NURS 611 Exams: Advanced Pathophysiology Questions and Answers

NURS 611 Exams: Advanced Pathophysiology Questions and Answers

1. Describe the pathophysiological changes associated with hypoparathyroidism.

– Hypoparathyroidism is disorder of parathyroid hormone (PTH) deficiency.

– There is Primary hypoparathyroidism and Secondary hypoparathyroidism.

Primary hypoparathyroidism is inadequate PTH activity. When PTH activity is inadequate PTH, the ionized calcium concentration in the extracellular fluid falls below the reference range. Primary hypoparathyroidism is therefore a syndrome resulting from one of many rare diseases.

Secondary hypoparathyroidism is a physiologic state in which PTH levels are low in response to a primary process that causes hypercalcemia.

 2. Explain what occurs in panhypopituitarism.

Panhypopituitarism refers to ailment whereby production of all hormones by the pituitary gland is reduced.

 

3. List the clinical manifestations of

– Decreased heat rate also known as bradycardia

– Constipation

– Lethargy.

When thyroid hormone levels are low result to decreased energy metabolism which results to decreased heart rate, constipation and lethargy.

 

4. Differentiate diabetes insipidus, diabetes mellitus and SIADH.

Diabetes mellitus also known as diabetes refers to several conditions involving how your body turns food into energy. Whereas diabetes insipidus is condition where the body has too little antidiuretic hormone (ADH) and SIADH is when the body has too much antidiuretic hormone (ADH)

 

5. What causes the microvascular complications of DM.

Microvascular complications result from capillary basement membranes thickening and endothelial cell hyperplasia.

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6. What is the cause of diabetes insipidus.

Diabetes insipidus is caused by insufficient antidiuretic hormone (ADH). NURS 611 Exams: Advanced Pathophysiology Questions and Answers.

 

7. Describe the pathophysiological changes associated with Addison’s Disease.

Addison disease is adrenocortical insufficiency due to the dysfunction or destruction of adrenal cortex and it affects mineralocorticoid and glucocorticoid function. The start of disease occurs when 90% or more of adrenal cortices are destroyed.

 

8. Explain the pathophysiology associate with Type 1 and Type 2 DM.

Type 1 diabetes occurs as a result of the body’s immune system attacking the insulin producing beta cells of the pancreas, although it is not clear why this happens. A lack of insulin in the blood means inadequate amounts of glucose are taken up by cells of the body to provide energy for cellular functions. Consequently, glucose remains in the blood leading to a high blood sugar level. Exactly what causes the immune system to do this is not yet clearly understood. Type 2 diabetes mellitus consists of an array of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion.

 

9. What are the causes and pathophysiological changes associate with ketoacidosis?

– Diabetic ketoacidosis is a result of dehydration due to insulin deficiency associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis mostly occurs in people with type 1 diabetes mellitus.

– Diabetic ketoacidosis can as well develop in any person with diabetes. Type 1 diabetes mostly starts before age 25 years and therefore diabetic ketoacidosis is common in this age group but it may occur at any age and affecting both male and female.

 

10. What is acromegaly?

Acromegaly is a hormonal disorder and it develops after pituitary gland produces too much growth hormone during adulthood. This makes bones increase in size and can affect hands, feet and face bones and usually affects middle-aged adults.

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11. Differentiate hypothyroidism and Graves’ disease.

Graves’ disease is over production of thyroid hormone while hypothyroidism is lack of thyroid hormone.

 

12. Describe the pathophysiology related to chronic DM.

Chronic symptoms of diabetes are due to vascular damage from persistent hyperglycemia. Vascular damage leads to end-organ damage. Other conditions associated with diabetes, such as hypertension, dyslipidemia (as well as smoking) accelerate the development of vascular damage and the chronic complications of diabetes, which are the following: Microvascular complications are a significant cause of morbidity. Persistent hyperglycemia is the major cause for the microvascular complications which are highly specific for diabetes. retinopathy with potential loss of vision, nephropathy leading to kidney failure, peripheral neuropathy leading to pain, foot ulcers, and limb amputation, autonomic neuropathy causing gastrointestinal, genitourinary, cardiovascular symptoms and sexual dysfunction. Macrovascular complications are the main cause of mortality. Although persistent hyperglycemia may contribute to macrovascular complications, it is the associated conditions (hypertension, dyslipidemia, and smoking) that account for most of the burden of the macrovascular complications. Coronary heart disease is the major cause of death for patients with diabetes, peripheral vascular disease, and cerebrovascular disease. Unfortunately, many patients with diabetes remain asymptomatic for long periods, so that the first presentation of the disease is frequently a chronic complication. Indeed, about 50% of newly diagnosed type 2 diabetes will already have developed a vascular. NURS 611 Exams: Advanced Pathophysiology Questions and Answers.

 

13. What happens during hypoglycemia?

– Hypoglycemia is a condition with abnormal low level of blood sugar (blood glucose) and this is a result of excess insulin. Therefore, hypoglycemia interferes with the brain’s ability to function properly since brain depends on blood sugar as a source of energy. Hence it can cause dizziness, headache, blurred vision, difficulty concentrating and other neurological symptoms.

– Hypoglycemia can also triggers the release of epinephrine and norepinephrine body hormones which the brain relies on to raise blood sugar levels. When such hormones are increased can cause additional symptoms of tremor, sweating, rapid heartbeat, anxiety and hunger.

 

14. What is the metabolic syndrome?

Metabolic syndrome is a collection of various conditions occurring together and they are; –

– High blood sugar level

– Increased blood pressure

– Abnormal cholesterol levels

– Excess body fat around the waist

 

15. Describe how Diabetic neuropathies (DM) causes peripheral neuropathy.

– Diabetic neuropathies is a nerve disorders caused by diabetes. Some people with nerve damage have no symptoms while others may have symptoms such as pain, tingling, or numbness (loss of feeling) in the hands, arms, feet, and legs. Nerve problems can occur in every organ system, including the digestive tract, heart, and sex organs.

– About 60 to 70 percent of people with diabetes have some form of neuropathy. People with diabetes can develop nerve problems at any time, however risk rises with age and not duration of diabetes.

– People who have had diabetes for at least 25 years have the highest rates of neuropathy.

– Diabetic neuropathies seem to be more common to the following people; –

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16. What causes diabetic neuropathies?

– Different types of diabetic neuropathy have different causes.

– The following is a likely combination of factors which can cause nerve damage.

17. Identify the location of the neurotransmitters in the heart.

Coronary vessels and myocardium

18. Define adrenergic receptors.

Class of receptors named after the action of adrenalin(e), the alternative name for epinephrine. Alpha receptors, which are stimulated by norepinephrine and blocked by agents such as phenoxybenzamine, are categorized into two classes, α1 and α2, which have different actions. α1 adrenergic actions include contraction of the iris, decreased motility in the intestine, and potassium and water secretions from the salivary glands. α2 adrenergic receptors inhibit adenylate cyclase, rather than activating it. Beta receptors, which are stimulated by epinephrine and blocked by agents such as propranolol, are also categorized into two types; β1 adrenergic receptors, which produce lipolysis and cardio stimulation, and β2 adrenergic receptors, which produce bronchodilatation and vasodilatation.

 

19. Discuss left-ventricular end diastolic pressure.

As a pump, the ventricle generates pressure (to eject blood) and displaces a volume of blood. The normal relationship between left ventricular pressure generation and ejection can be expressed as a plot of left ventricular pressure versus left ventricular volume. At end–diastole, the fibers have a particular stretch or length, which is determined by the resting force, myocardial compliance, and the degree of filling from the left atrium. This distending force is the preload of the muscle.

 

20. Define Frank-Starling law.

Frank-Starling law; cardiac muscle, like other muscle, increases its strength of contraction when it is stretched. As stated in Frank-Starling law, the volume of blood in the heart at the end of diastole (the length of its muscle fibers) is directly related to the force (strength) of contraction during the next systole.

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21. Discuss the effect of angiotensin II on the heart.

Increasing the peripheral vascular resistance. Angiotensin II also causes structural changes in blood vessels (remodeling) that contribute to permanent increases in peripheral resistance and make vessels more vulnerable to endothelial dysfunction and platelet aggregation.

 

22. Define pulsus paradoxus.

Pulsus paradoxus means that the arterial blood pressure during expiration exceeds arterial pressure during inspiration by more than 10 mmHg. This clinical finding reflects impairment of diastolic filling of the left ventricle plus reduction of blood volume within all four cardiac chambers.

 

23. List the indicators for an acute myocardial infarction (AMI).

Elevated levels of troponin, creatine kinase (CK), and lactic dehydrogenase (LDH). Cardiac troponins (troponin I and troponin T) are the most specific indicators of MI. Other biomarkers released by myocardial cells include CK-MB (creatine kinase-MB) and LDH.

 

24. List the clinic indicator for a coronary thrombus.

Acute coronary syndrome usually occurs when an acute thrombus forms in an atherosclerotic coronary artery. Athermanous plaque sometimes becomes unstable or inflamed, causing it to rupture or split, exposing thrombogenic material, which activates platelets and the coagulation cascade and produces an acute thrombus. Platelet activation involves a conformational change in membrane glycoprotein (GP) IIb/IIIa receptors, allowing cross-linking (and thus aggregation) of platelets. Even atheroma causing minimal obstruction can rupture and result in thrombosis; in > 50% of cases, pre-event stenosis is < 40%. Thus, although the severity of stenosis helps predict symptoms, it does not always predict acute thrombotic events. The resultant thrombus abruptly interferes with blood flow to parts of the myocardium. Spontaneous thrombolysis occurs in about two thirds of patients; 24 h later, thrombotic obstruction is found in only about 30%. However, in virtually all cases, obstruction lasts long enough to cause tissue necrosis. Initial consequences vary with size, location, and duration of obstruction and range from transient ischemia to infarction. Measurement of newer, more sensitive markers indicates that some cell necrosis probably occurs even in mild forms; thus, ischemic events occur on a continuum, and classification into subgroups, although useful, is somewhat arbitrary.

Sequelae of the acute event depend primarily on the mass and type of cardiac tissue infarcted. NURS 611 Exams: Advanced Pathophysiology Questions and Answers

 

25. Define pericarditis.

Most individuals with acute pericarditis describe several days of fever, myalgias, and malaise followed by the sudden onset of severe chest pain that worsens with respiratory movements and with lying down. Although the pain may radiate to the back, it is generally felt in the anterior chest and may be confused initially with the pain of acute myocardial infarction. Individuals with acute pericarditis also may report dysphagia, restlessness, irritability, anxiety, and weakness.

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26. List the causes and types of cardiomyopathy.

Dilated cardiomyopathy causes decreased ejection fraction, increased end-diastolic and residual volumes, decreased ventricular stroke volume, and biventricular failure.

 

27. Discuss the effect of HTN on the kidney.

Vasoconstriction and the resultant decreased renal perfusion cause tubular ischemia and preglomerular arteriopathy.

 

28. Describe the blood flow through the heart.

Blood enters the heart through two large veins, the inferior and superior vena cava, emptying oxygen- poor blood from the body into the right atrium of the heart. As the atrium contracts, blood flows from your right atrium into your right ventricle through the open tricuspid valve. When the ventricle is full, the tricuspid valve shuts. This prevents blood from flowing backward into the atria while the ventricle contracts. As the ventricle contracts, blood leaves the heart through the pulmonic valve, into the pulmonary artery and to the lungs where it is oxygenated. Left Side of the Heart: The pulmonary vein empties oxygen-rich blood from the lungs into the left atrium of the heart. As the atrium contracts, blood flows from your left atrium into your left ventricle through the open mitral valve. When the ventricle is full, the mitral valve shuts. This prevents blood from flowing backward into the atrium while the ventricle contracts. As the ventricle contracts, blood leaves the heart through the aortic valve, into the aorta and to the body.

 

29. Differentiate β1 and β2 receptors in the heart.

B1-receptors are largely postsynaptic and are located mainly in the heart but are also found in platelets, the salivary glands and the non-sphincter part of the gastrointestinal tract (GIT). They can however be found presynaptically. Activation causes an increase in the rate and contractile force of the heart, relaxation of the non-sphincter part of the GIT, aggregation of platelets and amylase secretion from the salivary glands. Presynaptically, their activation causes an increase in noradrenaline release. B2-receptors are also mainly postsynaptic and are located on a number of tissues including blood vessels, bronchi, GIT, skeletal muscle, liver and mast cell. Activation results in vasodilatation, bronchodilation, relaxation of the GIT, glycogenolysis in the liver, tremor in skeletal muscle and inhibition of histamine release from mast cells.

Diagram the action potential of the myocardial cell.

Action potential diagram –NURS 611 Exams: Advanced Pathophysiology Questions and Answers

 

30. Discuss surfactant in the lung.

Two major types of epithelial cells appear in the alveolus. Type I alveolar cells provide structure, and type II alveolar cells secrete surfactant, a lipoprotein that coats the inner surface of the alveolus and facilitates its expansion during inspiration, lowers alveolar surface tension at end- expiration, and thereby prevents lung collapse.

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31. Discuss the pulmonary anatomy as it relates to pressure.

Pulmonary ventilation is the main process by which air flows in and out of the lungs. This is done through the contraction of muscles, as well as through a negative pressure system that is accomplished by the pleural membrane covering the lungs. When the lungs are completely sealed in this membrane, they remain at a pressure that is slightly lower than the pressure of the lungs at rest. As a result of this, the air passively fills the lungs until there is no more pressure difference. At this point, if necessary, additional air can be inhaled by contracting the diaphragm as well as the surrounding intercostal muscles. During exhalation, the muscles relax and this reverses the pressure dynamic, increasing the pressure on the outside of the lungs and forcing air to escape them until both pressures equalize again. Thanks to the elastic nature of the lungs, they revert back to their state at rest and the entire process repeats itself.

 

32. What part of the brainstem is responsible for automatic rhythm of respiration?

The basic automatic rhythm of respiration is set by the DRG, a cluster of inspiratory nerve cells located in the medulla that sends efferent impulses to the diaphragm and inspiratory intercostal muscles.

 

33. Describe how to effectively monitor a person’s alveolar

The adequacy of alveolar ventilation cannot be accurately determined by observation of ventilatory rate, pattern, or effort. If a healthcare professional needs to determine the adequacy of ventilation, an arterial blood gas analysis must be performed to measure PaCO2.

 

34. Describe the cause of

Dyspnea refers to the sensation of difficult or uncomfortable breathing. It is a subjective experience perceived and reported by an affected patient.

 

35. What cause proximal nocturnal dyspnea (PND)?

Another type of positional dyspnea is PND, in which individuals with heart failure or lung disease wake up at night gasping for air as a result of fluid accumulation in the lungs and must sit up or stand to relieve the dyspnea.

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36. Discuss oxygen transport in the blood.

Oxygen is transported in the blood in two forms. A small amount dissolves in plasma, and the remainder binds to hemoglobin molecules.

 

37. How is respiration stimulated?

The respiratory center is composed of several groups of neurons located bilaterally in the brainstem: the dorsal respiratory group (DRG), the ventral respiratory group (VRG), the pneumotaxic center, and the apneustic center. Stimulation of any of these centers can stimulate respiration. The usual stimulant of respiration is a rising CO2.NURS 611 Exams: Advanced Pathophysiology Questions and Answers

 

38. Discuss β receptors in the lung.

The lungs are innervated by both the sympathetic and parasympathetic nervous systems, which entails the activation of adrenergic and muscarinic receptors, respectively. Both the adrenergic and muscarinic receptors are G-protein-coupled receptors, and they share many similar signal transduction molecules. These receptors are widely expressed in the lung and the specific receptor expression can vary among the species. The location and the subtype of receptor expressed are important in the regulation of normal airway function. Acetylcholine released from the parasympathetic fibers activates the M3 muscarinic receptors located on the airway smooth muscle, causing bronchoconstriction. To counter this activity, M2 muscarinic receptors located on the parasympathetic nerves inhibit release of acetylcholine. Beta2-adrenergic receptors are expressed on the airway smooth muscle where activation causes bronchodilation. Adrenergic receptors are also on the autonomic nerves where they can modulate neurotransmitter release. The crosstalk between these G-protein-coupled receptors and downstream pathways ensures normal airway function. The prejunctional and post junctional muscarinic and adrenergic receptors control autonomic tone and any imbalance or selective blockade of the receptors can compromise the system and cause the airways to become hyperreactive. The location, function, and crosstalk of the adrenergic and muscarinic receptors must be considered in the design, development, and use of drugs to combat airway diseases.

 

39. What substances can cause bronchoconstriction?

Bronchoconstriction (definition) is defined as the narrowing of the airways in the lungs (bronchi and bronchioles). Air flow in air passages can get restricted due to 3 factors: – a spasmodic state of the smooth muscles in bronchi and bronchioles- an inflammation of the airways- excessive production of mucus due to an allergic reaction or irritation caused by mechanical friction of air (due to shear stress), overcooling or drying of airways. NURS 611 Exams: Advanced Pathophysiology Questions and Answers.

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40. What cause pulmonary artery constriction.

Pulmonary hypertension is a condition in which blood pressure in the arteries of the lungs (the pulmonary arteries) is abnormally high. Many disorders can cause pulmonary hypertension. People usually have shortness of breath upon exertion and loss of energy, and some people feel light-headed or fatigued on exertion. Chest x-rays, electrocardiography (ECG), and echocardiography give clues to the diagnosis, but measurement of blood pressure in the right ventricle and the pulmonary artery is needed for confirmation. Treatment of the cause and use of drugs that improve blood flow through the lungs are helpful. Blood travels from the right side of the heart through the pulmonary arteries into the lungs. There, carbon dioxide is removed from the blood and oxygen is added. Normally, the pressure in the pulmonary arteries is low, allowing the right side of the heart to be less muscular than the left side (because relatively little muscle and effort are needed to push the blood through the lungs via the pulmonary arteries). In contrast, the left side of the heart is more muscular because it has to push blood through the entire body against a much higher pressure. If the pressure of the blood in the pulmonary arteries increases to a sufficiently high level, the condition is called pulmonary hypertension. With pulmonary hypertension, the right side of the heart must work harder to push the blood through the pulmonary arteries into the lungs. Over time, the right ventricle becomes thickened and enlarged and heart failure develops. In people with heart failure, the heart does not pump blood adequately.

 

41. What changes occur in the lung due to Asthma, emphysema and chronic bronchitis.

Inflammatory mediators are produced in asthma including Histamine, prostaglandins and leukotrienes. These cause edema of the mucous lining of the airways, bronchoconstriction and stimulation of mucous production in response to a trigger. Emphysema is characterized by the loss of elastic recoil of the lung and destruction of the supporting structures of the alveolus. Chronic bronchitis is a change in the lining of the bronchus due to repeated infections and loss of ciliated epithelium and replacement with goblet cells and increased mucous production.

 

42. What are the risk factors for pulmonary emboli?

Pulmonary embolus is the end result of a deep vein thrombosis or blood clot elsewhere in the body. Most commonly, the DVT begins in the leg, but they also can occur in veins within the abdominal cavity or in the arms. The risk factors for a pulmonary embolism are the same as the risk factors for deep vein thrombosis. These are referred to as Virchow’s triad and include: prolonged immobilization or alterations in normal blood flow (stasis), increased clotting potential of the blood (hypercoagulability), damage to the walls of the veins.

 

43. List the changes in the aging lung.

Normal alterations include (1) loss of elastic recoil, (2) stiffening of the chest wall, (3) alterations in gas exchange, and (4) increases in flow resistance.

 

44. Which of the following anemias is classified as a macrocytic-normochromic anemia?

Macrocytic anemia (MCV >100 µm3 [>100 fL]) are less common than normocytic or microcytic anemia. Macrocytic anemia may be subdivided into those with a normal RDW (principally those caused by bone marrow failure, such as aplastic anemia and myelodysplasia), and those with a high RDW (caused by either deficiencies of vitamin B12 or folic acid; by autoimmune hemolysis or cold agglutinins). NURS 611 Exams: Advanced Pathophysiology Questions and Answers.

 

45. What causes the paresthesia that occurs in vitamin B12deficiency anemia?

Vitamin B12 (cobalamin) plays an important role in DNA synthesis and neurologic function. Deficiency can lead to a wide spectrum of hematologic and neuropsychiatric disorders that can often be reversed by early diagnosis and prompt treatment. The true prevalence of vitamin B12 deficiency in the general population is unknown. The incidence, however, appears to increase with age. In one study,1 15 percent of adults older than 65 years had laboratory evidence of vitamin B12 deficiency. The nearly ubiquitous use of gastric acid–blocking agents, which can lead to decreased vitamin B12 levels, may have an underappreciated role in the development of vitamin B12 deficiency. Taking the widespread use of these agents and the aging of the U.S. population into consideration, the actual prevalence of vitamin B12 deficiency may be even higher than statistics indicate. Despite these facts, the need for universal screening in older adults remains a matter of controversy.

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46. How does the body compensate for anemia?

Increased oxygen extraction of anemic blood by the tissues produces increased concentration of deoxyhemoglobin in the rbc, which stimulates the production of 2,3-diphosphoglycerate (2,3-DPG). 2,3-DPG shifts the hemoglobin-oxygen dissociation curve to the right, thus allowing the tissues to more easily strip the hemoglobin of its precious electron-accepting cargo: In anemia selective vasoconstriction of blood vessels subserving certain nonvital areas allows more blood to flow into critical areas. The main donor sites who sacrifice their aerobic lifestyle are the skin and kidneys. Shunting of blood away from cutaneous sites is the mechanism behind the clinical finding of pallor, a cardinal sign of anemia. Although the kidney can hardly be thought of as a nonvital area, it receives (in the normal state) much more blood flow than is needed to meet its metabolic requirements.

Although (by definition) total body red cell mass is decreased in anemia, in the chronically anemic patient the total blood volume paradoxically is increased, due to increased plasma volume. It is as if the body were trying to make up in blood quantity what it lacks in quality. The heart can respond to tissue hypoxia by increased cardiac output. The increased output is matched by decreased peripheral vascular resistance and decreased blood viscosity (thinner blood flows more freely than thick blood), so that cardiac output can rise without an increase in blood pressure. Generally, anemia must be fairly severe (hemoglobin < 7 g/dL) before cardiac output rises.

 

47. Deficiencies in folate and vitamin B12 alter the synthesis of which cell component?

Vitamin B12 is involved in cellular metabolism in two active coenzyme forms methyl cobalamin and 5-deoxyadenosylcobalamin. Vitamin B12 cooperates with folic acid (folate) in the synthesis of deoxyribonucleic acid (DNA). A deficiency of either compound leads to disordered production of DNA and, hence, to the impaired production of red blood cells. Vitamin B12 also has a separate biochemical role, unrelated to folic acid, in the synthesis of fatty acids in the myelin sheath that surrounds nerve cells. NURS 611 Exams: NURS 611 Exams: Advanced Pathophysiology Questions and Answers.

 

48. What type of anemia has a defective secretion of intrinsic factor, which is essential for the absorption of vitamin B12.

Pernicious anemia is a chronic illness caused by impaired absorption of vitamin B-12 because of a lack of intrinsic factor (IF) in gastric secretions. It occurs as a relatively common adult form of anemia that is associated with gastric atrophy and a loss of IF production and as a rare congenital autosomal recessive form in which IF production is lacking without gastric atrophy.

 

49. Additional information that will be on the test per the Panopto recording:

-There are 2 characteristics that allow erythrocytes to function as gas carriers: they are reversible deformability and biconcavity.