D236 Pathophysiology Final Exam Study Guide

D236 Pathophysiology Final Exam Study Guide

Student Name

Western Governors University

D236 Pathophysiology

Prof. Name:

Date

Clinical Case Review and Physiological Interpretations

1. Acid–Base Imbalance and Respiratory Compensation

Question:
A patient with a viral illness and severe vomiting presents with an elevated CO₂ level and a blood pH of 7.53. The patient is breathing slowly. What condition does the patient have?

• Respiratory acidosis

• Respiratory alkalosis

• Metabolic acidosis

• Metabolic alkalosis

Answer:
The correct diagnosis is metabolic alkalosis.

Explanation:
In this case, both the pH and CO₂ levels are elevated, moving in the same direction. This pattern is consistent with a metabolic origin rather than a respiratory one. The vomiting leads to a loss of hydrogen ions and chloride, raising the blood pH. The respiratory system compensates by slowing the respiratory rate, which increases CO₂ retention and helps balance the alkalosis.

Table 1
Summary of Acid–Base Relationship

2. Fluid Balance and Hormonal Response in Dehydration

Question:
What happens in a dehydrated patient?

• ADH levels decrease and RAAS is activated.

• ADH levels decrease and RAAS is inactivated.

• ADH levels increase and RAAS is inactivated.

• ADH levels increase and RAAS is activated.

Answer:
The correct response is that ADH levels increase and RAAS is activated.

Explanation:
When dehydration occurs, osmoreceptors in the hypothalamus detect increased plasma osmolality and signal the posterior pituitary to release antidiuretic hormone (ADH). ADH acts on the kidneys to reabsorb water. Simultaneously, decreased renal perfusion activates the renin-angiotensin-aldosterone system (RAAS), leading to sodium and water retention and vasoconstriction. These combined actions restore blood pressure and fluid balance.

3. Mechanism of ACE Inhibitors

Question:
How do ACE inhibitors lower blood pressure?

• The decrease in the production of angiotensin II keeps blood vessels more dilated, lowering blood pressure.

Answer:
ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. The reduction in angiotensin II levels promotes vasodilation, decreases aldosterone secretion, and ultimately reduces blood pressure.

Table 2
Effects of ACE Inhibition on Blood Pressure Regulation

4. Anion Gap in Diabetic Ketoacidosis (DKA)

Question:
In diabetic ketoacidosis, what happens to the anion gap?

• Because HCO₃⁻ is consumed, the anion gap increases.

Answer:
In DKA, ketone bodies accumulate in the blood, consuming bicarbonate (HCO₃⁻) as a buffering response. This results in a decreased measured bicarbonate level and an increased anion gap.

Table 3
Anion Gap Calculation and Interpretation

5. Potassium Regulation in Dialysis

Question:
In patients with end-stage renal disease, how should potassium be removed during dialysis?

• The dialysate should have a lower concentration of potassium than that of the bloodstream.

Answer:
Dialysis removes solutes through diffusion. When the dialysate has a lower potassium concentration, potassium naturally moves from the blood into the dialysate, reducing serum potassium levels and minimizing cardiac complications.

6. Genetic Probability in Hemophilia

Question:
If a woman is a carrier for hemophilia and her baby is a boy, what is the probability her son will have hemophilia?

• 50%

Answer:
Because hemophilia is X-linked recessive, a carrier mother (one affected X chromosome) has a 50% chance of passing the defective gene to her son, who would then express the disease due to having only one X chromosome.

7. Sickle Cell Disease and Gene Therapy

Question:
How does sickle cell anemia affect the body, and how can gene therapy help?

Answer:
Sickle cell anemia results from a mutation in the β-globin gene, leading to defective adult hemoglobin (HbS). The body still retains the normal gene for fetal hemoglobin (HbF). Gene therapy reactivates HbF production, compensating for the defective HbS and improving oxygen transport.

8. Effects of Alcohol on Fetal Brain Development

Question:
Which effect does alcohol consumption during pregnancy have on brain development?

• It decreases brain volume.

Answer:
Prenatal exposure to alcohol results in fetal alcohol spectrum disorders (FASD), which are associated with reduced overall brain volume, particularly affecting the corpus callosum, cerebellum, and frontal lobes, leading to cognitive and behavioral deficits.

9. Down Syndrome Etiology

Question:
What causes Down syndrome?

• An extra copy of chromosome 21.

Answer:
Down syndrome (Trisomy 21) occurs due to the presence of a third copy of chromosome 21, resulting in characteristic facial features, developmental delays, and increased risk for congenital heart disease and hypothyroidism.

10. Blood Loss and Hormonal Response

Question:
What physiological response is expected following significant blood loss?

• ADH will stimulate the kidneys to reabsorb more water.

Answer:
In response to hypovolemia, ADH (vasopressin) is released to conserve water by promoting reabsorption in the renal tubules. This compensatory mechanism helps stabilize blood volume and pressure after hemorrhage.

11. Respiratory Rate and pH Balance During Exercise

Question:
How does increased respiratory rate during exercise help maintain pH homeostasis?

• The increased exhalation of CO₂ helps to increase pH.

Answer:
During exercise, elevated metabolism produces excess CO₂. Faster breathing eliminates CO₂, reducing carbonic acid formation and preventing acidosis, thereby maintaining a near-neutral pH.

12. Arterial Blood Gas Imbalance in ICU Patient

Question:
An ICU patient’s arterial blood gas results show a low pH and low CO₂ levels, and the patient’s respiratory rate is increased. What condition does the patient have?

• Metabolic acidosis

• Metabolic alkalosis

• Respiratory alkalosis

• Respiratory acidosis

Answer:
The correct diagnosis is metabolic acidosis.

Explanation:
The simultaneous decrease in both pH and CO₂ indicates that CO₂ reduction is a compensatory mechanism rather than the primary cause. In metabolic acidosis, the body increases the respiratory rate to expel more CO₂, reducing the acidity caused by metabolic disturbances such as lactic acid accumulation or renal failure.

13. Dialysis and Home-Based Kidney Management

Question:
Which dialysis method allows a patient with kidney disease to manage treatment at home?

• Peritoneal dialysis

Answer:
Peritoneal dialysis (PD) uses the patient’s own peritoneal membrane as a semi-permeable barrier to filter wastes and excess electrolytes. This treatment can be performed at home, providing greater independence for patients with chronic renal failure.

Table 4
Comparison of Dialysis Modalities

14. Compensation for Pulmonary Edema

Question:
How does the body compensate for elevated CO₂ levels in pulmonary edema?

• The kidneys excrete more H⁺ and conserve HCO₃⁻.

Answer:
In pulmonary edema, CO₂ retention leads to increased carbonic acid formation and a reduced pH (respiratory acidosis). The renal system compensates by excreting hydrogen ions and conserving bicarbonate to help normalize the pH.

15. Inflammatory Response Mechanisms

Question:
A patient stung by a bee exhibits redness and swelling. Which response is unlikely to occur?

• Vasoconstriction at the site of the sting causing fluid accumulation.

Answer:
Vasodilation, not vasoconstriction, is the hallmark of inflammation. Histamine release from mast cells increases capillary permeability, allowing immune cells and plasma proteins to enter the affected tissue, producing redness (erythema) and swelling (edema).

16. Function of Helper T Cells

Question:
What is the role of helper T cells?

• They produce cytokines, which activate B cells and cytotoxic T cells.

Answer:
Helper T cells (CD4⁺) coordinate immune responses by releasing cytokines that stimulate B cells to produce antibodies and activate cytotoxic T cells to destroy infected or malignant cells. They play a central role in adaptive immunity.

17. Genetic Basis of Red–Green Color Blindness

Question:
What is red–green color blindness?

• Sex-linked genetic disorder.

Answer:
Red–green color blindness is an X-linked recessive trait. Males are more frequently affected since they possess a single X chromosome; thus, inheriting the defective allele results in color vision deficiency.

18. Neurobehavioral Congenital Abnormality (ND-PAE)

Question:
What causes ND-PAE?

• Prenatal exposure to alcohol.

Answer:
Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE) arises from maternal alcohol consumption during pregnancy. It results in cognitive deficits, impaired impulse control, and abnormal brain structure development.

19. Neural Tube Defect: Spina Bifida

Question:
Which developmental defect occurs in spina bifida?

• Failure of the neural tube to close results in a fluid-filled sac on the lower back.

Answer:
Spina bifida develops when the neural tube fails to close during embryonic development. Depending on severity, it can involve protrusion of meninges or spinal cord elements, leading to neurological impairment.

20. Fracture with Bone Fragments

Question:
An x-ray shows visible bone fragments after a hip fracture. What type of fracture is this?

• Comminuted fracture.

Answer:
A comminuted fracture involves the bone breaking into multiple fragments, commonly resulting from high-impact trauma. Surgical stabilization is often required for proper healing.

D236 Pathophysiology Final Exam Study Guide

21. Ankle Sprain Severity

Question:
A patient presents with a swollen, bruised ankle and difficulty bearing weight. What type of injury is this?

• Grade II sprain.

Answer:
A grade II sprain involves partial tearing of ligaments, moderate swelling, and pain with limited joint function. It typically requires rest, compression, and physical therapy.

22. Glucocorticoids and Bone Health

Question:
Why are patients on glucocorticoids more susceptible to bone diseases such as rickets?

• Glucocorticoids inhibit vitamin-D–dependent calcium absorption.

Answer:
Chronic glucocorticoid use reduces intestinal calcium absorption, leading to hypocalcemia and impaired bone mineralization, increasing the risk of rickets in children and osteoporosis in adults.

23. Cervical Degenerative Disc Disease

Question:
Which symptom is not associated with cervical degenerative disc disease?

• Low back pain.

Answer:
Cervical disc disease primarily causes neck pain, arm weakness, and tingling sensations in the upper extremities. Low back pain is typically linked to lumbar disc disease.

24. Compartment Syndrome After Tibial Fracture

Question:
What complication arises from elevated compartment pressure after a fracture?

• Compartment syndrome.

Answer:
Compartment syndrome occurs when swelling and bleeding increase pressure within a closed muscle compartment, compromising blood flow and nerve function. Immediate fasciotomy is required to prevent tissue necrosis.

25. Melanoma Identification

Question:
A flat, irregularly shaped, dark lesion on the back measuring 8 mm is observed. What is the most likely diagnosis?

• Melanoma.

Answer:
Melanoma presents as an irregular, asymmetrical lesion with variegated pigmentation and diameter >6 mm. Early detection is critical due to its high metastatic potential.

26. Burn Classification After Sun Exposure

Question:
An adolescent with bright red, painful, swollen skin after sun exposure most likely has what type of burn?

• Superficial burn.

Answer:
A superficial burn (first-degree) affects only the epidermis and is characterized by redness, pain, and swelling without blistering. Healing typically occurs within a few days without scarring.

27. Burn Surface Area Estimation

Question:
Using the Rule of Nines, what is the total body surface area burned if the anterior face and neck, both arms, lower legs, and upper torso are affected?

• 58.5%.

Answer:
By applying the Rule of Nines, partial regions of the body are summed to estimate the affected area. Accurate BSA estimation is vital for calculating fluid replacement using the Parkland formula.

28. Vitiligo and Skin Depigmentation

Question:
A patient presents with smooth, white patches of skin that burn easily in sunlight. What is the most likely diagnosis?

• Vitiligo.

Answer:
Vitiligo results from the autoimmune destruction of melanocytes, leading to depigmented areas of skin. It is benign but can have psychosocial impacts due to cosmetic appearance.

29. Fungal Infection of the Scalp

Question:
A child has a scaly, itchy scalp lesion that fluoresces yellow-green under a Wood’s light. What is the diagnosis?

• Tinea capitis.

Answer:
Tinea capitis is a dermatophyte infection of the scalp, typically caused by Microsporum or Trichophyton species. It presents with scaling, hair loss, and pruritus and is treated with antifungal agents.

30. Hemorrhagic Stroke Mechanism

Question:
What happens during a hemorrhagic cerebrovascular accident (CVA)?

• A blood vessel ruptures in the brain, causing bleeding and lack of blood flow to the area.

Answer:
A hemorrhagic stroke results from the rupture of a cerebral artery, often due to hypertension or aneurysm rupture, leading to intracerebral bleeding, increased intracranial pressure, and neuronal death.

31. Peripheral Neuropathy in Diabetes

Question:
What causes peripheral neuropathy in patients with diabetes mellitus?

• High blood glucose levels damage the vasa nervorum, leading to nerve ischemia.

Answer:
Persistent hyperglycemia results in microvascular injury to the small blood vessels supplying nerves (the vasa nervorum). This impairs oxygen delivery, causing demyelination and axonal degeneration. Symptoms include numbness, tingling, and burning pain, particularly in the feet and hands.

32. Iron-Deficiency Anemia

Question:
A patient presents with pallor, fatigue, and low hemoglobin and hematocrit levels. What type of anemia is most likely?

• Iron-deficiency anemia.

Answer:
Iron deficiency reduces hemoglobin synthesis, producing microcytic, hypochromic red blood cells. Common causes include chronic blood loss, dietary deficiency, or malabsorption.

Table 5
Characteristics of Common Anemias

33. Pernicious Anemia

Question:
Which vitamin deficiency causes pernicious anemia, and why?

• Vitamin B₁₂ deficiency due to lack of intrinsic factor.

Answer:
Pernicious anemia arises when autoimmune destruction of gastric parietal cells leads to decreased intrinsic factor production, impairing vitamin B₁₂ absorption. This deficiency disrupts DNA synthesis in developing red blood cells, resulting in macrocytosis and neurological symptoms.

34. Leukemia and Bone Marrow Function

Question:
How does leukemia affect blood cell production?

• It causes uncontrolled proliferation of abnormal white blood cells, crowding out normal cell lines.

Answer:
Leukemia originates in bone marrow stem cells, producing immature, dysfunctional leukocytes. The overcrowding suppresses erythropoiesis and thrombopoiesis, leading to anemia, infection, and bleeding tendencies.

35. Disseminated Intravascular Coagulation (DIC)

Question:
What is disseminated intravascular coagulation?

• A pathological activation of coagulation causing both clotting and bleeding.

Answer:
In DIC, widespread activation of the coagulation cascade forms microthrombi that consume clotting factors and platelets. The paradoxical result is simultaneous thrombosis and hemorrhage, often secondary to sepsis or trauma.

36. Hypertension Pathophysiology

Question:
What is a major physiological change in primary hypertension?

• Increased systemic vascular resistance.

Answer:
Chronic arteriolar vasoconstriction elevates afterload and blood pressure. Structural vascular remodeling perpetuates this resistance, leading to left ventricular hypertrophy and end-organ damage if untreated.

37. Atherosclerosis Development

Question:
Describe the steps leading to atherosclerosis.

Answer:
Atherosclerosis begins with endothelial injury, allowing LDL cholesterol infiltration. Oxidized LDL triggers macrophage recruitment, forming foam cells and fatty streaks. Over time, fibrous plaques narrow arterial lumens, predisposing to ischemia and thrombosis.

Table 6
Stages of Atherosclerotic Plaque Formation

38. Myocardial Infarction (MI)

Question:
What causes chest pain in myocardial infarction?

• Ischemia leading to anaerobic metabolism and lactic acid accumulation.

Answer:
When coronary arteries are occluded, oxygen delivery to the myocardium declines. The cells switch to anaerobic metabolism, producing lactic acid that irritates nerve endings and causes the characteristic chest pain.

39. Heart Failure

Question:
Why do patients with left-sided heart failure experience pulmonary symptoms?

• Blood backs up into pulmonary circulation, increasing hydrostatic pressure.

Answer:
Left ventricular dysfunction impedes forward blood flow, causing pulmonary venous congestion. Elevated capillary pressure leads to transudation of fluid into alveoli, manifesting as dyspnea and pulmonary edema.

40. Right-Sided Heart Failure

Question:
What signs are typical of right-sided heart failure?

• Peripheral edema, ascites, and jugular venous distension.

Answer:
Right ventricular failure results in systemic venous congestion. Venous return from peripheral tissues slows, causing fluid accumulation in dependent areas and abdominal organs.

D236 Pathophysiology Final Exam Study Guide

41. Shock States

Question:
How does shock lead to cellular injury?

• Inadequate tissue perfusion causes hypoxia and anaerobic metabolism.

Answer:
All shock types share insufficient oxygen delivery to cells. The resulting switch to anaerobic metabolism increases lactic acid, decreases ATP production, and leads to cellular dysfunction and death if untreated.

Table 7
Major Types of Shock

42. Deep Vein Thrombosis (DVT)

Question:
What triad of factors predisposes to DVT?

• Venous stasis, endothelial injury, and hypercoagulability (Virchow’s triad).

Answer:
Prolonged immobility, vascular trauma, or hypercoagulable states promote clot formation in deep veins. Detached thrombi can migrate to the lungs, causing pulmonary embolism—a medical emergency.

43. Pulmonary Embolism (PE)

Question:
What is the physiological consequence of a large pulmonary embolism?

• Impaired gas exchange and increased pulmonary vascular resistance.

Answer:
A large embolus obstructs pulmonary arteries, preventing perfusion of ventilated alveoli. This ventilation-perfusion mismatch leads to hypoxemia, elevated pulmonary pressures, and potentially right ventricular failure.

44. Endocarditis

Question:
What is the pathogenesis of infective endocarditis?

• Bacterial colonization of damaged heart valves leads to vegetative lesions.

Answer:
Turbulent blood flow or congenital defects damage endocardial surfaces, allowing bacterial adherence during transient bacteremia. Vegetations form, impairing valve function and releasing emboli into circulation.

45. Rheumatic Heart Disease

Question:
How does rheumatic fever cause heart valve damage?

• Autoimmune cross-reactivity between streptococcal antigens and cardiac tissue.

Answer:
Following Streptococcus pyogenes infection, antibodies targeting bacterial M proteins cross-react with myocardial and valvular proteins, resulting in inflammatory scarring and chronic valvular stenosis or regurgitation.

46. Peripheral Arterial Disease (PAD)

Question:
Why does PAD cause intermittent claudication?

• Ischemia during exertion limits oxygen to skeletal muscles.

Answer:
Atherosclerotic narrowing of peripheral arteries reduces blood flow. During activity, oxygen demand exceeds supply, causing pain or cramping that subsides with rest.

47. Varicose Veins

Question:
What leads to varicose veins?

• Incompetent venous valves cause blood pooling and venous dilation.

Answer:
Valve insufficiency in superficial veins allows backflow, increasing hydrostatic pressure and causing tortuous, distended veins, often in the lower extremities.

48. Aneurysm Formation

Question:
What structural weakness predisposes to aneurysm formation?

• Degeneration of the arterial media layer.

Answer:
Loss of elastin and smooth muscle integrity in the tunica media weakens the vessel wall, promoting localized dilation. Rupture risk increases with size and blood pressure.

49. Hypertensive Crisis

Question:
Why is hypertensive crisis life-threatening?

• Rapidly elevated pressure damages endothelium, leading to encephalopathy or renal failure.

Answer:
Severe hypertension (>180/120 mm Hg) overwhelms autoregulatory mechanisms, causing vascular leakage, cerebral edema, and acute end-organ dysfunction.

50. Raynaud’s Phenomenon

Question:
What triggers Raynaud’s phenomenon?

• Vasospasm of small arteries in response to cold or stress.

Answer:
Episodic constriction of digital arterioles reduces blood flow, causing color changes (white-blue-red) and numbness or pain. It is commonly secondary to autoimmune diseases like scleroderma.