Exam 3 Flashcards

Question

Disorders of erythrocytes Macrocytic anemia: in Vit B12 or Folate deficiency

Answer 1

Macrocytic anemia: in Vit B12 or Folate deficiency

Answer 2

Sickle cell disease: inherited condition, defective hemoglobin molecule Erythrocytes distort into a sickle shape

Answer 3

Leukemia: a form of cancer | Classified as lymphoblastic or myeloblastic

Answer 4

Thrombocytopenia | Abnormally low concentration of platelets

Answer 5

First blood cells develop with the earliest blood vessels Mesenchyme cells cluster into blood islands Late in the second month liver and spleen take over blood formation Bone marrow becomes major hematopoietic organ at month 7

Answer 6

Polycythemia AKA polyvera over production of erythrocytes by bone marrow could be primary or secondary primary – main problem is in bone marrow sign/symptoms – patient has increased RBC, WBC, Platelets increased RBC can cause severe headache, vertigo(from hypertension) spleen accumulates dead RBC = enlargement of spleen(splenomegaly) and liver(hepatomegaly) increased hematocrit weak immune system due to immature WBC increased platelets leads to blood clotting which can lead to organs and block, myocardial infarction or stroke Secondary – artificial due to over secretion of hormone Erythropoietin(on production of RBCs slide) 90% of hormone is secreted by kidney and 10% liver Erythropoietin stimulates bone marrow for production of RBC this is temporary

Answer 7

Normocytic anemia – losing blood volume during pregnancy | normal ish

Answer 8

Microcytic anemia – due to deficiency of ion

Answer 9

Macrocytic anemia – due to deficiency of B12 or folic acid

Answer 10

Sickle cell disease is an inherited blood disorder that affects red blood cells. People with sickle cell disease have red blood cells that contain mostly hemoglobin* S, an abnormal type of hemoglobin. Sometimes these red blood cells become sickle-shaped (crescent shaped) and have difficulty passing through small blood vessels. Hemoglobin – is the main substance of the red blood cell. It helps red blood cells carry oxygen from the air in our lungs to all parts of the body. Normal red blood cells contain hemoglobin A. Normal red blood cells are soft and round and can squeeze through tiny blood tubes (vessels). Normally, red blood cells live for about 120 days before new ones replace them. Hemoglobin S and hemoglobin C are abnormal types of hemoglobin.

Answer 11

RBC has abnormal hemoglobin which carry 4 oxygen molecules deficiency of hemoglobin leads to deficiency of oxygen supply hypoxemia(deficiency of oxygen)

Answer 12

``` Sickle cells are destroyed rapidly in the body of people with the disease causing anemia, jaundice and the formation of pigment gallstones. Almost all patients with sickle cell anemia have painful episodes (crises), which can last from hours to days. These crises can affect the bones of the back, the long bones, and the chest. Attacks of abdominal pain Bone pain Breathlessness Delayed growth and puberty Fatigue Fever Jaundice Paleness Rapid heart rate Ulcers on the lower leg ``` Treatment: They should take supplements of folic acid. Antibiotics and vaccines are given to prevent bacterial infections. ----- Oxygen is last molecule for ATP electron acceptor deficiency of oxygen supply leads to severe headache, weakness, irritates the sensory nerves(abdominal and joint pain), respiratory problems, weak immune system(fever), Jaundice Jaundice is yellowish color of skin due to high level of bilirubin(dead RBCs) 3 types of Jaundice prehepatic damaged RBCs hemolytic hepatic cause is in liver Alcoholics failure of liver important protein production and iron which is important for RBC formation posthepatic closure or obstruction of common bile duct by stone common bile duct carries bile from liver to intestine for emulsification of fat obstruction and closure of duct means failure of release into small intestine bile contains bilirubin Treatment folic acid, iron supplements if bacterial infection then antibiotic too

Answer 13

Oxygen is last molecule for ATP electron acceptor deficiency of oxygen supply leads to severe headache, weakness, irritates the sensory nerves(abdominal and joint pain), respiratory problems, weak immune system(fever), Jaundice Jaundice is yellowish color of skin due to high level of bilirubin(dead RBCs) 3 types of Jaundice prehepatic damaged RBCs hemolytic hepatic cause is in liver Alcoholics failure of liver important protein production and iron which is important for RBC formation posthepatic closure or obstruction of common bile duct by stone common bile duct carries bile from liver to intestine for emulsification of fat obstruction and closure of duct means failure of release into small intestine bile contains bilirubin Treatment folic acid, iron supplements if bacterial infection then antibiotic too

Answer 14

is cancer of the blood cells. It starts in the bone marrow, the soft tissue inside most bones. Bone marrow is where blood cells are made. The bone marrow starts to make a lot of abnormal white blood cells, called leukemia cells. They don't do the work of normal white blood cells, they grow faster than normal cells, and they don't stop growing when they should. Types of leukemia: Acute Chronic Lymphocytic (or lymphoblastic) leukemia affects white blood cells called lymphocytes, it produces large numbers of mature white blood cells (lymphocytes). Myelogenous leukemia affects white blood cells called myelocytes. It produces large numbers of immature and mature white blood cells (myelocytes). ---- Over production of immature WBC immature WBC are not functional and can not protect the body Lymphocytic – patient has large number of mature WBC, extremely high Myeleocytic – mature and immature WBCs

Answer 15

Symptoms: ``` Fever and night sweats Headache Bleeding easily Bone or joint pain Swollen lymph nodes in the armpit, neck Getting a lot of infections weakness Losing weight ``` Treatment: 1. Chemotherapy to kill leukemia cells using strong anti-cancer drugs; 2. Interferon-alpha (INFa) therapy to slow the reproduction of leukemia cells and promote the immune system's anti-leukemia activity; 3. Radiation therapy to kill cancer cells by exposure to high-energy radiation. 4. Stem cell transplantation (SCT) to enable treatment with high doses of chemotherapy and radiation therapy. ``` ---- Patient has weak immune system risk for bacterial infection fever inflammation of lymphatic system weakness, losing weight ``` ``` Treatment chemotherapy interferon-alpha – controls maturation of WBCs radiation stem cell transplantation ```

Answer 16

Composed of three layers (tunics) Tunica intima: composed of simple squamous epithelium Tunica media: sheets of smooth muscle Contraction: vasoconstriction Relaxation – vasodilation Tunica externa: composed of connective tissue Lumen: central blood-filled space of a vessel

Answer 17

Aorta(largest artery in body) -> artery -> arterioles -> capillary -> veniole -> large vein -> SVC/IVC Aorta carries large amount of blood from left ventricle. By contraction of left ventricle we have ejection of large amount of blood into aorta. The pressure that exist in aorta comes from the LEFT VENTRICULAR CONTRACTION which is about 100mmHg. When the blood flow reaches the artery and arteriole the blood pressure decreases to 50mmHg. When it reaches the smaller diameter of the capillary and intersectional area with vein side the capillary shows resistance to blood flow. This is calls “Total Peripheral Resistance(TPR). The pressure drops to 20mmHg. In the veniole and large vein the pressure drops further to 4mmHg. The pressure in SVC and IVC is only 4mmHg. Veins have smooth muscle in their walls which controls blood pressure which is controlled by ANS BP is controlled by alpha 1 neurotransmitter by NE BP = TPR * CO Blood pressure TPS – in capillary for total peripheral resistance CO = cardiac output – the amount of blood ejected from the aorta per minute approximately 5 liters per minute

Answer 18

Arteries: carry blood away from the heart Veins: carry blood toward the heart Capillaries: smallest blood vessels The site of exchange of molecules between blood and tissue fluid

Answer 19

``` 1- Elastic arteries: the largest arteries, High elastin Diameters range from 2.5 cm to 1 cm (aorta and its major branches), also called conducting arteries, ``` 2- Muscular (distributing) arteries 3- Arterioles: Smallest arteries

Answer 20

Conduct blood from capillaries toward the heart Blood pressure is much lower than in arteries Smallest veins – called venules, diameters from 8–100 µm Smallest venules – called postcapillary venules, Venules join to form veins Tunica externa is the thickest tunic in veins Some veins particularly in the limbs have valves Skeletal muscle pump: muscle press the veins and push the blood toward heart vascular anastomoses Vasa vasorum

Answer 21

``` Smallest blood vessels, Diameter from 8–10 µm, RBCs pass through single file Capillary bed: Network of capillaries running through tissues ``` Low permeability capillaries: Blood-brain barrier Highly selective, only vital substances pass through. Not a barrier against O2, CO2 and some anesthetics. Sinusoids: Wide, leaky capillaries found in spleen, liver…

Answer 22

When TPR or CO increases then BP increases = hypertension BP = TPR * CO

Answer 23

Pericardium is a thin membrane which covered heart

Answer 24

Your heart is located between your lungs in the middle of your chest. Pericardium Myocardium Papillary muscle, Chordae tendineae The heart has 4 chambers: left and right atria, left and right ventricles. A wall of muscle called the septum separates the left and right atria and the left and right ventricles. The left ventricle is the largest and strongest chamber in your heart. The left ventricle's chamber walls are only about a half-inch thick, but they have enough force to push blood through the aortic valve and into your body.

Answer 25

Pericardium protects heart from external trauma Myocardium heart muscle Endocardium internal layer of heart walls Chordae tendineae connects valve and papillary muscle 3 papillary on right and 2 on left

Answer 26

Four types of valves regulate blood flow through your heart: 1. The tricuspid valve regulates blood flow between the right atrium and right ventricle. 2. The pulmonary valve controls blood flow from the right ventricle into the pulmonary arteries, which carry blood to your lungs to pick up oxygen. 3. The mitral valve lets oxygen-rich blood from your lungs pass from the left atrium into the left ventricle. 4. The aortic valve opens the way for oxygen-rich blood to pass from the left ventricle into the aorta, your body's largest artery, where it is delivered to the rest of your body.

Answer 27

The tricuspid valve regulates blood flow between the right atrium and right ventricle.

Answer 28

The pulmonary valve controls blood flow from the right ventricle into the pulmonary arteries, which carry blood to your lungs to pick up oxygen.

Answer 29

The mitral valve lets oxygen-rich blood from your lungs pass from the left atrium into the left ventricle.

Answer 30

The aortic valve opens the way for oxygen-rich blood to pass from the left ventricle into the aorta, your body's largest artery, where it is delivered to the rest of your body.

Answer 31

After flowing through the body, blood enters the heart at the right atrium. From the right atrium, it passes through the right atrioventricular valve and into the right ventricle. When the right ventricle contracts, it ejects the blood out of the heart through the pulmonary valve and into the pulmonary artery to the lungs. After passing through the lungs, removing CO2 and picking up oxygen (O2), the blood returns through the pulmonary vein to the left atrium. From here the blood enters the left ventricle through the left atrioventricular valve. When the left ventricle contracts, blood is ejected through the aortic valve into the aorta and out to the body.

Answer 32

Superior and inferior vena cava collect deoxygenated blood from upper and lower parts of the body and release the content into the right atrium. RA contracts and releases its contents into right ventricle through tricuspid valve. The RV contracts and ejects large amount of blood into pulmonary artery. Pulmonary artery then becomes left and right pulmonary arteries which carry deoxygenated blood to lung tissue for gas exchange. After gas exchange in lungs then the lung tissue releases oxygen molecules into pulmonary capillary . The pulmonary capillary becomes the pulmonary veins. Pulmonary veins carry fresh oxygenated blood to left atrium. LA contracts and releases fresh oxygenated blood into left ventricle through the mitral(bicuspid) valve. The LV contracts and ejects large amount of blood into aorta. The aorta carries fresh blood to head and neck, upper limb, and lower part of body. ``` Aorta has 3 parts ascending arch descending enters into abdominal cavity and becomes abdominal aorta which branches to supply organs ```

Answer 33

Systemic circulation is the portion of the cardiovascular system which carries oxygenated blood away from the heart, to the body, and returns deoxygenated blood back to the heart. The term is contrasted with pulmonary circulation. Oxygenated blood from the lungs leaves the left heart through the aorta, from where it is distributed to the body's organs and tissues, which absorb the oxygen, through a complex network of arteries, arterioles, and capillaries. The deoxygenated blood is then collected by venules, from where it flows first into veins, and then into the inferior and superior venae cavae, which return it to the right heart, completing the systemic cycle. The blood is then re-oxygenated through the pulmonary circulation before returning again to the systemic circulation. Systemic circulation connection between body and heart by SVC and IVC which carry deoxygenated blood from body to heart Aorta takes back fresh blood from heart to entire body

Answer 34

Systemic circulation connection between body and heart by SVC and IVC which carry deoxygenated blood from body to heart Aorta takes back fresh blood from heart to entire body

Answer 35

Pulmonary circulation is the portion of the cardiovascular system which carries oxygen-depleted blood away from the heart, to the lungs, and returns oxygenated blood back to the heart. The term is contrasted with systemic circulation. Oxygen-depleted blood from the body leaves the right heart through the pulmonary arteries, which carry it to the lungs, where red blood cells release carbon dioxide and pick up oxygen during respiration. The oxygenated blood then leaves the lungs through the pulmonary veins, which return it to the left heart, completing the pulmonary cycle. The blood is then distributed to the body through the systemic circulation before returning again to the pulmonary circulation. Connection between heart and lungs 2 pulmonary arties carry deoxygenated blood from heart to lungs 4 pulmonary veins carry fresh oxygenated blood from lungs to heart

Answer 36

Connection between heart and lungs 2 pulmonary arties carry deoxygenated blood from heart to lungs 4 pulmonary veins carry fresh oxygenated blood from lungs to heart

Answer 37

Aorta, artery, arteriole contain smooth muscle Innervation is by Alpha 1(vasoconstriction) and Beta 2(relaxation) adrenergic receptors by ANS The pressure that exist in the arteriole system is much higher than in the venous system the pressure comes from ventricular contraction of heart the volume of blood which circulates in arteriole is “stressed volume”(under high pressure) Capillary lacks smooth muscle contains pores for gas exchange, nutrients, fluid to pass through

Answer 38

Arteries - deliver oxygenated blood to the tissues. - are thick-walled, with extensive elastic tissue and smooth muscle. - are under high pressure. - The blood volume contained in the arteries is called the stressed volume.

Answer 39

Arterioles - are the smallest branches of the arteries. - are the site of highest resistance in the cardiovascular system. - have a smooth muscle wall that is extensively innervated by autonomic nerve fibers. - Arteriolar resistance is regulated by the autonomic nervous system (ANS). - Alpha1-Adrenergic receptors are found on the arterioles of the skin, splanchnic, and renal circulations. - Beta2-Adrenergic receptors are found on arterioles of skeletal muscle.

Answer 40

Capillaries - consist of a single layer of endothelial cells surrounded by basal lamina. - are thin-walled. - are the site of exchange of nutrients, water and gases.

Answer 41

Venules | -are formed from merged capillaries.

Answer 42

Veins –progressively merge to form larger veins. The largest vein, the vena cava, returns blood to the heart. -are thin-walled. -are under low pressure. -contain the highest proportion of the blood in the cardiovascular system. -The blood volume contained in the veins is called the unstressed volume. -have alpha 1-adrenergic receptors.

Answer 43

-can be expressed by the following equation: V= Q/A V=velocity (cm/sec) Q=blood flow (ml/min) A= cross-sectional area (cm2) Velocity is directly proportional to blood flow and inversely proportional to the cross-sectional area at any level of the cardiovascular system. For example, blood flow velocity is higher in the aorta than in the sum of all of the capillaries . The lower velocity of blood flow in the capillaries optimizes conditions for exchange of substances across the capillary wall. Velocity depends on cross-sectional area capillary has higher cross sectional area so blood flows slower in capillaries

Answer 44

Velocity depends on cross-sectional area | capillary has higher cross sectional area so blood flows slower in capillaries

Answer 45

-can be expressed by the following equation: Q=P/R Or Cardiac output= Mean arterial pressure- Right atrial pressure Total peripheral resistance (TPR) Q=flow or cardiac output (ml/min) P= pressure gradient (mm Hg) R =resistance or total peripheral resistance (mm Hg/ml/min) - The equation for blood flow (or cardiac output) is analogous to Ohm’s law for electrical circuits (I= V/R), where flow is analogous to current, and pressure is analogous to voltage. - The pressure gradient (P) drives blood flow. - Thus, blood flows from high pressure to low pressure. - Blood flow is inversely proportional to the resistance of the blood vessels. Blood flow depends on QPR and cardiac output

Answer 46

Blood flow depends on QPR and cardiac output

Answer 47

-Poiseuille’s equation gives factors that change the resistance of blood vessels. R= (8 n l)/ (r)(4) R= resistance n= viscosity of blood l=length of blood vessel r4= radius of blood vessel to the fourth power - Resistance is directly proportional to the viscosity of the blood. For example, increasing viscosity by increasing hematocrit will increase resistance and decrease blood flow. - Resistance is directly proportional to the length of the vessel. Resistance depends on diameter of blood vessel(radius) concentration of blood stream(viscosity) length of blood vessel

Answer 48

Resistance depends on diameter of blood vessel(radius) concentration of blood stream(viscosity) length of blood vessel

Answer 49

- describes the distensibility of blood vessels. - is inversely related to elastance. The greater the amount of elastic tissue in a blood vessel, the higher the elastance, and the lower the compliance. - is expressed by the following equation: C=V/P C= capacitance or compliance (ml/mm Hg) V= volume (ml) P=pressure (mm Hg) - is directly proportional to volume and inversely proportional to pressure. - describes how volume changes in response to a change in pressure. - is much greater for veins than for arteries. As a result, more blood volume is contained in the veins (unstressed volume) than in the arteries (stressed volume). - Changes in the capacitance of the veins produce changes in unstressed volume. For example, a decrease in venous capacitance decreases unstressed volume increases stressed volume by shifting blood from the veins to the arteries. - Capacitance of the arteries decreases with age, as a person ages, the arteries become stiffer and less distensible.

Answer 50

More elastic fiber means the wall is thicker(stronger) Less elastic fiber means thinner(weaker) When thick wall in blood vessel then the thickness covers more internal environment and is thicker than venous system The blood flow that exist in artery is a little bit lower than venous system BUT arteriole pressure is much higher than venous system The pressure in venous system is only 4mm Hg Capacity depends on amount of elastic fiber thicker fiber = lower capacity but increased pressure

Answer 51

- As blood flows through the systemic circulation, pressure decreases progressively because of the resistance to blood flow. - Thus, pressure is highest in the aorta and large arteries and lowest in the vena cavae. - The largest decrease in pressure occurs across the arterioles because they are the site of highest resistance. Mean pressure in the systemic circulation are as follows: Aorta, 100 mm Hg Arterioles, 50 mm Hg Capillaries, 20 mm Hg Vena cava, 4 mm Hg

Answer 52

``` Blood pressure (BP) is a force exerted by circulating blood on the walls of blood vessels. -is not constant during a cardiac cycle. It is pulsatile. ``` 1. Systolic pressure - is the highest arterial pressure during a cardiac cycle. - is measured after the heart contracts (systole) and blood is ejected into the arterial system. 2. Diastolic pressure - is the lowest arterial pressure during a cardiac cycle. - is measured when the heart relaxed (diastole) and blood is returning to the heart via the veins. 3. Pulse pressure -is the different between the systolic and diastolic pressures. -The most important determinant of pulse pressure is stroke volume. As blood is ejected from the left ventricle into the arterial system, systolic pressure increases because of the relatively low capacitance of the arteries. Because diastolic pressure remains unchanged during ventricular systole, the pulse pressure increases to the same extent as the systolic pressure. -Decreases in capacitance, such those that occur with the aging process, cause increases in pulse pressure. 4. Mean arterial pressure - can be calculated approximately as diastolic pressure plus one-third of pulse pressure.

Answer 53

Systolic pressure pressure that exist in ventricle during contraction Diastolic pressure pressure that exist in in ventricle during relaxation Pulse pressure difference between systolic and diastolic ``` Clinical point arteriole pressure(any artery) is higher than venous pressure venous pressure is higher than atrial pressure(atrium in heart) ```

Answer 54

- is very low. - The veins have a high capacitance and therefore, can hold large volumes of blood at low pressure. 2 factors valve in vein skeletal muscle covers veins contraction of skeletal muscle then it increases pressure which is helpful for blood flow in venous system

Answer 55

Atrial pressure - is even lower than venous pressure. - Left atrial pressure is estimated by the pulmonary wedge pressure. A catheter, inserted into the smallest branches of the pulmonary artery, makes almost direct contact with the pulmonary capillaries. The measured pulmonary capillary pressure is approximately equal to the left atrial pressure.

Answer 56

Environmental factors (dietary Na+, obesity, and stress), whatever the responsible pathogenic mechanisms, they must lead either to increased total peripheral vascular resistance (TPR) by inducing vasoconstriction or to increased cardiac output (CO), or both. Because BP =CO x TPR (resistance). Sympathetic nervous system and renin-angiotensin-aldosteron system have received the most attention for the pathophysiology of hypertension, both can increase CO and TPR. Na+: Abnormal Na+ transport across the cell wall due to a defect in or inhibition of the Na+/K+ pump or because of increased permeability to the Na+. Increased intracellular Na+, which makes the cell more sensitive to sympathetic stimulation. Since Ca2+ follows Na+, accumulation of intracellular Ca2+ is responsible for the increased sensitivity. Deficiency of a vasodilator substance: prostaglandin, bradykinin.

Answer 57

Know this slide. Its on test What is blood pressure? the pressure that exist in blood vessels from blood flow on wall of blood vessel BP = CO * TPR TPR – resistance in capillaries CO – cardiac output the amount of blood per minute is about 5 liters Hyper tension types Primary Secondary We do not know the exact cause of primary hypertension secondary we know and can treat Obesity which is associated with endocrine disorder(like type 2 diabetes) stress increases cortisol hormone(stress hormone) increases appetite which causes obesity increases TPR and systolic and diastolic pressures Clinical point Tumor in sympathetic system over stimulation/secretion of NE leads to alpha 1 oversecretion = vasoconstriction ***any factor(s) which leads to contraction or vasoconstriction, obstruction, or destruction of BV leads to hypertension After depolarization then calcium enter cells Ca2+ is extremely important for contraction of any muscle Hypercalcemia leads to hyper tension hypocalcemia can impact heart function and blood pressure Prostaglandid and bradykinin are vasodilators deficiency of these causes hypertension

Answer 58

Secondary hypertension can be caused by conditions that affect your kidneys, arteries, heart or endocrine system. Secondary hypertension can also occur during pregnancy. 1. Disorders of the adrenal gland 2. Cushing's syndrome (a condition caused by an overproduction of cortisol) 3. Hyperaldosteronism (too much aldosterone) 4. Pheochromocytoma (a rare tumor that causes over secretion of hormones like adrenaline and NA). 5. Kidney disease: polycystic kidney disease, kidney tumor, kidney failure, or a narrow or blocked main artery supplying the kidney. 6. Drugs: such as corticosteroids (anti-inflammatory drugs like prednisone), leads to increased systolic, diastolic pressures and increases arterial resistance.7. Nonsteroidal anti-inflammatory drugs (Motrin, Aleve,), weight loss drugs (such as Meridia). Salt and water retention, sympathetic activity, loss of renal vasodilation. 8. Coarctation of the aorta, a birth defect in which the aorta is narrowed 9. Preeclampsia, a condition related to pregnancy, endothelial dysfunction in the maternal blood vessels. 10. Thyroid and parathyroid problems

Answer 59

Know this slide – on test Adrenal gland adrenal cortex surrounds adrenal medulla adrenal cortex secretes 3 hormones aldosterone when BP is low then enzyme Renin is secreted from kidney Renin converts Angiotensinogen(from liver protein) into Ag1(inactive form) ACE(from lung tissue) converts AG1 -> Ag2 Ag2 acts as vasoconstrictor aldosterone release from adrenal cortex in to blood stream blood stream carries Aldosterone to nephron in kidney Aldosterone binds to its receptor on nephron collecting tubule Capillary then absorbs Na+, Cl-, H2O, and HCO3- into blood H+ and K+ release into urine ***this means fluid absorption which increases blood pressure cortisol increases TPR, systolic, and diastolic pressures androgen adrenal medulla adrenaline(aka epinepherine) noradrenaline(aka NE) binds to alpha 1 adrenergic receptor leading to vasoconstriction all but androgen if oversecreted lead to hypertension

Answer 60

``` Usually asymptomatic Headache Fatigue Shortness of breath Dizziness Convulsion Changes in vision (Blurred vision, Double vision) Nausea Vomiting Anxiety Increased sweating Nose bleeds Tinnitus - ringing or buzzing in ears Heart palpitations General feeling of unwellness Increased urination frequency Flushed face Pale skin ``` ---- Severe headache, vomiting, anxiety, sweating, sleep disorder, vertigo, palpitation, nose bleeding, weakness

Answer 61

Angiotensin-converting enzyme (ACE) inhibitors, Captopril, Ramipril Angiotensin || receptor blockers (ARBs) , Valsartan Diuretics, Thiazide diuretics such as hydrochlorothiazide Calcium channel blockers, Felodipine, Benidipine Beta-adrenergic blocking agents, Propranolol ---- ACE inhibitors can block ACE Ag2 receptor blockers Aldosterone receptor blockers spironolactone

Answer 62

The P wave represents the wave of depolarization that spreads from the SA node throughout the atria, and is usually 0.08 to 0.1 seconds (80-100 ms) in duration. -represents atrial depolarization. -does not include atrial repolarization, which is buried in the QRS complex. ``` ---- P wave first half is depolarization and contraction of right atrium second half is left atrium relaxation phase can not be seen on EKG might be part of Q ```

Answer 63

The period of time from the onset of the P wave to the beginning of the QRS complex is termed the P-R interval, which normally ranges from 0.12 to 0.20 seconds in duration. This interval represents the time between the onset of atrial depolarization and the onset of ventricular depolarization. *** If the P-R interval is >0.2 sec, there is an AV conduction block. ``` ---- PR interval between P wave and QRS complex depolarization and stimulation of AV node 0.1 -0.2 seconds ```

Answer 64

The duration of the QRS complex is normally 0.06 to 0.1 seconds. This relatively short duration indicates that ventricular depolarization normally occurs very rapidly. *** If the QRS complex is prolonged (> 0.1 sec), conduction is impaired within the ventricles. This can occur with bundle branch blocks or whenever a ventricular foci (abnormal pacemaker site) becomes the pacemaker driving the ventricle. ***Ectopic foci are abnormal pacemaker sites within the heart (outside of the SA node) that display automaticity. Such an ectopic foci nearly always results in impulses being conducted over slower pathways within the heart, thereby increasing the time for depolarization and the duration of the QRS complex. ---- QRS complex duration 0.06-0.1 second shows depolarization and contraction of both ventricles Ectopic foci abnormal contraction of ventricle example post myocardial infarction the healed tissue may have spontaneous depolarization which can send signals to different parts of heart may shows multiple QRS back to back on EKG

Answer 65

-is the segment from the end of the S wave to the beginning of the T wave. -represents the period when the ventricles completely are depolarized. *** The ST segment is important in the diagnosis of ventricular ischemia or hypoxia because under those conditions, the ST segment can become either depressed or elevated. ---- ST segment between WRS complex and T wave T wave is relaxation phase of ventriculars between depolarization and repolarization of ventricles Clinical point elevated or depressed ST segment shows positive sign for myocardial infarction

Answer 66

The T wave represents ventricular repolarization and is longer in duration than depolarization (i.e., conduction of the repolarization wave is slower than the wave of depolarization). Sometimes a small positive U wave may be seen following the T wave. This wave represents the last remnants of ventricular repolarization. Inverted or prominent U waves indicates underlying pathology or conditions affecting repolarization. ----- T Wave repolarization and relaxation of ventricles

Answer 67

-is the interval from the beginning of the Q wave to the end of the T wave. The Q-T interval represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential. This interval can range from 0.2 to 0.4 seconds depending upon heart rate. * ** At high heart rates, ventricular action potentials shorten in duration, which decreases the Q-T interval. Because prolonged Q-T intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias. - represents the entire period of depolarization and repolarization of the ventricles. ---- QT interval 0.2-0.4 seconds shows contraction and relaxation of both ventricles Tachyarrhythmias abnormal especially the contraction

Answer 68

-have stable resting membrane potentials of about -90mV. This value approaches the K+ equilibrium potential. -Action potential are of long duration, especially in Purkinje fibers, where they last 300 msec. -is the upstroke of the action potential. -is caused by a transient increase in Na+ conductance. This increase results in an inward Na+ current that depolarizes the membrane. At the peak of the action potential, the membrane potential approaches the Na+ equilibrium potential. ---- Phase 0 opening of sodium channels which enters cells leads to depolarization of atrial ventricular Purkinje fiber cells Phase 1 potassium ions leave cells

Answer 69

- is a brief period of initial repolarization. - Initial repolarization is caused by an outward current, in part because of the movement of K+ ions (favored by both chemical and electrical gradients) out of the cell and in part because of a decrease in Na+ conductance.

Answer 70

–is the plateau of the action potential - is caused by a transient increase in Ca2+ conductance, which results in an inward Ca2+ current, and by an increase in K+ conductance. - During phase 2, outward and inward currents are approximately equal, so the membrane potential is stable at the plateau level.

Answer 71

- is repolarization. - During phase 3, Ca2+ conductance decreases, and K+ conductance increases and therefore predominates. - The high K+ conductance results in a large outward K+ current (Ik) which hyperpolarizes the membrane back toward the K+ equilibrium potential.

Answer 72

- is the resting membrane potential. - is a period during which inward and outward current (Ik1) are equal and the membrane potential approaches the K= equilibrium potential.

Answer 73

- is normally the pacemaker of the heart. - has an unstable resting potential. -is upstroke of the action potential. -is caused by an increase in Ca2+ conductance. This increase causes an inward Ca2+ current that drives the membrane potential toward the Ca+ equilibrium potential. -The ionic basis for phase 0 in SA node is different from that in the ventricles, atria and Purkinje fibers (where it is result of an inward Na+ current.)

Answer 74

Phases 1 and 2 | -are not present in the SA node action potential.

Answer 75

- is repolarization. - is caused by an increase in K+ conductance. This increase results in an outward K+ current that causes repolarization of the membrane potential.

Answer 76

- is slow depolarization. - accounts for the pacemaker activity of the SA node (automaticity). - is caused by an increase in Na+ conductance, which results in an inward Na+ current called If (slow depolarization, produced by the opening of Na+ channels and an inward Na+ current called If). (“f” which stands for funny).

Answer 77

Upstroke of the action potential in the AV node is the result of an inward Ca+ current (as in the SA node).

Answer 78

- reflects the time required for excitation to spread throughout cardiac tissue. - depends on the size of the inward current during the upstroke of the action potential. The larger the inward current the higher the conduction velocity. - is fastest in the Purkinje system. - is slowest in the AV node, allowing time for ventricular filling before ventricular contraction. If conduction velocity through the AV node is increased, ventricular filling may be compromised.

Answer 79

- is the ability of cardiac cells to initiate action potentials in response to inward, depolarizing current. - reflects the recovery of channels that carry the inward currents for the upstroke of the action potential. - Changes over the course of the action potential. These changes in excitability are described by refractory periods. ``` 1. Absolute refractory period (ARP) No action potential can be initiated. (absolute means absolutely no stimulus is large enough to generate another action potential). ``` 2. Effective refractory period (ERP) ERP is slightly longer than. (effective means that a conducted action potential cannot be generated). 3. Relative refractory period (RRP) Action potential can be elicited but more than the usual inward current is required. RRP begins at the end of the absolute refractory period and continues until the cell membrane has repolarized to about -70mV. During RRP it is possible to generate a second action potential (which is an abnormal configuration and shortened plateau phase).

Answer 80

No action potential can be initiated. (absolute means absolutely no stimulus is large enough to generate another action potential).

Answer 81

ERP is slightly longer than. (effective means that a conducted action potential cannot be generated).

Answer 82

Action potential can be elicited but more than the usual inward current is required. RRP begins at the end of the absolute refractory period and continues until the cell membrane has repolarized to about -70mV. During RRP it is possible to generate a second action potential (which is an abnormal configuration and shortened plateau phase).

Answer 83

SA node depolarization sends signal to AV node AV node is located in right atrium intraatrial septum and intraatrial membrane Then bundle of HIS AKA AV bundle becomes 2 branches left and right branches

Answer 84

Clinical point | elevated or depressed ST segment shows positive sign for myocardial infarction

Answer 85

Phase 0 opening of sodium channels which enters cells leads to depolarization of atrial ventricular Purkinje fiber cells Phase 1 potassium ions leave cells Phase 2 during p2 opening of Ca2+ channels to enter cell Phase 3 opening of K+ channels to leave the cell Phase 4 K+ should reach equilibrium potential(-85mv)

Answer 86

Absolute refractory period when there is second stimulus during phase 0 the cell membrane cannot accept the stimulus and it can not show any reaction to the second stimulus Effective refractory period when there is second stimulus during phase 1 or 2 it can accept it but cannot show any reaction has effect but no reaction Relative refractory period when there is second stimulus during phase 3 the cell membrane accepted and it shows reaction to second stimulus

Answer 87

The second type of cells found in the heart are nodal or conducting cells. These cells contract very weakly because they contain very few contractile elements (myofibrils). These special cells are able to spontaneously generate action potentials without the help of nervous input like regular neurons. Along with this special property of self-excitability, they can also rapidly conduct the action potentials to atrial and ventricular muscle. Thus, these specialized cells provide a self-excitatory system for the heart to generate impulses and a transmission system for rapid conduction of the impulses throughout the heart. Although nearly all of the cells in the heart can spontaneously generate action potentials, the sinoatrial node (or SA node) is generally the site of origin. The SA node is located in the upper posterior wall of the right atrium, and it is the first area to spontaneously depolarize, producing an action potential; this is why it is called the pacemaker of the heart. The action potential travels through the atria to the atrial-ventricular node (AV node) and then to the Bundle of His. From the Bundle of His, the action potential travels through the Purkinje Fibers and then to the ventricular muscle.

Answer 88

Once the action potential is generated at the SA node, it travels throughout the heart in a highly coordinated manner. From the SA node, the action potential spreads throughout the atrial muscle, causing it to contract. From the atria, the action potential travels to the ventricles. However, the atria are electrically isolated from the ventricles by a fibrous tissue. Therefore, the action potential cannot jump directly down to the ventricles. The action potential must first travel through the atrio-ventricular (AV) node. Once through the AV node, the action potential travels through each branch of the Bundle of His down to the apex of the heart. From here, the action potential propagates through the Purkinje Fibers, which rapidly distribute the action potential to the ventricular muscle which then contracts. ------ Myocardial tissue is full of mitochondria to produce ATP for ion pump and strong contraction The type of junctions used are tight and gap junctions

Answer 89

Chronotropic effects - produce changes in heart rate. - A negative chronotropic effect decreases heart rate by decreasing the firing rate of the SA node. - A positive chronotropic effect increases heart rate by increasing the firing rate of the SA node. Dromotropic effects - produce changes in conduction velocity, primarily in the AV node. - dromotropic effect decreases conduction velocity through the AV node, slowing the conduction of action potentials from the atria to the ventricles and increasing the PR interval. - A positive dromotropic effect increases conduction velocity through the AV node, speeding the conduction of action potentials from the atria to the ventricles and decreasing the PR interval. Inotropic effects A negative inotropic decreases force of contraction, a positive inotropic effect increases force of contraction.

Answer 90

Chronotropic = heartrate Dromotropic = conduction velocity Inotropic = contractility of myocardium

Answer 91

Sympathetic - β1-rec: +ve Chronotropic - β1-rec: +ve Dromotropic - β1-rec: +ve inotropic vasodilatation Parasympathetic - ve Chronotropic - ve inotropic - ve Dromotropic vasoconstriction

Answer 92

At rest, a normal heart beats around 50 to 99 times a minute.

Answer 93

It results from abnormalities in impulse formation or in impulse conduction, Disturbances in the formation of impulses lead to change in the sinus rhythm. Sinus tachycardia: If sinus frequency rises above 100/min (exercise, psychic excitation, fever, rise of 10 beats/min. Sinus bradycardia: If it drops below 50-60/min.In both cases the rhythm is regular. ---- Arrhythmia means abnormal contraction which is not enough for ejection of large amount of blood into blood vessels could be atrial or ventricular

Answer 94

At rest, a normal heart beats around 50 to 99 times a minute. Sinus tachycardia: If sinus frequency rises above 100/min (exercise, psychic excitation, fever, rise of 10 beats/min.

Answer 95

At rest, a normal heart beats around 50 to 99 times a minute. Sinus bradycardia: If it drops below 50-60/min.In both cases the rhythm is regular.

Answer 96

Abnormal or ectopic (heterotopic) impulses may arise in the atria (atrial), in the AV node (nodal) or in the ventricle (ventricular). The impulses from an atrial (or nodal) ectopic focus are transmitted to the ventricle, which thus thrown out of its sinus rhythm :supraventricular arrhythmia due to atrial or nodal extrasystole (ES). In atrial ES the P wave is deformed but the QRS complex is normal. In nodal extrasystole, stimulation of the atria is retrograde; the P wave is thus negative and is either masked by the QRS wave or appears shortly after it. Because in supraventricular extrasystole the sinus nodes often also depolarize.

Answer 97

Supraventricular arrhythmia AKA atrial arrhythmia when atrium receives extra signal(stimulus) from different part of ventricle which is not part of conductive system 2 factors post myocardial infarction the healed tissue may have spontaneous depolarization which sends signal to different part of ventricle and atrium. When atrium receives that type of signal the P wave is negative on EKG could be due to different ions such as hypercalcemia. Increased blood calcium can impact contractility of myocardium and increases the heart rate

Answer 98

Ventricular premature complexes (VPCs) are ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular arrhythmia In this case the QRS complex of the ES is deformed. Two common mechanisms exist for VPCs, (1) automaticity, (2) reentry, and as follows: 1. Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC. Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium. 2. Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. The slow-conducting tissue could be due to damaged myocardium, as in the case of a healed MI. ---- Ventricular extrasystole(ventricular arrythmia) after T wave there is the QRS complex.

Answer 99

Ischemia hypoxemia due to obstruction of BV which leads to deficiency of oxygen supply to tissues Medicine side effects long term or high dosage of medicines Digoxin – medicine for patients with flutter/fibrillation. The medicine helps for strong contractions of ventricles and atriums. Decreases the heart rate. High dosage of this medicine can cause extracystole Myocarditis inflammation of myocardium impacts the contractility of the muscle Cardiomyopathy hypertrophic or dilated when the muscle ventricle becomes hypertrophile(thicker) then it occupies the internal environment of the ventricle and impacts the contractility of the myocardium Hypoxia respiratory disorder, lung disorder, anemia, heart problem, decreased RBC, or some diseases Hypercapnia(CO2 poisoning) rate of CO2 is high in blood due to lung problems, abnormal cell respiration tissue cannot receive sufficient amounts of oxygen for cell respiration. The heart should compensate and contract faster Mitral valve collapse if there is any problem with mitral valve then it impacts the contractility Smoking, alcohol, drugs, cocaine decreases oxygen and increases CO2 levels Magnesium and potassium deficiency Mg controls Calcium deficiency of Mg can lead to hypercalcemia K+ deficiency means failure of repolarization phase which is relaxation phase of muscle after each contraction Calcium excess hypercalcemia Thyroid problems stimulates the beta 1 adrenergic receptor and noradrenaline beta 1 = contractility of myocardium hyperthyroidism has palpitation and excess contractility of myocardial, heartrate, and hypertension Heart attach postmyocardial infarction

Answer 100

List of possible causes: ``` Ischemia Certain medicines such as digoxin, which increases heart contraction Myocarditis Cardiomyopathy hypertrophic or dilated Hypoxia Hypercapnia (CO2 poisoning) Mitral valve prolapse Smoking Alcohol Drugs such as cocaine Caffeine Magnesium and potassium deficiency Calcium excess Thyroid problems Heart attack ```

Answer 101

Symptoms Chest pain Faint feeling Fatigue Hyperventilation (after exercise) Frequent episodes of continuous PVCs becomes a form of ventricular tachycardia (VT), which is a rapid heartbeat, because there is an extra electrical impulse, causing an extra ventricular contraction.

Answer 102

PVCs can often be resolved by 1. restoring the balance of magnesium, calcium and potassium within the body. 2. Pharmacological agents Class I agents Sodium channel blockers . Class I agents are grouped by what effect they have on the Na+ channel, and what effect they have on cardiac action potentials. Lidocaine, Phenytoin. Class II agents Beta blockers. They act by blocking the effects of catecholamines at the β1-adrenergic receptors, thereby decreasing sympathetic activity on the heart. They decrease conduction through the AV node. Class II agents include atenolol, propranolol, and metoprolol. Class III Block the potassium channels, thereby prolonging repolarization. Since these agents do not affect the sodium channel, conduction velocity is not decreased. Sotalol ``` Class IV agents Calcium channel blockers. They decrease conduction through the AV node, and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure. However, in contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility.Class IV agents include verapamil and diltiazem. ----- Know lidocaine sodium channel blocker ``` Know class 1 and 2 agents

Answer 103

Atrial tachycardia is a rhythm disturbance that arises in the atria. Heart rates during atrial tachycardia are highly variable, with a range of 100-250 beats per minute (bpm). The atrial rhythm is usually regular.

Answer 104

It results from a rapid sequence of ectopic ventricular impulses. Beginning with ES. Ventricular filling and cardiac output decrease and ventricular fibrillation can even ensue, that is a high frequency uncoordinated twitching of the myocardium. Unless treated the failure to eject blood can be just as dangerous as cardiac arrest.with a rate between 120 and 250 beats per minute.

Answer 105

PR is depolarization of AV node sometimes AV node block First degree a little longer then 0.2 seconds between Second degree multiple P between QRS Third degree multiple P one QRS then no more QRS

Answer 106

PR interval in the normal heart, this time is 0.12 to 0.20 second in duration, damage to AV node causes slowing of impulse conduction and is reflected by changes in the PR interval. This condition is AV node block. First degree AV node block PR interval exceeds 0.20 second Second degree AV node block occurs when the AV node is damaged so severely that only one out of every two, three, or four atrial electrical waves can pass through to the ventricles. ECG: P waves without associated QRS waves. Third-degree, or complete, AV node block, non of the atrial waves can pass through the AV node to the ventricles. Result is bradycardia.

Answer 107

There are two principal types of myocardial cells (myo = muscle, cardio = heart): contractile cells, which have similar features to skeletal muscle cells and nodal/conducting cells that have features similar to nerve cells. The contractile cells of the heart contain the same contractile proteins actin and myosin arranged in bundles of myofibrils surrounded by a sarcoplasmic reticulum. ---- Gap junction act as channel for K, Na, Ca ions Tight junctions

Answer 108

They differ from skeletal muscle by having only one nucleus but far more mitochondria. In fact, one-third of their volume is taken up by mitochondria. These cells are extremely efficient at extracting oxygen; they extract roughly 80% of the oxygen from the passing blood—about twice the amount of other cells. The cells are much shorter, are branched, and are joined together by special structures called intercalated discs. These structures contain tight junctions that bind the cells together, while gap junctions allow for the movement of ions and ion currents between the myocardial cells. Because of the gap junctions, the myocardial cells of the heart can conduct action potentials from cell to cell without the need for nerves.

Answer 109

The action potential (AP) spreads from the cell membrane into the T tubules. During the plateau of AP, Ca2+ conductance is increased and Ca2+ enters the cell from extracellular fluid (inward Ca2+ current). This Ca2+ entry triggers the release of even Ca2+ from the SR (Ca2+ induced Ca2+ release). As a result of this Ca2+ release, intracellular (Ca2+) increases. Ca2+ binds to troponin C, and tropomyosin is moved out of the way, removing the inhibition of action and myosin binding. Actin and myosin binds, the thick and thin filaments slide past each other, and the myocardial cell contracts. Relaxation occurs when Ca2+ is reaccumulated by the SR by an active Ca2+-ATPase pump.

Answer 110

- is the intrinsic ability of the cardiac muscle to develop force at a given muscle length. It is also called inotropism. - is related to the intracellular Ca2+ concentration. - can be estimated by the ejection fraction (stroke volume/end-diastolic volume), which is normally 0.55 (55%). - Positive inotropic agents produce an increase in contractility. - Negative inotropic agents produce a decrease in contractility. Factors that increase contractility (positive inotropism) 1. Increased heart rate - More AP occur per unit time, more Ca2+ enters the myocardial cells during the AP plateaus, more Ca2+ is released from the SR, and greater tension is produced during contraction. 2. Sympathetic stimulation - Increases the inward Ca2+ current during the plateau of each cardiac action potential. - It increases the activity of the Ca2+ pump of the SR as a result more Ca2+ is accumulated by the SR and thus more Ca2+ is available for release in subsequent beats. 3.Cardiac glycoides (digitalis)

Answer 111

Calcium is extremely important ion for muscle contraction any calcium disorder either hypercalcemia or hypocalcemia can impact the muscle contraction of ventricle ``` The factors that increase the contractility(inotropic) of myocardium blood calcium stimulation of sympathetic system over secretion of norepinephrine digitalis(dioxine medicine) ```

Answer 112

- Parasympathetic (Ach) via muscarinic receptors - decrease the force of concentration in the atria by decreasing the inward Ca2+ current during the plateau of the cardiac action potential. ---- Parasympathetic, vagus nerve, and Ach

Answer 113

1. Preload - is equivalent to end-diastolic volume, which is related to right atrial pressure. - When venous return increases, end-diastolic volume increases and stretches or lengthens the ventricular muscle fibers. 2. Afterload -for the left ventricle is equivalent to aortic pressure. Increases in aortic pressure cause an increase in afterload on the left ventricle. -for the right ventricle is equivalent to pulmonary artery pressure. Increases in pulmonary artery pressure cause an increase in afterload on the right ventricle. 3. Saromere length - determines the maximum number of cross-bridges that can form between actin and myosin. - determines the maximum tension, or force of contraction. 4. Velocity of contraction at a fixed muscle length - Velocity of contraction is maximal when the afterload is zero. - Velocity of contraction is decreased by increases in afterload. 5. Frank-Starling relationship

Answer 114

Preload AKA end diastolic volume the volume of blood which exist in ventricle during relaxation phase and the pressure in ventricle the amount of blood in each ventricle is approximately 140mL during relaxation phase(dilation phase) Afterload the pressure that comes to aorta or pulmonary trunk by each ventricular contraction Frank-Starling relationship

Answer 115

Describes the increases in stroke volume and cardiac output that occur in response to an increase in venous return or end-diastolic volume. - is based on the length-tension relationship in the ventricle. Increases in end-diastolic volume cause an increase in ventricular fiber length, which produces an increase in developed tension. - is the mechanism that matches cardiac output to venous return. The greater the venous return, the greater the cardiac output. - Changes in contractility shift the Frank-Starling curve upward (increased contractility) or downward (decreased contractility). - --Increases in contractility cause an increase in cardiac output for any level of right atrial pressure or end-diastolic volume. - --Decreases in contractility cause a decrease in cardiac output for any level of right atrial pressure or end-diastolic volume.

Answer 116

When length of fiber increases then the contractility of myocardium is increased Increase VR -> up EDV -> up L/T -> up CO Up VR -> 140ml -> up Ca2+ release from SR -> binding Ca2+ with Troponin C because of this we have strong contraction of myocardium which increases cardiac output(CO)

Answer 117

a. 1---2 (isovolumetric contraction) b. 2---3 (ventricular ejection) c. 3---4 (isovolumetric relaxation) d. 4---1 (ventricular filling)

Answer 118

This begins with the ventricles depolarizing (QRS complex) then contracting. The left ventricle is filled with blood from the left atrium and its volume is about 140 ml (end-diastolic volume). Ventricular pressure is low because the ventricular muscle is relaxed. On excitation, the ventricle contracts and ventricular pressure increases. The mitral valve closes when left ventricular pressure is greater than left atrial pressure. Because all valves are closed, no blood can be ejected from the ventricle (isovolumetric).

Answer 119

The aortic valve opens at point 2 when pressure in the left ventricle exceeds pressure in the aorta. Blood is ejected into the aorta, and ventricular volume decreases. The volume that is ejected in this phase is the stroke volume. The volume remaining in the left ventricle at point 3 is end-systolic volume.

Answer 120

At point 3, the ventricle relaxes. When ventricular pressure decreases to less than aortic pressure, the aortic valve closes. Because all of the valves are closed again, ventricular volume is constant (isovolumetric) during this phase.

Answer 121

Once left ventricular pressure decreases to less than left atrial pressure, the mitral (AV) valve opens and filling of the ventricle begins. During this phase, ventricular volume increases to about 140 ml (the end-diastolic volume).

Answer 122

a. Increased preload - refers to an increase in end-diastolic volume and is the result of increased venous return. - causes an increase in stroke volume based on the Frank-Starling relationship. - The increase in stroke volume is reflected in increased width of the pressure-volume loop. b. Increased afterload - refers to an increase in aortic pressure. - The ventricle must eject blood against a higher pressure, resulting in a decrease in stroke volume. - The decrease in stroke volume is reflected in decreased width of the pressure-volume loop. - The decrease in stroke volume results in an increase in end-systolic volume. c. Increased contractility - The ventricle develops greater tension than usual during systole, causing an increase in stroke volume. - The increase in SV results in a decrease in end-systolic volume.

Answer 123

1. Stroke volume - is the volume ejected from the ventricle on each beat. Stroke volume= End-diastolic volume - End-systolic volume 2. Cardiac output CO= Stroke volume x Heart rate 3. Ejection fraction - is the fraction of the end-diastolic volume ejected in each stroke volume. - is related to contractility. - is normally 0.55, or 55%. EF = Stroke volume End-diastolic volume

Answer 124

- is directly related to the amount of tension developed by the ventricles. - is increased by: Increased afterload (increased aortic pressure) Increased size of the heart Increased contractility Increased heart rate

Answer 125

CA (Cardiac output) = O2 consumption/O2 pulmonary vein-O2 pulmonary artery

Answer 126

In order for blood to be ejected from the heart, the pressure in the ventricles must be greater than the pressure in the aorta. When the pressure in the left ventricle rises above 80 mmHg (which is the pressure in the aorta), the aortic valve opens. Immediately, blood pours out of the ventricles, while the pressure continues to increase to 120 mmHg. The period during which the ventricles empty blood into the aorta is known as the ejection period.

Answer 127

The opening of heart valves is a slowly developing process and produces no sound. However, when they close, the vanes of the valves and the surrounding fluid vibrate under the influence of sudden pressure differences, producing sounds that travel in all directions through the chest. The first heart sound is produced (indirectly) by the closure of the AV valves; it is of low pitch and of relatively long duration. The second heart sound is produced (indirectly) by the closing of the aortic and pulmonary semilunar valves; this is of high pitch and of relatively smaller duration. A third heart sound sometimes occurs in the middle of diastole. This is caused by blood flowing with rumbling motion into the almost filled ventricles; it is difficult to hear with a stethoscope.

Answer 128

Cardiac output (CO) is the amount of blood each ventricle can pump in one minute. At rest, the cardiac output is roughly 5 liters (1.3 gallons) of blood every minute. During vigorous exercise, this can increase up to 20 l/min (5.2 gallons/min) in a normal individual and up to 35 to 40 l/min (10 gallons/min) in a highly trained athlete. CO can be calculated using equation 5. Heart rate (HR) is the number of times the heart beats in one minute, and stroke volume (SV) is the amount of blood pumped by one ventricle during one contraction/heartbeat. At rest, the heart rate is 70 beats per minute (bpm) and the stroke volume is roughly 70 ml/beat. Using equation 5, a CO of roughly 5 l/min is determined. During exercise, CO increases dramatically in order to supply the working muscles with more oxygen and nutrients. This increase in CO is achieved by increasing either HR, SV, or both.

Answer 129

CO = (SV)(HR) volume of blood leacing the heart/time = (amount of blood leaving the heart with ventricular contraction)(# of times the heart beats/time)

Answer 130

The autonomic nervous system (ANS) exerts a powerful control over heart rate and force of contraction. This is because the heart is innervated by both the parasympathetic nervous system (PSYN) and the sympathetic nervous system (SYN). The parasympathetic nerves are distributed mainly to SA and AV nodes and to a lesser extent to atrial and ventricular muscles. Sympathetic nerves are distributed to the same areas but with a stronger innervation to the ventricular muscle. The PSYN will decrease heart rate by affecting both the SA node and AV node and will (to a lesser extent) decrease the force of contraction of the heart. The SNS, on the other hand, will have the opposite effect, increasing the heart rate and force of contraction. If all these influences from the ANS were removed, the heart would beat at its own natural rhythm of roughly 100 bpm. Yet, the resting heart rate of a normal individual is roughly 70 bpm. Why this difference? The answer is quite interesting: in an individual at rest, there is constant activity from the PSYN keeping the heart rate slowed to roughly 70 bpm!

Answer 131

Atherosclerosis is patchy intimal plaques (atheromas) in medium and large arteries; the plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue. This disease happens when the arteries get blocked by fats and cholesterol. Atherosclerosis can affect all large and medium-sized arteries, including the coronary, carotid, and cerebral arteries, the aorta, its branches, and major arteries of the extremities

Answer 132

Causes: Dyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension Smoking The hallmark of atherosclerosis is the atherosclerotic plaque, which contains lipids (intracellular and extracellular cholesterol and phospholipids) inflammatory cells (eg, macrophages, T cells) smooth muscle cellsconnective tissue (eg, collagen, elastic fibers)thrombiCa++ deposits. Symptoms: Shortness of breath Tightening pain in the chest Complications: Strokes Damage of muscles, body organs and blood vessels Deficiency of blood supply due to obstruction (angina)

Answer 133

All stages of atherosclerosis—from initiation and growth to complication of the plaque—are considered an inflammatory response to injury. Endothelial injury is thought to have a primary role. - Endothelial dysfunction and inhibits endothelial production of nitric oxide, a potent vasodilator and anti-inflammatory molecule. - Such blood flow also stimulates endothelial cells to produce adhesion molecules, which recruit and bind inflammatory cells. The net effect is endothelial binding of monocytes and T cells, migration of these cells to the subendothelial space, and initiation and perpetuation of a local vascular inflammatory response. Monocytes in the subendothelium transform into macrophages. macrophages in the plaque produce some enzymes which digest the fibrous cap, particularly at the edges, causing the cap to thin and ultimately rupture. Lipids in the blood, particularly low density lipoprotein (LDL) and very low density lipoprotein (VLDL), also bind to endothelial cells and are oxidized in the subendothelium.

Answer 134

Atrial fibrillation and flutter are abnormal heart rhythms in which the atria are out of sync with the ventricles. In atrial flutter, the atria beat regularly and faster than the ventricles. In atrial fibrillation, the heart beat is completely irregular. The atrial muscles contract very quickly and irregularly; the ventricles beat irregularly but not as fast as the atria. When the atria fibrillate, blood that is not completely pumped out can pool and form a clot. In atrial flutter, the heart beat is usually very fast but steady. The atria beat faster than the ventricles. Atrial fibrillation often occurs in people with various types of heart disease. Atrial fibrillation may also result from an inflammation of the heart's covering (pericarditis), chest trauma or surgery, pulmonary disease, and certain medications

Answer 135

``` In most cases, the cause of atrial fibrillation and flutter: many types of heart disease stress and anxiety caffeine alcohol tobacco diet pills open heart surgery ```

Answer 136

are generated by turbulent flow of blood, which may occur inside or outside the heart. Murmurs may be physiological (benign) or pathological (abnormal). ``` Abnormal murmurs can be caused by : Stenosis restricting the opening of a heart valve, causing turbulence as blood flows through it. Valve insufficiency (or regurgitation) allows backflow of blood when the incompetent valve is supposed to be closed. ```

Answer 137

There are three standard leads, usually designated as I, II and III. They are bipolar (i.e., they detect a change in electric potential between two points) and detect the electrical potential change in the frontal plane. Lead I: is between the right arm and left arm electrodes, the left arm being positive. Lead II: is between the right arm and left leg electrodes, the left leg being positive. Lead III: is between the left arm and left leg electrodes, the left leg again being positive.

Answer 138

Chest Electrode Placement V1: Fourth intercostal space to the right of the sternum. V2: Fourth intercostal space to the Left of the sternum. V3: Directly between leads V2 and V4. V4: Fifth intercostal space at midclavicular line. V5: Level with V4 at left anterior axillary line. V6: Level with V5 at left midaxillary line. (Directly under the midpoint of the armpit) Chest Leads a. V1 & V2 b. V3 & V4 c. V5 & V6 View a. Right Ventricle b. Septum/Lateral Left Ventricle c. Anterior/Lateral Left Ventricle

Answer 139

The blood supply to certain areas of the myocardium is obstructed. The muscle tissue at the center of the infarct dies off. Causes: In atherosclerosis, plaque builds up in the walls of your coronary arteries. This plaque is made up of cholesterol and other cells. A heart attack can occur. Stress Male gender Diabetes Family history of coronary artery disease (genetic or hereditary factors) High blood pressure Smoking Unhealthy cholesterol levels, especially high LDL ("bad") cholesterol and low HDL ("good") cholesterol. Chronic kidney disease

Answer 140

Chest pain (angina pectoris): Feeling the pain in only one part of your body, or it may move from your chest to your arms, shoulder, neck, teeth, jaw, belly area, or back. The pain can be severe or mild. It can feel like: A tight band around the chest Bad indigestion Something heavy sitting on your chest Squeezing or heavy pressure The pain usually lasts longer than 20 minutes. Rest and a medicine do not completely relieve the pain of a heart attack. Symptoms may also go away and come back. ``` Other symptoms of a heart attack include: Sweating Anxiety Cough Fainting Dizziness Nausea or vomiting Palpitations (feeling like your heart is beating too fast) Dyspnea ```

Answer 141

1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes. 2. Changes in serial ECG tracings. 3. Rise and fall of serum cardiac biomarkers such as creatine kinase -MB fraction and troponin T and I and myoglobin, Lactate dehydrogenase as they are more specific for myocardial injury. (The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks). 4. If there is a high positive R, there is also a Larger negative Q waves, ST segment elevation or depression, or coronary intervention are diagnostic of MI. Management: A MI is a medical emergency which requires immediate medical attention. Oxygen, aspirin, and nitroglycerin.

Answer 142

Endocarditis is inflammation of the inside lining of the heart chambers and heart valves (endocardium). Endocarditis is usually a result of a blood infection. Bacteria or other infectious substance can enter the bloodstream during certain medical procedures, including dental procedures, and travel to the heart, where it can settle on damaged heart valves. The bacteria can grow and may form infected clots that break off and travel to the brain, lungs, kidneys, or spleen. The following increase chances for developing endocarditis: - Artificial heart valves - Congenital heart disease (atrial septal defect, patent ductus arteriosus) - Heart valve problems (such as mitral insufficiency). -History of rheumatic heart disease.

Answer 143

``` Abnormal urine color Chills (common) Excessive sweating (common) Fatigue Fever (common) Joint pain Muscle aches and pains Night sweats Nail abnormalities (splinter hemorrhages under the nails) Paleness ```

Answer 144

Blood culture and sensitivity (to detect bacteria) Chest x-ray Complete blood count (may show mild anemia) Echocardiogram (ultrasound of the heart) Erythrocyte sedimentation rate (ESR) Transesophageal echocardiogram Treatment: Long-term, high-dose antibiotic treatment is needed to get rid of the bacteria. Treatment is usually given for 4-6 weeks, depending on the specific type of bacteria. Blood tests will help your doctor choose the best antibiotic. Surgery may be needed to replace damage heart valves.

Answer 145

Mitral stenosis is a heart valve disorder that involves the mitral valve. Stenosis refers to a condition in which the valve does not open fully, restricting blood flow. Causes: the valve area becomes smaller, less blood flows to the body. The upper heart chamber swells as pressure builds up. Blood may flow back into the lungs. Fluid then collects in the lung tissue (pulmonary edema), making it hard to breathe. - Rheumatic fever - Congenital mitral stenosis

Answer 146

Symptoms: May begin with an episode of: -Atrial fibrillation -Chest discomfort (rare): Increases with activity, decreases with rest -Radiates to the arm, neck, jaw, or other areas Tight, crushing, pressure, -Cough, possibly bloody (hemoptysis) Difficulty breathing during or after exercise or when lying flat; may wake up with difficulty breathing -Fatigue, becoming tired easily - Bronchitis -Palpitations -Swelling of feet or ankles Complications: - Atrial fibrillation and atrial flutter - Blood clots to the brain (stroke), intestines, kidneys, or other areas - Heart failure - Pulmonary edema - Pulmonary hypertension

Answer 147

There is atrial fibrillation. No P waves are visible. The rhythm is irregularly irregular (random). With severe pulmonary hypertension, right ventricular hypertrophy can be seen. Treatment: Medical treatment includes: -Cardiac Glycosides: These agents alter the electrophysiologic mechanisms responsible for arrhythmia. Digoxin (Lanoxin). - Diuretics - β-blockers - Ca2+ channel blockers - Anticoagulants - balloon valvotomy - surgical commissurotomy - valve replacement *Digoxin: Negatively chronotropic - i.e. slowing the heart rate by decreasing conduction of electrical impulses through the AV node, making it a commonly used antiarrhythmic agent in controlling the heart rate during atrial fibrillation or atrial flutter. Positively inotropic - i.e. increasing the force of heart contraction via inhibition of the Na+/K+ ATPase pump.

Answer 148

Negatively chronotropic - i.e. slowing the heart rate by decreasing conduction of electrical impulses through the AV node, making it a commonly used antiarrhythmic agent in controlling the heart rate during atrial fibrillation or atrial flutter. Positively inotropic - i.e. increasing the force of heart contraction via inhibition of the Na+/K+ ATPase pump.

Answer 149

Mitral regurgitation is a long-term disorder in which the heart's mitral valve does not close properly, causing blood to flow backward (leak) into the upper heart chamber when the left lower heart chamber contracts. The condition is progressive, which means it gradually gets worse. Causes: - Mitral valve prolapse - Congenital - Atherosclerosis - Endocarditis - Heart tumors - High blood pressure - Marfan syndrome - Untreated syphilis

Answer 150

Symptoms: -Cough -Fatigue -Palpitations (related to atrial fibrillation) -Shortness of breath during activity and when lying down -Urination, excessive at night enlarged liver Treatment: The choice of treatment depends on the symptoms present and the condition and function of the heart. - Antibiotics reduce the risk of infective endocarditis in patients with mitral valve prolapse who are having dental work. - Antihypertensive drugs and vasodilators. - Anticoagulant or antiplatelet medications prevent clot formation in patients with atrial fibrillation. - Digitalis may be used to strengthen the heartbeat, along with diuretics to remove excess fluid in the lungs.

Answer 151

Cardiac output is distributed among various organs: Cerebral=15% Coronary=5% Renal=25% Gastrointestinal=25% Skeletal muscle=25% Skin=5%

Answer 152

Fast mechanism: neural, (baroreceptor) Slow mechanism: hormonal (renin-angiotensin-aldosterone) Baroreceptor reflex - includes fast, neural mechanisms. - is a negative feedback system that is responsible for the minute-to-minute regulation of arterial pressure. - Baroreceptors are stretch receptors located within the walls of the carotid sinus near the bifurcation of the common carotid arteries.

Answer 153

a. A decrease in arterial pressure decreases stretch on the walls of the carotid sinus. - Because the baroreceptors are most sensitive to changes in arterial pressure, rapidly decreasing arterial pressure produces the greatest response. - Additional baroreceptors in the aortic arch respond to increases, but not to decreases, in arterial pressure. b. Decreased stretch decreases the firing rate of the carotid sinus nerve cranial nerve IX, which carries information to the vasomotor center in the brain stem. c. The set point for mean arterial pressure in the vasomotor center is about 100 mm Hg. Therefore, if mean arterial pressure is less than 100 mm Hg, a series of autonomic responses is coordinated by the vasomotor center. These changes will attempt to increase blood pressure toward normal. d. The responses of the vasomotor center to a decrease in mean arterial blood pressure are coordinated to increase the arterial pressure to 100 mm Hg. The responses are decreased parasympathetic (vagal) outflow to the heart and increased sympathetic outflow to the heart and blood vessels.

Answer 154

1. Increases heart rate 2. Increases contractility and stroke volume 3. Increases vasoconstriction of arterioles 4. Increases vasoconstriction of veins * Example of the baroreceptor reflex: response to acute blood loss

Answer 155

- is a slow, hormonal mechanism. - Regulation by adjustment of blood volume. - Renin is an enzyme. - Angiotensin I is inactive. - Angiotensin II is physiologically active. - Angiotensin II is degraded by angiotensinase. * Example : response of the RAA system to acute blood loss.

Answer 156

Regulation by Aldosterone | Renin-Angiotensin-Aldosterone system

Answer 157

1. Cerebral ischemia 2. Chemoreceptors in the carotid and aortic bodies 3. Vasaopressin (antidiuretic hormone) 4. Atrial natriuretic peptide (ANP)

Answer 158

a. Pco2 pressure increases in brain tissue. b. Chemoreceptors in the vasomotor center respond by increasing sympathetic outflow to the heart and blood vessels. Constriction of arterioles causes intense peripheral vasoconstriction and increased TPR. Blood flow to other organs (kidneys) is significantly reduced in an attempt to preserve blood flow to the brain. c. The Cushing reaction in an example of the response to cerebral ischemia. Increases intracranial pressure cause compression of the cerebral blood vessels, leading to cerebral ischemia and increased cerebral Pco2. The vasomotor center directs an increase in sympathetic outflow to the heart and blood vessels, which causes a profound increase in arterial pressure.

Answer 159

- are located near the bifurcation of the common carotid arteries and along the aortic arch. - have very high rates of O2 consumption and are very sensitive to decreases in the partial pressure of oxygen (Po2). - Decreases in Po2 activate vasomotor centers that produce vasoconstriction, an increase in TPR, and an increase in arterial pressure.

Answer 160

too little water in blood -> detected by hypothalamus -> more ADH secreted into blood by pituitary gland -> kidneys absorb less water from blood -> less urine produced -> blood water level back to normal too much water in blood -> detected by hypothalamus -> less ADH secreted into blood by pituitary gland -> kidneys absorb more water from blood -> lots of dilute urine produced -> blood water level back to normal

Answer 161

Physiological effects ANP binds to a specific set of receptors. Receptor-agonist binding causes a reduction in blood volume and therefore a reduction in cardiac output and systemic blood pressure. - Inhibits renin secretion, thereby inhibiting the renin-angiotensin system. - Reduces aldosterone secretion by the adrenal cortex. - Relaxes vascular smooth muscle in arterioles and venules.

Answer 162

- At the junction of the arterioles and capillaries is a smooth muscle band called the precapillary sphincter. - True capillaries do not have smooth muscle; they consist of a single layer of endothelial cells surrounded by a basement membrane. - Clefts (pores) between the endothelial cells allow passage of water-soluble substances. The clefts represent a very small fraction of the surface area (<0.1%). - Blood flow through the capillaries is regulated by contraction and relaxation of the arterioles and the precapillary sphincters.

Answer 163

1. Lipid-soluble substances (o2 and CO2) 2. Small water-soluble substance - cross via the water-filled clefts between the endothelial cells. - include water, Glucose, and amino acid. - Proteins molecules are too large to pass freely through the clefts. - In the brain, the clefts between endothelial cells are exceptionally tight (blood-brain barrier). - In the liver and intestine, the clefts are exceptionally wide and allow passage of protein. These capillaries are called sinusoids. 3. Large water-soluble substances - can cross by pinocytosis.

Answer 164

a. Normally, filtration of fluid out of the capillaries is slightly greater than absorption of fluid into the capillaries. The excess filtered fluid is returned to the circulation via the lymph. Lymph also returns any filtered protein to the circulation. b. Unidirectional flow of lymph - one-way flap valves permit interstitial to enter, but not leave, the lymph vessels. - Flow through larger lymphatic vessels is also unidirectional, and is aided by one-way valves and skeletal muscle contraction. c. Edema - occurs when the volume of interstitial fluid exceeds the capacity of the lymphatic to return it to the circulation. - can be caused by excess filtration or blocked lymphatics.

Answer 165

It maintains constancy of ECF volume and of osmolality by balancing intake and excretion of Na+ and water. Furthermore, the kidney achieves constancy of extracellular K+ concentration and of blood and cellular PH by adjusting excretion of H+ and HCO3- . It conserves nutrients (e.g. glucose, aminoacids) and excretes end products of metabolism (urea, uric acid). It also has numerous metabolic functions (arginine formation, gluconeogenesis, peptide hydrolysis). It is a source of hormones (angiotensin II, erythropoietin, prostaglandins)

Answer 166

*** Reabsorption: Whence the greater part of this ultrafiltrate is transported across the tubule wall and reenters the blood. *** Excretion: The fraction that is not reabsorbed remains in the tubules and appears in the terminal urine. *** Secretion: Some urinary solvents enter the nephron lumen from tubule cells by secretion.

Answer 167

- A nephron consists of a glomerulus and renal tubule. 1. The glomerulus is a glomerular capillary network, which emerges from an afferent arteriole. 2. Renal tubule comprises the following segments: - Proximal tubule - Loop of Henle (thin decending limb, a thin ascending and a thick ascending limb) - Distal tubule - Collecting ducts.

Answer 168

Blood enters each kidney via renal artery, which branches into interlobar a., arcuate a. and cortical radial . The smallest arteries subdivide into first set of arterioles, the afferent arterioles. The afferent arterioles deliver blood to the first capillary network, the glomerular capillaries. Then blood leaves the glomerular capillaries, via a second set of arterioles, the efferent arterioles, which deliver blood to a second capillary network, the peritubular capillaries. The peritubular capillaries surround the nephrons. Solutes and water are reabsorbed into the peritubular capillaries and a few solutes are secreted from the peritubular capillaries. Blood from the peritubular capillaries flows into small veins and then into the renal vein. In the juxtamedullary nephrons, the peritubular capillaries have a specialization called the vasa recta. Vasa recta serve as osmotic exchangers for the production of concentrated urine. (a=artery)

Answer 169

- Total body water (TBW) is approximately 60% of body weight. - The percentage of TBW is highest in newborns and adult males and lowest in adult females and in adults with a large amount of adipose tissue.

Answer 170

* Plasma is ¼ of the ECF. * Interstitial fluid is ¾ of the ECF. 60-40-20 rule: - TBW is 60% of body weight. - ICF is 40% of body weight - ECF is 20% of body weight

Answer 171

The glomerular capillaries have large pores in their walls, and the layer of Bowman’s capsule in contact with the glomerulus has filtration slits. Water, together with dissolved solutes (but not proteins) can thus pass from the blood plasma to the inside of the capsule and the nephron tubules. The volume of this filtrate produced by both kidneys per minute is called the glomerular filtration rate (GFR).

Answer 172

The fluid that enters the glomerular capsule is called ultrafiltrate. Because glomerular capillaries are extremely permeable and have an extensive surface area, this modest net filtration pressure produces an extraordinarily large volume of filtrate. The glomerular filtration rate (GFR) is the volume of filtrate produced by both kidneys per min. The GFR averages 115 ml per min in woman and 125 ml per min in men. It 180 L per day. Most of the filtered water must obviously be returned immediately to the vascular system, or a person would literally urinate to death within minutes.

Answer 173

Measurement of GFR-clearance of inulin-Inulin is filtered, but not reabsorbed or secreted by the renal tubules. GFR= U inulin V/ P inulin U=Urine concentration of inulin (mg/ml) P=Plasma concentration of inulin (mg/ml)

Answer 174

Clearance equation - indicates the volume of plasma cleared of a substance per unit time. - The units of clearance are ml/min and ml/24hr. C=UV/P C=clearance (ml/min or ml/24hr) U= urine concentration (mg/ml) V=urine volume/time (ml/min) P-plasma concentration (mg/ml)

Answer 175

a. Na+-glucose cotransport in the proximal tubule reabsorbs glucose from tubular fluid into the blood. There are a limited number of Na+-glucose carriers. b. At plasma glucose concentrations less than 250 mg/dl, all of the filtered glucose can be reabsorbed because plenty of carriers are available; in this range, the line for reabsorption is the same as that for filtration. c. At plasma glucose concentration greater than 350 mg/dl, the carriers are saturated. Therefore, increases in plasma concentration above350 mg/dl do not result in increased rates of reabsorption. The reabsorptive rate at which the carrires are saturated is the transport maximum ™.

Answer 176

a. At plasma concentrations less than 250 mg/dl, all of the filtered glucose is reabsorbed and excretion is zero. Threshold is approximately 250mg/dl. b. At plasma concentrations greater than 350 mg/dl, reabsorption is saturated ™. Therefore, as the plasma concentration increases, the additional filtered glucose cannot be reabsorbed and is excretes in the urine.

Answer 177

General information about Na+ reabsorption - Na+ is filtered across the glomerular capillaries; therefore, the Na+ in the tubular fluid of Bowman’s space equals that in plasma - Na+ is rabsorbed along the entire nephron, and very little is excreted in urine <1% of the filtered load. Na+ reabsorption along the nephrone 1. Proximal tubule - reabsorb 2/3, or 67%, of the filtered Na+ and H2O, more than any other part of the nephron. - is the site of glumerulo-tubular balance. - The reabsorption of Na+ and H2O in the proximal tubule are exactly proportional. Early proximal tubule-special features - reabsorbs Na+ and H2O with HCO3-, glucose, amino acids, phosphate, and lactate. - Na+ is reabsorbed by cotransport with glucose, AAs, phosphate, and lactate. These cotransport processes account for the reabsorption of all of the filtered glucose and AAs. - Na+ is also reabsorbed by countertransport via Na+-H+ exchange, which is linked directly to the reabsorption of filtered HCO3-.

Answer 178

- Filtered glucose, amino acids, and HCO3- have already been completely removed from the tubular fluid by reabsorption in the early proximal tubule. - In the middle and late proximal tubules, Na+ is reabsorbed with Cl-.

Answer 179

- reabsorbs 25% of the filtered Na+. - contains a Na+-K+-2Cl- cotransporter in the luminal membrane. - is impermeable to water. NaCl is reabsorbed without water. As a result, tubular fluid Na+ and tubular fluid osmolarity decrease to less than their concentrations in plasma This segment, therefore, is called the diluting segment.

Answer 180

- together reabsorb 8% of the filtered Na+. a. Early distal tubule-special features. - reabsorbs NaCl by a Na+-Cl- cotransporter. - is impermeable to water. - is called the cortical diluting segment.

Answer 181

- reabsorb Na+ and H2O. - secrete K+. - Aldosterone increases Na+ reabsorption and increases K+ secretion. - Antidiuretic Hormone increases H2O permeability by directing the in secretion of H2O channels in the luminal membrane. In the absence of ADH, the principal cells are virtually impermeable to water.

Answer 182

- secrete H+ by a H+ adenosine triphosphatase (ATP ase), which is stimulated by aldosterone. - reabsorb K+ by a H+, K+-ATPase.

Answer 183

- Most of the body’s K+ is located in the ICF. - A shift of K+ out of cells causes hyperkalemia. - A shift of K+ into cells causes hypokalemia.

Answer 184

- K+ is filtered, reabsorbed, and secreted by the nephron. - K+ balance is achieved when urinary excretion of K+ exactly equals intake of K+ in the diet. - K+ excretion can vary widely from 1% to 110% of the filtered load, depending on dietary K+ intake, aldosterone levels, and acid-base status.

Answer 185

-Filtration occurs freely across the glomerular capillaries.

Answer 186

reabsorbs 67% of the filtered K+ along with Na+ and H2O.

Answer 187

-reabsorbs 20% of the filtered K+. Reabsorption involves the Na+-K+-2Cl- cotransporter in the luminal membrane of cells in the thick ascending limb.

Answer 188

either reabsorb or secrete K+, depending on dietary K+ intake.

Answer 189

- occurs in the principal cell. - is variable and accounts for the wide range of urinary K+ excretion. - depends on factors such as dietary K+, aldosterone levels, acid-base status, and urine flow rate.

Answer 190

- A diet high in K+ increases K+ secretion, and a diet low in K+ decreases K+ secretion. - On a high-K+ diet, intracellular K+ increases so than the driving force for K+ secretion also increases. - On a low-K+ diet, intracellular K+ decreases so that the driving force for K+ secretion decreases. Also, the alpha-intercalated cells are stimulated to reabsorb K+ by the H+, K+-ATPase.

Answer 191

- increases K+ secretion. - The mechanism involves increased Na+ entry into the cells across the luminal membrane and increased pumping of Na+ out of the cells by the Na+-K+ pump. Stimulation of the Na+-K+ pump simultaneously increases K+ uptake into the principal cells, increasing the intracellular K+ concentration and the driving force for K+ secretion. Aldosterone also increases the number of luminal membrane K+ channels. * Hyperaldosteronism increases K+ secretion and causes hypokalemia. * Hypoaldosteronism decreases K+ secretion and causes hyperkalemia.

Answer 192

- Effectively, H+ and K+ exchange for each other across the basolateral cell membrane. - Acidosis decreases K+ secretion,. The blood contains excess H+; therefore, H+ enters the cell across the basolateral membrane and K+ leaves the cell. As a result, the intracellular K+ concentration and the driving force for K+ secretion decrease. - Alkalosis increases K+ secretion. The blood contains too little H+; therefore, H+ leaves the cell across the basolateral membrane and K+ enters the cell. As a result, the intracellular K+ concentration and driving force for K+ secretion increase.

Answer 193

-Fifty percent of the filtered urea is reabsorbed passively in the proximal tubule. Rest are impermeable. -ADH increases the urea permeability of the inner medullary collecting ducts.

Answer 194

- Eighty-five percent of the filtered phosphate is reabsorbed in the proximal tubule by Na+-phosphate cotransport. 15% of the filtered load is excreted in urine. - Parathyroid hormone inhibits phosphate reabsorption in the proximal tubule by activating adenylate cyclase, PTH causes phosphaturia and increased urinary cAMP.

Answer 195

- Sixty percent of the plasma Ca+ is filtered across the glomerular capillaries. - Together, the proximal tubule and thick ascending limb reabsorb more than 90% of the filtered Ca+ by passive processes that are coupled to Na+ rabsorption. - Together, the distal tubule and collecting duct reabsorb 8% of the filtered Ca+ by an active process. * PTH increases Ca+ reabsorption by activating adenylate cyclase in the distal tubule.

Answer 196

- is reabsorbed in the proximal tubule, thick ascending limb of the loop of Henle, and distal tubule. - In the thick ascending limb, Mg2+ and Ca+ compete for reabsorption; therefore, hypercalcemia causes an increase in Mg2+ excretion (by inhibiting Mg+ reabsorption ).

Answer 197

- is also called hyperosmotic urine, in which urine osmolarity> blood osmolarity. - is produced when circulating ADH levels are high (e.g., water deprivation, hemorrhage, SIADH).

Answer 198

- is the gradient of osmolarity from the cortex (300mOsm/L to the papilla (1200mOsm/L), and is composed primarily of NaCl and urea. - is established by countercurrent multiplication and urea recycling. - is maintained by countercurrent exchange in the vasa recta.

Answer 199

- The osmolarity of the glomerular filtrate is identical to that of plasma (300mOsm/L). - Two-thirds of the filtered H2O is reabsorbed isosmotically (with Na+, Cl-, HCO3-. Glucose, AAs, ) in the proximal tubule. TF/P osm= 1.0 throughout the proximal tubule because H2O is reabsorbed isosmotically with solute.

Answer 200

- is called the diluting segment. - reabsobs NaCl by the Na+-K+-2Cl- cotransporter. - is impermeable to H2O. Therefore, H2O is not reabsorbed with NaCl, and the tubular fluid becomes dilute. - The fluid that leaves the thick ascending limb has an osmolarity of 100 mOsm/L and TF/P osm<1.0 as a result of the dilution process.

Answer 201

- is called the cortical diluting segment. - like the thick ascending limb, the early distal tubule reabsorbs NaCl but is impermeable to water. Consequently, tubular fluid is further diluted.

Answer 202

- ADH increases the H2O permeability of the principal cells of the late distal tubule. - H2O is reabsorbed from the tubule until the osmolarity of distal tubular fluid equals that of the surrounding interstitial fluid in the renal cortex (300mOsm/L) - TF/Posm=1.0 at the end of the distal tubule because osmotic equilibration occurs in the presence of ADH.

Answer 203

- as in the late distal tubule, ADH increases the H2O permeability of the principal cells of the collecting ducts. - As tubular fluid flows through the collecting ducts, it passes through the corticopapillary gradient (regions of increasingly higher osmolarity), which was previously established by counterrecurrent multiplication and urea recycling. - H2O is reabsorbed from the collecting ducts until the osmolarity of tubular fluid equals that the surrounding interstitial fluid. - The osmolarity of the final urine equals that at the bend of the loop of Henle (1200mOsm/L)

Answer 204

Glomerulonephritis (nephritic syndrome) is a disorder of glomeruli. It is characterized by body tissue swelling (edema), high blood pressure, and the presence of red blood cells in the urine.

Answer 205

Glomerulonephritis can be: Primary, affecting only the kidneys, Secondary, caused by a vast array of disorders that affect other parts of the body.

Answer 206

Acute glomerulonephritis most often occurs as a complication of throat or skin infection by streptococcus, a type of bacteria. Acute glomerulonephritis that occurs after a streptococcal infection (post-streptococcal glomerulonephritis). Infections with other types of bacteria, such as -staphylococcus and pneumococcus, -viral infections, such as chickenpox, -parasitic infections, such as malaria. -Noninfectious causes of acute glomerulonephritis include: -membranoproliferative glomerulonephritis, -immunoglobulin A (IgA) nephropathy, -systemic lupus erythematosus (lupus), Acute glomerulonephritis that develops into rapidly progressive glomerulonephritis most often results from conditions that involve an abnormal immune reaction.

Answer 207

Occasionally, chronic glomerulonephritis is caused by hereditary nephritis, an inherited genetic disorder. In many people, the cause of chronic glomerulonephritis cannot be identified.

Answer 208

``` -Edema: Puffiness of the face Eyelids but later is prominent in the legs. -Blood pressure -headaches -visual disturbances -coma -nausea -general feeling of illness (malaise) -weakness, fatigue -fever -Loss of appetite, nausea, vomiting -abdominal pain -joint pain ```

Answer 209

Following a diet that is low in protein and sodium may be necessary until kidney function recovers. - Diuretics may be prescribed to help the kidneys excrete excess sodium and water. - High blood pressure needs to be treated. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs). - When a bacterial infection is suspected as the cause of acute glomerulonephritis, antibiotics. - Restricting the amount of protein in the diet is modestly helpful in reducing the rate of kidney deterioration. - End-stage kidney failure can be treated with dialysis or a kidney transplant.

Answer 210

Pyelonephritis is a bacterial infection (90% is by Escherichia Coli) of one or both kidneys. Infection can spread up the urinary tract to the kidneys, or the kidneys may become infected through bacteria in the bloodstream. Symptoms: Chills, fever, back pain, nausea, and vomiting can occur. Urine and sometimes blood tests are done to diagnose pyelonephritis. Treatment: Antibiotics are given to treat the infection.

Answer 211

Stones (calculi) are hard masses that form anywhere in the urinary tract and may cause pain, bleeding, obstruction of the flow of urine, or an infection. Causes Stones may form because the urine becomes too saturated with salts that can form stones or because the urine lacks the normal inhibitors of stone formation. Citrate is such an inhibitor. About 80% of the stones are composed of calcium, and the remainder are composed of various substances, including uric acid, cystine. Stones are more common in people with hyperparathyroidism.

Answer 212

Small stones that are not causing symptoms, obstruction, or an infection usually do not need to be treated. - Drinking plenty of fluids has been recommended to help stones pass, but it is not clear that this approach is helpful. - Drugs that may help the stone pass include alpha-adrenergic blockers (such as tamsulosin). - Potassium citrate - Calcium channel blockers (such as Verapamil) Once a stone has passed, no other immediate treatment is needed. -The pain of renal colic may be relieved with nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids.

Answer 213

Two types of acid are produced in the body(Volatile acid and Nonvolatile acid) - is CO2. - is produced from the aerobic metabolism of cells. - CO2 combines with H2O to form the weak acid H2CO3 which dissociates into H+ and HCO3 by the following reactions -Carbonic anhydrase, which is present in most cells, catalyzes the reversible reaction between CO2 and H2O.

Answer 214

Two types of acid are produced in the body(Volatile acid and Nonvolatile acid) - are also called fixed acids. - include sulfuric acid H2SO4 (a product of protein catabolism) and phosphoric acid (a product of phospholipid catabolism) - are normally produced at a rate of 40-60mmoles/day. - other fixed acids that may be overproduced in disease or may be ingested include ketoacids, lactic acid, and salicylic acids.

Answer 215

- prevent a change in pH when H+ ions are added to or removed from a solution. - are most effective within 1.0 pH unit of the pK of the buffer. a. The major extracellular buffer is HCO3-, which is produced from CO2 and H2O. b. Phosphate is a minor extracellular buffer. - Phosphate is most important as a urinary buffer; excretion of H+ as H2PO4- is called titratable acid.

Answer 216

- prevent a change in pH when H+ ions are added to or removed from a solution. - are most effective within 1.0 pH unit of the pK of the buffer. a. Organic phosphates b. Proteins - Hemoglobin is a major intracellular buffer.-In the physiologic pH range, deoxyhemoglobin is a better buffer than oxyhemoglobin.

Answer 217

-occurs primarily in the proximal tubule. A. Key features of reabsorption of filtered HCO3- 1. H+ and HCO3- are produced in the proximal tubule cells from CO2 and H2O. CO2 and H2O combine to form H2CO3 Carbonic acid , catalyzed by intracellular carbonic anhydrase; H2CO3 dissociates into H+ and HCO3-. H+ is secreted into the lumen via the Na+-H+ exchange mechanism in the luminal membrane. The HCO3- is reabsorbed. 2. In the lumen, the secreted H+ combines with filtered HCO3- to form H2CO3, which dissociates into CO2 and H2O, catalyzed by brush border carbonic anhydrase. CO2 and H2O diffuse into the cell to start the cycle again. 3. The process results in net reabsorption of filtered HCO3-. However, it does not result in net secretion of H+.

Answer 218

-Increases in the filtered load of HCO3- result in increased rates of HCO3- reabsorption. However, in the plasma HCO3- concentration becomes very high (metabolic alkalosis), the filtered load will exceed the reabsorptive capacity, and HCO3- will be excreted in the urine.

Answer 219

- Increases in Pco2 result in increased rates of HCO3- reabsorption because the supply of intracellular H+ for secretion is increased. - Decreases in Pco2 result in decreased rates of HCO3- reabsorption because the supply of intracellular H+ for secretion is decreased. - These effects of changes in Pco2 are the physiologic basis for the renal compensation for respiratory acidosis and alkalosis

Answer 220

- ECF volume expansion results in decreased HCO3- reabsorption. - ECF volume concentration results in increased HCO3- reabsorption (contraction alkalosis)

Answer 221

stimulates Na+-H+ exchange and thus increases HCO3- reabsorption, contributing to the contraction alkalosis that occurs secondary to ECF volume contraction.

Answer 222

-Fixed H+ produced from the catabolism of protein and phospholipid is excreted by two mechanisms, titratable acid and NH4+. Excretion of H+ as titratable acid (H2PO4) - the amount of H+ excreted as titratable acid depends on the amount of urinary buffer present and the pK of the buffer. 1. H+ and HCO3- are produced in the cell from CO2 and H2O. The H+ is secreted into the lumen by an H+-ATPase, and the HCO3- is reabsorbed into the blood (new HCO3). In the urine, the secreted H+ combines with filtered HPO4-2 to form H2PO4-, which is excreted as titratable acid. 2. This process results in net secretion of H+ and net reabsorption of newly synthesized HCO3-. 3. As a result of H+ secretion, the pH of urine becomes progressively lower. The minimum urinary pH is 4.4. 4. The amount of H+ excreted as titratable acid is determined by the amount of urinary buffer and the pK of the buffer.

Answer 223

A. Overproduction or ingestion of fixed acid or loss of base produces an increase In arterial (H+) (acidemia). B. HCO3- is used to buffer the extra fixed acid. As a result, the arterial (HCO3) decreases. This decrease in the primary disturbance. C. Acidemia causes hyperventilation (Kussmaul breathing), which is the respiratory compensation for metabolic acidosis. D. Renal correction of metabolic acidosis consists of increased excretion of the excess fixed H+ as titratable acid and NH4+, and increased reabsorption of new HCO3-, which replenishes the HCO3- used in buffering the added fixed H+. -In chorionic metabolic acidosis, an adaptive increase in NH3 ammonia synthesis aids in the excretion of excess H+.

Answer 224

A. Loss of fixed H+ or gain of base produces a decrease in arterial H+ (alkalemia) b. As a result, arterial HCO3- increases. This increase is the primary disturbance. - For example, in vomiting H+ is lost from the stomach, HCO3- remains behind in the blood, and the HCO3- increases. C. Alkalemia causes hypoventilation, which is the respiratory compensation for metabolic alkalosis. D. Renal correction of metabolic alkalosis consists of increased excretion of HCO3- because the filtered load of HCO3- exceeds the ability of the renal tubule to reabsorb it. -If metabolic alkalosis is accompanied by ECF volume contraction (vomiting), the reabsorption of HCO3- increases (secondary to ECF volume contraction), worsening the metabolic alkalosis.