Final Exam Flashcards

1
Q

What do pathologists do?

A

Pathologists analyze microbial tests to identify illness, characterize disease, use molecular genetics to increase the use of preventative medicine, and understand and treat disease with allocation of resources.

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2
Q

What is pathology?

A

Pathology is the study of disease, looking at its cause, effects, current state, treatments, and outcomes with tests and procedures.

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3
Q

Explain the patient journey.

A

The ideal patient journey shows how Canada’s healthcare system is ideally built to manage disease.

Well: subjective state of health defined by factors and social determinants
Health Decline: decline in health that can be managed by the patient or treated with prescription medication
Triage: patient presents themselves at a hospital or is taken by ambulance and seen by a triage nurse that assesses the urgency of treatment and care.
Admittance: patient is admitted when their illness is too severe, is unidentified and needs further testing, or requires treatment and monitoring by specialists
Diagnosis: tests are done to assess the condition. This is the stage where families begin to seek support
Treatment: after given a diagnosis and prognosis, the patient and physician discuss treatment options
Discharge: patient is sent home with medication and follow-up support
Monitoring: patients have check-ins so that physicians can monitor compliance and treatment safety
Palliative Care: patient is made comfortable until death

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4
Q

Explain the disease paradigm.

A

The disease paradigm is used to conceptualize the characteristics of a disease.

Etiology: the root cause of the disease
Pathogenesis: the development mechanisms of the disease
Testing: tests are done to analyze the presence of the disease
Biochemical Changes: changes to the chemical processes in the body seen through the test results
Morphological Changes: how the change in cells and tissues appear
Functional Changes: changes to physiology that appear in symptoms
Natural History: the prognosis of the disease
Treatment: how the disease is treated
Complications: further complications that can be caused by the disease

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5
Q

At what stage in the patient journey do pathologists play the largest role?

A

The primary role of pathologists in healthcare is to determine a diagnosis of the patients ailment.

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6
Q

How do indigenous groups learn and inherit knowledge?

A

Indigenous groups learn through experiential learning which is actively done through observation, action, and reflection. This learning is strengthened by ancestors, guides, and the Creator to form views on disease.

They inherit knowledge through oral tradition with the use of songs, poems, storytelling, and prayers. They have identified individuals who carry oral tradition. These people are knowledge keepers who remember and recite history, longhouse leaders who recite traditional speeches, and elders who tell stories to influence behaviour.

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7
Q

How do indigenous individuals view health?

A

Indigenous groups view health through a holistic perspective, viewing systems as wholes with inclusion of the four interconnected dimensions that are expressed on the medicine wheel.

Spiritual: cultural safety, strength, and resilience
Physical: capacities, mobility, comorbidity, awareness, and prevention
Mental: housing, family, community, and ceremony
Emotional: causality, and access to services

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8
Q

What are cells?

A

Cells are the basic unit structure of life that are composed of DNA. They differentiate into specialized cells that work together to do functions of tissues, in organs, within body systems, that come together as the human body. They always need nutrients, waste removal, and oxygen and are subjected to stresses that cause the cell to die and be replaced by new cells.

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9
Q

Define and explain the function of the cells organelles. (10)

A

Plasma membrane: made of phospholipids that control what can enter and exit the cell. Some molecules can freely pass through the membrane while others cannot. The molecules that can’t freely pass require transporters or the binding of receptors.

Nucleus: contains the genome within DNA that replicates, transcribes, and translates.

Mitochondria: produces energy in the form of ATP with the use of the Krebs cycle and oxidative phosphorylation.

ER: transports molecules around the cell and produces proteins and lipids.

Golgi apparatus: packages protein and cargo into vesicles for transport.

Lysosomes: digest waste and destroy bacteria with the use of enzymes.

Endosomes: sort, store, and organize content that comes into the cell.

Peroxisomes: break down hydrogen peroxide producing molecules and reactive oxygen species to neutralize the cell. Peroxisomes also need neutralized by catalase as they can be dangerous to the cell.

Cytoplasm: fluid within the plasma membrane with tightly regulated composition.

Cytoskeleton: structure filaments that provide structure and generate force for motion.

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10
Q

Explain the Central Dogma.

A

The central dogma covers the main parts of cellular function: replication, transcription, and translation.

Replication: cell duplicates it’s DNA before dividing
Transcription: DNA is transcribed into RNA
Translation: mRNA is translated into amino acid sequences that fold into proteins

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11
Q

How does gene regulation occur?

A

Gene regulation gives gene expression profiles by turning genes on or off, allowing an effective response to stimuli.

1) ligand binds to a receptor
2) receptor initiates cellular signalling
3) the signal up-regulates transcription of specific proteins
4) transcription produces mRNA
5) mRNA is translated into a protein
6) the protein is secreted from the cell so that it can do its function

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12
Q

Briefly explain the cell cycle.

A

G0: nerve and muscle cells are in a state of rest
G1: cells are actively living and growing in preparation to divide
S: genome replication occurs
G2: cell grows, increasing its amount of organelles
M: mitosis occurs where organelles are reorganized or dissolves, chromosomes are lined up and moved to each side of the cell, and cytokinesis divides the cell into two daughter cells

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13
Q

What are stem cells?

A

Stem cells are asymmetric cells that can differentiate into specialized cells to preform a function. They are extremely important for cellular repair or replacement. Stem cells specialize into progenitor cells that can differentiate into specialized cells to renew damaged tissue.

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14
Q

Briefly explain the two processes of cell death.

A

Necrosis is a result of trauma that causes the cell the real ease harmful reactive oxygen species and enzymes that cause inflammation and cell death in surrounding cells.

Apoptosis is regulated cell death that causes the cell to release its components without inducing inflammation.

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15
Q

What is cancer?

A

Cancer is the uncontrolled growth and division of abnormal cells that have the ability to invade tissues. It is the number one cause of death to Canadians.

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16
Q

What are neoplasms and tumours?

A

A neoplasm is abnormal tissue that grows when cells divide and do not die. A tumour is swelling or an abnormal mass that can be benign or malignant. Benign tumours cannot spread, can become large without killing the patient, and have a smooth round contour. Malignant tumours are cancerous tumours that can metastasize, kill patients when they are small, and have a spiky contour.

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17
Q

What is metastasis?

A

Metastasis is the ability of malignant tumours to spread around the body, through the bloodstream, to colonize different sites. This is what makes controlling cancer difficult as it can spread through the body, killing patients and making it difficult to determine the tumours place of origin. To find its place of origin, full body imaging and gene expression is used.

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18
Q

What are the different classifications of cancer? (5)

A

Carcinoma: solid tumours that affect epithelial cells
Sarcoma: begin in tissues that support the body like fat, muscle, nerves, blood vessels, bone, and tendons
Lymphoma: cancer that begins in lymphocytes
Glioma: arise in connective tissues of the brain
Leukaemia: cancer of the blood and bone marrow

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19
Q

What are the risk factors of cancer?

A

Family history, tobacco, age, HPV, and UV radiation are all carcinogens with tobacco being the most preventative. Generally tissues with higher stem cell divisions are at a higher lifetime risk of cancer.

Tobacco leads to the accumulation of tissue damage and the smoke kills epithelial cells so that stem cells need to repair the damage. The stem cells rapidly divide to restore the epithelial level and return to a resting state. With repeated exposure to smoke, stem cell division occurs more often, increasing the risk and vulnerability to oncogenic mutations.

Genetics are a major factor in cancer as a mutation occurs due to chromosomal damage that alters genes.

Direct UV exposure causes cumulative damage that increases the risk of damaging the genome which then accumulates to provide selective growth advantages, allowing mutated cells to thrive.

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20
Q

How does cancer start and evolve?

A

Cancers starts with a single cell that undergoes an oncogenic mutation. Typically mutations are silent, which don’t change the amino acid sequence or protein produced, or oncogenic which directly contributes to cancer development. The first step of cancer development is transformation, where a normal cell undergoes a genetic change that leads to a tumour cell that can divide rapidly. Over time, the tumour cells divide, causing an accumulation of mutations in daughter cells that can be the same as the initial tumour cell, or genetically different with other mutation variants. These cells are called clones. As the tumour cells proliferate, additional mutations occur, forming subclones that derive from the initial clone, which provide further growth advantages. With various sets of different mutations, the cancer is heterogenous representing hundreds of different cancer cells and subclones that offer different physiological characteristics.

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21
Q

Compare oncogenes and tumour suppressor genes.

A

Oncogenes derive from proto-oncogenes that mutate into oncogenes and produce proteins with altered functions that are involved with growth receptor pathways to mediate homeostasis and injury repair. Oncogenes only require 1 mutated allele and are typically form a sporadic type of cancer.

Tumour suppressor genes, when mutated, disable the ability of cells to prevent growth and induce cell death. These genes require both alleles to be mutated and typically are a familial type of cancer.

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22
Q

Explain the TP53 gene.

A

The TP53 is a tumour suppressor gene that produces p53 protein to regulate division. p53 Response to genomic damage by activating repair or cell death that prevents mutated cells from dividing. p53 Deficiency allows the cell to thrive with oncogenic mutation. Initially, the p53 binds to damaged DNA inducing G1 cell cycle arrest and repair with transcription. Proteins must repair mutations to proceed, but if that fails p53 triggers apoptosis or senescence. With inactive p53 no cell cycle arrest or repair occurs and damaged cells can proliferate into tumors.

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23
Q

Explain the ERBB-1 gene

A

ERBB-1 is an oncogene that encodes for epidermal growth factor receptors (EGFR). There are 20 different EGFR Proto-oncogenes that detect ligands, form dimers, and transmit signals associated with growth or survival to prevent unwanted proliferation. EGFR is a tyrosine kinase receptor that induces gene expression. initially a ligand binds to a receptor causing a confirmational change. Secondary messengers are then phosphorylated to transmit signals to the nucleus inducing transcription for proliferation, migration, and angiogenesis. Afterwards, the ligand releases or the receptor is broken down to stop the signal. Is there is a mutation to the ERBB-1, hyperactivation occurs where more secondary messengers are activated increasing the signal response and pro cancer processes. It also induces constitutive activation where signals are sent without a stimulus so pro cancer processes do not stop.

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24
Q

How does colorectal cancer develop?

A

Colorectal cancer arises from epithelial neoplasms called adenomas that are in the mucosa. Their development begins when cells with oncogenic mutations hyperproliferate. The mass that grows then projects into the intestinal lumen as a colonic polyp that takes 7 to 10 years to progress and can be removed in that time. Without removal, the polyp eventually invades adjacent tissue layers causing adenocarcinoma. The cancerous stage is when the polyp grows and evades tissues by entering the bloodstream to metastasize

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25
Q

How is screening and removal done for colorectal cancer?

A

Screening detects cancer early so that it is easier to treat. This is done on patients with increased risk of cancer due to age or family history. For colorectal cancer, a fecal immunochemical test which examines stool for blood from polyps, colonoscopy that looks for any masses, and CT scan which use medical imaging with x-rays to check for metastasis can be completed. Typically people do not get screened because of fear, lack of family history, misconception, or costs.

To remove colorectal cancer, a hemicolectomy can be done to remove the part of the colon that contains cancer and its surrounding lymph nodes.

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26
Q

How are tumours characterized?

A

Histology looks for changes to tissue structure to determine tumour progression by cutting and staining thin sections of tissue. Tumours are characterized by their stage and grade.

Stages of cancer include T, N, and M. The T indicates the depth of invasion, N indicates the spread to lymph nodes, and M denotes the presence or absence of metastasis. Lower stage numbers indicate less progression and better outcomes.

Cancer grades show how abnormal cells appear on a scale of 0 to 4 where higher numbers show more abnormality. Normal cells have hollow glands while G1 have less circular glands, G2 have different cells shapes, G3 has less glands and a variation in shape, and G4 have no glands, are not hollow, and do not have a specific structure.

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27
Q

What is genetic testing done on colorectal cancer patients done for?

A

When patients have colorectal cancer, genetic counsellors can get a blood test to see if there’s a mutation in the MSH2 gene of non-cancer cells to confirm Lynch syndrome. Lynch syndrome is a hereditary non-polyposis colorectal cancer that is the most common hereditary colorectal cancer syndrome. It is caused by a germline mutation to a mismatch repair gene. Since lynch syndrome is hereditary, one allele is already mutated so only one more mutation needs to occur for cancer to develop.

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28
Q

What is sporadic and familial colorectal cancer?

A

Sporadic: mutation spontaneously occurs on both alleles of the APC gene
Familial: inherited mutation of the mismatch repair genes (MSH2)

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29
Q

What affects the prognosis of colorectal cancer?

A

The prognosis of colorectal cancer depends on prognostic factors like age, general health, response to treatment, stage and grade, genetics, access to care, and compliance.

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30
Q

Explain blood cancers.

A

Blood cancers are caused when malignant cells, that begin in the bone marrow and fail to mature, are detected in the blood. Decreased red blood cells and oxygen results in fatigue and immune issues, while bleeding and clotting occurs from a loss of platelets.

31
Q

Describe the genomic events that cause acute myeloid leukemia.

A

Hematopoiesis is the development of mature blood cells from hematopoietic stem cells. Unspecialized stem cells can live for years and differentiate into progenitor cells which are multipotent cells with the ability to differentiate into specialized cells like myeloid, bone marrow, and lymphoid, connective tissue. Myeloid cells include red blood cells, platelets, and white blood cells. Lymphoid cells include T cells, B cells, and natural killer cells. Blood cancer occurs when progenitors do not fully differentiate and rapidly divide to create blasts.

In the first step, a tumour suppressor gene is lost in the HSC’s or the common progenitors. This leads to the initial accumulation of immature blood cells called blasts. At some point another proto-oncogene Is mutated, resulting in a major increase of proliferation. When these mutations occur, malignant blasts crowd normal HSCs and produce the symptoms associated with blood cancer.

32
Q

What are the different types of leukemia?

A

Leukaemia is classified by its proliferation speed and cell of origin. It can either be acute or chronic and lymphocytic or myeloid leukemia.

Acute: rapid progression of poorly differentiated cells that needs to be treated immediately
Chronic: slow progression of well differentiated cells that can be monitored overtime
Myeloid: myeloid progenitors become malignant
Lymphoid: lymphoid cell becomes malignant

33
Q

What factors affect the prognosis of acute myeloid leukemia?

A

The factors that affect the prognosis of acute myeloid leukaemia include age, weight, previous blood disorders, and genetics.

34
Q

What is PML-RARA?

A

Chromosomes can break and fuse together incorrectly in translocation, coding for fusion proteins that can be on cogenic. PML-RARA is a fusion protein hybrid sequence that occurs during a fusion of chromosomes 15 and 17 at the sites of PML and RARA genes. PML-RARA normally produces RARa to allow differentiation, but after fusion does not respond to signals, accumulating blasts. ATRA is a treatment that causes blast cells to mature into specialized myeloid cells.

35
Q

Describe new technological advances for cancer.

A

Cancer research, technologies, and clinical management has progressed, influencing how cancer is diagnosed, characterized, and treated.

A new treatment that is used is immunotherapy which uses immune checkpoint inhibitors to block the signal that allows cancer cells to hide from the bodies immune system, further allowing T cells to attack.

For testing, biomarkers like chemical products, enzymes, DNA, RNA, cancer cells, and proteins are tested for in screening for purpose of diagnostic, prognostic, and predictive testing. Diagnostic testing confirms disease presence. Prognostic testing indicates the likelihood of progression or reoccurrence. And predictive testing predicts the response to treatment. Genome sequencing is also used to understand the complete nucleotide sequence of DNA. This has been seen in the human genome project, tumour sequencing, data analysis, and further application.

Goals for the patient journey include improving wellness, with routine screening, and treatment, by finding better treatments to cure cancer.

36
Q

Who would benefit from immunotherapy?

A

Patients that have high levels of immune checkpoint gene expression in cancer cells would benefit from immunotherapy.

37
Q

What is metabolism?

A

Metabolism is the process in which macromolecules are converted to energy providing a balance of energy requirements by taking in, storing, breaking, and creating macromolecules. How bodies use and store energy depends on food intake and expenditure, stored fat, and the central nervous system‘s basal metabolic rate. It is regulated by hormones that influence sensation, storage, and consumption. At equilibrium there are equal amounts of anabolic and catabolic processes. Anabolism is when there is a lack of exercise or food intake that causes the favouring of sugar storage so that macromolecules are created to grow and repair damage. Catabolism is seen during exercise and fasting that causes sugar breakdown to create energy.

38
Q

What is the importance of insulin?

A

Insulin is produced by pancreatic beta cells to maintain healthy glucose levels. It binds to insulin receptors, activating anabolic activity and stimulating movement of glucose transporters from the endosome to the plasma membrane allowing glucose to enter the cell. If there is no insulin no glucose transporter will be moved to the plasma membrane and glucose cannot enter cells.

39
Q

Explain lipid transport.

A

Plasma Lipo proteins known as cholesterol forms spherical complexes around lipids to transport them in the bloodstream as they are water soluble. LDL transports cholesterol to tissues and is the bad cholesterol that we want to keep low. HDL transports extra cholesterol back to the liver and is the good cholesterol that we want to keep high. Triglycerides are the stored fats that should also be kept low.

40
Q

Explain obesity.

A

Obesity develops when someone consumes more energy then is used, causing excess fat to be stored as adipose tissue. We store energy to use the reservoir in times of fight or flight, but now consume too much energy that causes physical, biochemical, and morphological changes. Obesity can lead to diabetes, cardiovascular disease, cancer, and arthritis.

41
Q

Explain the difference between subcutaneous and visceral fat.

A

Subcutaneous fat is found under the skin in the abdomen, hip, and thighs and has a slow fat metabolism rate. It causes people to have a pair body shape. Visceral fat is found around the abdominal organs and allows for fast fast turnover. It increases the risk of metabolic disease as a result of excess hormone signalling and causes people to have an apple body shape.

42
Q

What is metabolic syndrome?

A

Metabolic syndrome is a health disorder characterized by visceral obesity, increased blood sugar, hypertension, increased triglycerides, and the low HDL cholesterol. In order to be diagnosed with metabolic syndrome, patients need to have three out of the five factors. Metabolic syndrome increases the risk of chronic illness.

43
Q

What is diabetes?

A

Diabetes is it disease characterized by high blood sugar that occurs when the body either does not produce enough insulin or does not correctly respond to insulin. Diabetes can be type 1 or type 2. In healthy bodies, pancreatic beta cells produce insulin that signals glucose uptake. in type 1 diabetes an autoimmune disorder kills beta cells so that insulin is not produced at all. Patients with type one diabetes require insulin replacement. Type 2 diabetes occurs when cells become insulin resistant, reducing glucose uptake.

44
Q

How does insulin resistance occur?

A

Insulin resistance occurs when blood glucose spikes so that insulin secretion also increases. With continuous glucose uptake, insulin receptors change so that they bind to less insulin. Overtime tissues become less responsive to regular insulin levels and uptake less glucose. Because less glucose is taken into the cells, an increased insulin production occurs, overtaxing and damaging Beta cells.

45
Q

What are the symptoms, medications, progressions, and risk factors of type 2 diabetes?

A

The symptoms of type two diabetes include polyuria, polydipsia, and polyphagia.

In order to treat type 2 diabetes, lifestyle changes like exercise, decreased caloric intake, medications, and glucose monitoring is done. Medication’s, like Metformin, activate signalling pathways for sugar and fat metabolism in order to increase insulin sensitivity, decreased glucose absorption, and promote glucose cannibalism.

If type two diabetes is not treated, the eyes, heart, pancreas, kidneys, and feet can be impacted. Retinal damage causes vision loss, the heart is impacted increasing risk of cardiovascular disease, heart attack, or stroke, the pancreas fails to produce insulin, the kidneys have damaged blood vessels resulting in kidney failure, and peripheral neuropathy causes numbness in the feet and hands.

The risk factors of type two diabetes include age, lifestyle, and family history.

46
Q

What are strokes?

A

Strokes occur when blood clots prevent blood from reaching the brain. They can be treated with TPA through thrombolytic therapy used to dissolve clots.

47
Q

What is atherosclerosis?

A

Atherosclerosis is the thickening of arteries from inflammation or plaque buildup that can cause heart attacks and strokes. It occurs when vessels are repeatedly damaged, injuring endothelial cells. Healthy blood vessels have lumen surrounded by endothelial cells that cover smooth muscle and connective tissue. Atherosclerosis occurs when the force of blood causes friction so that LDL accumulates under the endothelium. Because LDL accumulates under the endothelium, infiltration can occur where platelets infiltrate the vessel wall. Immune cells try to remove this buildup but LDL apoptosis increases inflammation. Eventually collagen, debris, and immune cells increase plaque buildup narrowing and weakening the blood vessel. If this plaque ruptures, it can lodge and create a blockage elsewhere. This is known as an embolism.

48
Q

What are tests done, risk factors, common sites, and treatments for atherosclerosis?

A

In order to determine the diagnosis of atherosclerosis, blood tests, ECG‘s, carotid Doppler‘s, and ultrasounds can be used.

The risk factors of atherosclerosis include diabetes, weight, smoking, and pre-existing heart diseases. Protective factors can be used to lower disease potential.

Atherosclerosis typically occurs in the carotid, coronary, and ilio-femoral arteries

Treatments for atherosclerosis include carotid endarterectomy‘s, statin therapy, bypass, angioplasty, and stenting. Carotid endarterectomy‘s are used to surgically open the artery and remove blood clots. Statin therapy is used to lower cholesterol. bypass is done when veins are harvested and grafted to skip over a blockage. Angioplasty uses a balloon catheter to expand the vessel. Stenting uses metal or plastic stents to keep the vessel open.

49
Q

What are future treatment options for metabolic disorders?

A

Prevention and early intervention are important to control metabolic disorders but treatment is hoped to slow and reverse effects. The future of monitoring includes nanoparticles that could attack plaque and prevent buildup. It also includes the idea that the presence of blood clots can be used to predict potential danger to other parts of the body. The future of treatment includes the use of smart devices that can read blood glucose levels, immunotherapy to protect beta cells, and the identification of predictive markers.

50
Q

What is the nervous system? What does it consist of? What cells are involved?

A

The nervous system coordinates, controls, and regulates processes by creating a motor response, interpreting sensory information, and maintaining the internal environment of cells. It controls emotion, memory, learning, and high-level cognitive functions. It consists of the central nervous system, including the brain and spinal cord, and the peripheral nervous system, including all nerve tissue outside of the central nervous system. It is composed of neurons and glial cells.

Neurons communicate to transmit information between the central and peripheral nervous systems. They contain a cell body, dendrites, axon, myelin sheath, and axon terminals.
Cell body: Contains the nucleus and organelles
Dendrites: Protrusions that receive incoming signals
Axon: Transmits signals away from the cell body
Myelin Sheath: Fatty coating that insulates signals increasing transmission speed
Axon Terminals: The axons and where signals are transmitted to adjacent neurons
Electrochemical signalling through neurons is known as nerve impulse. It occurs when a signal is received by the dendrites, causing electrical action potential to move through the cell body and down the axon. When the electrical action potential reaches the axon terminals, neurotransmitterchemicals are released into the synapse to trigger action potential in an adjacent cell.

Glial cells support neurons by regulating the environment, maintaining neuron position, and repairing damage. These include Schwann cells, oligodendrocytes, microglial cells, and astrocytes.
Schwann Cells: Support and insulate with myelin in the peripheral nervous system by spiralling around the axon length
Oligodendrocytes: Produce and maintain myelin in the central nervous system, myelinating multiple adjacent neurons at a time
Microglial Cells: The brains immune system that clears damage, prunes synapses, and removes debris
Astrocytes: cells that look like stars and provide growth factors and nutrients, maintain the blood brain barrier, and repair tissues

51
Q

What is mental health vs mental illness?

A

Mental health is a physiological and emotional state that can lead to mental or physical illness and may need interventions to support.

Mental illness is a diagnosable and treatable condition that does not involve structural abnormalities, but reduces functionality over a prolonged period of time.

52
Q

What are ACEs?

A

ACEs Are adverse childhood experiences that increase the risk for developing mental, physical, and social problems. Addressing these symptoms and building resiliency can improve health by considering individual, family, and community factors.

53
Q

What are neurodegenerative disorders and their risk factors?

A

Nerodegenerative diseases are heterogeneous and slow progressing disorders that occur when the nervous system cells lose function and die. There is no way to slow or halt the progression of neurodegenerative diseases and no cures found. Neurodegenerative diseases are classified based off pathological features, like the parts of the nervous system involved.

The risk factors of neurodegenerative disorders are age, reactive oxygen species, cell death, protein misfolding, aggregation, synaptic dysfunction, and cell death.

54
Q

What is dementia?

A

Dementia is a term for cognitive decline that impacts memory, thinking, and reasoning. It results from neurodegeneration associated with Alzheimer’s disease or Lewy body dementia.

The risk factors of dementia include age, genetics, diabetes, increase blood pressure, increased cholesterol, smoking, inactivity, obesity, drugs, poor diet, PTSD, depression, and schizophrenia.

An issue to the indigenous culture is that they describe dementia as natural mind changes that bring them closer to the creator so that they do not access healthcare in the early stages. I-CAARE is an association that provides fact sheets about dementia in order to help the situation.

55
Q

What is Alzheimer’s disease?

A

Alzheimer’s disease is characterized by personality change, memory loss, and withdrawal. It is diagnosed with cognitive tests like clock drawing, pattern recognition, and memorization in order to check judgment, orientation, memory, and visuoconstructive skills. Alzheimer’s disease is a progressive neurodegenerative disease that is the most common cause of dementia and gives a prognosis of 4 to 20 years.

The risk factors of Alzheimer’s disease include genetics, where inherited mutations affect amyloid-beta processing causing sporadic Alzheimer’s disease; sex, where incidence is two times higher in women due to hormones; and lifestyle risk factors like diabetes, obesity, depression, and smoking.

Initially amyloid-beta is produced by APP cleavage in the cell membrane of neurons. The amyloid-beta oligomers disrupt synaptic function then aggregate into plaques that disrupt neuron function. Amyloid beta deposits activate microglial cells, triggering inflammatory responses. Misfolded tau then aggregate into tau tangles, displacing intracellular organelles. Misfolded tau then pass the synapse and catalyze further misfolding of tau.

56
Q

Describe the microscopic and macroscopic changes in Alzheimer’s disease and it’s progression.

A

Alteration to amyloid-beta and tau proteins causes misfolding, aggregation, and cellular death.

Microscopic Changes:
Amyloid-beta: Small proteins from cleavage of amyloid precursor proteins in the cell membrane of neurons are amyloid-beta proteins. In Alzheimer’s disease, amyloid-beta aggregates and oligomers concentrate in the synapse then further aggregate into amyloid-beta plaques that activate microglia, increase inflammation, and injure neurons, damaging the brain blood vessels causing cerebral amyloid angiopathy.
Tau: binds to microtubules to promote stability. In Alzheimer’s disease, tau protein misfolds, disassembling and disrupting neurotransmission and forming oligomers that aggregate in neurons as tau tangles that are toxic and can spread.

Macroscopic Changes:
Cerebral cortical atrophy: Brain weight and size decreases
Ventricles: Ventricles in large due to debris
Hippocampal atrophy: Hippocampus shrinks

Progression:
In the early stages of Alzheimer’s disease, the hippocampus is affected, altering memory and spatial navigation. In the middle stages, the cerebral cortex fills with amyloid-beta plaques and tau tangles. In the late stages, aggregation increases over several years causing further complications.
Amyloid-beta plaques are found early, while tau tangles are found later, closer to the onset of symptoms.

57
Q

What is Charcot-Marie-Tooth Disease?

A

CMT onset is in childhood, characterized by muscle weakness and atrophy, diminished muscle stretch reflexes, and sensory deficits. CMT can be classified as type 1 or type 2. it affects the peripheral nervous system with over 100 genes linked to disease.

Type 1: Demyelinating neuropathy affects Schwann cells, slowing conduction. Shows a slow progression of weakness and atrophy in the legs. This is caused by the mutation to the PMP22 gene.

Type 2: Axonal neuropathy that causes axonal degeneration, resulting in loss of nerve supply to muscle and atrophy of skeletal muscle. Typically has more mild symptoms with less disability seen in childhood.

CMT is diagnosed with nerve conduction studies, that test electrical signals with electrodes that transmit electricity, electromyography, that uses a needle in muscle to measure muscles electrical activity, and genetic testing, which uses blood samples to check for hereditary neuropathy‘s.

There is no cure for CMT, but it is not life-threatening and physiotherapy can be done to maintain muscle. Only light exercise should be done, but current states can be maintained for several years.

58
Q

Future of neurological disease management.

A

Health Decline: prevent protein missfolding, clear plaque, find biomarkers with spinal tap, use PiB to find amyloid-beta peptides with pet scans, clear accumulations

Treatment: Bypass genetic mutations, silence Jean copies, replace jeans, and use antisense oligionucleotides

Monitoring: Increase nursing and personal care, use reminiscing kits, increase therapy, I-CAARE

59
Q

What causes infectious disease?

A

Infectious agents and microbes are organisms capable of producing infectious disease. They are grouped based on features.
Bacteria: Unicellular prokaryotes with double stranded circular DNA and cell walls
Viruses: Obligate microbes that invade the host to replicate. They have DNA or RNA and protein coat
Fungi: Eukaryotes with carbohydrate cell walls that cause superficial infection and invade tissue
Parasites: eukaryotes that cause disease including worms, insects, and arachnids. They can also be ectoparasites that cause disease from the outside

The microbiome, normal flora, has microbes that live symbiotically on the skin and mucous membranes to digest, prevent inflammation or infection, and produce vitamins. If there is an imbalance of good and bad microbes, disease can be caused.

60
Q

What are pathogens? How do they affect the body?

A

Pathogens cause disease with an imbalance of good and bad microbes. The body has barriers in place to remove or prevent pathogens from entering. These include innate response, adaptive response, and barriers.

Innate: Instant response to prevent pathogens spread with immune cells and barriers
Adaptive: Specific response that take days after detecting antigens. After attacking the antigen, adaptive response puts the antigen into memory for a faster response if the disease reoccurs
Barriers: Physical, including the skin and mucus, chemical, including enzymes from tears and saliva, and immune cells, that cause inflammation

Initially pathogens enter the body through passages then attach to human cells and use a specific tactic to invade the cell. After evasion, the pathogen can reproduce and spread. for infection to establish, there must be a reservoir, mode of transmission, and opportunistic conditions.

61
Q

How can infectious disease be prevented?

A

Transmission can be prevented with reservoir removal, barriers, vaccines, and medication. Vaccines are the most powerful tools for protection, but certain groups like children, elderly, pregnant women, and immunocompromised patients can’t get vaccinated. Because of this, herd immunity is used to indirectly prevent risk for those patients.

62
Q

Describe the structure of bacteria.

A

Bacteria fall within two groups based on their cell wall structure. They can be gram-positive with a thick peptidoglycan wall, or gram-negative with a thin wall of peptidoglycan within the outer membrane. All bacteria have a bacterial cell envelope that contains the internal pressure of the cytoplasm to prevent bursting. It is composed of the membrane and cell wall.

63
Q

Explain antibiotic types.

A

Antimicrobials: Natural and synthetic agents that stop growth of and kill microorganisms
Antibiotics: Molecules from microorganisms that stop growth of and kill microorganisms
Bacteriostatic: Inhibit bacterial growth with help of immune system
Bactericidal: Kill bacteria without the help of the immune system
Broad-spectrum: Attack a wide range of bacteria
Narrow spectrum: Attack a small group of organisms

64
Q

What are the targets of antibiotics?

A

Cell wall synthesis inhibitors: Prevent cell wall formation by binding to enzymes that cross-link peptidoglycan, causing osmotic rupture.

Cell membrane disruptors: Daptomycin creates leaks in the plasma membrane to halt protein synthesis and change chemical gradients.

Protein synthesis inhibitors: Prevent mRNA translation by targeting ribosomes.

Nucleic acid synthesis inhibitors: inhibit DNA guyrase, preventing DNA super coiling and causing unravelling in order to degrade DNA and kill the cell.

Metabolic pathway disruptors: Two antibiotics are used in conjunction to separate enzymes involved in folate synthesis.

65
Q

What is antibiotic resistance? How does it develop?

A

Antibiotic resistance occurs when bacteria develop mechanisms to evade antibiotics. This can include altering targets or having enzymes take over the target function, restricting target access so that the drug cannot enter or is immediately pumped out, and using drug specific enzymes that are developed to destroy or modify the antibiotic.

Initially the host is infected with some drug resistant pathogenic bacteria. When the patient is treated, antibiotics kill the bacteria that is not drug resistant. The drug resistant bacteria do not die, and are able to proliferate inside the host. These drug resistant bacteria then transfer their resistance to drug susceptible bacteria through progeny or horizontal gene transfer for a fast and widespread resistance. Horizontal gene transfer can occur through transformation, where DNA is taken up and incorporated into the genome, conjugation, where cell to cell contact allows plasmid gene transfer, and transduction, where infection occurs with a bacteriophage. Maintaining resistance requires energy, so it is only maintained with antibiotics stimulus. This is known as selective pressure

66
Q

How did global antibiotic resistance occur?

A

Selective pressure from antibiotic use made nearly all bacteria resistant through beta-lactamase‘s and carbapanem resistance. Antibiotic overuse in hospitals, pharmaceutical companies, agriculture, and aquaculture created this resistance, increasing the cost of antibiotics and adverse events.

67
Q

How is antibiotic resistance prevented?

A

Surveillance: continuous monitoring
Stewardship: Careful use of antibiotics across all industries
Research and innovation: Research for antibiotic discovery
Prevention and control: Adherence to hygiene, sanitation, and infection control

In high income countries, antibiotics are restricted in food, med school prescriptions, gifts, and usage is tightly monitored. In low income countries, antibiotics are not regulated due to a lack of testing, funding, and leadership. As well antibiotic quality is lower, increasing antibiotic resistance.

68
Q

What are viruses? How do they infect people?

A

Viruses are obligate infectious agents that can only replicate in hosts. Virions carry the minimum equipment to replicate, including an envelope and genome. They should not be considered living because they are not made of cells, do not grow, and do not produce their own energy. Viruses continually mutate and evolve into new types. They have a single or double stranded DNA or RNA genome and are surrounded by a capsid and an outer envelope derived from host membranes. The outer layer of viruses has viral proteins that interact with host receptors to enter cells.

Initially the viral attachment to the host receptor grants access inside the cell. The virus then synthesizes its genome, translates proteins, and assembles into virions. afterward, the virus utilizes a process to release into the extracellular environment in order to infect new cells.

69
Q

Explain the 1918 Influenza pandemic.

A

Influenza had several outbreak waves, with the second being the most lethal and third evolving into the annual influenza season. At the time, little was known about viruses, making it difficult to manage the disease. It was believed that the overactive inflammatory immune response led to secondary pneumonia and tissue damage that caused death in healthy young adults. At this time there was no quarantine, but gatherings were prohibited and isolation of sick occurred.

70
Q

Describe COVID-19 and how it infects hosts.

A

Covid is caused by SARS-CoV-2 and is characterized by a fever, cough, and fatigue. As part of the coronavirus family, it is spherical, envelope with spike proteins, and has a single-stranded RNA genome. it spreads via droplets and aerosols and does not stay on surfaces long.

Covid infects hosts through entry, attachment, replication, release, and infection. Initially, virions enter the body through the oral or a nasal pathway and travel to the lungs where spike proteins can bind to ACE2 receptors. After binding to the receptors, the virus hijacks cellular machinery to replicate. The SARS-CoV-2 virions then bud out of the host cell and infect other tissues, people, or organisms.

71
Q

What are the different types of variants?

A

The different types of variance include variants under monitoring, variants under interest due to their characteristics, previously circulating variants, variants of concern due to transmissibility, and subvariants.

The biggest variant of concern for Covid is currently omicron.

72
Q

How is the infection of CoVID-19 controlled?

A

The infection of Covid is controlled with distancing, closures, masking, washing, staying inside, quarantine, and tracing.

73
Q

What are the different types of vaccines?

A

Viral vector: Harmless virus used for gene to encode protein of interest
mRNA: Synthetic mRNA is used to code for a piece of protein
Whole virus: Attenuated or weakened viruses are used to expose the immune system to the disease
Protein subunit: harmless virus antigens are used to generate immunity
Virus-like particles: bio technology makes virus like particles with antigens but no genetic information

74
Q

Discuss the future management of disease.

A

Screening: Early detection can help control disease. Future screening improvements include cancer screening with gene sequencing or biomarkers for monitoring and PCR testing which allows for rapid diagnosis.

Medication: Government assistance is required to improve and identify drug development. New antibiotics and vaccines are almost always required.

Healthcare disparities: It is important to identify and address the social determinants of health.

Patient communication: Open communication with patients can improve outcomes by allowing doctors to obtain complete information, enhance diagnosis, and facilitate treatment or support. It is also important that indigenous goals and needs are met with protective factors, prevention, and spirituality which promotes health and safety.