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Stage 1 pressure ulcers present with intact skin showing non-blanchable redness, typically over bony prominences, due to localized ischemia from sustained pressure. No skin loss or blistering occurs, as the epidermis remains intact, indicating early tissue stress without ulceration. This does not match the described blister and skin loss, making it incorrect.

Stage 4 pressure ulcers involve full-thickness tissue loss, exposing underlying structures like muscle, bone, or tendons. Severe necrosis and deep tissue damage occur due to prolonged pressure, disrupting blood supply extensively. The described superficial skin loss with a blister does not involve such deep structures, ruling out Stage 4.

Stage 3 pressure ulcers feature full-thickness skin loss, extending into subcutaneous tissue but not to muscle or bone. They may show undermining or tunneling due to tissue necrosis. The described blister with top-layer skin loss suggests partial-thickness damage, not deep enough for Stage 3, making this choice incorrect.

Autosomal dominant disorders affect both genders equally, as they are not sex-linked. Heterozygous individuals express the disorder, not just males, due to the dominant allele on an autosome. The idea of females being carriers only applies to X-linked recessive disorders, making this choice scientifically inaccurate.

Autosomal dominant disorders are caused by mutations on autosomes, not the Y chromosome, which is sex-linked and primarily affects males. These disorders do not typically skip generations, as the dominant allele is expressed in every affected individual, making this choice incorrect.

In autosomal dominant disorders, there is no "carrier" state as in recessive disorders, because heterozygous individuals express the disorder. The 50% probability applies to inheriting the disorder itself, not a carrier genotype, which is a concept relevant to autosomal recessive disorders, making this choice incorrect.

This result shows a slightly acidic pH (7.34) with normal PaCO2 and low HCO3, suggesting metabolic acidosis. Nasogastric suctioning causes loss of acid, not base, so it does not lead to acidosis. This imbalance is inconsistent with the alkalosis expected from gastric acid loss, making it incorrect.

This result indicates a low pH (7.32) and elevated PaCO2, suggesting respiratory acidosis with partial compensation (normal HCO3). Nasogastric suctioning affects gastric acid, causing metabolic, not respiratory, alkalosis. The respiratory parameters here do not align with the condition’s pathophysiology, making this choice incorrect.

This result shows an elevated pH (7.46) and low PaCO2, indicating respiratory alkalosis, likely from hyperventilation, with normal HCO3. Nasogastric suctioning causes metabolic alkalosis due to acid loss, not respiratory changes. The low PaCO2 does not fit the expected metabolic profile, making this choice incorrect.

Facial trauma may increase aspiration risk if swallowing is impaired, but a 21-year-old typically has a robust immune system, reducing pneumonia risk. The trauma does not directly compromise lung defenses or immune function significantly, making this individual less likely to develop pneumonia compared to an immunocompromised person.

Osteoarthritis and chronic knee pain in a 72-year-old may limit mobility, slightly increasing pneumonia risk due to reduced lung expansion. However, this condition does not directly impair immune function or lung clearance mechanisms, making it a lower risk compared to immunodeficiency, which severely predisposes to infections.

Elevated cholesterol in a 48-year-old increases cardiovascular risk but does not directly affect lung function or immune response to infections. Without respiratory or immune compromise, this individual has a lower risk of pneumonia compared to someone with a primary immunodeficiency disorder, making this choice incorrect.

Bradycardia, or slow heart rate, is not typically associated with dehydration. Dehydration reduces blood volume, triggering compensatory tachycardia to maintain cardiac output. Bradycardia may occur in severe cases with electrolyte imbalances, but it is not a primary manifestation, making this choice incorrect for dehydration.

Eupnea refers to normal breathing. Dehydration does not directly alter respiratory rate unless severe metabolic acidosis occurs, prompting compensatory hyperventilation. The described symptoms suggest hypovolemia, not respiratory changes, so eupnea is not an additional manifestation of dehydration, making this choice incorrect.

Elevated blood pressure is not associated with dehydration. Hypovolemia from fluid loss causes low blood pressure due to decreased cardiac output. The body’s compensatory mechanisms, like vasoconstriction, aim to maintain pressure but do not elevate it above normal, making this choice incorrect.

Increased skin pigmentation is associated with Addison’s disease due to elevated ACTH stimulating melanocytes. Cushing syndrome, caused by excess cortisol, typically causes skin thinning and bruising, not hyperpigmentation. The excess cortisol does not directly affect melanin production, making this choice incorrect.

Cushing syndrome leads to weight gain, not weight loss, due to cortisol’s promotion of fat deposition in central areas (e.g., abdomen, face). Increased appetite and altered metabolism contribute to obesity, not weight loss, making this choice incorrect as it contradicts the metabolic effects of hypercortisolism.

Cushing syndrome often causes hypertension, not decreased blood pressure, due to cortisol’s mineralocorticoid effects, increasing sodium retention and vascular resistance. Decreased blood pressure is more associated with adrenal insufficiency, making this choice incorrect as it does not align with Cushing syndrome’s pathophysiology.

An abnormal immune response causing synovitis and cartilage deterioration describes rheumatoid arthritis, not osteoporosis. Rheumatoid arthritis involves autoimmune inflammation of joints, not bone density loss. Osteoporosis primarily affects bone matrix, not cartilage or synovial tissues, making this choice incorrect.

Cartilage erosion from mechanical stress describes osteoarthritis, a degenerative joint disease, not osteoporosis. Osteoporosis affects bone density, not articular cartilage. Mechanical stress may exacerbate joint issues but does not cause the systemic bone loss characteristic of osteoporosis, making this choice incorrect.

A bacterial bone infection describes osteomyelitis, not osteoporosis. Osteomyelitis involves localized bone inflammation and destruction due to pathogens, not a systemic imbalance of bone remodeling. Osteoporosis is a metabolic condition, not an infectious one, making this choice incorrect for the described pathophysiology.

Hypoalbuminemia results from liver cirrhosis due to decreased hepatic protein synthesis but is not a direct manifestation of portal hypertension. It contributes to ascites by reducing oncotic pressure but is a separate consequence of liver dysfunction, making this choice incorrect.

Hypoglycemia is not typically caused by portal hypertension. Cirrhosis may impair glucose regulation due to reduced glycogen storage, but portal hypertension primarily affects vascular dynamics, leading to ascites or varices, not low blood sugar, making this choice incorrect.

Hyperkalemia is not a direct result of portal hypertension. Cirrhosis may cause electrolyte imbalances indirectly, but portal hypertension primarily leads to fluid shifts and vascular complications like ascites, not potassium elevation, making this choice incorrect for the described condition.

A metabolic deficit of dystrophin causing muscle cell necrosis describes muscular dystrophy, not osteoarthritis. Osteoarthritis involves joint cartilage degradation, not muscle pathology. Dystrophin deficiency affects muscle fiber integrity, unrelated to the joint-specific degenerative process of osteoarthritis, making this choice incorrect.

Bone infection, or osteomyelitis, is caused by bacteria or fungi, leading to bone destruction. Osteoarthritis is a non-infectious degenerative condition affecting cartilage and subchondral bone due to mechanical stress and aging, not infection, making this choice incorrect for osteoarthritis’s pathophysiology.

Loss of bone matrix causing fragile bones describes osteoporosis, not osteoarthritis. Osteoarthritis primarily involves cartilage breakdown and joint inflammation, with secondary bone changes like osteophytes, not systemic bone density loss, making this choice incorrect for the joint-focused pathology.