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NR 507 Mid Term Study Guide (Set-3)/ NR 507 Week 4 Midterm Study Guides, NR 507: Advanced Pathophysiology, Chamberlain $12.49   Add to cart
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NR 507 Mid Term Study Guide (Set-3)/ NR 507 Week 4 Midterm Study Guides, NR 507: Advanced Pathophysiology, Chamberlain

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NR 507 Mid Term Study Guide (Set-3)/ NR 507 Week 4 Midterm Study Guides, NR 507: Advanced Pathophysiology, Chamberlain

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  • May 10, 2023
  • 142
  • 2022/2023
  • Exam (elaborations)
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  • chamberlain
  • nr 507 mid term study guide set 3 nr 507 week 4 midterm study guides
  • nr 507 advanced pathophysiology

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NR 507 Week 4 Midterm Study Guides
NR 507: Advanced Pathophysiology

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Study Guide Mid Term Week 4

Pulmonary Review

Concepts Related to Anticholinergic Drugs & Treatment for Asthma:
Fast-acting Medications:
- Tiotropium & ipratropium
- Anticholinergic drugs block acetylcholine binding > bronchodilation through
decreased parasympathetic response

Bronchitis & Associated Pathogenesis:
Bronchitis – bronchial inflammation, hypersecretion of mucus, chronic productive cough
Exposure to airborne irritants activates bronchial:
- Smooth muscle constriction
- Mucus secretion
- Release of inflammatory mediators

Chronic Bronchitis & Related Acid/Base Disturbances:

, Hypercapnia (CO2 retention) > respiratory acidosis

Perfusion:
Perfusion – the actual exchange of O2 and CO2 in the bloodstream, occurs via the
alveoli and pulmonary capillaries
Ventilation – air movement in/out of the lung, is critical to ensure sufficient perfusion

Blood Flow Between the Heart & Lungs:
R heart – receives deoxygenated systemic blood and returns it to the lungs = pulmonary
circulation
L heart – receives oxygenated blood from the lungs and returns it to systemic circulation
Right to Left “shunting” – blood passes from R ventricle to lungs to L ventricle without
perfusion (gas exchange)

Asthma Signs & Symptoms:
Coughing
Wheezing
Shortness of Breath
Rapid Breathing
Chest Tightness

Bronchioles:
Composed of a 3-layer tube surrounded the lumen or air passageway
- The innermost layer, closest to the lumen, is composed of ciliated solumnar
epithelial cells’ the constant sweeping action of the cilia are important to
help clear the bronchial passageways or irritants, including infectious agents.
This layer also contains mucus producing goblet cells which traps irritants and
microbes to prevent their passage into the alveoli
- The middle layer, called the lamina propria, is embedded with connective
tissue cells, as well as immune cells. These immune cells include a number of
different kinds of WBCs, located here to help protect the airways
- The outermost layer is composed of smooth muscle cells, responsible for the
ability of the airways to constrict and dilate

Alveolar Hyperinflation with Asthma:
Plugs of mucus and pus from the inflammatory process can block alveolar passageways
which leads to air-trapping and alveolar hyperinflation


Cardiovascular Review

Concepts Related to Cardiac Output & Cardiac Contractility:
Cardiac Output – volume of blood ejected by each ventricle per minute
CO = HR x SV (heart rate x stroke volume)
Cardiac Contractility – (inotropic state) – determined by Ca+2 availability and its
interaction with actin-myosin

, -Increased by sympathetic stimulation (fever, anxiety)
-Decreased by low ATP levels (ischemia, hypoxia, acidosis)

Preload/Afterload:
Preload – degree of myocardial fiber length stretch before contraction
- amount of blood entering ventricle during diastole
- increased by CHF, hypervolemia
- decreased by cardiac tamponade or hypovolemia (hemorrhage, dehydration)
Afterload – amount of tension each ventricle must develop during systole to open SL
valves and eject blood
- influenced by ventricle wall thickness, atrial pressure, ventricle chamber size
- increased by systemic hypertension, valve disease, or COPD
- decreased by hypotension or vasodilation (shock)

Systole/Diastole:
Diastole – the period of relaxation when blood fills the ventricles of the heart
Systole – ventricle contraction, propelling blood out of the ventricles into the body

Heart Valves (when they are open and closed; production of S1 & S2):
2 atrioventricular (AV) valves = tricuspid & bicuspid (mitral)
2 semilunar (SL) valves = pulmonary & aortic
- the valves open and close in response to myocardial contraction and pressure
changes within the heart
- when the AV valves close = 1st heart sound (S1)
- when the SL valves close = 2nd heart sound (S2)



Stenosis of the Heart Valves and Effects:
Valvular Stenosis – valve orifice is constricted and narrowed, impeding the forward
flow of blood and increasing the workload of the cardiac chamber proximal to the
diseased valve
Aortic Stenosis – diminished blood flow from the L ventricle into the aorta
Effects = angina, pulmonary edema, MI, heart failure
Mitral Stenosis – impairs blood flow from the L atrium to the L ventricle
Effects = pulmonary edema, atypical chest pain, respiratory infections

Stoke Volume:
Volume of blood ejected per beat during systole
Preload, afterload & contractility all interact with one another to determine stroke volume
and cardiac output
3 major factors determine force of contraction:
- changes in the stretching of ventricular myocardium caused by changes in
preload
- alteration in the inotropic stimuli of the ventricles
- adequacy of the myocardial oxygen supply

, Cor Pulmonale:
Also, known as Right Heart Failure
Inability of right ventricle (RV) to provide adequate blood flow into pulmonary
circulation
Causes:
- pulmonary disease, RV MI, RV hypertrophy, pulmonary SLV or tricuspid
valve damage secondary to L heart failure

Heart Failure & Physiologic Processes that Lead to Heart Failure Symptoms:
Heart Failure – cardiac dysfunction caused by inability of the heart to provide adequate
cardiac output, resulting in inadequate tissue perfusion
Symptoms – dyspnea, fatigue, edema, pulmonary HTN, decreased urine output,
orthopnea, cough with frothy sputum
Neurohumoral, inflammatory & metabolic processes:
- Catecholamine’s – sympathetic nervous system activation initially
compensates for a decrease in cardiac output by increasing heart rate and
peripheral vascular resistance
- RAAS (renin-angiotensin-aldosterone-system) – activation of RAAS causes
not only increase in preload and afterload but also causes direct toxicity to the
myocardium
- Aldosterone – causes salt and water retention by the kidney and contributes to
dysrhythmias
- Arginine Vasopressin (antidiuretic hormone) – causes peripheral
vasoconstriction and renal fluid retention
Parasympathetic stimulation – vasodilation and decreased HR
Sympathetic stimulation – vasoconstriction and increased HR

Hypertension:
Consistent elevation of systemic arterial blood pressure
Systolic blood pressure (SBP) of 130 or greater
Diastolic blood pressure (DBP) of 80 or greater
Risk Factors:
- Age, ethnicity, family history of HTN, tobacco use, sleep apnea, dietary
factors

Calcium Binding & Troponin:
Troponin – holds tropomyosin in position to block myosin-binding sites on actin
Ca+2 – binding to negatively charged troponin shifts tropomyosin to expose myosin
binding sites


Hematology Review

Concepts Related to Hematopoiesis:
Hematopoiesis – the site of blood cell formation

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