NURS 5315/ NURS5315 Exam 4 V2 – Advanced Pathophysiology Guide | UTA (Latest 2026/2027 Update) Verified Questions & Answers|100 out of 100

NURS 5315/ NURS5315 Exam 4 V2 – Advanced Pathophysiology Guide | UTA (Latest 2026/2027 Update) Verified Questions & Answers|100 out of 100 2026/2027 | GRADED A+ | 100% VERIFIED Question: Which condition may result from pressure exerted by a pituitary tumor? Answer Hypothyroidism Question: The term used to describe a person who experiences a lack of all hormones associated with the anterior pituitary is: Answer Panhypopituitarism Question: Visual disturbances are a result of a pituitary adenoma because of the: Answer Pressure of the tumor on the optic chiasm Question: Which disorder is considered a co-morbid condition of acromegaly? Answer Diabetes Question: Which disorder is caused by hypersecretion of the growth hormone (GH) in adults? Answer Acromegaly Question: Graves disease develops from a: Answer Thyroid-stimulating immunoglobulin that causes overproduction of thyroid hormones Question: The signs of thyrotoxic crisis include: Answer High levels of circulating thyroid-stimulating immunoglobulins Question: The level of thyroid-stimulating hormone (TSH) in individuals with Graves is usually: Answer Low Question: Palpation of the neck of a person diagnosed with Graves disease would detect a thyroid that is: Answer Diffusely enlarged Question: A deficiency of which chemical may result in hypothyroidism? Answer Iodine Question: What are clinical manifestations of hypothyroidism? Answer Constipation, decreased heart rate, and lethargy Question: Renal failure is the most common cause of which type of hyperparathyroidism? Answer Secondary Question: The most common cause of hypoparathyroidism is: Answer Parathyroid gland damage Question: A patient diagnosed with diabetic ketoacidosis (DKA) has the following laboratory values: arterial pH 7.20; serum glucose 500 mg/dl; positive urine glucose and ketones; serum potassium (K+) 2 mEq/L; serum sodium (Na+) 130 mEq/L. The patient reports that he has been sick with the "flu" for 1 week. What relationship do these values have to his insulin deficiency? Answer Decreased glucose use causes fatty acid use, ketogenesis, metabolic, acidosis, and osmotic diuresis Question: Polyuria occurs with diabetes mellitus becuase of the: Answer Elevation in serum glucose Question: Type 2 diabetes mellitus is best described as a: Answer Resistance to insulin by insulin-sensitive tissues Question: A person diagnosed with type 1 diabetes experiences hunger, lightheadedness, tachycardia, pallor, headache, and confusion. The most probable cause of these symptoms is: Answer Hypoglycemia caused by increased exercise Question: Which serum glucose level would indicate hypoglycemia in a newborn? Answer 28 mg/dl Question: When comparing the clinical manifestations of both diabetic ketoacidosis (DKA) and hyperglycemic hyperosmoler nonketotic syndrome (HHNKS), which condition is associated with only DKA? Answer Kussmaul respirations Question: Hypoglycemia, followed by rebound hyperglycemia is observed in those with: Answer The Somogyi effect Question: The first laboratory test that indicates type 1 diabetes is causing the development of diabetic nephropathy is: Answer Protein on urinalysis Question: Which classification of oral hypoglycemic drugs decreases hepatic glucose production and increases insulin sensitivity and peripheral glucose uptake? Answer Biguanide (metformin) Question: What causes the microvascular complications in patients with diabetes mellitus? Answer The capillary basement membranes thicken, and cell hyperplasia develops. Question: Retinopathy develops in patients with diabetes mellitus because: Answer Retinal ischemia and red blood cell aggregation occur. Question: A person had acne, easy bruising, thin extremities, and truncal obesity. These clinical manifestations are indicative of which endocrine disorder? Answer Cushing disease Question: If a patient with multiple sclerosis starts coughing frequently during meals and starts to eat significantly less food than normal, the patient may have: Answer dysphagia Question: For a patient with dysphagia, the food that would be most difficult to swallow is: Answer Chicken noodle soup Question: The most acute risk for patients with dysphagia is: Answer dehydration Question: What type of fracture occurs at a site of a preexisting bone abnormality as is a result of a force that would not normally cause a fracture? Answer Pathologic Question: By the time osteoporosis is visible on an x-ray examination, up to what percent of bone has been lost? Answer 30% Question: A bone density of 645 mg/cm2 would support which diagnosis? Answer Osteoporosis Question: Which type of osteoporosis would a person develop after having the left leg in a cast for 8 weeks to treat a compount displaced fracture of the tibia and fibula? Answer Regional Question: Considering the pathophysiologic process of osteoporosis, after being activated by receptor activator of nuclear factor KB ligand (RANKL), receptor activator of nuclear factor KB (RANK) activates which of the following? Answer Osteoclast survival Question: Considering the pathophysiologic process of postmenopausal osteoporosis, which changes are believed to play a significant role in the development of age-related bone loss? Answer Increased oxidative stress and increased intracellular reactive oxygen species Question: Considering the pathyphysiologic process of osteoporosis, which hormone exerts antiapoptotic effects on osteoblasts but proapoptotic effects on osteoclasts? Answer Estrogen Question: Considering the pathophysiologic process of osteoporosis, what are the effects of extracellular signal-regulated kinases (ERKs) and receptor activator of nuclear factor kB ligand (RANKL) on osteoblasts and osteoclasts? Answer ERKs and RANKL increase the life span of osteoclasts and decrease the life span of osteoblasts Question: What is the most common clinical manifestation of osteoporosis? Answer Bone deformity Question: Which disorder is characterized by the formation of abnormal new bone at an accelerated rate beginning with excessive resorption of spongy bone? Answer Paget disease Question: What is a primary defect in osteoarthritis? Answer Stromelysis and acid metalloproteinase break down articular cartilage In osteoarthritis, what is the effect of the disruption of the pumping action of proteoglycans? Answer Cartilage takes in too much fluid and is unable to withstand the stresses of weight bearing What is a characteristic of inflammatory joint disease? Answer Systemic symptoms of inflammation Which muscular dystrophy syndrome develops from an X-linked recessive mode of inheritance? Answer Duchenne Which protein, absent in muscle cells of Duchenne muscular dystrophy, mediates the anchoring of skeletal muscle fibers to the basement membrane? Answer Dystrophin What pulmonary complication in children with Duchenne muscular dystrophy contributes to their death? Answer Infection Generally, what is the first symptom of facioscapulohumeral muscular dystrophy? Answer Drooping shoulders Which statement is true regarding the thyroid hormone and the thyroid-stimulating hormone (TSH)? Answer TSH secretion is regulated by thyrotropin-releasing hormone (TRH) Obvious changes in cell function that are the result of stimulation by a particular hormone describe which factor? Answer Direct effects Which statement is true regarding the hypothalamus? Is divided into numerous nuclei Which hormone is secreted by the posterior pituitary? Oxytocin Which statement is true regarding the parathyroid glands? They play an important role in calcium regulation Which cell from the pancreas synthesizes insulin? Beta Which statement is true regarding glucagon? Hyperglycemia will inhibit glucagon release Which statement is true regarging acromegaly? Is commonly caused by GH-secreting pituitary adenoma Which is a symptom of graves disease? Lid lag (opthalmopathy) Which result may be used as a diagnosis for diabetes mellitus? Fasting glucose greater than 126 mg/dL Which statement is true regarding diabetic ketoacitosis (DKA)? Accelerated gluconeogenesis and ketogenesis are present A person develops severe deyhdration and hyperglycemia. An absence of ketosis has occurred. What condition does this patient have? Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS) Which statement best describes the Somogyi effect? Hypoglycemia, followed by rebound hyperglycemia Which is a true statement regarding adipose tissue? Adipose tissue has different rates of lipogenesis. Most adipose tissuein the bosy is what? WAT White adipose tissue Cranial Nerve I: Olfactory sensory, smell Sign of dysfunction: unable to identify aromatic substance Cranial Nerve II: Optic -Function: sensory - carries impulse for vision -Testing procedure: eye chart testing, visual field testing Cranial Nerve III: Oculomotor --Function: motor - fibers to the superior, inferior and medial rectus muscles of the eye and to the smooth muscle controlling lens shape. Medial and vertical eye movements; sensory - proprioception of the eye -Testing procedure: pupil sizes are compared for shape and equality, pupillary reflex is tested; visual tracking is tested Cranial Nerve IV: Trochlear Nerve Motor: eye movement, extra ocular superior oblique muscle Tested the same as CN III Cranial Nerve V: Trigeminal -Function: motor and sensory for face, conducts sensory impulses from mouth, nose, eyes; motor fibers for muscles of mastication. Control of jaw movements -Testing procedure: pain, touch, and temperature are tested with proper stimulus; corneal reflex tested with a wisp of cotton; person is asked to move jaw through full ranges of motion Cranial Nerve VI: Abducens -Function: motor and proprioceptor fibers to/from lateral rectus muscle. Lateral eye movements -Testing procedure: tested in conjunction with cranial nerve III relative to moving eye laterally Cranial Nerve VII: Facial -Function: mixed (sensory and motor) sensory fibers to taste buds and anterior 2/3 tongue; motor fibers to muscles of facial expression and to salivary glands -Testing procedure: check symmetry of face, ask person to attempt various facial expressions; sweet, salty, sour, and bitter substances are applied to tongue to test tasting ability Cranial Nerve VIII: vestibulocochlear Function: Sensory - special senses of hearing and balance; Foramen: internal auditory canal; Consequence of Loss: loss of hearing, loss of balance and equilibrium, nausea, vertigo, vomiting Cranial nerve IX: glossopharyngeal -Function: motor fibers for pharynx and salivary glands; sensory fibers for pharynx and posterior tongue. Taste sensation for sweet, bitter and sour -Testing procedure: gag and swallow reflexes are checked; posterior one third of tongue is tested for taste Cranial Nerve X: Vagus -Function: sensory/motor impulses for larynx and pharynx; parasympathetic motor fibers supply smooth muscles of abdominal organs; sensory impulses from viscera -Testing procedure: tested in conjunction with cranial nerve IX Cranial Nerve XI: Spinal Accessory Function: Motor - to sternocleidomastoid and trapezius; Foramen: foramen magnum, jugular foramen; Consequence of Loss: difficulty elevating scapula or rotating neck Cranial Nerve XII: Hypoglossal -Function: motor/sensory fibers to/from tongue. Movement of tongue -Testing procedure: ask person to stick out tongue, positional abnormalities are noted central nervous system consists of the brain and spinal cord peripheral nervous system consists of 12 pairs of cranial nerves and 31 spinal nerves subdivided into somatic and autonomic nervous system afferent nerves sensory transmitters that send impulses from receptors in the skin, muscles, and joints to the central nervous system efferent nerves Also called motor nerves; nerves that carry information from the CNS to cells, tissues and organs. Neuron a nerve cell; the basic building block of the nervous system fuel source: glucose Parts of a neuron cell body, dendrites, axon Cerebrum Location: largest part of the brain Function: Area of the brain responsible for all voluntary activities of the body Sign of injury/lesion/disorder: movements that are slow and uncoordinated cerebral cortex the gray matter surrounding the cerebrum white matter located beneath the cerebral cortex myelinated axons of the CNS Four lobes of the brain frontal, parietal, occipital, temporal frontal lobe located under forehead Function: directs voluntary skeletal actions; responsible for communication, emotions, intellect, reasoning, judgment and behavior. Contains Broca's area: responsible for speech Sign of injury/lesion/disorder: Head and eye movement to one side. Complete or partial unresponsiveness or difficulty speaking. Explosive screams, including profanities, or laughter. parietal lobe Located in the upper back half of the brain. Function: interprets tactile sensation such as touch, pain, temperature, shapes and 2-point discrimination Sign of injury/lesion/disorder: occipital lobe Located:behind the parietal lobe on the top of a membrane that helps in separating it from cerebellum function: houses the ability to read with comprehension and is the primary visual receptor center Sign of injury/lesion/disorder: vision and perception problems temporal lobe Located:The temporal lobes are located at the sides of the brain, and can be considered the "middle" region of each brain hemisphere. function: interprets impulses from the ear. contains Wernicke's area: auditory stimuli Sign of injury/lesion/disorder: Disturbance of auditory sensation and perception. Disturbance of selective attention of auditory and visual input. Disorders of visual perception. Impaired organisation and categorisation of verbal material. Disturbance of language comprehension. Impaired long-term memory. Cerebellum Location: the "little brain" at the rear of the brainstem; functions include processing sensory input and coordinating movement output and balance Sign of injury/lesion/disorder: ataxia, which may affect the limbs, trunk, or even speech Axonal reaction peripheral nerve self-repair Neuroglia cells that support and protect neurons Astrocytes, oligodendroglia, microglia, ependymal cells Schwann cells Supporting cells of the peripheral nervous system responsible for the formation of myelin. types of neurotransmitters Acetylcholine: excitatory and inhibitory Monoamines: histamine, serotonin, dopamine, epinephrine, norepinephrine deficiency of dopamine leads to Parkinson Disease Amino Acids: glutamate, GABA, glycine brain stem Location: area at the base of the brain that lies between the deep structures of the cerebral hemispheres and the cervical spinal cord Contains: midbrain, pons, medulla oblongata and reticular formation. Ten of the 12 cranial nerves arise from the brain stem. Function: It contains the respiratory and vasomotor centers, which are responsible, respectively, for breathing and the maintenance of blood pressure. Signs if injury/lesion/disorder: coma, irregular breathing, insomnia, balance issues, slurred speech, etc. reticular activating system (reticular formation) Responsible for alterations in arousal and sleep-wake transitions Extreme damage can cause coma Thalamus the brain's sensory switchboard, located on top of the brainstem; it directs messages to the sensory receiving areas in the cortex and transmits replies to the cerebellum and medulla Hypothalamus a neural structure lying below the thalamus; directs eating, drinking, body temperature; helps govern the endocrine system via the pituitary gland, and is linked to emotion limbic system neural system (including the hippocampus, amygdala, and hypothalamus) located below the cerebral hemispheres; associated with emotions and drives. Wernicke's area location: temporal lobe on the left side of the brain Function: speech comprehension, language development Signs of injury/lesion/defect: difficulty speaking in coherent sentences or understanding speech Broca's area Location: an area of the frontal lobe, usually in the left hemisphere, Function: Controls language expression - that directs the muscle movements involved in speech. Signs of injury/lesion/defect: Non-fluid primary progressive aphasia: this is a progressive deterioration of language. Supratentorial above the tentorium cerebelli Infratentorial below the tentorium cerebelli tentorium cerebelli separates cerebrum from cerebellum sympathetic nervous system the division of the autonomic nervous system that arouses the body, mobilizing its energy in stressful situations parasympathetic nervous system the division of the autonomic nervous system that calms the body, conserving its energy Beta 1 receptors located in the heart increase the heart's rate and strength of contraction Beta 2 receptors located in the bronchioles of the lungs and the arteries of the skeletal muscles cause vasodilation, reduces total peripheral resistance, bronchodilation Alpha 1 receptors Located in blood vessels, smooth muscles vasoCONSTRICTION - increase BP contraction of smooth muscles glucose metabolism Alpha 2 receptors Gi • decreases sympathetic outflow (suppress norepinephrine release) • decreases insulin release, induce glucagon release • decrease lipolysis • platelet aggregation • vasoconstriction • mediate synaptic transmission in nerve terminals cerebrospinal fluid (CSF) plasma-like clear fluid circulating in and around the brain and spinal cord Dermatone sensory neurons on the skin (the sensation is carried to the spinal nerves) autonomic nervous system (ANS) the part of the peripheral nervous system that controls the glands and the muscles of the internal organs (such as the heart). Its sympathetic division arouses; its parasympathetic division calms. Embryonic and infant Development of the Brain Conception: brain begins to develop 3-4 weeks gestation: neural tube forms entire nervous system. 2-3 months gestation: forebrain develps 3-5 months gest: neronal proliferation, brain develops rapidly, 5 months gest: synapses form Myelin is formed in the post-natal period and may take many years to complete half of the post-natal growth is achieved in the first year and 90% complete by age 6 2-3 months: posterior fontanel closes 18 months: anterior fontanel closes stepping reflex a neonatal reflex in which an infant lifts first one leg and then the other in a coordinated pattern like walking appears: Birth Disappears: 6 weeks Moro reflex (startle reflex) Sudden loud noise will cause symmetric abduction and extension of the arms followed by adduction and flexion of the arms over the body. appears: Birth Disappears: Disappears by 3 to 4 months. suckling reflex Sucking response when roof of mouth is touched appears: Birth Disappears: 4 months awake, 7 months asleep rooting reflex a baby's tendency, when touched on the cheek, to turn toward the touch, open the mouth, and search for the nipple appears: Birth Disappears: 4 months awake, 7 months asleep palmar grasp reflex in response to stroking a baby's palm, the baby's hand will grasp. appears: Birth Disappears: 6 months Plantar Grasp Reflex reaction to stimulation of the sole of the foot that causes the toes of the feet to "grasp" appears: Birth Disappears: 10 months Tonic neck reflex (fencer position) Turn newborn head turned to the right: Right arm/leg EXTEND Left arm/leg flex appears: 2 months Disappears: 5 months Neck righting reflex Hold the infant in a vertical position, then tilt to one side. Infant should attempt to maintain their line of vision parallel to the ground. appears: 4 months Disappears: 24 months Landau reflex Infant should attempt to raise the head and arch the back when placed in a prone position appears: 3 months Disappears: 24 months parachute reflex extension of both arms when thrust downward in the prone position appears: 9 months Disappears: persists for life age related nervous system changes structural: decreased brain weight and size, fibrosis o meninges, widening sulci and narrowing gyri, increase in ventricles cellular: decrease in neurons, myellin, dendritic and synaptic processes, increased neuroinflammation, declines in melatonin, atrophy of the epithelial cells in the choroid plexus cerebrovascular: arteriosclerosis, increased permeability of the blood-brain barrier, decreased vascular density functional changes: decreased deep tendon reflexes, skeletal muscle atrophy, progressive decrease in taste and smell, decreased vibratory sense, decrease control of gai and posture, sleep disturbances and memory impairments cerebral blood flow regulated to meet the metabolic needs of the brain. 20% of cardiac output altered by the concentration of CO2 and O2 CBF decreases when CO2 decreases and increases when the PaO2 50mmHg When PaO2 = 70-90 mmHg, CBF is maintained Cerebral Perfusion Pressure pressure required to maintain perfusion to the brain CPP = MAP - ICP Normal is 70-90 mmHg Low CPP caused by hypovolemia or hypotension brain ischemia High CPP caused by hypertension increased in hydrostatic pressure fluid moves into the interstitium in the brain and increased ICP decreased CPP intracranial pressure pressure in the intracranial vault that must be overcome to be perfused normal ICP = 5-15 mmHg increased ICP decreased CPP and impaired cerebral perfusion Four stages of ICP Stage 1: brain compensates with vasoconstriction and external compression - patient may be asymptomatic Stage 2: increasing amount of contents inside intracranial vault, brain unable to compensate; CM: confusion, restlessness, lethargy, pupil and breathing changes, decreased LOC Stage 3: ICP appraches arterial pressure - patient decompensates quickly. CM: decreased LOC, widening pulse pressure, bradycardia, pupils small and sluggish, CO2 accumulation causes vsodilation decreased hydrostatic pressure and increased blood volume Stage 4: equalization of arterial pressure and ICP no CPP cellular hypoxia, cell death cerebral herniation types supratentorial infratentorial Supratentorial: uncal herniation gyri moves through the tentorial notch and compresses the third cranial nerve and mesencephalon CM: change in LOC, ipsilateral pupil, Cheyne stokes respiration, decorticate posturing Supratentorial: central herniation diencephalon is forced down through the tentorial notch CM: lose consciousness quickly, develop apnea, reactive pupils that later dilate, decorticate posturing Supratentorial: cingulate gyrus herniation movement of the cingulate gyrus under the falx cerebri Supratentorial: transcalvarial herniation brain tissue which moves through an opening in the skull Infratentorial: cerebellar tonsillar herniation Most common downward movement of the cerebellum through the foramen magnum CM: stiff neck, decreased LOC, respiratory abnormalities and pulse variations Sodium imbalance effect on CNS hyponatremia causes water movement out of the vessels and into the interstitium and then into the cell. in the brain, they enter the neuron causing cerebral edema associated with CNS symptoms Hypernatremia is associated with a rapid decrease in intracellular water content and brain volume caused by an osmotic shift of free water out of the cells causing dehydrated neurons expressive dysphasia The inability to produce language ( despite being able to understand language) Location of dysfunction: Broca's area of the frontal lobe receptive dysphasia The inability to understand language (despite being able to hear it and produce it) Location of dysfunction: Wernicke's area of the temporal lobe global aphasia Nonfluent aphasia w/ impaired comprehension. Both Broca's and Wernicke's areas affected. Partial seizures types Simple partial with motor symptoms Simple partial with sensory symptoms Complex partial simple partial seizure with motor symptoms CM: motor symptoms which most often begin in the face and hands, tend to be clonic Simple partial seizure with sensory symptoms CM: tactile, visual auditory or olfactory sensations, most often in the lips, fingers and toes complex partial seizure CM: impairment in their consciousness during the seizure, usually have some sort of sensory experience prior to the onset of automatism. Automatisms may include lip smacking, chewing, facial grimacing, swallowing, movements, patting, picking, rubbing oneself generalized absence seizure - staring spell or brief loc no convulsions - can be precipitated by hyperventilation or flashing lights - can be short (30 sec) generalized tonic seizure CM: muscle contraction Generalized Clonic Seizure CM: quick repetitive jerks Generalized tonic-clonic (grand mal) CM: alternating stiffening and jerking, incontinent and disoriented after status epilepticus A condition in which seizures recur every few minutes or last more than 30 minutes. medical emergency Non-convulsive status epilepticus CM: no signs of seizure activity, altered mental status that is not explained by any other cause. Diagnosed with EEG spinothalamic tract Ascending sensory tract: carries info from skin to brain - includes anterior spinal thalamic tract and the lateral spinal thalamic tract. An afferent tract that transmits sensations of pain, temperature, itching, tickling, pressure, and crude touch crossover tract - so lesion/disorders are on the opposite side posterior column ascending sensory tract: includes fasciculus gracilis and fasciculus cuneatus tracts carries sensations of position (proprioception), vibration, stereognosis and fine touch crossover is high - so defects will be ipsilateral to a lesion. exception: if the lesion is in the cerebral cortex, it will be contralateral defect. pyramid tract descending motor tract: made of corticospinal and corticobulbar tracts impulses are generated in the brain and sent to control voluntary movements of purpose and skill. crossover at the junction between the spinal cord and brain defects in this tract will be contralateral to the brain. Upper motor neuron deficits manifest as spastic paralysis, hyperreflexia, and Babinski reflex i.e. Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease) lower motor neuron deficits manifest as flaccid paralysis, muscular atrophy, fasciculations, fibrillations or hyporeflexia. i.e. poliomyelitis extrapyramidal tracts descending motor tract: made of rubrospinal tract, the reticulospinal tract, tectospinal tract, and vestibulospinal tract crosses over at the junction between the brain stem and spinal cord. deficits are manifested contralaterally responsible for gross motor movements, automatic motor movements, facial expression, posture, muscle tone, speech, and swallowing. CM: spastic increase in muscle tone, abnormal postures, involuntary movements, tremors, i.e. Parkinson's Disease epilepsy primary seizure condition for which no underlying correctable cause can be found postictal state a state of decreased/altered level of consciousness following an epileptic seizure Increased ICP S/S Lethargy, decreased LOC Widening pulse pressure Bradycardia Increased Systolic Cushing's Triad Increased ICP: stage 1 Stage 1: brain compensates with vasoconstriction and external compression - patient may be asymptomatic increased ICP: stage 2 Stage 2: increasing amount of contents inside intracranial vault, brain unable to compensate; CM: confusion, restlessness, lethargy, pupil and breathing changes, decreased LOC increased ICP: stage 3 Stage 3: ICP approaches arterial pressure - patient decompensates quickly. CM: decreased LOC, widening pulse pressure, bradycardia, pupils small and sluggish, CO2 accumulation causes vasodilation decreased hydrostatic pressure, and increased blood volume increased ICP: stage 4 Stage 4: equalization of arterial pressure and ICP no CPP cellular hypoxia, cell death herniation occurs when the brain tissue moves from an area of high pressure to an area of low pressure Traumatic Brain Injury a blow to the head or a penetrating head injury that damages the brain Complications: post-concussion syndrome, posttraumatic seizures, chronic traumatic encephalopathy Primary brain injury An injury to the brain and its associated structures that is a direct result of impact to the head. Focal-limited to one area (closed head trauma) Diffuse-shaking force which strains the brain Secondary brain injury The "after effects" of the primary injury; includes abnormal processes such as cerebral edema, increased intracranial pressure, cerebral ischemia and hypoxia, and infection; onset is often delayed following the primary brain injury. closed traumatic brain injury brain injury in which damage may occur to the underlying vessels, dura sinus, brain and cranial nerves without harming the integrity of the skull May cause immediate loss of consciousness, loss of reflexes, transient loss of respiration, bradycardia and low BP Open Traumatic Brain Injury dura is damaged and the contents of the cranial vault are open to the environment Affecting a specific area of the brain tissue, Focal/localized damage. Example: Skull fracture. diffuse axonal injury occurs from shaking which strains the brain - type of brain injury characterized by shearing, stretching, or tearing of nerve fibers with subsequent axonal damage. post concussive syndrome (PCS) Symptoms of concussion 3 months. Generally occurs in about 80% of persons with mild and moderate TBI hemiparesis slight paralysis or weakness affecting one side of the body Kernig's sign inability to extend the leg completely when the thigh is flexed upon the abdomen and the person is sitting or lying down Brudzinski's sign Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed. transection of spinal cord ascending and descending tracts are partially or completely severed cord contusion Bruising of the neural tissue cord concussion temporary disruption of cord mediated functions spinal cord compression pressure placed on the cord from a lesion, mass or swelling. Leads to ischemia and tissue damage. spinal cord hemorrhage bleeding directly in to the spinal cord not usually associated with loss of function spinal shock complete but temporary loss of motor, sensory, reflex, and autonomic function immediately after injury- resolves 7-20 days s/s: flaccid, bradycardia, hypotension, paralytic ileus Autonomic Dysreflexia patients with spinal cord injuries are at risk for developing autonomic dysreflexia (T-6 or above) parasympathetic nervous system is unable to send signals below the area of injury. Above injury: flushing sweating and bradycardia below injury: pale and cool skin Other CM: SBP up to 300mmHg, HA, blurred vision and nausea Anterior Cord Lesion Cause: trauma, ruptured intervertebral disk, anterior spinal artery occlusion, primary spinal cord tumors or metastatic CA CM: loss of pain and temperature sensation, motor weakness Central cord lesion Cause: primary spinal cord tumors and hyperextension injuries CM: loss of pain and temperature at level of lesion with other modalities preserved posterior cord lesion Cause: cervical spondylosis, epidural abscess, vit B12 deficiency, syphilis, multiple sclerosis, primary spinal cord tumors, metastatic CA CM: loss of fine touch, loss of vibratory sensation, loss of proprioception, motor weakness Migraine Phases Premonitory Phase - early warning signs, can occur several hours before the headache (e.g. depression, irritability, craving for foods etc.) Aura Phase - 1 in 5 people have an aura phase with: visual ( can include hallucinations), skin ( pin prick or needles) or language (expressing thoughts) difficulties HA Phase - throbbing pain and can last from several hours to days; may have fatigue, N/V or dizziness Recovery: After the Storm -patient feels extreme tiredness, weakness and or confusion, irritability, may take days to resolve Anencephaly defect in closure of the cephalic portion of the neural tube that results in incomplete development of the brain and bones of the skull; the most drastic neural tube defect usually results in a stillbirth encephalocele herniation of brain tissue, most commonly the occipital area meingocele sac-like protrusion through the bony defect in the spinal defect containing meninges and cerebral spinal fluid. Does not involve the spinal cord and it is possible that the infant will not have any neurologic deficits myelomeningocele hernia of the spinal cord and meninges most common development abnormality of the nervous system most commonly located in the lumbar and lumbosacral areas, the last of the neural tube to close stroke: anterior cerebral artery blood supplies: basal ganglia, the corpus callosum, the medial surface of the cerebral hemispheres, the superior surface of the frontal and parietal lobes CM: contralateral paralysis and loss of sensation, more pronounces in lower extremities Stroke: Middle Cerebral Artery (MCA) Blood supplies: frontal, parietal, temporal lobes CM: aphasia in the dominant hemisphere, contralateral paralysis and loss of sensation Stroke: Posterior cerebral artery Blood supplies: occipital lobe CM: visual changes contralateral to the occlusion Stroke: basilar artery Blood supplies: pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular cranial nerve CM: quadriplegia, loss of voluntary facial, mouth, tongue movements, loss of horizontal eye movements, consciousness remains intact Stroke: anterior inferior cerebellar artery Blood supplies: lateral pons, vestibular nuclei, facial nucleus, spinal trigeminal nucleus, cochlear nuclei, sympathetic fibers CM: vomiting, vertigo, nystagmus, decreased lacrimation, decreased taste, a decreased corneal reflex, decreased pain and temp sensation in the face, decreased ipsilateral hearing Stroke: middle and inferior cerebellar artery blood supplies: cerebellum CM: ataxia, dysmetria Stroke: posterior cerebellar artery blood supplies: lateral medulla, spinal trigeminal nucleus, nucleus ambiguous, sympathetic fibers, inferior cerebellum CM: vomiting, vertigo, nystagmus, decreased pain and temperature sensation in teh ipsilateral face and contralateral body, dysphagia, hoarseness, decreased gag reflex, ataxia, dysmetria Dysmetria inability to control the distance, power, and speed of a muscular action (lack of coordination) substance use disorder continued substance craving and use despite significant life disruption and/or physical risk substance intoxication the acute effects of substance use Substance Withdrawal Disorder Each substance has its own unique syndrome as symptoms of abrupt cessation of heavy and prolonged use vasogenic edema clinically the most important type and is caused by the increased permeability of the capillary endothelium of the brain after injury to the vascular structure cytotoxic edema toxic factors directly affect the cellular elements of the brain causing failure of the active transport systems interstitial edema (hydrocephalic edema) occurs especially around the lateral ventricles when an increase in intravascular pressure causes an abnormal flow of fluid from the intraventricular CSF across the ependymal lining to the periventricular white matter contracoup injury brain slams against cranium in one direction and then back in the other direction What are the types of bone cells? osteoblasts, osteocytes, osteoclasts What is the function of an osteoblast? formation of bone through ossification or osteogenesis What is the function of osteocytes? bone maintenance What is the function of osteoclasts? Bone resorption and remodeling. What are the components of the bone matrix? Organic: collagen and proteoglycane (35%) Inorganic: Hydroxyapatite. (65%) What are the steps in bone remodeling? Quiescent Activation Resorption Formation Mineralisation How does Vitamin D contribute to bone growth and what diagnosis is associated with deficiency? For absorption of calcium from intestines Deficiency: Rickets and osteomalacia How does Vitamin C contribute to bone growth and what diagnosis is associated with deficiency? For collagen synthesis by osteoblasts Deficiency: Scurvy What is the etiology, pathophysiology, and clinical manifestations of spondylitis? Etiology: Unknown Strong association with HLA-B27 antigen HLA-B7 in African Americans Patho: Inflammation of fibrocartilage Inflammatory cells and fibrocartilage erosion Repair and scar tissues Calcification leading to joint fusion Clinical manifestations: Early symptoms: low back pain in early 20's, progressing over time; stiffness; pain, restricted motion. Loss of normal lumbar curvature (lordosis) Increased concavity of upper spine (kyphosis) What is the etiology, pathophysiology, and clinical manifestations of osteoarthritis? Etiology: Idiopathic; genetic, biochemical and biomechanical stress. Patho: Local area of degeneration and loss of articular cartilage; Pro inflammatory cytokines; Thickening of the join capsule Osteophytes (bone spurs) Variable degrees of synovitis (inflammation) Clinical manifestations: Pain (worsens with activity) Stiffness (diminishes with activity) Swelling of the joint Tenderness Limited mobility Deformity What is the etiology, pathophysiology, and clinical manifestations of rheumatoid arthritis? Etiology: Multifactoral with strong genetic predisposition (HLA-DR4) More common in women than in men Patho: Primary site is synovial membrane Ab formed against joint tissue (rheumatoid factors, etc) Type IV hypersensitivity (T cell mediated) Inflammatory cells, cytokines (TNF-a) leads to destruction of catilage/bone Granulation tissue (pannus) Clinical manifestations: Insidious onset Affected joints, initially wrists, MCPS, MTPs Symmetric joint involvement Morning stiffness Constitutional symptoms Joint deformities Subcutaneous nodules Blood work; presence of RG and ANA (antinuclear antibodies) Identify the risks, clinical manifestations and pathophysiology of osteoporosis Risks: Aging Postmenopause (low estrogen & testosterone) Low Vitamin D Decreased physical activity level Excess intake of caffeine, phosphorus, alcohol, nicotine Drugs, such as corticosteroids Low BMI Family history Endocrine disorders Clinical manifestations: Bone aches Weakness and deformities Fractures Pathophysiology: Decreases estrogen - decreased OPG - Increased RANKL - increased RANK 0 increased formation (increased clasts and decreased clast apoptosis + estrogen needed for extracellular kinases (ERKs) to decrease apoptosis Increased blasts and increased apoptosis, clasts not balanced. What is scoliosis? sideways curvature of the spine When is scoliosis most likely to manifest? In muscular dystrophy or cerebral palsy What amount of spine curvature is clinically significant? Greater than 25 to 30 degrees If 45 to 50 degrees-severe. What is the general pathophysiology associated with muscular dystrophy? Most of the muscular dystrophy cases are caused by gene mutations affecting muscle proteins, such as dystrophin. Muscle fiber dropoutl muscle cells apoptosis or necrosis; inflammatory cytokines regeneration; fibrosis formation fatty infiltration and replacement. Muscle loses function. Describe the etiology, pathophysiology, and clinical manifestations of Duchenne Muscular Dystrophy Etiology: Mutation in dystrophin, an anchor protein for skeletal muscle cells. Patho: Poor anchored muscle fiber torn easily due to mescule contraction Calcium overload Cell death, fiber necrosis and apoptosis Inflammatory cytokines release Regeneration Fibrosis Fatty Infiltration Clinical manifestations: First- Muscle weakness that beings in the hips, pelvis, and legs Difficulty standing, walk and sit independently Unsteady, waddling gait Waling on the toes or balls of the feeth Falling Overtime - losing the ability to sit, walk, and life objects. Affecting heart, lung, and diaphragm. Describe the etiology, pathophysiology, and clinical manifestations of Sarcopenia Etiology: Aging, physically inactive, unhealthy diet Patho: Nutritional, hormonal, metabolic immunologic factors affect muscle, reduce muscle mass, and muscle strength. Clinical manifestations: Muscle weakness, decreased mobility, increased falls, disability, and loss of independence. How is obesity defined? A metabolic disorder the develops when caloric intake exceeds caloric caloric expenditure in genetically susceptible individuals. What is an adipocyte? Fat storing cell, store energy as triglycerides, synthesize triglycerides from glucose, mobilize, energy from free fatty acids and glycerol. What are adipokines and what are their functions? Secreted by adipocytes. Hormone-like cytokines. Secreted to regulate metabolic function and immune response. Food intake, energy expenditure, lipid storage, insulin sensitivity. Inflammatory response, coagulation, fibrinolysis; angiogenesis, BP regulation. The inflammatory response may lead to insulin resistance and metabolic dysfunction. What is white adipose tissue? Composes most of adipose tissues. Visceral (central) and SQ (peripheral) stores. Contributes to regulation of energy homeostasis. What is brown adipose tissue and what is its role in obesity? Composed of mitochondria and iron (brown color). Generate heat. Mitochondria oxidize glucose and FFA to generate heat (neonates and adults) No role in appetite or satiety. No negative metabolic effects. What is beige adipose tissue and what is its role in obesity? Appears in extreme cold weather with exercise. Protective against obesity, increases energy expenditure and weight loss. What is bone marrow adipose tissue and what is its role in obesity? In all bones including long bones. Releases adipokines with osteoblast activity. Excess osteoporosis and cause inflammation associated with rheumatoid arthritis. How are appetite and satiety controlled? Controlled by arcuate nucleus in hypothalamus - responsible for maintaining balance in metabolism. Regulated by "orexins" which increased appetite and decreased metabolism and anorexins which decrease appetite and increase metabolism. Describe Ghrelin and is role in obesity/satiety/appetite. Orexin Produced in the stomach in response to hunger. Ghrelin receptors in hypothalamus - growth hormone: releases gastric acid, increases gastric motility, pancreatic secretion of insulin: stimulates appetite. Describe Endocannabinoids and its role in obesity/satiety/appetite. Orexin Produced in the brain and peripheral nerves. Increases appetite, nutrient absorption, and lipogenesis. Increase peripheral and central adipose tissue accumulation Describe Leptin and its role in obesity/satiety/appetite. Anorexin Produced by adipocytes, acts on hypothalamus Decreases appetite and energy expenditure. As adipocytes increase, leptin secretion increased high levels of lepto lose effectiveness (leptin resistance) disrupts hypothalamus signals satiety - overeat - increase weight (levels increase with stress, simple carbs, and decreased sleep) Describe Glucagon like peptide 1 and its role in obesity/satiety/appetite. Anorexin. Stimulates pancreatic glucose- dependent insulin secretion. Decreases gastric emptying. Decreased appetite and increased satiety. Semaglutide is a GLP-1 receptor agonist. Describe Adiponectin and its role in obesity/satiety/appetite. Anorexin Produced primarily in adipose tissue; less in muscle and brain. Considered an adipokine. Regulates glucose levels and fatty acid breakdown (lipid metabolism) and insulin sensitivity: anti-inflammatory, anti fibrotic and antioxidant effects. Peptide stimulates fatty acid oxidation and glucose uptake in skeletal muscle and adipose tissue. Levels decrease in obesity-increases insulin resistance, increased CAD risk, increase inflammatory markers. How does the apple shape clinical manifestation associate with obesity risks? Due to visceral obesity, accelerated lipolysis, increased inflammation and metabolic syndrome. List three underlying etiologies of the chronic complications of obesity Chronic inflammation Metabolic disorders Increased free fatty acids. How does the pear shape clinical manifestation associate with obesity risks? Due to peripheral obesity. Fat is less metabolically active. Release of fewer adipocytokines. The risk of obesity is less severe.