Exam 3

pathophysiology chapters

valve dysfunction and blood flow changes

injury or damage to valves disrupts the one-way flow of blood through the heart, causing backup, infection, MI, trauma, or congenital defects, murmur, less efficient blood movement, excess workload; this can range from mild and asymptomatic to lethal

stenotic valve

narrowed valve opening; caused by narrow orifice or valve not opening completely; does not allow blood to flow freely across it

valve insufficiency (regurgitant)

loose valve; valve does not close properly which allows leakage of blood

valvular dysfunction

typically symptomatic of physical exertion; dyspnea, excessive fatigue, exercise intolerance, syncope; severe disorders cause of palpitations and symptoms of HF like cough, edema, ascites, orthopnea, paroxysmal nocturnal dyspnea

murmur

different characteristics of murmur can reflect various cardiac issues, such as heart valve deformity, valve dysfunction, or defects of the heart wall, or there could be no issue at all

mitral valve stenosis

patho: common sequel to rheumatic fever; impedes blood flow from LA to LV; decreased CO as less blood flow into LV; LA to lungs causing pulmonary edema, congestion, and high pressure; increases risk of atrial fibrillation; mitral valve is thickened, fibrotic narrowed; the LA becomes overloaded, overstretched, and dilated; can stretch conduction fibers causing atrial fibrillation; stasis of blood can cause thrombus formation which can become detached and travel and cause ischemia

clinical presentation: present with dyspnea with exertion, cough, paroxysmal nocturnal dyspnea, and orthopnea; may have a diastolic murmur or opening snap on auscultation

mitral valve insufficiency

patho: mitral valve fails to close sufficiently; caused by mitral valve prolapse, rheumatic heart disease, infective endocarditis, drugs, myxomatous degeneration, mitral annular calcifications, MI, and Marfan’s and Ehlers-Danlos syndromes; backup into LA causes overload and distension; can cause pulmonary edema due to hydrostatic pressure increase and pulmonary vein congestion

clinical symptoms: may be asymptomatic, but when it is severe it causes chest pain and exercise intolerance, pulmonary symptoms due to fluid back up in lungs, atrial fibrillation, diminished S1 sound, holosystolic murmur at apex; weakness, fatigue, pallor, diaphoresis, dyspnea

mitral valve prolpase

patho: one or both leaflets are loose, floppy, and thickened; common cause of mitral insufficiency; can arise from CT disorders, RF, ischemic HD, cardiomyopathies; commonly affects females 14-30

clinical presentation: commonly asymptomatic with unknown cause; most don’t require treatment; if severe it has the typical symptoms of mitral insufficiency or angina as well as similar diagnosis and treatment; systolic murmur

aortic valve stenosis

patho: caused by aortic sclerosis, RHD, congenital valve defect; difficult for LV to eject blood due to increased resistance, leading to LVH or angina pectoris; aortic valve is narrowed and LV outflow is obstructed

clinical presentation: symptoms when valve area less than 1cm2, has prolonged initial asymptomatic period; exertional dyspnea, exercise intolerance, pulmonary edema, and angina pectoris, systolic murmur that is low-pitched and in second intercostal space; if severe there are symptoms of HF, syncope, and angina

hypertrophic cardiomyopathy

patho: increased risk for both atrial and ventricular dysrhythmias; can cause sudden death especially due to ventricular dysrhythmias; LV is asymmetrically hypertrophied, stiff, noncompliant, and LV outflow obstruction

clinical presentation: commonly asymptomatic and can cause sudden death; symptoms can be palpitations, dyspnea, chest pain, fatigue, dizziness, and syncope, irregular pulse; systolic murmur (harsh, diamond shaped)

aortic valve insufficiency

patho: deformed aortic valve does not close properly, backflow of blood from aorta into LV, dilation and decreased contraction of LV, backup of blood into pulmonary circulation; caused by RHD, endocarditis, Marfan’s syndrome, ankylosing spondylitis

clinical presentation: causes high-pitched diastolic murmur; Austin Flint murmur; can have symptoms of right and left HF like orthopnea, paroxysmal dyspnea, diaphoresis, hepatomegaly, ascites, peripheral edema; diastolic trill

anoxic encephalopathy

if there is rupture of large cerebral artery, ischemia, cerebral edema, lack of cerebral circulation, and significant lack of oxygen delivery to brain tissue can lead to this condition which causes decreased levels of consciousness

lack of oxygen delivery causes decreased level of consciousness

aphasia

difficulty to understand or speak language

arteriovenous malformation (AVM)

congenital abnormality that connects an artery with a vein within the brain tissue; causes weakened areas in vessel walls that are vulnerable to rupture; can lead to intracerebral bleeding

carotid stenosis

atherosclerosis of the carotid artery; common cause of ischemic stroke

cerebral infarction

caused by ischemia of brain tissue; death of brain cells

circle of Willis

located at base of brain; provides collateral circulation in event that one of the major cerebral vascular routes should occlude

contralateral

relating to or denoting the side of the body opposite to that on which a particular structure or condition occurs

corticobulbar tract

neurons run parallel to corticospinal tract; descend from cortex down into brain stem where cranial nerves emerge

Cushing’s triad

bradypnea/irregular respirations, bradycardia, hypertension

corticospinal tract

major region of upper motor neurons that descend from the brain down the spinal cord

decussation

area in medulla where most upper motor neurons cross from one side of the brain to control the opposite side of the body

Any type of cerebral injury manifests in sensory or motor deficits on the contralateral side of the body

expressive aphasia

caused by dysfunction of Broca’s area; affected individual cannot make words but does understand what others are saying

glutamate

neurotransmitter that is considered a major mediator of excitatory signals in the CNS and is involved in cognition, memory, and learning

hemorrhagic stroke

caused by rupture and hemorrhage of cerebral artery leading to compression and toxicity of brain cells and loss of cerebral blood flow

ipsilateral

belonging to or occurring on the same side of the body

ischemic penumbra

perimeter around the core of the ischemic area

ischemic stroke

caused by thrombus or embolus that lodges in a cerebral artery and blocks blood flow to the brain tissue

lacunar infarct

small areas in the brain that endure ischemia from occluded tiny blood vessels

neurological deficit

brain cell death leads to loss of neurological functions

receptive aphasia

caused by dysfunction of Wernicke’s area; affected individual can speak but cannot understand words and uses illogical language

spinothalamic tract

major region of sensory neurons that travel from the periphery up into the brain

subarachnoid hemorrhage

specific type of cerebral hemorrhage that occurs when arterial branch in subarachnoid space ruptures

transient ischemic attack (TIA)

ischemic injury of the brain; often called a mini-stroke; disruption of cerebral circulation with neurological deficits that are reversible and last for less than 24 hours; body naturally dissolves the clot and circulation returns with no permanent neurological injury; can be warning sign for future stroke

Temporary and resolves; neurological changes may go unnoticed by patient but observed by bystanders, may be resolved by time medical help is receives, interview of patient and observers is key

vertebral-basilar insufficiency (VBI)

syndrome where there is decreased vertebral and basilar artery blood flow and consequent decreased blood supply to the cerebellum

cerebral ischemia

often occurs gradually and the symptoms are progressive; appears over several hours; the core area can increase over time, if completely occluded the neurons in the core area will suffer irreversible infarction within minutes; ischemic penumbra has less perfusion but not irreversible damage, rapid reperfusion is critical to recover cells

ischemic cerebrovascular accident (stroke)

Risk factors: afib, carotid stenosis, cerebral ateriosclerosis

Patho: caused by cerebral arteriosclerosis, carotid stenosis, afib causing stasis and clot formation

Clinical presentation: speech, motor, and sensory deficits; neurological deficits on one side of body, slurred speech, loss of gag reflex, facial droop, hemiparesis, hemiparalysis, loss of sensation, vision loss, disorientation, confusion

hemorrhage CVA

Risk factors: HTN, oral anticoagulation, cerebral aneurysm

Patho: artery rupture results in bleeding, caused by HTN, aneurysm rupture, subarachnoid hemorrhage, blood flow into brain compresses and displaces brain tissue, vasospasm of adjacent blood vessels, Cushing’s triad

Clinical presentation: speech, motor, and sensory deficits; neurological deficits on one side of body, slurred speech, loss of gag reflex, facial droop, hemiparesis, hemiparalysis, loss of sensation, vision loss, disorientation, confusion

septic shock

Severe sepsis with persistent life-threatening hypotension; medical emergency; hypotension doesn’t respond to fluid replacement and vasopressors; immunocompromised are most at risk; infection of great severity which is the result of a highly virulent microbe; criteria include alteration in mental state, hypoxemia, elevated plasma lactate level, oliguria, or systolic hypotension <100 mmHg

cardiogenic shock

failure of the heart; commonly caused by MI, heart unable to maintain pressure to perfuse tissues

hypovolemic shock

large depletion of blood or fluids; low body volume, may induce coronary ischemia, renal tubular necrosis, RAAS and SNS activated

anaphylactic shock

severe allergic reaction; due to overwhelming immune response to allergen, urticaria, bronchospasm, angioedema, swelling of throat, bronchoconstriction, vasodilation, increased capillary permeability

neurogenic shock

injury to spinal cord or brain; SNS disrupted, can occur during anesthesia, reduced venous return to heart from widespread vasodilation

common pathway for 5 types of shcok

shock trigger to inadequate blood flow to tissues to cellular hypoxia to anaerobic metabolism to lactic acidosis

clinical signs of impending death

Coma, absence of motor responses, absence of pupillary light response, absence of corneal reflexes, absence of caloric responses, absence of gag reflex, absence of coughing in response to tracheal suctioning, absence of sucking and rooting reflexes, absence of respiratory drive at PaCO2 that is 60 mmHg or 20mmHg above normal baseline

focal seizure

can be aware of have impaired awareness which can further classify them as onset aware or onset impaired awareness; located within 1 cerebral hemisphere; patient will experience involuntary movements of the contralateral side; can cause motor, sensory, autonomic, or psychic symptoms with or without impairment of cognition

generalized

involved both hemispheres; may have motor and/or nonmotor symptoms like clonic, tonic, or myoclonic activity, epileptic spasms; absence seizures (staring spells)

aura

unique sensations before a seizure of perception of a strange light, unpleasant smell, or confusing thoughts or experiences; allows individual time to prepare for a seizure and prevent injury

ictal period

episode of the seizure

postictal

phase after completion of seizure where a person enters an altered state of consciousness that usually lasts from 5-30 minutes

interictal

between seizures; time between seizures when multiple seizures occur in a short time frame; when brain activity is more normal

triad of Parkinson’s

bradykinesia, resting tremor, muscle rigidity

bradykinesia

state of slowed movement that can inhibit independent functioning; first see effects in distal muscles of arms and legs; may have difficulty initiating gait or rising from a seat; decreased arm swing, hand writing micrographia, decreased fine motor function; may also experience akinetic episodes

resting tremor

classically a resting, “pill-rolling” tremor of hand and finger that begins unilaterally before progressing bilaterally and spreads to legs and sometimes the head, jaws, and face; resting tremor ceases when purposeful movement of limb occurs

muscle rigidity

often felt by patient as tightness or stiffness in arms, legs, neck, and trunk and begins unilaterally but progresses gradually to both sides; physical exam will find cogwheeling or ratchety movements; in face can cause facial masking or emotionless stare; may also experience decreased blinking, soft, monotonous, low-volume speech, and difficulty swallowing

dopamine and Parkinson’s disease

In Parkinson’s, there is a progressive loss of dopamine-producing cells. Dopamine and Ach modulate the body’s movements. Dopamine has an inhibitory effect on movement. The imbalance of the neurotransmitters creates the tremors and abnormal spastic movements.

postural instability and Parkinson’s disease

The postural instability with Parkinson’s is caused by a loss of postural reflexes, which when coupled with rigidity and decreased corrective ability for balance increase the fall risk. The patient may take very short, quick steps forward or may step backward rapidly and uncontrollably.

multiple sclerosis

Patho: a chronic demyelinating disorder that affects the brain, spinal cord, and optic nerves; characterized by remissions and exacerbations; unknown etiology

Clinical presentation: weakness, numbness, tingling sensations, balance problems, blurred vision, fatigue, tinnitus, decreased hearing, nystagmus, diplopia, dysarthria, dysphagia, may progress to paralysis, muscle spasticity, ataxia, vertigo, urinary retention, spastic bladder, constipation

blunt trauma

object hit skull forcefully causing fractures of the skull and damage to underlying brain

accleration-deceleration

when the skull stops abruptly and the brain continues to move forward, rotating within the skull and causing shearing of brain tissue against the skull’s rough interior edges; brain bounces off skull and moves in opposite direction then strikes back of skull and damages opposite area

penetrating injury

when a foreign object penetrates the skull and brain, the skull is fractured and brain tissue is damaged; amount of damage depends on the size of the foreign object and its velocity

blast injury

extent of injury caused by explosion depends on type and amount of explosive material and distance to blast; initial injury from pressure wave that can produce acceleration-deceleration injury; secondary injury from penetrating and blunt injuries from debris; tertiary injury from individuals being thrown by blast; quaternary injury from burns, inhalation, and angina

Cushing’s Triad

hypertension, bradycardia, irregular respirations

concussion

mild traumatic brain injury, traumatic force causes disruption in brain function (may or may not involve loss of consciousness), cease sporting activity until evaluation and assessment; can be simple or complex; previous ones increase risk for future concussions; manifested by temporary memory loss and alteration of mental status

epidural hematoma

bleed in space below skull bone and above dura mater; most serious complications of head injury commonly caused by skull bone fracture lacerating middle meningeal artery causing voluminous arterial bleeding; midline shift of brain can be viewed on imaging with an hour; injury leads to decreased LOC, followed by lucid period and rapid deterioration

subdural hematoma

bleeding in space below dura mater usually due to bridging veins in subdural space; slow leak/bleeding but blood accumulates over time; most common type of traumatic intracranial hematoma; neurological deficits do not occur until substantial bleeding; can be acute or subacute

subarachnoid hemorrhage

aneurysm or trauma causes rupture of artery that causes blood to fill subarachnoid space; blood irritates tissues and puts pressure on brain; can cause obstructive hydrocephalus or brain herniation

traumatic subarachnoid hemorrhage

tearing of cerebral and meningeal vessels within subarachnoid space, post-traumatic cerebral vasospasm in response to blood

aneurysmal subarachnoid hemorrhage

weakened area of vessel may rupture, half the time symptoms precede rupture, thunderclap headache

between C1 and C3 SCI

unable to breathe without respirator, loss of bowel control, unable to move arms and legs

between C4 and C7 SCI

severe weakness in arms with no motor function or sensation in legs, loss of bowel and bladder control

thoracic spine SCI

paralysis of legs but arms can still function, truncal instability, loss of bowel and bladder control

lumbar sacral SCI

loss of bowel and bladder control, upper body strength and sensation normal, motor weakness or paralysis and sensory loss in hips and legs

spinal shock

altered physiological state immediately after spinal cord injury; state of areflexia, paralysis, absence of sensation at and below level of injury, and bowel and bladder dysfunction

autonomic dysreflexia

caused by a complication below the level of injury such as bowel impaction, bladder distension, or pressure sores; involuntary functions such as breathing, BP, HR become unregulated

sprain

overstretch ligament with possible tear; 3 grades: no tear, partial tear, complete tear

strain

overstretch of muscle or tendon

closes (complete)

fracture in which bone fragments separate completely, are not displaced, and remain beneath underlying tissue

open (compound)

fracture of bone that protrudes to the outside of the body

incomplete

fracture in which bone fragments are still partially joined

compression

fracture that consists of the crushing of cancellous bone

transverse

fracture where parts of the bones are separated but close to each other

spiral

twisting force to the thigh causes a fracture line that encircles the shaft of the femur

comminuted

fracture with more than one fracture line and more than 2 bone fragments that may be shattered or crushed

stress fracture

failure of one cortical surface of the bone often caused by repetitive activity

repetitive stress on bone; second and third metatarsals, tibia, and fibula most common; extensive microdamage before bone adequately remodeled; may not be apparent on x-ray initially

risk factors: genetics, female sex, low body weight, amenorrhea

avulsion

separation of small fragment of bone at the site of attachment of a ligament or tendon

greenstick

incomplete break in the bone with the intact side of the cortex flexed (one side is broken and the other is bent); usually seen in children

impacted

fracture in which one part of the fracture is compressed into an adjacent part of the bone

neurovascular injury

damage to brain, spinal cord, nerve roots, and peripheral nerves can cause irreversible dysfunction if untreated like loss/decrease in LOC, weakness/paralysis, pain, paresthesia, sensory deficits; damage to bone or tissue can also damage vascular system and cause hemorrhage, hematoma, and ischemia

stage 1 of bone healing

fracture and inflammatory phase

bleeding between edges of fractured bone

stage 2 of bone healing

granulation tissue formation

fibroblasts are attracted to the area of injury, growth of vascular itssue

stage 3 of bone healing

callus formation

consists of osteoblasts and chondroblasts, synthesis of extracellular organic matrix of woven bone and cartilage

stage 4 of bone healing

lamellar bone deposition

strengthening phase, ossification occurring

stage 5 of bone healing

remodeling

remodeling of bone at site of fracture, adequate strength commonly occurs in 3 to 6 months

kyphosis

hunched over posture

lordosis

inward curvature of the spine

scoliosis

sideways curvature of the spine

fat embolism

fat globules from the marrow of the fracture bone enter the circulation; associated with long-bone and pelvic fractures; these fat droplet emboli can obstruct the pulmonary microvasculature and other microvascular beds; the systemic manifestation of this is fat embolism syndrome

compartment syndrome

tissue pressure exceeds perfusion pressure in enclosed anatomical space; patient complains of pain out of proportion of degree of injury; ischemia, necrosis, and functional impairment; weak distal pulse or pulselessness; immediate surgical evaluation

vertebral compression fractures

patho: collapse of internal lattice like mesh-work of the vertebral bone; bone becomes thin or flattened; can be caused by osteoporosis, cancer, infection, ischemia, trauma

risk factors: advanced age, bilateral ovariectomy, Caucasian or Asian race, early menopause, female, history of fractures in adulthood, history of fractures in first-degree relatives, premenopausal amenorrhea for more than a year, dementia, alcohol use, dietary Ca or Vitamin D deficiency, estrogen deficiency, frailty, insufficient physical activity, low body weight, osteoporosis, prolonged glucocorticoid/anticonvulsant use, tobacco use