Week 9 Flashcards

1
Q

When do papillary muscles contract

A

When the valve flaps are closed at the same time that the ventricles contract. They serve to keep the valve flaps tightly closed and avoid them flipping in the wrong way. Chordae Teninaea connect papillary muscles to valves and are pulled tight

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2
Q

What are the semilunar valves? Name the two types and what their purpose is

A

Pulmonary semilunar valve: located between the right ventricle and the pulmonary artery (pulmonary trunk)
Aortic semilunar valve: located between the left ventricle and the aorta. This valve has two little holes, otherwise looks the same as pulmonary.

These valves open during ventricular contraction to allow blood to enter circulation. They don’t deal with very much pressure so are not supported by chordae tendineae. They snap shut as ventricles relax to prevent back flow of blood into ventricles.

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3
Q

Why are there no one-way valves for blood flow into the atria? what other features of the atria create this effect (four total)

A

The atria has continuous, uninterrupted blood flow! Four characteristics make this possible:

  1. No valves to interrupt blood flow
  2. Atrial systole contractions do not contract to the extent that would block blood flow, blood continues to flow into atria during atria systole
  3. Atrial contractions must be gentle enough to not exert any back pressure
  4. Atria relaxation is timed to relax before the start of ventricular contraction

Overall this allows atria 70% more cardiac output.

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4
Q

Which valve is most likely to fail?

A

Left / mitral / bicuspid. Left side of heart has way more pressure and so is more prone to failure.

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5
Q

What is heard during auscultation on the chest

A

First sound or Lub or S1: produced by closing of AV valves during ventricular contraction or Systole
Second sound or Dub or S2: produced by closing of semilunar valves when ventricles relax or Diastolate. Louder than the first sound.

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6
Q

Name common causes of heart murmurs*

A
  1. Defective heart valves: for example aortic valve stenosis (narrowing) due to calcium deposits produces mid-systolic heart murmur
  2. Rheumatic Endocarditis: streptococcal bacterial infection causes antibodies to attack heart valves “Rheumatic fever”
  3. Mitral Stenosis: mitral valve thickens and calcifies causing a rise in left atrial and pulmonary vein pressure resulting in hypertension
  4. Mitral Valve Prolapse: most common cause of mitral regurgitation (blood flows backward into atrium). Both congenital (excess leaflet material) and acquired. Most people lack symptoms and have normal lifespan. Chordae Tendinae rupture can worsen regurgitation and replacement with mechanical or biological valve may be needed
  5. Septal defects: holes in the septum between right and left sides. Congenital. May lead to hypertension and edema
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7
Q

Describe all the steps in the cardiac cycle. *Which step contributes the most blood volume to the ventricles?

A
  1. Quiescent period (relaxation phase): When atria and ventricles are both relaxed, venous blood fills the atria. When atria pressure is greater than ventricular, the AV valves open allowing blood to flow from atria to ventricles. While all 4 chambers are relaxed is when 80% of the blood fills the ventricles (rapid filling stage)
  2. Atrial Contraction (systole): Contraction of the atria adds the final 20% volume to the End-Diastolic Volume
  3. Isovolumetric contraction: Ventricles begin to contract (systole) and AV valves shut (produce S1 lub). Both AV and semilunar valves are closed
  4. Ejection: Ventricle pressure becomes greater than aorta and opens semilunar valves to eject two thirds (ejection fraction) of the blood they contain. This is the Stroke Volume. The one third that remains is the End-Systolic volume
  5. Isovolumetric Relaxation: ventricle pressure falls below artery pressure and semilunar valves close (produce S2 dub). Both AV and semilunar valves are closed and heart is in diastole
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8
Q

what is contraction and relaxation of the heart called

A
Systole = contraction
Diastole = relaxation

When the words are used without reference to specific chambers they usually refer to the ventricles. However atria do have systole and diastole, we just care more about the ventricles

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9
Q

What happens to the function of the heart if the atria don’t contract? why?

A

The heart still pumps and people can survive with an atria that does not contract. They are more at risk for blood clots leading to stroke, however. This is because most of the blood flow from atria to ventricles is accomplished passively and atrial contraction only contributes about 20% to the final ventricular volume. So the heart is still functioning at like 80% capacity

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10
Q

What blood pressure measurements occur at each state of the cardiac cycle? Mostly focus on left ventricle, short description of right ventricle. Where do we measure blood pressure?

A

In diastole: arteries 80 mmHg
Ejection (when left ventricle pressure is greater than aorta): both ventricle and aorta 120 mmHg
Isovolumetric relaxation (when ventricle pressure is below arteries pressure): left ventricle 0 mmHg and aorta 80 mmHg

Similar events occur in right ventricle (pulmonary circulation) but at lower pressure which a maximum of 25 mmHg during systole and 8 mmHg at diastole

*A persons blood pressure is measured at the brachial artery

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11
Q

What is the dicrotic notch

A

On a graph of arterial pressure, there is a short inflection in the descending portion that is produced by the closing of the elastic aortic and pulmonic semilunar valves. The closed semilunar valves are stretched and lead to a slight drop in blood pressure, then they recoil which leads to a quick upsurge in blood pressure. This dicrotic notch is associated with the second heart sound S2 created by closing of the semilunar valves

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12
Q

Review the electrical conduction of the myocardium. What is a term to describe the single functioning unit?

A

Myocardial cells are interconnected by gap junctions which are electrical synapses. The entire mass of interconnected cells is the myocardium and it can be called a Functional Syncytium because any action potentials that originate in any cell in the mass can be transmitted to all the other cells.

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13
Q

What creates the automaticity or intrinsic rhythmicity of the heart? Name the cells, not the mechanism

A

Pacemaker cells

  1. Sinoatrial node (the pacemaker): located in right atrium near superior vena cava, serves as the primary pacemaker.
  2. AV node: normally suppressed by SA node. Has slower diastolic depolarization and action potential production. Also called an ectopic pacemaker or ectopic focus because it is abnormal to use
  3. Purkinje fibers: normally suppressed by SA node. Has slower diastolic depolarization and action potential production. Also called an ectopic pacemaker or ectopic focus because it is abnormal to use
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14
Q

*Describe the mechanism that creates intrinsic rhythmicity in the heart

A

Sinoatrial Node cells exhibit a slow spontaneous depolarization called the Pacemaker Potential, which occurs during diastole (also called diastolic depolarization). This is created by ion channels:

  1. HCN channels: open in response to HYPERpolarization to allow Na+ to enter and cause depolarization (“Funny Current”). They also open in response to cAMP (from beta adrenergic signaling nor/epinephrine)
  2. Dihydropyridine Receptors: once diastolic depolarization reaches threshold of -40 mV, DHP receptors open and allow Ca2+ to flow inside the cell. The Ca2+ binds RyR2 ryanodine receptors to cause huge calcium increase to depolarize cell. (Ca2+ induced Ca2+ release mechanism)
  3. Voltage gated K+ channels: open after depolarization max is reached and repolarize cell by outward K+ migration
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15
Q

How is heart rate increased or decreased? What specific molecules are involved and what do they bind to?

A

Increase: sympathoadrenal stimulation produces (nor)epinephrine which causes cAMP production in pacemaker cells which opens HCN channels and promotes entry of Ca2+. Causes an increased diastolic depolarization which produces a faster cardiac rate and strength of contraction

Decrease: parasympathetic vagus nerve (X) releases acetylcholine which bind muscarinic receptors and (through G proteins) open K+ channels. This outward diffusion of K+ slows diastolic depolarization and slows cardiac rate

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16
Q

Is the SA node a single uniform structure? What is the name for the normal rhythm produced by the SA node and how does it time the atrial and ventricular contractions appropriately?

A

Not a uniform structure. Consists of different pacemaker regions around the right atrium that are electrically separated and communicate through Sinoatrial Conduction Pathways. Action potentials spread through these pathways to depolarize atria and ventricles, but path to ventricles is longer (AV node, bundle of His, Purkinje fibers) so that ventricles will contract slightly after atria. This is how the sinoatrial node produces a Normal Sinus Rhythm.

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17
Q

*Describe the unique feature of a myocardial action potential

NOTE: there are 2 separate action potentials required for a heart: the sinoatrial node produces the pacemaker potential which THEN stimulates the myocardium to produce its own action potential

A

Myocardial cells are stimulated by pacemaker potentials that depolarize to a threshold where Fast Na+ Channels open. The level of depolarization is maintained during a Plateau Phase before repolarization! Plateau phase is a result of a slow inward diffusion of Ca2+ through Slow Ca2+ Channels (dihydropyridine receptors) which balances a slow outward K+ diffusion. Rapid repolarization at the end of the plateau phase is achieved by opening of voltage gated K+ channels

The plateau phase is unique and needed to give time for contraction to occur! The Ca2+ that enters during this phase signals contraction (RyR2) so that contraction is complete before the membrane recovers from refractory period. This prevents summation from occurring

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18
Q

How are action potentials conducted from the atria to the ventricles (through the nonconductive fibrous skeleton)

A

Specialized conducting tissue is required: the Atrioventricular (AV) Node, the bundle of His, and the Purkinje Fibers.

Action potentials generated by the SA node spread through atria into the AV node (located on interatrial septum). After a brief delay, the impulse continues through the bundle of His (atrioventricular bundle) at the top of the inter ventricular septum. This descends through the fibrous skeleton and divides into left and right bundle branches, which are continuous with the Purkinje fibers in the ventricle walls. The delay at the AV node is important for timing ventricular contraction 0.1-0.2 seconds after atrial contraction

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19
Q

Review the excitation-contraction coupling mechanism of the myocardial cells

A

Ca2+ induced Ca2+ release is stimulated by action potentials which open Dihydropyridine voltage gated Ca2+ channels in the plasma membrane and allow a puff of calcium into the cytoplasm. This calcium binds the ryanodine RyR2 receptors in the sarcoplasmic reticulum and opens them, allowing a large influx of calcium into the cytoplasm. The calcium binds troponin C and allows contraction.
These events occur at Signaling Complexes, where sarcolemma is close to sarcoplasmic reticulum.

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20
Q

How is relaxation of the muscle during repolarization of the myocardial cells achieved?

A

Ca2+ concentration is lowered by Sarcoplasmic Reticulum Ca2+ ATPase (SERCA) pumps which actively transport calcium into the SR. Calcium is also extruded into the extracellular fluid by the Sodium Calcium Exchanger (NCX) via secondary active transport and the Ca2+ ATPase pump via primary active transport. These ensure myocardium relaxes during repolarization during diastole.

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21
Q

What prevents the heart from sustaining a contraction? Why is this important?

A

Because of the plateau phase which creates a long refractory period where the heart cannot be stimulated until it has relaxed from the previous contraction. This ensures rhythmic pumping of the heart

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22
Q

Describe the normal ECG waves. How does the device record an ECG? What action of the heart produces each wave?

A

Electrocardiograph’s record ion flow (not action potentials directly) to produce an electrocardiogram (ECG or EKG).
1. P wave: depolarization of the atria. When about half of the atria is depolarized the upward deflection is at max value. When the entire atria is depolarized the ECG returns to baseline.
(atria repolarization is covered up by the QRS wave)
2. QRS wave: depolarization of the ventricles. Same as with atria, it peaks at half depolarized and returns to baseline at full depolarization.
(S-T segment is the plateau phase)
3. T wave: repolarization of the ventricles. Note that the wave points in the same direction as QRS despite being opposite potential changes, this is because depolarization occurs from endocardium to epicardium while repolarization spreads in the opposite direction.

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23
Q

Which sounds are associated with each wave on and ECG

A

QRS wave occurs at systole (depolarization) so the shutting of the AV valves occurs immediately after the QRS wave. This is the first heart sound (S1 or lub)

T wave occurs during diastole (repolarization) of ventricles so the shutting of the semilunar valves occurs shortly after the T wave. This is the second heart sound (S2 or dub)

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24
Q

What are the three coats that compose the walls of arteries and veins (not capillaries!)

A
Tunica externa: connective tissue
Tunica media: smooth muscle
Tuncia interna (intima): has three parts, an innermost epithelium (endothelium) which lines all vessel lumina, a basement membrane (glycoproteins0, and an internal elastic lamina formed from elastin fibers.
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25
Q

How are the structures of arteries and veins different?

A

arteries have more muscle (larger tunica media) and appear more rounded in cross section while veins are usually partially collapsed. Veins also have one-way valves which arteries do not.

26
Q

*How do arteries contribute to the continuous one-way flow of blood into the heart?

A

Aorta and other large arteries are large elastic arteries that expand when the pressure of the blood rises after ventricle contraction. They then recoil when blood pressure falls during ventricle relaxation. This elastic recoil drives the blood during the diastolic phase when the heart is resting and not providing a driving pressure. Elastic recoil continuous to push blood out while the heart is relaxed so that blood flow never stops!

27
Q

What arteries have the greatest resistance to blood flow? What other vessels do they feed into?

A

Muscular arteries, which are small arteries and arterioles. They are less elastic and have a thicker layer of smooth muscle (tunica media) so their diameter only changes slightly in response to rising and falling blood pressure.
Arterioles may enter venules directly through arteriovenous anastomoses, but in most cases arterioles pass into capillaries which connect to venules.

28
Q

What is the diameter of a capillary and why it is notable?

A

7 to 10 µm, the narrowest blood vessels. A red blood cell is 7 µm in diameter, so capillaries are a tight fit!

29
Q

What hormones are secreted by the corpus luteum? What do peak levels of these hormones cause?

A

Both estradiol and progesterone (developing follicles only secrete estradiol). Progesterone rises to peak levels during the luteal phase, one week after ovulation. The luteal phase is very stable at 14 days long (starting day 14 and ending day 28). The high progesterone and estradiol (and also inhibin!) from the corpus luteum exerts a negative feedback effect on FSH and LH secretion so that no other follicles develop and no ovulation occurs. Basically prevents multiple ovulations and pregnancies!

30
Q

Describe the events of the late luteal phase. What hormones are involved?

A

New follicles start to develop toward the end of the luteal phase as inhibin production is decreased and estrogen and progesterone levels fall as corpus luteum regresses. The decline of the corpus luteum in other animals is caused by a hormone called luteolysin, secreted by the uterus. In humans the cause is less known, but may be prostaglandin F2alpha. luteolysis is prevented by high LH levels, but LH levels are low during the luteal phase due to estrogen and progesterone secretions from the corpus luteum. It causes it’s own demise!

At the very end of the luteal phase the corpus luteum declines until estrogen and progesterone are at very low levels, and this causes menstruation to occur.

31
Q

What are the three phases of the female cycle as defined by changes in the endometrium? Which ovarian phases are they associated with?

A
  1. Proliferative Phase: while the ovary is in follicular phase, estradiol is secreted and stimulates growth of the stratum functionale in the endometrium. Spiral arteries develop
  2. Secretory Phase: while ovary is in luteal phase, increased progesterone secretion (from corpus luteum) stimulates uterine gland development. Endometrium becomes thick and “spongy” while uterine glands are engorged with glycogen. The endometrium is well prepared to course an embryo
  3. Menstrual Phase: while ovary is in late luteal phase, estradiol and progesterone levels fall and necrosis and sloughing of the stratum functionale of the endometrium results from Spiral artery constriction. The spiral arteries are responsible for menstrual bleeding! Nausea, vomiting, headache, water retention (bloating) also occur due to hormone changes
32
Q

What other changes (besides endometrium and ovarian) occur in the female reproductive tract due to cyclic hormone changes (particularly mucus)

A

High estradiol also causes cornification of the vaginal epithelium (upper cells die and become filled with keratin). Also causes production of a thin, stretchy (like rubber cement) cervical mucus that can be easily penetrated by sperm, this is called Spinnbarkeit and is present when fertility is at its peak. It has guiding channels to direct sperm towards cervical opening.

High progesterone (luteal phase) causes cervical mucus to thicken and become sticky after ovulation. This is a barrier agains sperm entry or bacteria

33
Q

What causes the dormitory effect

A

Dormitory effect = females who live together will synchronize their menstrual cycles.

Due to pheromonal effects that stimulate the Vomeronasal Organ (VNO) in the nasal mucosa which controls the hypothalamus’s release of GnRH

34
Q

What factors may cause Hypothalamic (or Functional) Amenorrhea and how?

A

Hypothalamic (or Functional) Amenorrhea is cessation of menstruation caused by inadequate stimulation of ovaries by FSH and LH due to inadequate GnRH release from hypothalamus. Caused by:

  1. Stress: axons connect the limbic system to GnRH neurons in the hypothalamus, so emotions can effect GnRH secretion
  2. Low body fat (very thin or athletic): Intense exercise can suppress GnRH secretion. Leptin is secreted by adipocytes and also effects GnRH secretion. A sufficient amount of adipose tissue (and leptin secretion) is required for ovulation and reproduction.
35
Q

What is the main factor that increases or decreases resistance to blood flow

A

Arterioles contraction. Resistance increases by vasoconstriction of arterioles which decreases blood flow to capillaries. Vasodilation of arterioles (by relaxation) decreases resistance and increases flow to capillaries. Vasoconstriction caused by norepinephrine and vasodilation caused by acetylcholine can be propagated for some distance along the arteriole wall through gap junctions which connect cells of the arteriole walls.

36
Q

In some organs, like intestine, blood flow is regulated by ____ as in addition to the primary driver ____

A

Precapillary sphincters: circular muscle bands at the origin of the capillaries
Normal driver is arteriole vasoconstriction (decrease blood flow) and vasodilation (increase blood flow)

37
Q

What are the walls of capillaries composed of

A

just one cell layer, a simple squamous epithelium or endothelium surrounded by basement membrane. This permits rapid exchange of materials between blood and tissue

38
Q

Describe the three types of capillaries, where are they located and what is their structure

A
  1. Continuous capillaries: closely adjacent to endothelial cells in muscles, lungs, adipose, and central nervous system. They lack intercellular channels in the CNS and contribute to the blood-brain barrier. In other organs, they have narrow intercellular channels to pass molecules (other than proteins!)
  2. Fenestrated capillaries: in kidneys, endocrine glands, and intestines. Have wide intercellular pores covered by mucoprotein (basement membrane) which restricts passage of certain molecules (especially proteins)
  3. Discontinuous capillaries (Sinusoids): in liver, bone marrow, and spleen. Distance is great between endothelial cells so these look like little cavities, sinusoids, in the organ. These have low regulation
39
Q

How do capillaries contribute to the blood brain barrier?

A

Continuous capillaries in the CNS lack intercellular channels. Endothelial cells, however, have pinocytotic vesicles which may perform intracellular transport across capillary walls. This type of transport is the only type present in the CNS and accounts for the selective nature of the BBB. There are also cells called pericytes along the capillaries which contract (but are not smooth muscle) and regulate cerebral blood flow and produce transport proteins that function in the BBB

40
Q

What happens to capillaries in hypoxic conditions?

A

Hypoxic (low oxygen) tissue grows new capillary networks to increase oxygen flow. *Vascular Endothelial Growth Factor (VEGF) promotes capillary growth. Adenosine also stimulates vasodilation of arterioles and increases blood flow to tissue

41
Q

what two mechanism help return venous blood to the heart? (normal venous pressure is too low to get blood from lower limbs to heart)

A

Skeletal muscle pump: skeletal muscles near veins provide a massaging action that squeezes veins to push blood toward heart. The one-way flow is ensured by venous valves in the vein walls. Aids in blood return from lower limbs

Respiratory pump: helps move blood from abdominal to throracic veins. When inhaling, the diaphragm contracts and flattens to descend inferiorly to abdomen. This increases abdomen pressure and decreases thoracic pressure, causing blood to flow into thoracic veins that will return blood to heart

42
Q

When is the skeletal muscle pump active or inactive and what does its activity cause?

A

Less active while standing still or bedridden. Blood accumulates in the veins and causes them to budge (may lead to blood clot formation). When standing still for a long time the lack of blood return to the heart can cause low blood flow to the brain and fainting (syncope)

More active when a person is exercising.

43
Q

What is atherosclerosis and what causes it

A

Atherosclerosis is the most common arteriosclerosis (hardening of arteries). Localized plaques (atheromas) build up and protrude into the artery (NOT veins), reducing blood flow. The atheroma are also sites for thrombus formation which further occludes blood supply.
Caused by “insult” to endothelium such as smoking, hypertension, high blood cholesterol, and diabetes. The insults can appear during teens to 20s and cause heart attack/stroke later in life (highest cause of death in United States!)

44
Q

describe the progression of atherosclerosis in the arteries. What is the first recognized change? what do they develop into?

A

First change is appearance of Fatty Streaks (gray-white areas protruding in arteries) that consist of lipid-filled macrophages and lymphocytes in the tunica interna. Progression of disease is promoted by inflammation caused by cytokines which attract monocytes that penetrate the tunica interna and become macrophages, engulf lipids, and appear as Foam Cells. The more advanced lesions are Fibrous Plaques which have a cap of connective tissue. Cytokines stimulate production of collagenase enzymes that weaken the plaque’s cap. When it ruptures and exposes the underlying collagen tissue, thrombi form.

45
Q

What factors promote high cholesterol and what is the consequence of high cholesterol

A

Diet rich in saturated fat or an inherited condition called Familial Hypercholestermia. Inherited high cholesterol usually causes heart attacks during childhood, regardless of cholesterol. High cholesterol is associated with atherosclerosis and increased heart attacks and stroke risk.

46
Q

What is the bad cholesterol? describe the pathway this molecule takes in the body

A

Low Density Lipoproteins (LDLs) carry cholesterol TO the arteries. LDLs are derived in the liver from very low density lipoproteins (VLDLs). Cells in different organs contain receptors for apolipoproteins on LDLs. When they bind, the cell engulfs LDL particles by receptor-mediated endocytosis. Most LDL particles are removed this way by the liver. However, apolipoprotein B signals uptake into artery tissue and initiates atherosclerotic plaque formation. This is enhanced by OXIDATION that promotes monocyte entry, which convert to macrophages and ingest lipoproteins, become foam cells, progressing disease

People who eat high cholesterol/fat have low LDL receptors in liver so high blood LDL

47
Q

what is the good cholesterol? describe the pathway this molecule takes through the body

A

High density lipoprotein (HDL) carries cholesterol AWAY from arteries. HDL accepts cholesterol from foam cells and carries it to the liver for metabolism. Levels of HDL are largely determined by genetics. Women (pre-menopause) have higher HDL and people who exercise regularly have higher HDL

48
Q

Atherosclerosis is believed to be what type of disease? What evidence supports this idea?

A

Inflammatory disease. C-reactive protein is a marker of inflammation (not a cause!) which is also a strong predictor of atherosclerotic heart disease.

49
Q

What is PCOS and what are its symptoms? What treatments are commonly prescribed

A

Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder, and the major reason for female infertility. The ovaries contain fluid-filled cysts visible in an ultrasound. Cause is unknown, but may be related to high anti-Müllerian hormone (AMH) that promotes increased LH secretion.

Symptoms: amenorrhea (the absence of menstruation), dysmenorrhea (painful menstruations), reduced fertility, excessive growth of body hair, male pattern baldness, and acne. Symptoms are caused by excessive androgens (testosterone, DHT, dehydroepiandrosterone (DHEA), and androstenedione) secreted from the ovaries, and sometimes from the adrenal. PCOS also increases risk of obesity, hypertension, and insulin resistance, creating danger of developing type 2 diabetes and metabolic syndrome.

Treatments: contraceptives and sustained weight loss

50
Q

What is the female athlete triad?

A
  1. energy deficiency due to inadequate food intake
  2. menstrual disturbances and amenorrhea
  3. osteopenia (decreased bone mineral density) and possibly osteoporosis.
    Younger female athletes may be particularly vulnerable due to an excessive focus on thinness; the eating disorders of anorexia and bulimia may or may not be present. Exercise and low body fat, acting through the suppression of the hypothalamic-pituitary-ovarian axis and reduced estradiol secretion, cause an increase in osteoclast activity that reduces bone mineral density to increase the risk of fractures. In a healthy athlete without the triad, bone mineral density actually improves as a result of the physical stresses on bones.
51
Q

What auscultatory positions are best for hearing each valve? What factors can affect the positions?

A

Closing of the tricuspid valve is best heard when the stethoscope is placed to either side of the lower sternum, just above the xiphoid process. Closing of the mitral valve is best heard at the apex of the heart, in the fifth left intercostal space. Closing of the pulmonary and aortic semilunar valves is heard best at the second left and right intercostal spaces, respectively.
these auscultatory positions are affected by obesity, pregnancy, and other conditions.

52
Q

What are the symptoms of atrial fibrillation and what drugs help treat it?

A

Atrial fibrillation (when atria fail to contract) often has no symptoms as the amount of blood that fills the ventricles and that the ventricles eject is sufficient. The person may experience fatigue and difficulty exercising. More seriously, the pooling of blood in the atria increases the chances of blood clot formation, causing an increase in the risk of stroke and clot in the right atria can cause pulmonary embolism. This may be prevented with anticoagulants including aspirin, warfarin (which blocks the activation of vitamin K), and rivaroxaban (Xarelto), which inhibits factor X activity in the clotting sequence

53
Q

What are arrhythmias? What treatments exist (4 groups) and what do they target? Name specific examples of drugs

A

Arrhythmias are abnormal patterns of electrical activity that result in abnormalities of the heartbeat. Drugs target cardiac action potentials. Group 1 drugs are those that block the fast Na+ channels (quinidine, procainamide, lidocaine). Group 2 drugs are beta-blockers, interfering with the ability of catecholamines to stimulate beta-adrenergic receptors (propranolol, atenolol). Group 3 drugs block K+ channels (amiodarone), slowing repolarization. Group 4 drugs block the slow Ca2+ channels (verapamil, diltiazem). Different arrhythmias are best treated by the specific actions of each drug.

54
Q

How does digitalis work and what does it treat? remember all three names for this drug

A

Digitalis, or digoxin (Lanoxin), is a “cardiac glycoside” drug often used to treat people with congestive heart failure or atrial fibrillation. Digitalis inactivates the Na+/K+–ATPase pumps in the myocardial cell plasma membrane, interfering with their ability to pump Na+ out of the cell. This increases the reverse activity of the Na+/Ca2+ exchange pumps in the plasma membrane, so that they pump more Na+ out of the cell and more Ca2+ into the cell. As the intracellular concentration of Ca2+ rises, so does the amount of Ca2+ stored in the sarcoplasmic reticulum. This increases the contractility (strength of contraction) of the myocardium, which helps to treat congestive heart failure, and also slows the conduction of the impulses through the AV node, helping to treat atrial fibrillation.

55
Q

What is an aneurysm? Where do they most commonly occur (name two types at this location)? What is dissection? What causes aneurysms?

A

An aneurysm is a balloonlike swelling in an artery or in a weakened ventricular wall. It most commonly occurs in the aorta—either as a thoracic aortic aneurysm or an abdominal aortic aneurysm, but can occur in cerebral and other arteries. A dissected aorta is a tear in the wall of the aortic aneurysm, which often can be detected and corrected before it completely bursts. Aneurysms may result from congenital causes and atherosclerosis, but conditions such as hypertension and diabetes can increase the risk.

56
Q

What is angiogenesis and what conditions is it involved in? What two regulators stimulate angiogenesis? Name two drugs that treat angiogenesis related diseases

A

Angiogenesis is formation of new blood vessels from preexisting vessels, usually venules. It is required for the growth of neoplasms (tumors) and the development of neovascular age-related macular degeneration (wet macular degeneration).
Paracrine regulators fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) stimulate angiogenesis via tyrosine kinases. Bevacizumab (Avastin) is monoclonal antibody that inactivates VEGF to treat cancers of the colon, lung, breast, cervix, ovaries, and kidneys. Ranibizumab (Lucentis), also a monoclonal antibody against VEGF, can be injected into the vitreous humor of the eye to inhibit the angiogenesis of wet macular degeneration.

57
Q

What are varicose veins? What treatments exist?

A

Varicose veins are enlarged surface veins, generally in the lower limbs, which occur when venous congestion stretches the veins to the point that the venous valves no longer close effectively. Walking, compression stockings, and leg elevation can reduce venous congestion. In bedridden patients, flexing and extending the ankle joints helps move blood from the legs to heart. Surgical treatments of varicose veins include sclerotherapy (where chemicals are injected into the veins to scar them), laser therapy (using lasers to destroy the veins), ligation and stripping (tying off and removing the veins), and other techniques.

58
Q

What complications are associated with varicose veins? What prevention and treatments are used?

A

Inadequate venous flow in a bedridden patient increases the risk of Deep Vein Thrombosis (DVT), a dangerous condition that can lead to a venous thromboembolism (a traveling blood clot). Walking around as soon as possible after a surgery reduces the risk, as does the use of compression stockings and devices that compress the leg. Anticoagulant drugs or thrombolytic agents may sometimes be necessary to prevent or treat a thromboembolism so that it doesn’t result in a potentially fatal pulmonary embolism

59
Q

What are Statins? What specific molecule do they target and what is the effect on the body?

A

Statins are drugs that help lower LDL-cholesterol concentrations to reduce the risk of atherosclerosis. Statins are inhibitors of HMG-coenzyme A reductase, the enzyme that catalyzes the rate-limiting step in cholesterol synthesis. The lowered intracellular cholesterol then stimulates the production of more LDL receptors in the plasma membrane, allowing the liver cells to engulf more LDL-cholesterol from the blood. This lowers the blood LDL-cholesterol concentration so that less will enter the endothelial cells of the arteries. Statins also slightly increase the HDL level and they reduce inflammation which promotes atherosclerosis.

60
Q

What should you do to lower the risk of atherosclerosis

A

Exercise! Regular physical activity and exercise provide a degree of “cardioprotection” that reduces the risk of cardiovascular disease directly and through beneficial effects on risk factors such as high blood pressure and high blood lipids. Diet! Should encompass all food groups and contain low amounts of high-calorie/low-nutrient items. Saturated fat and trans fats should be limited to 5% to 6% of total calories (fast food is 40-50% fat calories). Eat fish! They are rich in omega-3 (or n-3) fatty acids, which provide protection against cardiovascular disease. Walnuts, soybeans, and rapeseed (canola) oil are also rich in EPA and DHA, the n-3 fatty acids found in fish. Don’t Smoke! Smoking greatly increases the risk of coronary heart disease, stroke, aortic aneurism, and peripheral vascular disease.