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Pathology - Subarachnoid Bleeding
Pathophysiology
In this instance, the bleeding is most likely the result of a berry aneurysm rupturing. Because of the uneven collagen deposition in the vasculature, berry aneurysms are frequently connected with Marfan's syndrome, which the patient's height implies may be the cause of. The symptoms of ipsilateral oculomotor nerve palsy, also known as cranial nerve III palsy, include an extorted, laterally turned eye with a dilated pupil. Berry aneurysms of the posterior connecting artery can induce this condition. Compression of the nearby oculomotor nerve is the cause of this. In addition to frank blood on lumbar puncture, patients with subarachnoid hemorrhage may also have xanthochromia, or yellow staining of CSF, as a result of RBC breakdown. Subarachnoid blood irritates the meninges, causing nuchal stiffness. In addition to nimodipine, a dihydropyridine calcium channel blocker that prevents reactive vasospasm and consequent ischemia to the tissue fed by the afflicted arterial, surgically cutting the aneurysm is the method of treatment.
Pathophysiology
In this instance, the bleeding is most likely the result of a berry aneurysm rupturing. Because of the uneven collagen deposition in the vasculature, berry aneurysms are frequently connected with Marfan's syndrome, which the patient's height implies may be the cause of. The symptoms of ipsilateral oculomotor nerve palsy, also known as cranial nerve III palsy, include an extorted, laterally turned eye with a dilated pupil. Berry aneurysms of the posterior connecting artery can induce this condition. Compression of the nearby oculomotor nerve is the cause of this. In addition to frank blood on lumbar puncture, patients with subarachnoid hemorrhage may also have xanthochromia, or yellow staining of CSF, as a result of RBC breakdown. Subarachnoid blood irritates the meninges, causing nuchal stiffness. In addition to nimodipine, a dihydropyridine calcium channel blocker that prevents reactive vasospasm and consequent ischemia to the tissue fed by the afflicted arterial, surgically cutting the aneurysm is the method of treatment.
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Pathology - Amaurosis Fugax
Pathophysiology
Amaurosis fugax is a temporary, unilateral blindness.
He has a number of risk factors, including hypertension, diabetes, hyperlipidemia, and tobacco use, which indicate the underlying problem of atherosclerosis.
LDL molecules accumulate and oxidize inside the vessel wall over time, triggering an inflammatory reaction. The oxidized LDL is phagocytosed by macrophages, resulting in foam cells that have the potential to burst and intensify inflammation. The vessel thickens as a result, forming a membrane to seal off the inflammatory process. This contributes to the physical examination finding of a carotid bruit by decreasing the luminal width of the vessel and increasing the velocity of blood flow through that location. Ruptures of the carotid atherosclerotic plaque have the potential to induce stroke by releasing emboli into the cerebral circulation. In the event of amaurosis fugax, the emboli may only momentarily obstruct a vessel, such as the ciliary, ophthalmic, or retinal arteries. Amaurosis fugax can have numerous different causes, such as temporal arteritis and hypercoagulable conditions. It is crucial to keep in mind that individuals suffering with amaurosis fugax have a heightened likelihood of experiencing a stroke.
Pathophysiology
Amaurosis fugax is a temporary, unilateral blindness.
He has a number of risk factors, including hypertension, diabetes, hyperlipidemia, and tobacco use, which indicate the underlying problem of atherosclerosis.
LDL molecules accumulate and oxidize inside the vessel wall over time, triggering an inflammatory reaction. The oxidized LDL is phagocytosed by macrophages, resulting in foam cells that have the potential to burst and intensify inflammation. The vessel thickens as a result, forming a membrane to seal off the inflammatory process. This contributes to the physical examination finding of a carotid bruit by decreasing the luminal width of the vessel and increasing the velocity of blood flow through that location. Ruptures of the carotid atherosclerotic plaque have the potential to induce stroke by releasing emboli into the cerebral circulation. In the event of amaurosis fugax, the emboli may only momentarily obstruct a vessel, such as the ciliary, ophthalmic, or retinal arteries. Amaurosis fugax can have numerous different causes, such as temporal arteritis and hypercoagulable conditions. It is crucial to keep in mind that individuals suffering with amaurosis fugax have a heightened likelihood of experiencing a stroke.
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Pathology - Thromboembolic stroke in the cerebral arteries
Pathophysiology
Due to the high rate of stimulation, the left atrium in this condition is unable to contract completely, which causes blood stasis within the atrial and increases the risk of thrombus formation. Either the cerebral or peripheral circulation may become embolize by the thrombus. Characteristic clinical manifestations of cerebral artery occlusion correspond to the ischemia-affected brain areas. A large portion of the left lateral cerebral cortex, including the area involved in vocal expression, is supplied by the left middle cerebral artery. Aphasia, facial and extremity paralysis, and contralateral paralysis are all possible outcomes of local ischemia. Because Broca's area is involved in this instance, the patient has expressive aphasia; she can understand but cannot speak. Early in the course of a stroke, gaze deviation toward the side of the lesion is possible. Interestingly, this patient's CHADS2 score of 2 indicates that she probably did not have an atrial fibrillation diagnosis earlier because she is not using an anticoagulant. It's critical to identify these people very away and start treating them right away.
Sustaining elevated or standard blood pressure is crucial in order to stop more tissue ischemia.
Pathophysiology
Due to the high rate of stimulation, the left atrium in this condition is unable to contract completely, which causes blood stasis within the atrial and increases the risk of thrombus formation. Either the cerebral or peripheral circulation may become embolize by the thrombus. Characteristic clinical manifestations of cerebral artery occlusion correspond to the ischemia-affected brain areas. A large portion of the left lateral cerebral cortex, including the area involved in vocal expression, is supplied by the left middle cerebral artery. Aphasia, facial and extremity paralysis, and contralateral paralysis are all possible outcomes of local ischemia. Because Broca's area is involved in this instance, the patient has expressive aphasia; she can understand but cannot speak. Early in the course of a stroke, gaze deviation toward the side of the lesion is possible. Interestingly, this patient's CHADS2 score of 2 indicates that she probably did not have an atrial fibrillation diagnosis earlier because she is not using an anticoagulant. It's critical to identify these people very away and start treating them right away.
Sustaining elevated or standard blood pressure is crucial in order to stop more tissue ischemia.
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Pathology - Lacunar Infarcts
Pathophysiology
Hypertension is a significant risk factor for this illness, which can arise from obstruction of the perforating arteries that supply the interior structures of the brain. This disease's pathogenesis is caused by lipohyalinosis or microthrombi. Larger proximal arteries with atherosclerotic plaques are the source of microthrombi. The narrowing of tiny veins in lipohyalinosis is caused by either fibrinoid necrosis or inflammation and edema. Pure motor strokes are the most prevalent type of lacunar infarct syndrome, while there are five other types as well. The internal capsule, which contains fibers from the corticospinal tract that aid in voluntary movement, is involved in the paresis. Dysarthria may develop as a result of basal ganglia involvement. Similar to other forms of stroke, it's critical to keep in mind that maintaining cerebral perfusion is necessary to stop more ischemia in spite of the patient's elevated blood pressure.
Pathophysiology
Hypertension is a significant risk factor for this illness, which can arise from obstruction of the perforating arteries that supply the interior structures of the brain. This disease's pathogenesis is caused by lipohyalinosis or microthrombi. Larger proximal arteries with atherosclerotic plaques are the source of microthrombi. The narrowing of tiny veins in lipohyalinosis is caused by either fibrinoid necrosis or inflammation and edema. Pure motor strokes are the most prevalent type of lacunar infarct syndrome, while there are five other types as well. The internal capsule, which contains fibers from the corticospinal tract that aid in voluntary movement, is involved in the paresis. Dysarthria may develop as a result of basal ganglia involvement. Similar to other forms of stroke, it's critical to keep in mind that maintaining cerebral perfusion is necessary to stop more ischemia in spite of the patient's elevated blood pressure.
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Pathology - Major Depressive Disorder
Even though many psychiatric diagnoses have several criteria, it's crucial to first commit the time requirements and quantity of symptoms to memory. A minimum of two weeks must pass between the onset of one of the five symptoms of major depressive illness, which is either anhedonia (lack of interest) or a gloomy mood. The remaining nine symptoms include disturbed sleep, low energy, impaired concentration, feelings of guilt or worthlessness, altered appetite or weight, psychomotor agitation or retardation, and suicidal thoughts. The mnemonic SIG E CAPS is helpful.
A diagnosis of adjustment disorder could be made if the patient did not meet at least five criteria. This is because the patient's symptoms were brought on by a significant life stressor that started within three months of the stressor and did not last for longer than six months. A patient with dysthymic illness manifests a milder form of depression on more than half of their days for a duration exceeding two years.
Even though many psychiatric diagnoses have several criteria, it's crucial to first commit the time requirements and quantity of symptoms to memory. A minimum of two weeks must pass between the onset of one of the five symptoms of major depressive illness, which is either anhedonia (lack of interest) or a gloomy mood. The remaining nine symptoms include disturbed sleep, low energy, impaired concentration, feelings of guilt or worthlessness, altered appetite or weight, psychomotor agitation or retardation, and suicidal thoughts. The mnemonic SIG E CAPS is helpful.
A diagnosis of adjustment disorder could be made if the patient did not meet at least five criteria. This is because the patient's symptoms were brought on by a significant life stressor that started within three months of the stressor and did not last for longer than six months. A patient with dysthymic illness manifests a milder form of depression on more than half of their days for a duration exceeding two years.
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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.
