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Beginning with a large volume, even if diluted, can overwhelm the GI tract, potentially causing gastric distention, increased risk of aspiration, and motility issues, leading to adverse GI symptoms like diarrhea or nausea. Gradual introduction is key to successful long-term tolerance.

While continuous feeding is a common method, starting with an immediate 24-hour continuous feed without allowing for rest or assessment of tolerance is not the best approach for an initial feeding transition in a malnourished client. Intermittent or trophic feeding often precedes full continuous feeding.

Administering formula at a cold temperature can actually stimulate the vagus nerve and increase GI motility, leading to cramping and diarrhea, which are undesirable side effects. Enteral formulas should generally be administered at room temperature or slightly warmer to improve tolerance.



 

While the hepatic lymphatic system contributes to ascites by producing and leaking excess lymph, the primary driver is the sustained increase in portal vein pressure and the underlying fluid imbalance due to poor albumin synthesis, not a simple physical obstruction of the overall lymphatic system.

Excess protein intake is not a cause of ascites in cirrhosis; rather, the low serum albumin (hypoalbuminemia) due to impaired liver synthesis is a major contributing factor. Low plasma oncotic pressure fails to retain fluid within the capillaries, allowing it to leak into the peritoneum.

Acute peritoneal infection, such as spontaneous bacterial peritonitis (SBP), can worsen existing ascites or lead to fluid buildup (exudate) through inflammation, but it is typically a complication of established ascites, not the primary cause of ascites development in chronic liver cirrhosis. .

 

Flushing a nasogastric tube (NGT) with normal saline is necessary to maintain patency before and after feeding or medication administration, but using only 10 mL is typically insufficient, and this action must occur after confirming correct tube placement to prevent accidental instillation into the respiratory tract, which is a life-threatening complication. Standard practice requires at least 30 mL.

Positioning the client flat in bed is contraindicated for tube feeding because it significantly increases the risk of pulmonary aspiration, where feeding contents enter the lungs, potentially leading to aspiration pneumonia. The client's head of bed should be elevated to at least 30 to 45 degrees, and this position must be maintained for at least 30 to 60 minutes after the feeding to facilitate gastric emptying.

Clamping the tube after feeding is not the standard procedure for an intermittent feeding. Instead, after flushing the tube to clear it of residual feeding, the tube is typically capped or plugged to prevent reflux of gastric contents or air entry. Clamping the tube might be done briefly during specific procedures but not routinely for 30 minutes post-feeding.

 

A family history of diabetes mellitus, which is a common endocrine disorder, does not directly increase the risk for acute pancreatitis, although severe chronic pancreatitis can eventually lead to secondary diabetes. Pancreatitis is more strongly linked to gallstones and chronic alcohol abuse, not a family history of diabetes, which primarily involves insulin regulation.

An appendectomy, the surgical removal of the appendix, is generally not a recognized risk factor for developing acute pancreatitis. Acute pancreatitis is typically precipitated by biliary tract disease (gallstones) or toxic/metabolic causes, such as chronic heavy alcohol use, and is unrelated to a routine, localized abdominal surgery like an appendectomy.

A history of hypertension, a chronic condition of elevated systemic blood pressure, is not directly implicated as a primary cause or risk factor for acute pancreatitis. The most significant risk factors remain gallstones (cholelithiasis) which cause obstruction, and heavy alcohol intake which causes direct cellular toxicity and enzyme autoactivation.
 

Diabetes mellitus, while sometimes a consequence of chronic pancreatitis due to the destruction of insulin-producing islet cells, is not typically a precipitating factor for acute pancreatitis. The acute condition is usually triggered by biliary obstruction (gallstones) or alcohol abuse, rather than pre-existing metabolic disorders like diabetes, making this an unlikely factor in the acute presentation history.

Shock, a state of profound and generalized inadequate tissue perfusion, is a severe complication of acute pancreatitis, often due to massive fluid shifting (third spacing) and systemic inflammatory response syndrome, rather than a pre-existing factor in the client's history that causes the condition. Pancreatitis often leads to hypovolemic shock, not the other way around.

Gastroesophageal Reflux Disease (GERD) is a disorder involving the backflow of gastric acid into the esophagus, primarily affecting the upper digestive tract. It has no established direct causal link or significant association with the development of acute pancreatitis, which is primarily caused by processes involving the biliary system (gallstones) or direct pancreatic tissue injury (alcohol).

Digestion is the mechanical and chemical breakdown of food into absorbable components, such as amino acids, simple sugars, and fatty acids, primarily occurring in the stomach and small intestine. If digestion were impaired, the body would struggle to break down nutrients from the food source, but not necessarily to utilize them once absorbed, which suggests a different metabolic issue.

Ingestion is the act of taking food into the body, which simply involves the mechanical process of eating and swallowing. Since the patient is reported to have a sufficient intake of food, the physical act of ingestion is likely unimpaired, making this process an unlikely cause for the downstream symptoms of nutrient deficiency.

Elimination is the process of removing unused or waste products from the body, primarily as feces or urine, after digestion and absorption have occurred. While elimination disorders can affect nutrient absorption (e.g., severe diarrhea), the primary impairment described—sufficient intake but deficiency symptoms—most directly points to an inability to utilize nutrients, which is a key metabolic function. .
 

Recurrent episodes of binge eating without subsequent compensatory or purging behaviors is the defining clinical manifestation of Binge Eating Disorder (BED). Unlike bulimia nervosa, individuals with BED do not regularly engage in methods to "undo" the effects of the binging, such as vomiting or laxative use. While bulimia includes binge eating, the absence of regular, inappropriate compensatory behaviors places the diagnosis in the BED category, thus differentiating it from bulimia nervosa.

Severe restriction of caloric intake leading to significantly low body weight (Body Mass Index < 17.5 in adults or less than minimally normal for age/height) and associated physiological effects like amenorrhea is the core clinical presentation of Anorexia Nervosa. In contrast, patients with bulimia nervosa, by definition, maintain a body weight that is typically within the normal range or overweight, and severe restriction with resultant low weight is not their primary characteristic.

While emotional distress focused on an intense fear of gaining weight and a disturbed body image is a common psychological component shared across eating disorders, including bulimia nervosa and anorexia nervosa, the feature of maintaining normal or above normal weight is not exclusive to bulimia. This feature is a key differentiator of bulimia from the significantly low weight seen in anorexia nervosa, but the combination of binging plus compensation (Choice A) is the best discriminator of bulimia from all other eating disorders

Introducing whole cow's milk prematurely at 9 months is not recommended because the infant's digestive and renal systems are not yet mature enough to handle the high protein and mineral load present in whole cow's milk compared to breast milk or formula. Additionally, cow's milk is a poor source of iron and may interfere with the absorption of iron from other sources, increasing the risk of developing iron deficiency anemia, which is a significant concern during this period of rapid growth.

Cow's milk is not appropriate for consumption by infants as a main milk source at 6 months of age. The fat and protein composition of whole cow's milk is not optimal for the rapid brain growth that occurs in the first year of life; for example, it has insufficient essential fatty acids and iron. The high solute load can strain the infant's still-developing kidneys, making it unsuitable as a primary nutritional source until after the first birthday, which is the recommended time.

Introducing whole cow's milk should be based on the infant's age and physiological maturation rather than just self-feeding readiness. While an infant may be developmentally ready to self-feed earlier than 12 months, their nutritional and systemic needs still necessitate breast milk or formula for optimal development and to prevent adverse effects. Cow's milk is nutritionally inadequate as a sole milk source before 1 year of age, regardless of the infant's ability to eat solids or self-feed.