causes increased secretion of renin from the kidney. Renin converts angiotensinogen (inactive) into angiotensin I (active). Then ACE (angiotensin converting enzyme) converts angiotensin I to Angiotensin II. Angiotensin II causes peripheral vasoconstriction, increased ADH secretion, and increased aldosterone secretion from the adrenal cortex, which combined result in increased MAP and water conservation
How does AHD (vasopressin) act as a vasoconstrictor
Low MAP, high plasma osmolarity, and decreased atrial stretch cause an increase number of AP in baroreceptor neurons. This causes an increased secretion of ADH from the posterior pituitary gland, where it binds to receptors in the kidney and vascular circular smooth muscle. This causes peripheral vasoconstriction and water conservation by the kidneys resulting in increased MAP
How does ANP (atrial natriuretic peptide) cause vasodilation
Excess fluid ingested causes an increase in blood volume. This increases causes an increase in atrial stretch resulting in an increase in the release of ANP from the heart. This causes more urine to be formed in the kidneys, and relaxation of VSM. Reducing blood volume and lower MAP.
“ANP makes you have to pee”
