Introduction
According to the case study, the patient, an 82-year-old female, Mrs. Y, was delivered to the Emergency Department by her daughter because of confusion, agitation, and irritable mood. According to chief complaints involving dysthymia, alteration of consciousness, agitation, and the age of the patient, the primary thoughts were of decline dementia and the most likely provisional diagnosis of Alzheimer’s disease. In this assignment, the examination and assessment of the patient will be provided along with a diagnostic and management plan. The paper also includes interpretation of clinical investigation findings, diagnostic tests results, differential and provisional diagnoses, and pathophysiology of the provisional diagnosis.
Dementia is a common disorder uniting a group of pathologies that are hardly treated and recognized. It was assessed that 298,000 people had dementia-connected disorders, and the commonness increases according to age (Cognitive Decline Partnership Centre, 2016). The most complicated factors about dementia-induced disorders are the under-researched risk factors, treatment methods, and oftentimes poor prognosis. Patients’ perception of the disease is another slowing issue as they rarely comprehend their actual condition and behavior. The family is the one noticing the changes in their elderly member; however, not all families have close interconnections and are able to highlight the differences in the early stages. On this occasion, health care professionals must be aware of dementia specialties and implement relevant treatment methods as well as build relationships with the patients according to the severity of the pathology. It is also essential to use principles of dignity in care and perform according to ethical standards when interacting with dementia patients.
Background History of the Patient
Mrs. Y is an 82-year-old female who was brought to the ER by her daughter because of confusion, agitation, and irritable mood. During the collection of the background history, Mrs. Y cannot name the current date and the place of the present location. The patient is in a conflicting mood, complains about someone stealing her things, feels unsafe and frightened. The daughter of Mrs. Y notes that her mother was agitated for about a week before being reviewed, even though the first signs of the disease were noticed approximately two years ago.
Within one year, the amnesia started to progress as Mrs. Y forgot the names of friends and relatives, of favourite TV shows and books. The daughter noticed that her mother stopped reading books and newspapers as she was struggling to memorise the information from them. Mrs. Y also started forgetting the pills she needs to take daily for arterial hypertension. The patient was brought to the family physician that stated memory changes were normal consequent changes for elderly people and recommended multivitamin therapy and rest. The therapy did not bring any significant outcomes.
Withing time, Mrs. Y became irritated and impatient, initiated conflicts with all family members, did not recognise them, and asked them to leave her alone. The patient got lost on five incidents when she was walking home from the market as well as her words and sentences often made no sense, she maintained her social adorns. All in all, over the subsequent two years of life her memory became shocking, worse, and she mostly mislaid her house keys and purse. Mrs. Y reiterated the questions to which she had obtained the reply only a minute ago. Mrs. Y started changing the location of the things in her apartment from time to time and was convinced that somebody could steal them if she did not change their places constantly.
The patient does not need assistance in daily activities, but she has struggled with expressing her opinions, reading, and communicating. Currently, the patient takes the following medications: Enalapril Maleate (Sandoz) 10 mg 2 times per day; Bisoprolol fumarate 5 mg once per day; Aspirin 100 mg 1 per day. From the past medical history, the patient has a family background of Alzheimer’s disease (grandmother), HTN, left ventricular myocardial hypertrophy, osteoarthritis of the left knee.
Physical Assessment of the Patient
According to general assessment, vital signs are in reference borders: height 165 cm, weight 75 kg, BMI 27.54 (pre-obesity), BP 129/74 mmHg, Temperature 36.4 C, Pulse 74 beats/min. Mrs. Y communicates with struggles, builds sentences that do not have a logical connection between each other. The patient responds to questions asked; however, she cannot name the date and current location, forgot the name of her mother and father, could name her daughter. Mrs. Y is afraid of other people stealing her things at home. The patient appears irritated, frightened, confused, and agitated. Pupils are equal, round, and reactive to light; conjunctivae and sclera are clear. Heart auscultation defines no murmurs, S1 and S2 are normal. The chest wall is symmetrical with its equal rise and fall. Percussion defines LVGTF (0.5 cm inside from the left midclavicular line). Lungs are clear to auscultation, no rales, rhonchi, wheezes were defined. Respiration is even and regular; harsh breathing is noted. The abdomen is soft, with no masses and bowel sounds present. Mrs. Y is not sexually active for the last 20 years, menopause at age 55.
Data Synthesis and Interpretation of Clinical Investigation Findings
The gathered information about medical history provides data about a patient’s health care experiences. The proper anamnesis collection, synthesis of previous and current conditions of the patient, data provided by close family members allow the physician to prioritize the major symptoms and syndromes of the disorder. With memory alterations, it is oftentimes complicated to gather data from the patient as he or she can provide an unclear picture of the disorder without comprehending the severity of the current condition. Sharda et al. (2021) showed that healthcare professionals facing dementia should exclude some comorbidities such as Parkinson’s disease, HIV infection, depression, a head injury, stroke, diabetes, HTN, or heart conditions. All the mentioned above disorders are vital parts of the medical history as these illnesses may cause confusion or other signs of dementia in some cases to delay in a definitive diagnosis confirmation.
The daily medication intake can also have a substantial impact on a patient’s condition and mood. For instance, one group of antihypertensive drugs, beta-blockers, are associated with depression (Kim et al., 2019). The patient from the case study takes beta-blockers daily, and the impact of this medication on her general condition should be reassessed and, if possible, changed to the other group of antihypertensive drugs. However, several proved that medications from the groups of beta-blockers, calcium antagonists, and angiotensin agents were not connected with depression initiation or worsening (Kessing et al., 2020). Furthermore, obtaining family history details would determine whether the consumer is at risk of illnesses of a genetic or familial nature. Family background can also help identify areas of health promotion and illness prevention. Planning the care of the patient should focus on the lifestyle, diet, daily activities, and interrelations with family members as these factors influence majorly on the patient’s treatment outcomes.
According to the data provided by the daughter, the first symptoms Mrs. Y developed two years ago, and since then the illness progressed slowly and became more distinguishing from the common changes of older age. The major symptom of Mrs. Y is amnesia that is followed by non-amnestic disorders such as light aphasia, agnosia, apraxia, visuospatial disorder, and behavioural disorder. Due to insidious inception, slow deterioration of the state, amnestic and cognitive function alterations and a family anamnesis of Alzheimer’s disease, the provisional diagnosis can be confirmed as Alzheimer’s disease.
Diagnostic Tests
Diagnostic tests include blood tests such as clinical blood analysis, biochemical blood analysis (K+, Na+, Ca2+, glucose, creatinine, ALT, ACT, alkaline phosphatase, total bilirubin), thyroid tests (TSH, T3, T4), serum vitamin B12, and folate levels (Cognitive Decline Partnership Centre, 2016). The social status and sexual activity of the patient claim no acute necessity of testing blood on syphilis antibodies and HIV infection. Electroencephalography might be done as a routine diagnostic test for people with dementia. Clinical cognitive assessment should involve Mini Mental State Exam (MMST) and Montreal Cognitive Assessment (MoCA).
The latter tests can help highlight cognitive disorders and will lead to a more apperceive evaluation of the gathered data. Structural imaging of the brain (MRI) can help distinguish the type of the disorder and possible combination of the pathologies. For example, Alzheimer’s disease can be accompanied by dementia with Lewy Bodies or cerebral vascular changes (Cognitive Decline Partnership Centre, 2016). Positron emission tomography (PET) can help identify areas of lower metabolism of glucose or reduced perfusion that can relate to trauma, injury, or some other pathology. According to the blood test results, the patient does not have clinically significant departures from reference intervals. Mrs. Y got 12 points on the MMST test and 15 points on the MoCA test. MRI of the brain highlighted thinning of the brain cortex and diffuse atrophy of the brain. PET scan highlighted amyloid plaques.
Diagnosis of Alzheimer’s disease
According to DSM-IV criteria for Alzheimer’s disease, the memory damage with insidious start and a history of ongoing worsening are major for the diagnosis. Furthermore, one of the subsequent cognitive insufficiencies can be involved: aphasia, apraxia, agnosia, or deterioration. Alzheimer’s disease should not be considered if there is any evidence of the other neurogenerative illness if the patient was priorly diagnosed with extensive cerebrovascular disease, if the patient has non-neurologic medical comorbidity, or if the patient intakes that can impact his current condition. Neuroimaging and cerebrospinal fluid supplement the diagnostic search. The highest-probability biomarker profile is the β-amyloid marker (found in CSF or imaging) and neuronal injury marker (CSF tau, FDG-PET, or structural MRI). Gene mutation, such as APP, PSEN1, or PSEN2, in accordance with clinical findings can point out Alzheimer’s disease.
Differential Diagnosis
Differential search is focused on other disorders that have dementia as a major sign. Mrs. Y has progressive amnesia, and less prevalently aphasia, apraxia, agnosia, visuospatial, and behavioural disorders. The two other pathologies that are uniting similar symptoms are vascular dementia and dementia with Lewy Bodies. Vascular dementia stands on the second place after Alzheimer’s disease in the development of cognitive deficit (Iadecola et al., 2019). This disorder accumulates a variety of pathologies that can cause damage to the vessels and lead to restricted brain blood flow. Brain cells are vulnerable to vessel damage as anatomically, neurovascular units exist closely as well as penetrating arteries that bring the blood to the deeper areas of the brain tissue (Vinters et al., 2018). Penetrating arteries also supply white matter of the brain, and the blood flow in this area is of low pressure and more vulnerable to damages. Depending on the localization of the vessel damage, various brain functions can suffer.
Most of the time, physicians face such cognitive disorders in their clinical practice as impairments in executive functions: initiation, decision-making, planning, cognitive flexibility, judgement, hypothesis synthesis (Iadesole et al., 2019). The other functions that can be involved in the pathological process are visuospatial function, attention, memory, and language (Iadesole et al., 2019). Several types of vascular dementia are distinguished: strategic-infarct dementia, mini-infarct dementia, and subcortical vascular dementia (Kalaria, 2018). The latter happens due to the damage of the small vessels of the brain leading to the deeper impairment of brain areas (subcortical). Small-sized vessels are involved in the pathology of diabetes mellitus or arterial hypertension as these pathologies target small diameters of vessels. Strategic infarct dementia is caused due to stroke of a large size. The damage depends on the localization of the stroke and the major characteristic of this type of dementia is fast-developing changes in brain functions such as thinking process and behavior. Usually, the changes are seen clearly, and the patient with a large-scale stroke needs urgent therapy.
Mini-infarct dementia occurs when several small-scale strokes happen, and such impairments are oftentimes asymptomatic, and the causes from them are viewed later because of the changed blood circulation. Mini-infarct dementia is characterized by a step-wise progression when after each small damage symptoms become more evident, and afterward stabilize at one level before the next mini-stroke. The most complicated issue in the differential diagnosis is that hemorrhages of various sizes can mimicry Alzheimer’s disease as both lead to neurocognitive decline (Vinters et al., 2018). Hereditary dementia interrelated with small vessel disease is described by various authors as the mutations in the NOTCH3 gene in accordance with cognitive mechanisms of apathy, subcortical infarcts, and leukoencephalopathy (Iadecola et al., 2019). In differential search, it is essential to pay attention to anamnesis of previous disorders because vascular dementia, except mini-infarct type, will be connected to the stroke in the medical background about 1 year ago.
The transient ischemic attack might also lead to vascular dementia; however, it less likely leads to irreversible changes compared to strokes. The identified risk factors can help with differential: diabetes, HTN, smoking, metabolic syndrome, and depression are believed to elevate the development of cerebrovascular disorders. Mini-infarct type is the most complicated to distinguish from Alzheimer’s disease as clinically they are very similar. Neuroimaging can identify infarctions and hemorrhages of small size and white matter deformations that can be recognized by using various scales (Iadecola et al., 2019). MRI is will also show general atrophy which conforms with Alzheimer’s disease alterations.
Lewy body dementia is another pathology for differential diagnosis as it also correlates with the cognitive deficit. The disorder can be called one of the storage diseases as the key factor in its pathogenesis is the storage of alpha-synuclein protein. The latter gathers in specific substantions, Lewy bodies, in various brain locations, nervous system and leads to nerve cell alteration and apoptosis (Sanford, 2018). The favourite location for Lewy bodies deposition is the neuron cytoplasm of glial cells and neurons. The histopathologic image of Lewy’s body is presented in Figure 1. The dissemination process of Lewy bodies is still being studied and is believed to be of a similar pattern describe for Parkinson’s disease. However, differential with Lewy bodies is easier as it involves a vast number of symptoms such as olfactory dysfunction (anosmia), sleep disturbances and alteration of motor functions, emotional and cognitive impairment. Constipation (due to the alteration of the nervus vagus) and rapid eye movements are believed to be the primary symptoms of this type of dementia (Sanford, 2018). Cognitive deficit develops within time, when the disease is progressive, which can be a significant factor in differential search.
In combination with other symptoms that are rarely met in Alzheimer’s disease, it might be easier to identify the major pathology. However, both pathologies can combine, and one patient might have two illnesses as Alzheimer’s disease and Lewy body dementia are accumulation disorders. The brain alteration might involve a mixed pathology with prevalent storage of alpha-synuclein, amyloid-beta plaques, and tau. (Sanford, 2018). Additionally, both dementias have relative vessel changes referring to ischemia that worsens neurogenerative disorders. On this occasion, it is essential to identify the pathology that is prevalent in comparison with others. Estimating diagnostic tests, Lewy body dementia cannot be directly imaged but the indirect evidence of alpha-synuclein can be found on MRI. The latter shows focal degeneration of the middle brain tissue, hypothalamus, and substantial innominate. Different from Alzheimer’s disease, Lewy body dementia shows milder decreases in brain volume on MRI (Sanford, 2018). PET and SPECT scans help identify the areas with different metabolic activity.
Provisional Diagnosis
Provisional diagnosis for Mrs. Y is Alzheimer’s disease as the chief symptom identified is amnesia that is accompanied by aphasia, agnosia, apraxia, visuospatial disorder, and behavioural disorder. However, amnestic changes are major and cause all the difficulties and struggles in a patient’s life. Due to insidious onset, slow worsening of the condition, amnestic and cognitive alterations and a family history of Alzheimer’s disease, the provisional diagnosis refers to it. Moreover, Mrs. Y got 12 points in the MMST test and 15 points in the MoCA test that refer to the cognitive deficit. MRI highlighted thinning of the brain cortex and diffuse atrophy of brain tissue that is more likely for the mentioned above pathology. PET scan highlighted amyloid plaques. Thus, all the DSM-4 criteria for the diagnosis are positive. For vascular dementia, a patient does not have a background of stroke or hemorrhages, no MRI data of micro-insults, and no comorbidities that could affect cerebral vessels. For Lewy body dementia, Mrs. Y has cognitive loss primarily and has no evidence of motor alterations, anosmia, constipation, sleep disturbances, and rapid eye movements. Moreover, the MRI picture shows diffuse brain atrophy, not focal damaging as it is classical for dementia with Lewy bodies.
Pathophysiology of the Provisional Diagnosis
The reasons of Alzheimer’s disease are still not comprehensively known. The disorder is believed to be multifactorial with the influence of both genetic and environmental factors. The early initiation of the illness (between ages 30 and 50) is connected with gene mutations: amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2). Amyloid plaques and neurofibrillary tangles are key elements in the pathophysiology of Alzheimer’s disease. Amyloid plaques are storages of amyloid-beta extracellularly (Lane et al., 2017). The protein accumulates in isocortex and subcortically in the progressive periods of the disease (Lane et al., 2017). Neurofibrillary tangles are spiraled filaments of hyperphosphorylated tau. Immunohistochemistry highlights amyloid plaques and tau accumulations that are presented in Figure 2.
Several studies have identified the early onset of amyloid formation and storage. Increased levels of beta-amyloid lead to its accumulation, inflammation, altered neuronal ionic homeostasis, oxidative injury, and widespread neuronal synaptic dysfunction. As a consequence, selective neuronal loss with attendant neurotransmitter deficits is developing. It is still being investigated how pathogenic proteins are reaching certain brain areas and they spread through the brain tissue. Some researchers claim that the proteins are transferred trans-synaptically (Lane et al., 2017). The latter processes cause nerve tissue damage that presented on MRI as thinning of the cortex layer and diffuse brain atrophy. Sych changes are shown in Figure 3. PET scan highlights beta-amyloid and tau that is shown in Figure 4.
Management plan
There is no treatment for Alzheimer’s disease guaranteeing total convalescence. The major principles of modern Alzheimer’s treatment are to stop neurogenerative progress. As always, a multidisciplinary approach involving medical specialists, nurses, social services, and support services is vital (Lanes et al., 2017). Acetylcholinesterase inhibitors (AChEIs) such as donepezil, galantamine, and rivastigmine are the first-line therapy of symptomatic treatment. The goal of AChEIs is to increase acetylcholine accessibility by inhibiting its breakdown in the synapse. Peripheral cholinergic side effects such as leg cramps and gastrointestinal upset are common but usually well tolerated. This group of drugs should not be prescribed to patients with impaired heart conduction systems as it can cause bradyarrhythmia (Lanes et al., 2017). The prolonged stay of acetylcholine increases the effectivity of neurotransmission in synapses and enhances all the neuron processes. An alternative treatment involves Memantine, a low-affinity N-methyl-D-aspartate receptor antagonist (Lanes et al., 2017). It reduces L-glutamate excitatory neurotoxicity with no interfering with its physiological actions. Memantine showed promising results in patients with agitation and is implemented in combined therapy with AChEIs.
Patient Mrs. Y needs primarily cupping of the agitation by neuroleptics or antipsychotics. When the condition of the patient stabilizes, it is recommended to initiate combined therapy with AChESI and Memantine as the first group of drugs increases cognitive functions, and memantine decreases symptoms of agitation. The non-pharmacological approach consists of communication skills training, music therapy, and person-centered care training.
Conclusion
Thus, Alzheimer’s disease is a complicated disorder that is widely spread and should be recognized well by physicians. In this assignment, the patient developed amnesia in accordance with aphasia, agnosia, apraxia, visuospatial disorder, and behavioral disorder. Dementia groups of disorders are oftentimes similar and might be mixed. Instrumental diagnostic tests such as MRI and PET scans can help highlight the major pathology and develop the best tactic for the patient. Vascular dementia and dementia with Lewy bodies can mimicry the early signs of the disease, and a physician needs to pay extra attention to patient’s anamnesis and comorbidities.
References
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