NR 507 Mid Term Study Guide Complete Solution
1. Concepts of anticholinergic drug and asthma:
Anticholinergic drugs: block acetylcholine binding
... [Show More] (primarily in the lungs) -promotes bronchiole dilation through decrease in the parasympathetic response (tiotropium & ipratropium) is fast acting
2. Bronchitis & associated pathogenesis:
Begins with an exposure to an irritant (tobacco smoke) – activates bronchiole smooth muscle constriction- mucus secretion- release of inflammatory mediators(histamine, prostaglandins & leukotrienes) normal response to occasional airborne site irritants- over bronchitis is over long term 3 months for over 2 consecutive years- = smooth muscle hypertrophy = increase bronchoconstriction, hypertrophy and hyperplasia of goblet cells= mucus hypersecretion, epithelia cell metaplasia = non-ciliated squamous cells, migration of more WBCs to site =
inflammation and fibrosis in bronchial wall, thickening and rigidity of bronchial basement membrane= narrowing of bronchial passageways : Increased mucus production- inflammation process = weight loss, loss of appetite, muscle weakness (interleukin controls appetite) increases protease activity= breakdown of elastin in the connective tissues of the lung= destruction of the wall between the alveoli and lungs = large ineffective air sacs develop-elastic recoil of bronchial wall -destroys bronchi and cant dilate and they stay constricted =air trapping : Chronic bronchitis =Dyspnea- air trapping increased mucus, increase WOB r/t chronic bronchoconstriction
Cough- irritated and inflamed bronchial epithelia membrane Hypoxia & Hypercapnia -from impaired gas exchange
3. Chronic bronchitis and related acid/base disturbance:
Hypercapnia (CO2 retention) = Respiratory acidosis
r/t anatomical changes ventilation is compromised esp. exhalation = alveolar hyperinflation) expanded thorax) hypercapnia CO2 retention = respiratory acidosis\
4. Perfusion:
the actual exchange of O2 and CO2 in the bloodstream occurs via the alveoli and pulmonary capillaries: the passage of fluid to an organ or a tissue usually referring to delivery of blood to an area
5. Blood flow between the heart and lungs in chronic bronchitis:
Poor ventilation leads to r to l shunting to occur= deoxygenated blood passes from r ventricle to the lungs to the l ventricle without adequate perfusion (gas exchange) the kidneys respond by secreting erythropoietin increasing RBC production the increase in RBC increase O2 carrying capacity -the increase blood volume increases the workload of the pulmonary and cardiovascular systems increasing blood volume and vasoconstriction = pulmonary HTN= increase workload on the R ventricle =cardiac hypertrophy= R side HF or Cor Pulmonale
6. Asthma signs and symptoms:
Coughing esp. at night, chest tightness, shortness of breath, wheezing on exhalation, and rapid breathing: Characteristics: airway inflammation, bronchial hyperactivity, smooth muscle spasms, = excessive mucus production, hypertrophy of bronchial smooth muscle -obstruction and decrease alveolar ventilation
7. Bronchioles in asthma:
There are 3 layers of the bronchiole which is a tube-like structure surrounding the lumen or airway passageway: innermost layer is composed of columnar epithelial cells and goblet cells-
The outermost layer is composed of smooth muscle cells responsible for the ability of the airway to constrict and dilate – the middle layer is the laminar propria and it is embedded with connective tissue and immune cells: in asthma these protective features go overactive =inflammation response= damage to host tissue=hypertrophy of the bronchioles smooth muscle and excessive mucus production: bronchioles spasm-mucus production-obstruction
8. Alveolar hyperinflation with asthma:
Increase mucus production from the goblet cells in the inflammation process forms plugs of mucus and pus and block alveolar passageways leading to air trapping and hyperinflation = erosion of airway tissue
9. Polycythemia Vera:
a rare blood disease in which the body makes too many RBCs making the blood thicker than normal causing blood clots; is often a result of chronic low levels of O2 in the blood, the kidney compensates by increase secretion of erythropoetin, the primary hormone responsible for stimulating RBC production= as a result patients with chronic bronchitis will often exhibit increased HCT levels and can develop a condition called secondary polycythemia vera.
10. Mechanism of action of anticholinergic drugs to treat asthma:
Anticholinergic drugs bind to muscarine receptors and block the action of acetylcholine They reduce Broncho motor tone =bronchodilation: block acetylcholine binding, bronchodilation, decrease parasympathetic response
Cardiovascular:
11. Review concepts of Cardiac Output:
Cardiac Output= Heart rate x Stroke volume\
Cardiac output: is the volume of blood ejected by each ventricle per minute
(75 bpm x 70ml = 5.25 L/min) 5 L of blood in the body= every drop of blood circulates the body -per heartbeat per minute
Cardiac output decrease with age at a rate of 1% per year after the age of 30 (other factors can accelerate the rate of decline)
Cardiac output is a key component of HF and is important to understand the connection b/t HR & SV:
DECRESE in HR (longer filling time) INCREASE in SV
INCREASE in HR (shorter fill time) DECREASE in SV
12. Concepts of cardiac contractility:
Contractility (ionotropic state)
Contractility is determined by Calcium availability and its interaction with actin and myosin
Contractility INCREASES by sympathetic stimulation (fever, anxiety, increased thyroxine levels; factors that increase the cellular metabolic rate will increase strength of muscle cell at least temporarily)
Contractility DECREASES by low levels of ATP (ischemia, hypoxia, acidosis;
Factors that decrease the amount of energy available to the muscle cell will decrease strength of contraction)
13. Preload and Afterload Concepts:
PRELOAD: is the degree of myocardial fiber length stretch before contraction; the degree of stretch will be influenced by the end diastolic ventricular volume (EDV) [edv= is the amount of blood entering each ventricle during diastoles {approx. 120- 130 ml}] PRELOAD IS LOADING THE HEART WITH BLOOD
Preload can be INCREASED by CHF, hypervolemia, (increased BV)
Preload can be DECREASED by cardiac tamponade, hypovolemia (hemorrhage or dehydration)
AFTERLOAD is the amount of tension the ventricle must develop during systole to open the semilunar valves and eject blood into circulation:
Afterload is influenced by: Ventricular wall thickness= muscle strength
Arterial pressure= resistance to ejection
Ventricle chamber size= blood volume capacity
Ventricular wall thickness: muscle strength (increase thickness the more muscle mass decrease tension force required for ejection)
Arterial pressure: resistance to ejection (increase pressure within the pulmonary or systemic vessels = increase tension required for ejection)
Ventricle chamber size: increased blood volume (increase tension required for ejection)
AFTERLOAD INCREASED by systemic HTN, valve disease, COPD = pulmonary HTN
AFTERLOAD DECREASED by hypotension or vasodilation, such as SHOCK
LAPELACE LAW: THE HEART MUST WORK HARDER (INCREASE TENSION) WHEN HEART MUSCLE IS WEAK: VENTRICLES ARE HYPERTROPHIED (HOLD MORE VOLUME) AND OR PULMONARY OR SYSTEMIC BP IS ELEVATED
14. Systole and Diastole:
Systole and Diastole are two phases of the cardiac cycle: they occur as the heart beats, pumping blood through the body.
Systole: occurs when the heart contracts to pump blood OUT
Diastole: occurs when the heart RELAXES after contraction
Systole causes the ejection of blood into the aorta and pulmonary trunk. Systole, period of contraction of the ventricles of the heart that occurs between the first and the second heart sound
Diastole period of relaxation of the heart muscle accompanied by the filing of the chambers with blood
15. Heart valves: When they open and close
4 valves of the heart
2 atrioventricular valves/ AV valves: tricuspid and bicuspid
2 semilunar valves/ SL : pulmonary and aortic
Valves are responsible for unidirectional flow of blood through the heart
The valves open and close in response to myocardial contractions and pressure changes within the heart
As the RV contracts the TRICUSPID valve closes and the PULMONARY valve opens; closure of the TRUCUSPID valve keeps blood from backing up into the RIGHT ATRIUM and the opening of the PULMONARY valve allows blood to flow into the pulmonary artery into the Lung
As the LV contracts the BICUSPID (mitral) valve closes, and the (SL) AORTIC valve opens, closure of the BICUSPID (mitral) valve prevents blood from backing into the LEFT ATRIUM and the opening of the AORTIC valve allows blood to flow into the aorta and into the Body
16. The production of heart sounds S1 and S2 :
S1 is the first heart sound; caused by the closure of the bicuspid (mitral) valve and the tricuspid valves at the start of systole
S2 is the second heart sound caused by the closure of the semilunar valves: the pulmonic and aortic valves marking the end of systole
17. Stenosis of the heart valves and effects;
Aortic valve stenosis occurs when the heart and aortic valves narrows; the narrowing prevents blood flow from the heart into the aorta and into the body (during systole) systolic murmur crescendo and decrescendo heart murmur can be hears S/sx: abnormal heart sound and angina, chest pain
Bicuspid (mitral)valve stenosis narrowing impairs blood flow from the L atrium to the L ventricle (most commonly due to rheumatic heart disease) low rumbling diastolic murmur at the apex radiating to the axilla hear during S1. s/sx of mitral valve stenosis: SOB, edema lower extremities, heart palpitations, chest pain dizziness, fatigue, coughing up blood
18. Stroke Volume:
Stroke volume is determined by: Preload, Contractility, and Afterload
Stroke volume is volume of blood which is about 70ml
19. Cor Pulmonale:
Cor Pulmonale is abnormal enlargement of the right side of the heart as a result of the lungs or the pulmonary vessels: R side HF (Cor Pulmonale) is defined as the inability of the RV to provide adequate blood flow into pulmonary circulation: Causes: pulmonary disease, (Pulmonary HTN) the most common (or worsening L side HF)
20. Heart Failure:
Heart failure is defined as a cardiac dysfunction caused by the inability of the heart to provide adequate cardiac output, resulting in inadequate tissue perfusion
Left side heart failure is CHF the inability of the LV to provide adequate blood flow into the systemic circulation caused by HTN, Cardiac hypertrophy, or MI
High systemic vascular pressure causes increase afterload and preload in the LV and LA, ultimately causing blood back up into the RV and RA causing back up of blood volume and pressure in the pulmonary veins= fluid into pulmonary capillaries into pulmonary tissues = pulmonary edema = dyspnea
Right side heart failure if back into the vena cava and systemic veins= jugular distention, hepatosplenomegaly, and peripheral edema
High Output heart failure HOF is caused by hyperthyroidism or nutritional deficiencies requiring an increased work load on the heart, at first the heart can keep up with the demands with adequate cardiac output and perfusion to tissues , but overtime will fail.
21. Hypertension: Patho:
Consistent elevation of systemic arterial blood pressure
Increased cardiac output and/or total peripheral resistance
CO increased by any condition that increase HR and/or SV
Peripheral resistance increases blood viscosity, reduce vessel diameter, vasoconstriction
Primary HTN: essential or idiopathic (Genetic or environment)
92 to 95% of individuals with HTN have primary HTN
Secondary HTN: HBP caused by effects of another dz (renal artery stenosis, kidney atrophy, increase in plasma renin)
• There is a genetic vulnerability link to HTN in combination with environment, which contribute to the dysfunction of the sympathetic nervous system: renin-angiotensin-aldosterone RAA system and natueretic hormones as well as inflammation and insulin resistance
• Insulin resistance and neurohumoral changes= sustained vasoconstriction and increased peripheral resistance
• Inflammation contributes to renal dysfunction and increase blood volume
• Increased peripheral resistance and increased blood volume are the 2 primary causes of sustained HTN
Target organs for HTN are: eyes: retinal changes, kidney; renal dz, heart: CHF and CAD, brain: stroke or dementia
22. Calcium binding and troponin:
Positively charged C ion is released from the sarcoplasmic reticulum: Ca has a affinity to bind with negatively charges troponin, this binding causes a physical shift of the tropomyosin (allowing exposure of the exposed myosin binding sites) the actin myosin proteins interact and the individual muscle fibers contract
ATP IS REQUIRED TO FACILLITATE THIS INTERACTION
Hematology:
23. Hematopoiesis: Hematopoiesis is blood cell formation
Hematopoiesis site varies by age: it occurs throughout the lifespan
Fetus: yolk sac to 3rd week gestation it is the initial site for hematopoiesis
By 8 weeks gestation in the fetal liver and spleen
By 5 months gestation in the bone marrow
Birth to 5 years: red marrow of the bone
After 20 years: red marrow of large bones: ilium, vertebrae, cranium, jaw, sternum, ribs, humerus, and femur
Hematopoiesis is stimulated by: infiltration of yellow (fatty) bone marrow with red marrow cells- faster proliferation and differentiation of stem cells and daughter cells.
24. Risk factors for developing any type of anemia:
Poverty
Age
Diet lacking in Fe vitamin B 12 and folic acid
Menstruation
Intestinal disorders: chrons or celiac
Pregnancy
Chronic conditions: Cancer, kidney dz, ulcers
Family history: autoimmune disorders, alcoholism, exposure to toxic chemical, medication
25. Iron Deficiency Anemia:
Iron deficiency anemia is a : microcytic hypochromic disorder= small cells low Hgb level
Most common problem contributing to IDA is insufficient Fe availability
Cause: inadequate dietary intake and chronic/occult bleeding (hemorrhage, GI ulcers, menorrhagia, colitis, cirrhosis, esophageal lesions)
Patho: insufficient Fe levels or inability for mitochondria to utilize Fe effectively= decrease in Hgb synthesis= smaller/paler cells
(2-4ml {1tsp} blood loss per day – 1-2mg Fe)
26. Erythrocyte function and lifespan:
Primary function id gas exchange: to transport O2 bound to Hgb molecules, also to transport small amount of CO2
Lifespan 100-120 days
27. Sickle cell anemia:
Sickle cell anemia; is a inherited disorder of the erythrocytes: Hemoglobinopathies: inherited autosomal recessive genetic disorder
Patho: single amino acid change on the beta chain (valine replaces glutamic acid) leads to elongated Hgb molecules which does not bind to O2 readily= oxidative stress occurs: anxiety, fever, cold, dehydration: which further decreases O2 binding to Hgb and increases sickling tendency of the Hgb.
The sickling of millions of Hgb molecules = distortion of RBC = weakening of RBC= rupture in 10 to 15 days
This type of hemolytic anemia presents with classic s/sx of anemia with the addition of more serious complications: lysis of large amount of RBC puts sickle cell patients at risk for circulatory [Show Less]