Pathophysiology and Pharmacology Essay Assignment

Pathophysiology and Pharmacology Essay Assignment

NUR-641E Midterm Exam Study Guide

39.Be familiar with the signs/symptoms and therapy for asthma.

Asthma is a chronic disease characterized by airway inflammation, bronchial hyperresponsiveness, and outflow obstruction. Exposure to allergens triggers symptoms Signs and symptoms include chest pain, chest tightness, coughing, wheezing on exhalation, shortness of breath, trouble sleeping.

Treatment approach; in the emergency setting, secure airway, breathing, and circulation. Start oxygen if oxygen saturations are low. Nebulization using a short-acting beta-agonist such as albuterol and ipratropium bromide. Outpatient treatment includes using an albuterol inhaler, corticosteroids such as prednisolone, and antibiotics to manage pneumonia that could exacerbate symptoms. Finally, allergen avoidance is key to preventing exacerbations.

40. Know what pathophysiologic factors increase respiratory rate. Pathophysiology and Pharmacology Essay Assignment

Either an increase in carbon dioxide or a decline in oxygen level can increase respiratory rate. For instance, a state of metabolic acidosis increases respiratory rate. In addition, several conditions, including asthma, pneumonia, anxiety, use of narcotics, congestive heart failure, chronic obstructive pulmonary disease, drug overdose, and diabetic ketoacidosis, can increase respiratory rate.

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41. Know how to interpret an arterial blood gas (ABG).

Acid-base imbalance is described in terms of either metabolic or respiratory derangement. It can be acidosis or alkalosis. Interpretation of ABG requires understanding various parameters included in the ABG report. These parameters include pH, partial pressures of Oxygen and Carbon dioxide (PaO2 and PaCO2), bicarbonate, base excess, and lactate levels. For instance, Normal _PH is between 7.35-7.45. any Ph <7.35 is acidic while >7.45 is alkalosis. Bicarbonate assesses the metabolic state and the functioning of kidneys. Normal level is 22-26 mEq/L. PCO2 assesses the respiratory function with normal between 35-45mmHg. The table below summarizes the patterns that could help identify either a metabolic or respiratory derangement.

Acid-base imbalance	Ph(7.35-7.45)	PCO2 (35-45)	Bicarbonate (22-26)
Respiratory alkalosis	Increased >7.45	Decreased <35	Decreased <22
Respiratory acidosis	Decreased <7.35	Increased >45	Increased >26
Metabolic alkalosis	Increased	Increased	Increased
Metabolic acidosis	Decreased	Decreased	Decreased

 

 

42. Know the ABGs for metabolic acidosis, metabolic alkalosis, respiratory alkalosis, and respiratory acidosis.

The table above summarizes different ABGs for various acid-base imbalance. Note that for respiratory derangement, if the PH is increased, then bicarbonate and PCO2 decrease and vice versa. However, in metabolic case, an increase in PH is associated with an increase of both bicarbonate and PCO2 and vice versa. Pathophysiology and Pharmacology Essay Assignment

43. Know the causes of respiratory acidosis.

Respiratory acidosis results from any condition that leads to reduced respiratory rate and accumulation of CO2 in the body. Causes include

1. Impaired respiratory drive; toxin overdose, head injury, and comatose state.
2. Airflow obstruction: foreign body, asthma, sleep apnea, pulmonary edema, COPD, pulmonary fibrosis
3. Be able to explain COPD and stepwise therapy (additions to current COPD medications) in its treatment.

COPD is a chronic inflammatory lung condition that leads to airway obstruction. It can either be emphysema or chronic bronchitis. Symptoms include cough, shortness of breath, wheezing, and difficulty breathing.

Stepwise therapy: Management is achieved through lifestyle modification, medications, and surgery step-wise. The first step is education on smoking cessation. The subsequent step includes short-acting bronchodilator (albuterol); long-acting bronchodilator (salmeterol); rehabilitation; inhaled corticosteroids (beclomethasone); oxygen, and surgery (lung transplant)

45. Know the cause for infant weight loss in the early postnatal period.
46. Acute infections
47. Allergy to milk protein
48. Child neglect
49. Malnutrition; limited caloric intake
50. Pyloric stenosis
51. Neonatal complications such as jaundice dehydration leading to renal failure
52. Be able to explain hypoxemia at altitude (reduced oxygen inspiration).

Hypoxemia results when an individual from low altitude areas visits high altitude areas (above 2500meters above sea level). In high-altitude areas, the oxygen concentration is constant while there is a reduction in barometric pressure. This reduction proportionately reduces oxygen partial pressure leading to reduced oxygen levels. Individuals compensate by hyperventilating.

47. Discuss how pulmonary arterial hypertension is associated with right ventricular hypertrophy and an enlarged pulmonary artery.

Pulmonary artery hypertension results from increased pressures within the pulmonary vessels. Consequently, the increased pressure leads to vascular engorgement and enlargement. In addition, the increased pulmonary pressure increases the pressures in the right ventricles with a resultant increase in afterload. To compensate for these changes, the right ventricle hypertrophies to overcome the pressures. Unfortunately, failure to offer early treatment leads to right-sided heart failure. Pathophysiology and Pharmacology Essay Assignment

48. Be able to explain fluid and electrolyte disorders.

Electrolyte and fluid derangement results from increased loss through vomiting, diarrhea, burns, sweating, or underlying conditions such as chronic kidney injury. These disorders can lead to increased or decreased fluids and electrolytes. Such disorders include

• Calcium- hypercalcemia or hypocalcemia
• Potassium: hyperkalemia or hypokalemia.
• Chloride: hypochloremia or hyperchloremia.
• Sodium: hypernatremia or hyponatremia.
• Phosphate: hypophosphatemia and hyperphosphatemia.
• Magnesium: hypermagnesemia or hypomagnesemia.

Signs and symptoms of electrolyte imbalances

Confusion, headache, irritability, muscle weakness and cramping, fatigue, lethargy, irregular heartbeat, lethargy, convulsions, vomiting, tachycardia, and abdominal cramping.

49. Know the laboratory values of magnesium, calcium, sodium, and potassium.

Normal electrolyte ranges.

1. Sodium; 136-144mEq/L
2. Potassium; 3.5-5.0mEq/L
3. Chloride 97-105mmol/L
4. Calcium: 2.16-2.60mEq/L
5. Magnesium: 1.4-1.9mEq/L

50.Be able to explain how aldosterone affects sodium and water.

Aldosterone causes an increase in the reabsorption of salt and water in the kidney nephrons. This leads to increased blood volume, stabilization of blood pressure, and restoration of salt levels.

51. Know the mechanism of action of each diuretic class.

Loop diuretics

Examples: furosemide

MOA: they inhibit the Na+/K+/2Cl- co-transporter in the ascending loop of Henle, leading to loss of sodium, potassium, and chloride through urine.

Thiazide diuretics

Example: hydrochlorothiazide

MOA: they inhibit NaCl reabsorption in the distal convoluted tubule by inhibiting the co-transporter.

Potassium sparing diuretic

Example: spironolactone, amiloride

MOA: they inhibit the entry of aldosterone into the principal cells of the collecting duct and distal tubule. The result is a loss of sodium and water while sparing potassium.

Carbonic anhydrase:

Example: acetazolamide

MOA: they inhibit the carbonic anhydrase enzyme in the proximal convoluted tubule resulting in reduced bicarbonate reabsorption. There is also reduced sodium absorption and potassium retention.

Osmotic diuresis

Example: mannitol

MOA: they inhibit water and sodium reabsorption, increasing the osmolarity of blood and renal infiltrate.

52. Know the effects of atrial natriuretic peptide (ANP).

ANP is a small peptide secreted by the heart in the presence of atrial stretch and high blood pressure. Upon secretion, it causes vasodilation of afferent arterioles leading to an increase in renal blood flow and increased glomerular filtration rate. This, in turn, leads to increased renal excretion of sodium and water. These actions lead to volume depletion with resultant lowering of blood pressure.

53. Be able to explain the relationship between edema and oncotic pressure.

A decrease in the oncotic pressure results in edema. Plasma oncotic pressure is maintained by proteins. Proteins are negatively charged, and large molecules cannot pass through the glomerular filtrate. However, in conditions such as nephrotic syndrome, there is a breakage of barrier leading to loss of proteins. This results in a reduction in oncotic pressure. A decrease in oncotic pressure combined with increased hydrostatic pressure and vascular permeability results in edema.

54. Be able to differentiate corticosteroids by potencies, mechanism of action, and pharmacokinetics.

Corticosteroids can be classified as either mineralocorticoids or glucocorticoids.  Glucocorticoids mimic the actions of cortisol to achieve anti-inflammatory and immunosuppression. On the other hand, mineralocorticoids mimic aldosterone function while causing anti-inflammation and immunosuppression. They are available in different forms, including tablets, injections, topical, and inhaled agents. In terms of potency, hydrocortisone is as potent as cortisol. Prednisone is four-time as potent as hydrocortisone. In terms of pharmacokinetics, they have a high oral bioavailability, are metabolized by hepatic enzymes, transported in the bloodstream bound to plasma proteins, and excreted in the urine.

55. Be able to explain how angiotensin affects the cardiovascular system.

Angiotensin II is known to increase blood pressure, activate the sympathetic nervous system, increase aldosterone secretion, and vasoconstriction of blood vessels. It also causes an increase in the synthesis of collagen type I and II that lead to the thickening of vascular walls and myocardium. Finally, it regulates cardiac contractility, remodeling, growth, and apoptosis.

56. Know the unique pharmacokinetics of amiodarone.

Absorption of amiodarone following oral intake is erratic and unpredictable, with an oral bioavailability range of 22-86%. It is highly lipophilic with a large volume of distribution.  Elimination is majorly by metabolism, with less than 1% of unchanged product excreted through urine.

57. Amiodarone can cause thyroid and pulmonary toxicity. How? Pathophysiology and Pharmacology Essay Assignment

Amiodarone has a large amount of iodine which can affect the functioning of the thyroid. It can cause either toxicity due to hypo or hyperthyroidism.  Pulmonary toxicity is a slow process on the long-term use of amiodarone. It manifests as either chronic interstitial pneumonitis or pulmonary fibrosis.

58. Know what drugs are used for angina: beta-adrenergic antagonists (beta-blockers), angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), nitrates, calcium channel blockers (CCBs).

Beta-blockers- they slow the heart rate to reduce oxygen demand of the heart and reduce the frequency of angina attacks.

59. Remember that many heart failure patients have more than just heart failure; look for underlying hypertension, angina, etc. why?

Heart failure is the presentation of an underlying disease. Its treatment necessitates understanding the underlying pathology while treating them. Various causes include diabetes mellitus, hypertension, hypercholesterolemia, atherosclerosis, coronary artery disease, thyroid disease, and valve disease, among others.

60. Be able to describe how electrolyte serum levels affect digoxin serum levels.

Electrolyte disturbances, including hypercalcemia, hypokalemia, and hypomagnesemia, cause increased sensitivity to digoxin, leading to digoxin toxicity even in a lower concentration of digoxin in the serum.

61. Know how hyperkalemia is caused by renal failure and Addison’s disease.

Hyperkalemia is a state of high potassium levels. In chronic kidney disease, both filtration and excretion of Potassium are inhibited, leading to the accumulation of potassium in the bloodstream leading to hyperkalemia. In Addison`s disease, there is a deficiency of aldosterone, a hormone that causes increased urinary potassium excretion. Therefore, in hypoaldosteronism, there is limited excretion with increased potassium retention, leading to hyperkalemia.

62. Know how to treat hypercalcemia with calcitonin and pamidronate (nitrogen-containing bisphosphonate).

A combination of calcitonin and pamidronate is effective in the rapid and long-term control of hypercalcemia. Calcitonin is a rapidly acting antiresorptive and causes calceuretic effects to reduce serum calcium. Pamidronate offers long-term control of calcium. They have no significant side effects.

63. What is compensatory hyperplasia?

Compensatory hyperplasia is the proliferation of human cells while maintaining their differentiated structure and function. It can occur due to either organ damage, removal of an organ, or cessation of one organ’s function. Examples include regeneration of liver cells after liver injury and unilateral kidney hyperplasia in conditions such as renal agenesis and ectopic multisystem kidney dysplasia.

64. What are the effects of nonsteroidal anti-inflammatory drugs (NSAIDs)?

NSAIDs are medications indicated for pain, fever, and other inflammatory processes. Side effects include peptic ulcer disease, acute renal dysfunction, nephrotic syndrome, hepatotoxicity, increased bleeding tendencies, atrial fibrillation, high blood pressure, tinnitus, headaches, abdominal pain, and dizziness.

65. An NSAID safe for use in CAD patients is naproxen.

Naproxen is a reversible inhibitor of COX-1. It limits platelet aggregation and clot formation. Unlike other NSAIDs, naproxen is safe for CAD with minimal risk of bleeding.

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66.NSAIDs can cause GI bleeding (indicated by the darkening of stools and epigastric pain); one recommendation is to switch to a COX-2 inhibitor (i.e., celecoxib).

NSAIDs block the COX-1 enzyme and disrupt prostaglandin production in the stomach. Reduced prostaglandins favor irritation and subsequent bleeding. Use of COX-2 inhibitors such as celecoxib limits GI bleeding.

67. Corticosteroids include glucocorticoids (e.g., prednisone, prednisolone, dexamethasone, hydrocortisone, methylprednisolone) and mineralocorticoids (e.g., aldosterone).
68. Patients on corticosteroids should be monitored for changes in the skin, muscle wasting, blood pressure, weight gain, blood glucose, vitamin D levels, and any vision changes.

The use of corticosteroids is associated with various side effects, including thinning of the skin, drug induced hypertension, muscle atrophy, fat deposition in the abdomen, back, and face leading to weight gain, glaucoma, cataracts, osteoporosis, vitamin D deficiency, and increased rate of infections due to immunosuppression. All these parameters must be monitored in patients taking corticosteroids. Pathophysiology and Pharmacology Essay Assignment

69. What are the side effects of diphenhydramine?

Side effects include drowsiness, vomiting, constipation, dizziness, dry mouth, nose and throat, loss of appetite, blurred vision, stomach upset, and allergic reactions. Long-term side effects include dementia, memory loss, anxiety, and dependence.

70. Understand the advantage of second-generation antihistamines like loratadine.

Advantages of the second generation over first-generation antihistamine include lack of sedation and impairment of the performance, longer duration of actions, and absence of anticholinergic side effects such as dry mouth.

71. Know how long after ingestion it takes dimenhydrinate (Dramamine) to prevent motion sickness.

Dimenhydrinate should be taken 30 minutes to 1 hour before traveling to prevent motion sickness. Repeated doses can be taken every 4 to 6 hours to prevent motion sickness.

72. Patients with a history of kidney stones should avoid products containing calcium.

Calcium oxalate is a major component of kidney stones. Increased serum calcium levels from calcium-containing compounds predispose to the formation of kidney stones. This may worsen pain in patients with kidney stones.

73. Know the factors predisposing individuals to antibiotic resistance.

Excessive and unnecessary use of antibiotics are the major contributors to antibiotic resistance. Other factors include over-prescription of antibiotics, failure to finish the course of antibiotic treatment, poor infection control measures in a healthcare setting, poor sanitation and hygiene, and emergence of resistant bacterial strains.

74. Fluoroquinolones have a boxed warning for tendon rupture.

Prolonged use or overdose of fluoroquinolones causes tendinitis and the rupture of the Achilles tendon. Effects can occur in acute setting of fluoroquinolones use or months after discontinuing these medications.

75. Know the predisposing factors for pseudomembranous colitis.

Predisposing factors include:

• Increasing age > 65 years
• Immunocompromised state from other medical conditions, including diabetes, hypertension, HIV, and heart failure.
• Long term intake of antibiotics/ prior history of antibiotic intake. They include clindamycin, ampicillin, fluoroquinolones, and cephalosporins.
• Following intestinal surgery.
• Presence of colon diseases such as inflammatory bowel disease
• Prolonged hospital stay or staying in a nursing home.
• Infection by clostridium defficile bacteria.
• History of pseudomembranous colitis in the past

 

76. Chronic pain is pain not due to cancer or a recognized medical condition lasting more than 3-6 months.

Chronic pain is long-standing pain persisting beyond the usual recovery time. It can be constant or intermittent. It affects the ability of an individual to work while lowering the quality of life. Chronic conditions such as cancers and underlying medical conditions that damage nerve cells leading to chronic pain. It can be permanent if the cause is not identified and treated. Pathophysiology and Pharmacology Essay Assignment