Nursing 611 Advanced Pathophysiology Study Guide, Exams of Pathophysiology

Download Nursing 611 Advanced Pathophysiology Study Guide and more Exams Pathophysiology in PDF only on Docsity! Nursing 611 Advanced Pathophysiology Study Guide Key Points Exam 1: Know Cell components and what they do: • Nucleus- contains and stores DNA • Ribosomes- Make proteins, vital for cell growth and survival • Mitochondria- powerhouse of the cell, make ATP • Golgi apparatus- Package newly synthesized proteins and lipids from the ER to send within the cytoplasm and to the plasma membrane • Lysosome- Break contents down using enzymes, release contents to be recycled • Peroxisome- (peroxide) break things down using oxygen, byproduct is H2O2 (hydrogen peroxide) too much can lead to free radicals • What are Free Radicals or Reactive Oxygen Species? How do they cause damage? o Unstable atoms that can cause damage (aging, illness) ▪ Atom with outer shell not full—will bond with another atom to complete its electron shell o Difficult to control and can initiate chain reactions o Can cause alteration of proteins or DNA, lipid peroxidation Cell membrane • What is the Plasma Membrane made up of? o Polar head (hydrophilic head) with nonpolar (hydrophobic tail) o Fluid mosaic model: fluidity of the lipid bilayer, the flexible, self- sealing properties, and selective impermeability of the plasma membrane. o Water moves freely by diffusion through the lipid bilayer through aquaporins • Why do we need a Cell membrane? o Keep ICF and ECF separate, hold cells together so they can function as a unit • How is Osmolality different between ICF and ECF? o Due to water permeability, osmolality should be equal. • What do proteins do for the cell? How much of the Cell membrane is made up of protein? o Carry out 55% of all physiologic processes o Recognition and binding units (receptors) for substances moving in and out of the cell o Pores or transport channels o Enzymes that drive active pumps o Cell surface markers, such as glycoproteins o Cell adhesion molecules • What is a protein? o Large, complex molecules that are required for the structure, function, and regulation of the body’s tissues and organs. o Made from amino acids (chains), each amino acid coded from 3 nucleotides→ major structural unit of the cell o Functions: antibody, enzyme, messenger, structural, transport/ storage (enzymatic and hormonal functions) 3 types of Cell junctions: • Describe what Tight junctions are and why we need them? o Help cells move together and don’t allow things in • Describe what Gap junctions are and why we need them? o Junctions are channels that allow for conductivity- like the heart and nerve cells o Provide the most intimate means of intercellular communication (don’t have to enter the extracellular fluid) o Protein channels • Describe what Desmosomes are and why we need them? o Hold cells together by forming either continuous bands of belts of epithelial sheets or button like points of contact Energy • What is Oxidative phosphorylation? o Occurs in the mitochondria and is the mechanism in which energy is produced from carbohydrates, proteins and fats and this energy is transferred to ATP • What is the Inside of cell main Cation? o Potassium • What is the outside of cell main Cation? o Sodium • Is the inside of the cell positively or negatively charged? o Negatively charged • Is the outside of the cell positively or negatively charged? o Positively charged Transport: • Diffusion o A passive movement of a solute from an area of higher solute concentration to an area of lower solute concentration • Facilitated diffusion o KEY and LOCK….. This is a carrier mediated process that will allow particles that are too big or charged to get through the membrane. AGAIN there is no energy to do this process, but you have a limited capacity. o Back up—glucose and ETOH Key Points WEEK 2: Altered Cell metabolism and Genetics Altered Tissue Define and give examples of each Condition Define Example Atrophy -Physiologic: with early development -Pathologic: Decrease in cell size (due to decreases in workload, use, pressure, blood supply, nutrition, hormonal or nervous stimulation Can affect any organ but most common in skeletal muscle, heart, secondary sex organs, and the brain -Physiologic: thymus gland during childhood -Pathologic: aging causes brain cells to atrophy Hypertrophy increase in the size of cells by increased work demands or hormonal stimulation-- increases the size of the affected organ; physiologic (increased demand, stimulation of hormone and growth factors) or pathologic (chronic hemodynamic overload) Physiologic hypertrophy: pregnancy (hormone-induced uterine enlargement) Pathologic hypertrophy: hypertension or heart valve dysfunction Hyperplasia increase in the number of cells caused by an increased rate of cellular division -Occurs as a response to injury that results when the injury has been severe and prolonged -Growth factors stimulate the remaining cells to synthesize new cell components -Compensatory hyperplasia enables certain organs to regenerate. (normal) *Removal of the liver leads to hyperplasia of the remain in liver cells to compensate for the loss -Hormonal hyperplasia is stimulated by hormones to replace lost tissue or support new growth, such as during pregnancy. (normal) -Pathologic hyperplasia is the abnormal proliferation of normal cells in response to excessive hormonal stimulation of growth factors on target cells. Metaplasia the reversible replacement of one mature cell type by another less mature cell type -Develop from a reprogramming of stem cells existing in most epithelia or of undifferentiated mesenchymal cells in connective tissue Long term smoker→ chronic irritation causes normal ciliated columnar epithelial cells of the trachea and bronchi to become replaced with stratified squamous epithelial cells (loss of protective mechanism) o Is Dysplasia considered a true adaptive process? o Also called atypical hyperplasia, abnormal change in size, shape, and organization of mature tissue cells, deranged cellular growth o Not a true adaptive process but is related to hyperplasia; mostly found in the epithelia → dysplasia is not cancer and may not progress to cancer; may be completely reversible depending on extent involved o What is the difference between physiological change and a pathological change? o Physiologic change: normal body change o Pathologic change: disease process Cell injury • Ischemia o Reduced blood supply o Often caused by gradual narrowing of arteries and complete blockage by blood clots ▪ Results in myocardial adaptation • Necrosis : the sum of the changes after local cell death (inflammation and cellular lysis/ autolysis); different types of necrosis in different tissues o Common type of cell death with severe cell swelling and breakdown of organelles • Define Infarction o Myocardial call death o Can be caused by an acute obstruction in a coronary artery What is the most common CAUSE of cell injury? HYPOXIA→ can result from reduced amount of oxygen in the air, loss of hemoglobin or hemoglobin function, decreased production of RBCs, consequences of respiratory or cardiovascular system diseases, and poisoning of the oxidative enzymes within cells (most common cause of hypoxia is ischemia) • Biochemical themes of cell injury o Depletion of ATP o Decreased levels of oxygen and increased levels of oxygen-derived free radicals, increased concentration of intracellular calcium and loss of calcium steady state, defects in membrane permeability Which is worse, Hypoxia or Ischemia? Why? • Ischemia causes hypoxia o Ischemia: cessation of blood flow to vessels that supply the cell with oxygen and nutrients ▪ Oxygen applied after can result in reperfusion injury o Hypoxia: can induce inflammation and inflamed lesions can become hypoxic What is the difference between necrosis and apoptosis? • Necrosis : the sum of all changes after local cell death (inflammation, cellular lysis, autolysis) o Rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction, lack of typical features of apoptosis o Cell SWELLS; plasma membrane disrupted; frequent adjacent inflammation • Apoptosis : programmed cell death characterized by the “dropping off” of cellular fragments called apoptotic bodies o CELL SHRINKS; plasma membrane intact o Occurs with severe cell injury, accumulation of misfolded proteins, infections (viral), obstruction in tissue ducts Necrosis: explain the difference • Gangrenous necrosis: death of tissue resulting from severe hypoxic injury • Dry gangrene o The result of coagulative necrosis: hypoxia caused by severe ischemia or hypoxia caused by chemical injury; coagulation is caused by protein denaturation→ causes Albumin to change from gelatinous, transparent state to a firm, opaque state→ area of infarct o Skin becomes very dry and shrinks, resulting in wrinkles, color change to dark brown/ black • Wet Gangrene o Develops when neutrophils invade the site, causing liquefactive necrosis o Occurs in internal organs→ site becomes cold, swollen and black, foul odor, pus Cells and Aging: • What happens to cells as we age? o Atrophy, decreased function, loss of cells (apoptosis)--> causes hypertrophy and hyperplasia which can lead to metaplasia, dysplasia, neoplasia o Are agents, such as radiation and chemicals, that increase the frequency of mutations • Which part of the cell can be damaged the most by radiation? o DNA from ionization Explain the process of how we make a Protein? • What is transcription? o The DNA strand is untwisted and unzipped. This occurs in Nucleus ▪ Single strand acts as a template→ creates mRNA ▪ mRNA (messenger) uses this DNA strand to make a template that can be carried outside of the nucleus happens within the nucleus ▪ RNA Splicing-- many RNA sequences are removed and the remaining sequences are spliced together to form functional mRNA that will migrate to the cytoplasm ▪ Excised sequences are called introns and exons are those that remains to code for proteins ▪ RNA polymerase ▪ Single stranded, ribose sugar molecule and Uracil rather than thymine ▪ Polymerase- . polymer- means long chain and -ASE means enzyme . So a polymerase IS an enzyme that helps to create a long chain. • What is translation? o mRNA and translating it into amino acids that will make a protein. o mRNA takes the “recipe” out of the nucleus o RNA directs the synthesis of a polypeptide via the interaction with transfer RNA (tRNA). o tRNA contains a sequence of nucleotides (anticodon) complementary to the triad of nucleotides on the mRNA strand (codon). • Where does protein synthesis occur? o The ribosome o Ribosome (rRNA) helps mRNA and tRNA make polypeptides. o When a ribosome arrives at a termination signal on the mRNA sequence, translation and polypeptide formation cease. o RNA is synthesized from the DNA template via RNA polymerase formation of mRNA mRNA moves out of the nucleus to cytoplasm capable of gene splicing (into introns and extrons) CHROMOSOMES: • How many pairs of chromosomes do we have? o 23: 22 homologous pairs and one sex linked pair (homologous (XX) or nonhomologous (XY)) • What is a Gamete cell? o Germline cells o Haploid cells (only 1 member of each chromosome pair) o Reproductive cells, sperm and egg cells; contain 23 chromosomes • What is a Somatic cell? o Any other cell than a reproductive cell o Contain 46 chromosomes-- 23 base pairs; 22 of the pairs are autosomes • What is a Karyotype? o An ordered display of chromosomes arranged according to length and centromere location Genetic Diseases: DEFINE THE FOLLOWING • Aneuploidy o A somatic cell that does not contain a multiple of 23; usually the result of nondisjunction o I.e. Trisomy (three copies of one chromosome), monosomy (one copy of any chromosome-- often fatal) ▪ Duplication of genetic material better than the loss of genetic material • Penetrance o Definition: the percentage of individuals with a specific genotype who also exhibit the expected phenotype o Incomplete penetrance ▪ Individual who has the gene for a disease but does not express the disease ▪ Has genotype but may not express phenotype ▪ Example: Retinoblastoma (eye tumor in children) (90%) o Age dependent ▪ Does not express a disease until a certain age is reached ▪ Has the genotype and will express disease but will not express until a certain age ▪ Example: Huntington disease • Expressivity o Is a variation in a phenotype associated with a particular genotype. o Can be caused by modifier genes, environmental factors, and mutations. o Example: von Recklinghausen disease ▪ Is autosomal dominant. ▪ Expressivity varies from brown spots on the skin to malignant tumors, scoliosis, gliomas, and neuromas. ▪ Can be expressed very differently Alleles • What is a Dominant allele? o Observable allele • What is a Recessive allele? o Effects are hidden • What is a Carrier? o Has a disease allele but is phenotypically normal→ can pass disease to offspring Relative Risk • What does relative risk mean? o A measure of the effect of a specific risk factor ▪ Factors include age, gender, diet, exercise, family history • What is incidence? How do you calculate it? o Number of new cases of a disease reported during a specific time period divided by the number of individuals in the population • What is prevalence? How do you calculate it? o Proportion of the population affected by the disease at a specific point in time Epigenetics • What is epigenetics? o Modifications that affect phenotype without altering DNA sequencing o Taking the genetics we have and manipulating them o A woman who smokes while pregnant induces epigenetic changes in three generations at once, herself, her unborn daughter, and her unborn daughter’s reproductive cells o Stably heritable phenotype resulting from changes in chromosome without alterations to the DNA sequence.; phenotype is going to be the physical appearances that you have. And so what epigenetics does is allow us to change the phenotypes without changing the underlining DNA sequence. And this is heritable. In other words, once we change that you can actually pass that on to the next generation. • How do environmental factors affect epigenetics? o Feed mother different amounts of nutrients, could create different offspring o What happens to a mother affects her, her baby and her baby’s unborn babies • Can epigenetic modifications be reversed? If so how? o Epigenetic modifications DNA sequences can be altered, unlike DNA mutations • What is hypermethylation associated with→ cancer Pediatric considerations: • Downs Syndrome o Best example of aneuploidy→ Trisomy 21 o Hormones ▪ Atrial natriuretic peptide (ANP)-produced by the myocardial atria ▪ Brain or B-type natriuretic peptide (BNP)- produced by the myocardial ventricles ▪ BNP is primarily secreted by the ventricles in the heart as a response to left ventricular stretching or wall tension ▪ They ↓BP and ↑of sodium and water excretion ▪ They are antagonists of the RAAS system • What initiates osmoreceptors? o Increased osmolality stimulates hypothalamic osmoreceptors that cause thirst, water drinking, and stimulating the release of ADH (promotes restoration of plasma volume and blood pressure) • What does the Antidiuretic hormone (ADH) do? o Renal water absorption o Increase the permeability of distal renal tubular cells to water, increase water reabsorption and promote the restoration of plasma volume and blood pressure o Released in posterior pituitary, in response to slight increases in tonicity of the ECFV. The presence or absence of ADH is the most important factor in determining whether final urine is concentrated or dilute. ADH increases the permeability of the renal collecting tubules to water. Electrolytes: Norma l Patho Manifestations Evaluation & treatment Hypernatremia (BRAIN) 135- 145 Blood vessels pull water out of brain cells into blood vessels causing brain cells to shrink Confusion, Convulsions, Cerebral Hem., Coma *elderly ⬇thirst *Obesity higher risk (adipose repels H2O) find and correct the faulty water control mechanism DI Insensible losses Treat-D5W Hyponatremia (BRAIN) 135- 145 Hypovolemic hyponatremia: loss of total body fluid. Caused by Headache, < 125: Lethargy, confus. < 120: Sz., coma Complete H&P, test serum and urine levels, CBC, BMP, emesis/diarrhea. ADH secretes to replete volume Euvolemic hyponatremia: Na+ loss w/o H2O loss. This is SIADH, hypothyroidism, PNA, glucocorticoid deficiency) Dilutional hypotonic hyponatremia (H2O intoxication): large intake of free water or replacement of fluid loss with D5W (glucose is metabolized, leaving hypotonic effect) (from cerebral edema/cellular swelling) *mild hyponatremia is usually asymptomatic Albumin, Urine osmolality and Na+ levels, as well as urine specific gravity, Differential dx includes: SIADH Dehydration Adrenal insufficiency Hypothyroidis m Infection (PNA) Glucocorticoid deficiency Hyperchloremia 95-105 Fluid retention, high BP, fatigue, muscle weakness, excessive thirst, dry mucous membranes. Hypochloremia 95-105 Typically accompanies Metabolic alkalosis, hyponatremia and elevated bicarb. Common in Cystic Fibrosis. Na+ deficit associated with diuretics or restricted intake is typically associated with hypochloremia. Weakness, fatigue, difficulty breathing. Often associated with vomiting and diarrhea - although these are what lead to the low levels. *Can be asymptomatic *In all cases treatment of the underlying cause is required ABGs, anion gap Good H&P required, review medications closely. Hyperkalemia 3.5-5 Insulin causes potassium to move into cells patients with deficient Insulin can develop EKG changes: Peaked T wave, prolonged PR, depressed ST, wide QRS EKG, labs, IV fluids if dehydrated. Treat underlying hyperkalemia *can be caused by decreased renal excretion Symptoms: dysrhythmias, tingling lips/fingers, muscle weakness cause. *buffered solutions (Sodium bicarb), Calcium gluconate Hypokalemia 3.5-5 EKG changes: slight prolonged PR, slight peaked P, ST depression, prominent U wave Symptoms: weakness/fatigue, muscle cramps, dysrhythmias Differential Includes: DKA, reduced K+ intake, aldosterone excretion (from increased Na+ levels) Hypercalcemia (PTH, Vit D, Calcitonin) 8.5-10 Hyperparathyroidism ; bone metastases with calcium resorption from breast, prostate, renal, and cervical cancer; sarcoidosis; excess vitamin D; many tumors that produce PTH; calcium-containing antacids Many nonspecific; fatigue, weakness, lethargy, anorexia, nausea, constipation; impaired renal function, kidney stones; dysrhythmias, bradycardia, cardiac arrest; bone pain, osteoporosis, fractures Hypocalcemia (PTH, Vit D, Calcitonin) 8.5-10 Inadequate intestinal absorption, massive blood administration, decreases in PTH and vitamin D levels; nutritional deficiencies – malnutrition; alkalosis, elevated calcitonin level; Increased neuromuscular excitability; tingling, muscle spasms (particularly in hands, feet, and facial muscles), intestinal cramping, • Metabolic acidosis: increased non-carbonic acids or loss of bicarb from extracellular fluid o Base is lost from the extracellular fluid and cannot be regenerated by the kidney o Causes: overproduction of acid, ketoacidosis, lactic acidosis, decreased acid excretion, advanced renal failure, diarrhea o S/S: headache and lethargy, anorexia, nausea, vomiting, diarrhea→ lead to confusion and coma→ Kussmaul respirations • Metabolic alkalosis : bicarbonate concentration increased, caused by excessive loss of metabolic acids o Vomiting, GI suctioning, excessive bicarb intake, hyperaldosteronism, diuretic therapy o Compensated by rate and depth of ventilation is decreased causing retention of CO2 • Respiratory acidosis : decreased alveolar ventilation, increased CO2 retention o Causes: depression of the respiratory center, paralysis of respiratory muscles, disorders of the chest wall, COPD, pulmonary edema o S/S: headache, restlessness, blurred vision, lethargy, muscle twitching, tremors, convulsions, coma • Respiratory alkalosis : alveolar hyperventilation, excessive reduction in CO2 • How do you determine if compensation is occurring? What does compensation mean? o Both Carbon dioxide and bicarb levels are not within normal range but pH is in normal range. Either the lungs or the kidneys are able to compensate to help the other system function normally • Understand how the renal and respiratory systems compensate for imbalances. o The kidney regulates HCO3- by ▪ 1. Reabsorption of virtually all of the filtered HCO3- by the proximal tubule ▪ Can reabsorb bicarbonate or regenerate new bicarbonate from CO2 and water ▪ Not as rapid as the lungs ▪ 2. Renal excretion of hydrogen ion ▪ Producing more acidic or more alkaline urine (hours to days) o The lungs regulate CO2 by ▪ Exhaling CO2 and leaving water ▪ Increasing or decreasing ventilation (minutes to hours Explain the neuronal discharge? • What do afferent, efferent and interneurons do? o Afferent neuron or sensory neuron picks up the stimuli o Interneuron associates the two signals to and from the brain o Efferent Neuron or Motor Neuron reacts to the message that was sent • How is the CNS divided? o Parasympathetic Nervous system ▪ Cholinergic ▪ NT- primarily Ach ▪ DAY to DAY – rest and digest o Sympathetic ▪ Noradrenergic ▪ NT- epinephrine- norepinephrine ▪ Fight or Flight How are the Parasympathetic and Sympathetic systems different? Parasympathetic Sympathetic Eyes Lacrimation; Pupils constrict Pupils dilate Lungs Constrict bronchial tubules Dilate bronchial tubules Cardiac response Slow HR Increase HR Peripheral Blood vessel response Dilate vessels Constrict vessels GI tract response Activates the gut -Salivation, Defecation, urination Inactivates the gut→ rectum contracted, decreased urinary output -Elevates plasma glucose, free fatty acids -Lowers recticular formation threshold • Which system controls DAY to DAY activity? o Parasympathetic NS • Which system does an anticholinergic work on? o Parasympathetic NS→ dry mouth, dry eyes, urinary retention etc. • What is the main NT of the parasympathetic nervous system? o Acetylcholine ▪ Acetylcholine performs as a transmitter at all neuromuscular (nerve-to- skeletal muscle) connections. It stimulates muscle contractions and, thus, all behavior. ▪ Acetylcholine is the transmitter of parasympathetic half of the autonomic nervous system. ▪ Acetylcholine is a transmitter in various brain regions (for instance, basal ganglia, cortex, and hypothalamus) and is required for proper memory and cognition, as well as motor control. The action of acetylcholine released at a synapse is ended through breakdown of ACh by enzyme acetylcholinesterase • What is the main NT of the sympathetic nervous system? o Norepinephrine • How do excitatory and inhibitory NT work? o Excitotory NT: increase the likelihood that a neuron will fire ▪ Ex: Acetylcholine, Glutamate, Norepinephrine, Seratonin o Inhibitory NT: decrease the likelihood that a neuron will fire ▪ Ex: GABA, Serotonin, Glycine, Dopamine • What is a seizure? o An excessive neuronal discharge o Partial or generalized, can have sudden death o Abnormal, excessive hypersynchronous discharges of cerebral neurons with transient alterations in brain function, generalized or foci o Epileptic syndrome location-related, generalized, undetermined • Can a brain injury cause a seizure? o Yes due to the sudden electrical disturbance in the brain. It can occur right away or several days or weeks • Could low blood sugar cause a seizure? • Yes because glucose is the main component for cell metabolism. Carbohydrates fulfill the task of being the energy transport system of the body. Glucose is made from the breakdown of carbohydrates. If glucose is low then the cells in the brain don’t have the energy they need to function properly resulting in a seizure. • Could withdrawal cause a seizure? How? o Alcohol withdrawal can cause seizures. Since alcohol is a central nervous system depressant and alcohol simultaneously enhances inhibitory (GABA activity) and inhibits excitatory tone (excitatory amino acid activity). An abrupt cessation can unmask the adaptive response to chronic alcohol (ethanol) use resulting in overactivity of the CNS. • Know the different types of CVA and their cause o Most frequently occurring neurologic disorder o Any abnormality of the blood vessels of the brain (is cerebrovascular disease) o Type C fibers (chemical) Only 10-25 % of fibers terminate in the thalamus. It goes through the reticular formation. It is impossible to sleep through this type of pain. This is why it is important to ask if the patient if the pain woke them up. • Chronic pain - Lasts 3-6 months beyond expected duration and after the acute cause has healed. o Is different, we can’t see the symptoms. It can be related to an acute injury with neuronal plasticity, but it is rarely associated with signs of sympathetic nervous system arousal. o Persistent low back pain (MOST COMMON) ▪ Most common chronic pain condition o Myofascial pain syndromes (MUSCLE) ▪ Second most common chronic pain condition ▪ Pain results from muscle spasm, tenderness, and stiffness ▪ Examples include myositis, fibrositis, myofibrositis, myalgia, and muscle strain—conditions that involve injury to the muscle and fascia o Phantom limb pain (Nerve) ▪ Pain experienced in amputated limb after stump has completely healed; may be immediate or occur months later • Deafferented pain→ Nerve pain o Painful condition resulting from damage to a peripheral nerve o Common types include severe burning pain triggered by various stimuli, such as cold, light touch, or sound, and reflex sympathetic dystrophies (occur after peripheral nerve injury and are characterized by continuous, severe, burning pain associated with vasomotor changes and muscle wasting) • Headaches o Tension ▪ Most common, acute and chronic, central and peripheral mechanisms, bilateral, tight band around head, last for hours or days ▪ Treated with OTC medications o Cluster ▪ Acute and chronic, occur in episodes several times during a day for a period of days at different times of the year, pain is unilateral, intense, tearing, burning ▪ Associated with ptosis, lacrimation, reddening of the eye, nausea ▪ Sympathetic CNS underactivity, parasympathetic overactivity ▪ More common in middle aged men. o Chronic Paroxysmal Hemicrania ▪ Cluster headaches with more frequent daily attacks o Migraines ▪ Familial episodic disorder, with and without aura and is precipitated by a triggering event ▪ Clinical Phases: premonitory phase, migraine aura, headache phase, recovery phase ▪ Cortical spreading depression followed by compensatory overactivity of the trigeminovascular system of the brain ▪ These are ONE sided (they happen on one side of the head) ▪ If it is a first migraine, full clinical work-up indicated to rule out other causes ▪ Migraine- with and without aura ▪ Without aura is more common variety o Temporal ▪ Inflammation of the temporal artery - can sometimes feel the cording of the artery ▪ Should be treated quickly - because the temporal artery supplies blood to the head and brain. Brain injury: • What is the difference between a focal or a diffuse brain injury? o Diffuse Brain Injury/ Diffuse Axonal Injury (DAI) ▪ Cause: effects of head rotation, brain experiences shearing stress causing axonal damage (Concussion to severe DAI state) ▪ Shaking, inertial effect, acceleration/ deceleration, axonal damage ▪ Acceleration/ deceleration rotational such as a concussion ▪ Elderly (and alcoholics) at increased risk for this due to cerebral atrophy o Focal: direct impact such as a skull fracture ▪ Observable brain lesion, cerebral edema, coup injury (injury directly below the point of impact), contrecoup (injury on the pole opposite the site of impact) produces contusions which can cause hemorrhage or hematomas • What happens in a concussion? o Disruption of axonal neurofilament organization impairs axonal transport, leading to axonal swelling, Wallerian degeneration, and transection [25]. Release of excitatory neurotransmitters acetylcholine, glutamate, and aspartate, and the generation of free radicals may contribute to secondary injury o Collateral damage • What is TBI? o Loss of consciousness for 6+ hours, most brain injuries are not severe o Causes: falls (28%), MVI (20%), moving objects (19%), assault (11%), sports related, military blasts o Trauma ▪ Closed-head: blunt, more common, Dura remains intact ▪ Open-head: penetrating, skull fracture—linear, comminuted, compound, basilar skull fracture, breaks through dura o Brain Injury ▪ Primary injury ▪ Focal (direct impact such as a skull fracture) or diffuse (acceleration/ deceleration rotational such as a concussion) ▪ Secondary injury ▪ Hypotension, hypoxia, cerebral ischemia, cerebral edema, oxidative stress, vascular injury, neuronal death, inflammation ▪ Brain trauma depolarizes the BBB causes channels to open and release amino acids causes mitochondrial dysfunction activate inflammatory mediators (failure of the BBB) cause ischemia and myelin injury neurologic defects o Focal Brain Injury ▪ Observable brain lesion, cerebral edema, coup injury (injury directly below the point of impact), contrecoup (injury on the pole opposite the site of impact) produces contusions which can cause hemorrhage or hematomas Mental issues • Explain what happens in schizophrenia? o 1% of population. Men and women equally. Genetic component. Still many unknowns. o Negative symptoms & Cognitive alterations: reduced dopaminergic neurotransmission o Positive symptoms: under activation of glutamate receptors o Three categories of symptoms: Positive, Negative and Cognitive ▪ Positive: delusions, hallucinations ▪ Negative: Removal of normal processes (decreased emotions), loss of interests, flat affect; Alogia (poverty of speech) ▪ Cognitive: Affects memory and learning (daily tasks such as where they put keys, balancing checkbook, etc) o Phases of schizophrenia: ▪ Prodromal - withdrawn ▪ Active - severe symptoms ▪ Residual - Cognitive symptoms.