In which autoimmune disease is a Type IV hypersensitivity reaction prominently involved?
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Multiple sclerosis
Graves’ disease
The Correct Answer is C
A. Rheumatoid arthritis primarily involves Type 3 hypersensitivity, where immune complexes deposit in the synovial joints to trigger inflammation. While T-cells are present, the formation of rheumatoid factor complexes is a central pathological feature. It represents a systemic autoimmune response characterized by both antibody-mediated and cell-mediated damage, but Type 3 is highly prominent.
B. Systemic lupus erythematosus (SLE) is the prototypical Type 3 hypersensitivity disorder involving the systemic deposition of antigen-antibody complexes. These complexes circulate and lodge in various tissues, such as the kidneys and skin, leading to complement activation and tissue destruction. It is not primarily defined by the delayed, cell-mediated mechanisms of Type IV hypersensitivity.
C. Multiple sclerosis is an autoimmune disorder driven by Type IV hypersensitivity, where autoreactive T-lymphocytes cross the blood-brain barrier to attack the myelin sheath. These T-cells release cytokines that activate macrophages, leading to the destruction of oligodendrocytes in the central nervous system. This delayed, cell-mediated immune response results in the characteristic plaque formation and neurodegeneration.
D. Graves’ disease is a Type 2 hypersensitivity reaction where autoantibodies specifically target and stimulate the thyroid-stimulating hormone (TSH) receptor. This leads to the autonomous overproduction of thyroid hormones, resulting in hyperthyroidism. The pathology is caused by direct antibody-receptor interaction rather than the sensitized T-cell activity that characterizes Type IV hypersensitivity.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A. Chronic obstructive pulmonary disease causes chronic alveolar hypoxia, which triggers pulmonary arteriolar vasoconstriction and subsequent pulmonary hypertension. This increased resistance in the pulmonary circuit forces the right ventricle to work harder, eventually leading to Cor Pulmonale. In this scenario, the right-sided failure is primary and independent of left ventricular dysfunction.
B. A myocardial infarction affecting the left ventricle is the most common cause of secondary right-sided heart failure. As the left ventricle fails, blood backs up into the pulmonary circulation, increasing the pressure that the right ventricle must overcome. This does not represent an isolated right-sided failure, as the pathology originated in the left heart.
C. Systemic hypertension primarily increases the afterload on the left ventricle, leading to left-sided hypertrophy and eventual failure. Any subsequent right-sided failure would be a secondary consequence of pulmonary venous congestion caused by the failing left side. This mechanism involves both chambers and does not explain isolated right-sided ventricular dysfunction or Cor Pulmonale.
D. Aortic valve stenosis creates a pressure gradient that the left ventricle must overcome to eject blood into the systemic circulation. This leads to left ventricular remodeling and failure, which eventually causes a backup of pressure into the lungs and right heart. It is a classic progression of global heart failure rather than an isolated right-sided event.
Correct Answer is D
Explanation
A. High-sensitivity C-reactive protein does not possess a direct enzymatic role in the lipolysis or breakdown of triglycerides. Adipose tissue metabolism is primarily regulated by hormones like insulin and catecholamines rather than inflammatory markers. While elevated CRP often correlates with metabolic syndrome, it does not function as a lipase in systemic circulation.
B. Increased levels of systemic inflammation, marked by high hs-CRP, are typically associated with decreased levels of high-density lipoprotein cholesterol. Inflammation can impair the reverse cholesterol transport system, leading to lower HDL-C levels and increased cardiovascular risk. This marker does not enhance the synthesis of protective lipoproteins but rather signals vascular stress.
C. Low-density lipoprotein production in the liver is governed by HMG-CoA reductase activity and intracellular cholesterol requirements, not by CRP levels. Although dyslipidemia and inflammation often coexist, hs-CRP is an acute-phase reactant rather than a direct metabolic stimulant for hepatic lipid synthesis. It serves as a biomarker for risk rather than a biosynthetic catalyst.
D. Elevated hs-CRP is a critical biomarker of low-grade systemic inflammation and vascular wall stress, which are essential drivers of atherogenesis. It contributes to the destabilization of atherosclerotic plaques and promotes the recruitment of monocytes into the arterial intima. Its presence indicates a heightened risk for coronary events independent of traditional lipid profiles.
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