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Pathology - Bipolar Disorder
Pathophysiology
In order to be diagnosed with major depressive disorder, a patient must have experienced at least one manic episode, typically accompanied by a history suggestive of one or more such episodes. A manic episode is defined as having three symptoms and requiring hospitalization, or as having an excessively high, expansive, or irritated mood for at least one week. The following are some of the symptoms: grandiosity (inflated self-esteem), distraction, insomnia or decreased need for sleep, flight of ideas (racing thoughts), psychomotor agitation or increase in goal-directed activities, pressured speech, and risk-taking (activities involving pleasure with painful consequences, i.e., excessive spending, sexual indiscretion, gambling). DIG FAST is an effective mnemonic. The mood disruption for bipolar I disorder must be severe enough to interfere with social or professional functioning, necessitate hospitalization, or have psychotic symptoms. Bipolar II disorder would be the diagnosis if this were not the case and at least three symptoms accompanied by a change in mood had persisted for at least four days. This would be referred to as a hypomanic episode. Since personality disorders are classified as axis II diagnosis, it is critical to differentiate the symptoms from personality disorders.
Pathophysiology
In order to be diagnosed with major depressive disorder, a patient must have experienced at least one manic episode, typically accompanied by a history suggestive of one or more such episodes. A manic episode is defined as having three symptoms and requiring hospitalization, or as having an excessively high, expansive, or irritated mood for at least one week. The following are some of the symptoms: grandiosity (inflated self-esteem), distraction, insomnia or decreased need for sleep, flight of ideas (racing thoughts), psychomotor agitation or increase in goal-directed activities, pressured speech, and risk-taking (activities involving pleasure with painful consequences, i.e., excessive spending, sexual indiscretion, gambling). DIG FAST is an effective mnemonic. The mood disruption for bipolar I disorder must be severe enough to interfere with social or professional functioning, necessitate hospitalization, or have psychotic symptoms. Bipolar II disorder would be the diagnosis if this were not the case and at least three symptoms accompanied by a change in mood had persisted for at least four days. This would be referred to as a hypomanic episode. Since personality disorders are classified as axis II diagnosis, it is critical to differentiate the symptoms from personality disorders.
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Pathology - Oppositional Defiant Disorder
Pathophysiology
This is typified by persistently antagonistic and defiant actions toward those in positions of power. This is different from conduct disorder in that there aren't any significant transgressions of social standards, such physical fights, property damage, cruelty to animals, stealing, or other actions that could raise an investigation from the police. After the age of 18, conduct problem also frequently leads to antisocial personality disorder. Other factors to take into account could be separation anxiety disorder, which usually begins at age 7 or 8 and is brought on by the loss of an attachment figure during a divorce.
Pathophysiology
This is typified by persistently antagonistic and defiant actions toward those in positions of power. This is different from conduct disorder in that there aren't any significant transgressions of social standards, such physical fights, property damage, cruelty to animals, stealing, or other actions that could raise an investigation from the police. After the age of 18, conduct problem also frequently leads to antisocial personality disorder. Other factors to take into account could be separation anxiety disorder, which usually begins at age 7 or 8 and is brought on by the loss of an attachment figure during a divorce.
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Pathology - Schizophrenia
Pathogenesis
Delusions, hallucinations, disorganized behavior/catatonia, disorganized speech, and negative symptoms are the DSM-IV criteria for schizophrenia. These criteria require more than six months of disturbed functioning with at least one month of at least two of the following symptoms (unless delusions are bizarre or voices provide running commentary, in which case only one criterion is required). The cause of these symptoms is a reduction in dopaminergic activity. Positive symptoms (delusions and hallucinations) originate from the mesolimbic system, whereas negative symptoms (anhedonia, flat affect, avolition) are sourced from the frontal cortical region. Dopamine antagonists are the standard of care. However, atypical antipsychotics are typically the first-line medication because to the high incidence of tardive dyskinesia and extrapyramidal symptoms linked to D2 dopamine receptor blockage in conventional antipsychotics.
Pathogenesis
Delusions, hallucinations, disorganized behavior/catatonia, disorganized speech, and negative symptoms are the DSM-IV criteria for schizophrenia. These criteria require more than six months of disturbed functioning with at least one month of at least two of the following symptoms (unless delusions are bizarre or voices provide running commentary, in which case only one criterion is required). The cause of these symptoms is a reduction in dopaminergic activity. Positive symptoms (delusions and hallucinations) originate from the mesolimbic system, whereas negative symptoms (anhedonia, flat affect, avolition) are sourced from the frontal cortical region. Dopamine antagonists are the standard of care. However, atypical antipsychotics are typically the first-line medication because to the high incidence of tardive dyskinesia and extrapyramidal symptoms linked to D2 dopamine receptor blockage in conventional antipsychotics.
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Pathology - Huntington's Disease
Pathophysiology
Chorea is an involuntary activity that resembles dancing that is brought on by the caudate nucleus's neuronal atrophy and loss.
Language, memory, and voluntary movement are all regulated by the caudate nucleus. The trinucleotide expansion of CAG repeats, which multiply with successive generations, is the inherited etiology of this disease. This occurrence illustrates the genetic concept of anticipation, which states that an earlier age of onset and a more severe disease are caused by an increased number of CAG repeats. The huntingtin protein, which is involved in a number of cellular processes including gene expression and trafficking, is encoded by a section of chromosome 4 that contains the CAG repeats.
Regretfully, this condition does not currently have a cure.
Pathophysiology
Chorea is an involuntary activity that resembles dancing that is brought on by the caudate nucleus's neuronal atrophy and loss.
Language, memory, and voluntary movement are all regulated by the caudate nucleus. The trinucleotide expansion of CAG repeats, which multiply with successive generations, is the inherited etiology of this disease. This occurrence illustrates the genetic concept of anticipation, which states that an earlier age of onset and a more severe disease are caused by an increased number of CAG repeats. The huntingtin protein, which is involved in a number of cellular processes including gene expression and trafficking, is encoded by a section of chromosome 4 that contains the CAG repeats.
Regretfully, this condition does not currently have a cure.
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Pathology - Protein-Energy Malnutrition (Kwashiorkor)
Kwashiorkor is a type of acute protein-energy malnutrition that can result from sepsis, severe infections, and the hypermetabolic state that follows. This disease is brought on by severe physiological stress, which also raises levels of the insulin counterregulatory stress hormones cortisol, glucagon, and adrenaline, which in turn stimulate proinflammatory cytokines. In order to fuel gluconeogenesis, protein catabolism removes protein from organs and muscles. A crucial finding is the presence of hypoalbuminemia, along with the loss of other serum proteins including transferrin and skin degeneration or inadequate wound healing. Loss of plasma oncotic pressure as a result of hypoalbuminemia is the cause of edema. The cytokine milieu leads to the suppression of cellular immunity (see the low lymphocyte count). Although mortality is still high, aggressive nutritional support is still required. Kwashiorkor is more prevalent in extremely underdeveloped nations when diets lack sufficient amounts of protein. Children under these circumstances will also develop ascites and hepatomegaly, which will cause their abdomen to protrude. You can compare kwashiorkor to marasmus, the traditional type of starvation-induced malnutrition. The treatment for marasmus, a hypometabolic state that causes cachexia, is progressive refeeding.
Kwashiorkor is a type of acute protein-energy malnutrition that can result from sepsis, severe infections, and the hypermetabolic state that follows. This disease is brought on by severe physiological stress, which also raises levels of the insulin counterregulatory stress hormones cortisol, glucagon, and adrenaline, which in turn stimulate proinflammatory cytokines. In order to fuel gluconeogenesis, protein catabolism removes protein from organs and muscles. A crucial finding is the presence of hypoalbuminemia, along with the loss of other serum proteins including transferrin and skin degeneration or inadequate wound healing. Loss of plasma oncotic pressure as a result of hypoalbuminemia is the cause of edema. The cytokine milieu leads to the suppression of cellular immunity (see the low lymphocyte count). Although mortality is still high, aggressive nutritional support is still required. Kwashiorkor is more prevalent in extremely underdeveloped nations when diets lack sufficient amounts of protein. Children under these circumstances will also develop ascites and hepatomegaly, which will cause their abdomen to protrude. You can compare kwashiorkor to marasmus, the traditional type of starvation-induced malnutrition. The treatment for marasmus, a hypometabolic state that causes cachexia, is progressive refeeding.
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Pathology - Vitamin A Deficiency
Pathophysiology
Vitamin A is necessary for both the upkeep of the surface of the eyes and eyesight, particularly in the dark.
Additionally, normal immunological response as well as the growth and repair of epithelial cells depend on it. While it is rare in affluent nations, vitamin A insufficiency is widespread in poor nations. The majority of vitamin A is stored in the liver and released into the bloodstream with the use of a carrier protein. Vitamin A is a fat-soluble vitamin that is absorbed in the small intestine through the chylomicron pathway. Fat malabsorption-related disorders will reduce the absorption of vitamin A in the intestines, whereas liver disorders will reduce the storage of vitamin A.
The cycling of visual pigment molecules in the retina is insufficient to support vision in low light when retinal concentration is too low. The patient exhibits symptoms of poor surface upkeep, such as "Bittot's spots" and dry eyes. In children in the underdeveloped world, corneal scarring is a major cause of blindness and can happen. Recurrent colds and coughing are indicative of lowered immunity. Oral vitamin pills are a simple way to address the disease.
Pathophysiology
Vitamin A is necessary for both the upkeep of the surface of the eyes and eyesight, particularly in the dark.
Additionally, normal immunological response as well as the growth and repair of epithelial cells depend on it. While it is rare in affluent nations, vitamin A insufficiency is widespread in poor nations. The majority of vitamin A is stored in the liver and released into the bloodstream with the use of a carrier protein. Vitamin A is a fat-soluble vitamin that is absorbed in the small intestine through the chylomicron pathway. Fat malabsorption-related disorders will reduce the absorption of vitamin A in the intestines, whereas liver disorders will reduce the storage of vitamin A.
The cycling of visual pigment molecules in the retina is insufficient to support vision in low light when retinal concentration is too low. The patient exhibits symptoms of poor surface upkeep, such as "Bittot's spots" and dry eyes. In children in the underdeveloped world, corneal scarring is a major cause of blindness and can happen. Recurrent colds and coughing are indicative of lowered immunity. Oral vitamin pills are a simple way to address the disease.
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Pathology - Common Obesity
Pathophysiology
Excess adipose tissue is the condition known as common obesity. More than 25 kg/m2 is considered overweight, more than 30 kg/m2 is considered obese, and more than 40 kg/m2 is considered severely obese.
In America, the majority of adults are either overweight or obese.
Hypertension, type 2 diabetes, dyslipidemia, joint disease, and certain malignancies are examples of many comorbidities. An imbalance between energy intake and expenditure causes obesity and excess fat storage. The patient reports eating high-calorie fast food frequently and leads a sedentary lifestyle. The complicated pathophysiology governs hunger and satiety and is mediated by numerous neuronal and endocrine mechanisms that work through the hypothalamus. Leptin is a hormone secreted by adipose tissue that indicates an excess of fat storage. Normally, leptin's physiological negative feedback reduces appetite and raises calorie expenditure. One way to think of obesity is as a leptin resistance syndrome. Excess adipose tissue also releases other cytokines that are linked to insulin resistance, type 2 diabetes, and dyslipidemia. Hypertension is more likely when there is an increase in central sympathetic activity. Here, the high frequency of obesity in the entire family suggests that genetic factors play a significant role in obesity.
With supportive behavioral therapy, this patient—who is motivated to reduce weight—should be assisted in increasing his physical activity and reducing his energy intake.
Pathophysiology
Excess adipose tissue is the condition known as common obesity. More than 25 kg/m2 is considered overweight, more than 30 kg/m2 is considered obese, and more than 40 kg/m2 is considered severely obese.
In America, the majority of adults are either overweight or obese.
Hypertension, type 2 diabetes, dyslipidemia, joint disease, and certain malignancies are examples of many comorbidities. An imbalance between energy intake and expenditure causes obesity and excess fat storage. The patient reports eating high-calorie fast food frequently and leads a sedentary lifestyle. The complicated pathophysiology governs hunger and satiety and is mediated by numerous neuronal and endocrine mechanisms that work through the hypothalamus. Leptin is a hormone secreted by adipose tissue that indicates an excess of fat storage. Normally, leptin's physiological negative feedback reduces appetite and raises calorie expenditure. One way to think of obesity is as a leptin resistance syndrome. Excess adipose tissue also releases other cytokines that are linked to insulin resistance, type 2 diabetes, and dyslipidemia. Hypertension is more likely when there is an increase in central sympathetic activity. Here, the high frequency of obesity in the entire family suggests that genetic factors play a significant role in obesity.
With supportive behavioral therapy, this patient—who is motivated to reduce weight—should be assisted in increasing his physical activity and reducing his energy intake.
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Pathology - Acute Pancreatitis
Pathophysiology
The intrapancreatic activation of enzymes is the etiology of this inflammatory disease. Common symptoms include pain, nausea, vomiting, and intestinal ileus (seen here by a lack of bowel noises). Acute pancreatitis is frequently caused by trauma, drug side effects, hypertriglyceridemia, gallstones, and alcohol consumption.
Pancreatic autodigestion is accompanied by bleeding, necrosis, interstitial edema, intra-abdominal fluid accumulation, and the release of vasoactive peptides. The sickness can vary in severity and has the potential to be lethal. Increased AST/ALT and alkaline phosphatase levels, together with elevated serum amylase and lipase, are found in laboratory examination. If gallstone blockage is present, these levels are frequently accompanied by hyperbilirubinemia. Patients are treated with pain management, hydration support, and close observation to prevent complications like necrotizing disease or damage to the surrounding vascular structures.
Pathophysiology
The intrapancreatic activation of enzymes is the etiology of this inflammatory disease. Common symptoms include pain, nausea, vomiting, and intestinal ileus (seen here by a lack of bowel noises). Acute pancreatitis is frequently caused by trauma, drug side effects, hypertriglyceridemia, gallstones, and alcohol consumption.
Pancreatic autodigestion is accompanied by bleeding, necrosis, interstitial edema, intra-abdominal fluid accumulation, and the release of vasoactive peptides. The sickness can vary in severity and has the potential to be lethal. Increased AST/ALT and alkaline phosphatase levels, together with elevated serum amylase and lipase, are found in laboratory examination. If gallstone blockage is present, these levels are frequently accompanied by hyperbilirubinemia. Patients are treated with pain management, hydration support, and close observation to prevent complications like necrotizing disease or damage to the surrounding vascular structures.
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Pathology - Chronic Pancreatitis
Pathophysiology
There is a connection between chronic pancreatic insufficiency and chronic pancreatitis. Exocrine pancreatic insufficiency causes maldigestion and malabsorption of food, which leads to diarrhea and nasty feces. The loss of endocrine pancreatic function is indicated by hyperglycemia. Malnutrition and a particular decrease of B12 absorption, which requires pancreatic enzymes, can cause anemia. Despite the usual acute spike in blood lipase and amylase due to pancreatitis, this patient has a little amount of functional pancreatic tissue mass because to fibrosis and is in the late stages of chronic illness. The most prevalent cause of pathogenesis is chronic alcohol consumption, although there are numerous additional factors as well, such as gallstone disease, immunological disorders, and inherited diseases like cystic fibrosis.
It is believed that oxidative stress, toxicity from alcohol metabolism, duct blockage, and necrosis-fibrosis responses that occur after acute inflammation are responsible for the gland's destruction. Inflammation results from the gland's trypsinogen being activated improperly. Because of the pancreatic duct blockage, ischemia, necrosis, and inflammation, pain is a common observation. Imaging frequently reveals pancreatic duct dilating.
Pathophysiology
There is a connection between chronic pancreatic insufficiency and chronic pancreatitis. Exocrine pancreatic insufficiency causes maldigestion and malabsorption of food, which leads to diarrhea and nasty feces. The loss of endocrine pancreatic function is indicated by hyperglycemia. Malnutrition and a particular decrease of B12 absorption, which requires pancreatic enzymes, can cause anemia. Despite the usual acute spike in blood lipase and amylase due to pancreatitis, this patient has a little amount of functional pancreatic tissue mass because to fibrosis and is in the late stages of chronic illness. The most prevalent cause of pathogenesis is chronic alcohol consumption, although there are numerous additional factors as well, such as gallstone disease, immunological disorders, and inherited diseases like cystic fibrosis.
It is believed that oxidative stress, toxicity from alcohol metabolism, duct blockage, and necrosis-fibrosis responses that occur after acute inflammation are responsible for the gland's destruction. Inflammation results from the gland's trypsinogen being activated improperly. Because of the pancreatic duct blockage, ischemia, necrosis, and inflammation, pain is a common observation. Imaging frequently reveals pancreatic duct dilating.
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Pathology - Anoxic Brain Injury
Pathophysiology
A history of prolonged cardiac arrest that resulted in diminished brain perfusion may produce anoxic brain damage. The brain tissue becomes ischemic due to decreased perfusion. Watershed areas, or the regions of the brain between two arterial supplies that lose perfusion and become ischemic earliest after vascular insult, are the most susceptible to anoxic brain injury. The neocortex, basal ganglia, and hippocampal regions are the brain's watershed regions. Unfortunately, there is no cure for this person because neurons have a limited capacity for regeneration.
Pathophysiology
A history of prolonged cardiac arrest that resulted in diminished brain perfusion may produce anoxic brain damage. The brain tissue becomes ischemic due to decreased perfusion. Watershed areas, or the regions of the brain between two arterial supplies that lose perfusion and become ischemic earliest after vascular insult, are the most susceptible to anoxic brain injury. The neocortex, basal ganglia, and hippocampal regions are the brain's watershed regions. Unfortunately, there is no cure for this person because neurons have a limited capacity for regeneration.
