Week 1 - Lecture 3 - Clinical Models Flashcards
what is cerebral atrophy
reduction in size of the cells in the cerebrum of the brain
- progressive reduction in the size of the brain
- reduction in brain tissue itself
Cerebral atrophy cont
neutrons are the functional cells in brain tissue
they conduct nerve impulses
- within the brain
- to other areas of the body
loss of neuronal function due to atrophy leads to neurological disease
- as we age, cerebral atrophy progresses
- clinical symptoms start to appear after a certain degree of atrophy
pathophysiology of cerebral atrophy
neurons are connected and communicate
- destruction of neutrons and loss of neurotransmitter in one part of the brain may lead to atrophy in another part of the brain
some injury types
- reduced perfusion : increased risk of deficit injury (oxygen and nutrient delivery impacted)
-intoxication : due to ischemia, metabolites accumulate
as neutrons decrease in size
- physical relationship with other neurons changes
- communication between neurones impaired due to increasing distance
neutrons are not able to replicate
neural cell death : permanent loss of cells and function
clinical manifestations of cerebral atrophy
focal : localised to a particular region
global : affecting entire brain
neurons in each area responsible for specific functions of the brain
as atrophy progresses, the associated function becomes altered
frontal lobe/temporal lobe : cognitive impairment
hippocampus/ cerebral cortex : alzheimer’s
basal ganglia : movement disorders
wide range of clinical manifestations
- depends on the location of atrophy and the extent
Diagnosis - cerebral atrophy
brain atrophy is a pathological finding
- identify possible etiology
- initiate possible treatment
medical history : signs, symptoms, onset, duration
- identifying onset is difficult (eg. self assessment of cognitive decline)
- insidious and subtle development of signs
- often signs first observed by others
- early identification of loss and function, better prognosis
neurological examination
imaging studies
Cerebral atrophy treatment
atrophied and damage neurons recovery is limited
- prevention is the best approach
- interruption process will stop or slow the course of disease
supportive care to maintain optimal functioning of the individual (physical, speech, occupational therapy)
pharmacologic treatment : to improve neurologic signal transmission
Cardiac hypertrophy
myocytes do not continually divide and replace themselves
- after 4 weeks of life : growth is only by hypertrophy
– you have the same number of functional cells (minus loss of injured/dead cells)
hypertrophy : increased cell size
cardiac hypertrophy : increased cardiac mass
Cardiac hypertrophy cont’
can be physiological or pathological
- physiological cardiac hypertrophy results from excessive exercise
pathophysiology cardiac hypertrophy
primary cardiac hypertrophy (hypertrophic cardiomyopathy)
idiopathic
inherited non-sex linked genetic trait
secondary cardiac hypertrophy (hypertrophic cardiomyopathy)
-due to an underlying condition increasing ventricular workload
increase in ventricular muscle mass results from an increase in myocardial cell size
can occur in both, right and left ventricle
cardiac hypertrophy pathophysiology cont’
ventricle walls become thickened and stiff due to increased cell size
-muscle is less effective at contracting despite the increased size
- result in lack of compliance (stiffness)
adequate filling is not possible
-cardiac output decreases
stiffness +small chamber size = cardiac failure
-clinical signs and symptoms develop slowly
cardiac hypertrophy : clinical manifestations
variable clinical expression
- mild to severe (some do not have symptoms)
left ventricle is the main pump
- decreased circulatory output
- back flow to left atrium
-backflow to pulmonary circulation
- heart own perfusion suffers and impacted, reducing oxygen and nutrient delivery
impaired cardiac function SOB syncope (fainting) irregular heart rate -myocutes enlarge, physical relationship of conducting cells altered -neurologic signalling disrupted
diagnosis for cardiac hypertrophy
family history of the condition
- genetic testing can aid preclinical diagnosis of primary cardiac hypertrophy
secondary cardiac hypertrophy
- identification of primary pathology
- treatment/management of primary pathology
routine screening
- hypertension
- reduced exercise tolerance
- ventricular arrhythmia
- altered signals in the cells of the ventricles
screening techniques
- EKG : electrical activity of the heart
- two dimensional echocardiogram : Ultrasound measurement of physical dimensions
- exercise stress testing : determine cardiovascular response to exercise
-P/E : heart murmur during cardiac contraction often heart
Cardiac hypertrophy treatment
main target: symptom relief and prevention of sudden cardiac death
- pharmacologic
- drugs that relax the ventricles
- drugs that reduce the workload of the heart
beta-adrenergic blockers
–reduce the rate and strength of muscle contraction by binding to and inhibiting norepinephrine and epinephrine receptors - surgery
- to reduce left ventricular mass
- repair heart valves
- complications associated - alcohol ablation of the interventricular septum : necrosis by injecting alcohol into small arteries, new therapy, not enough evidence to understand long term effects
- non-pharmacologic : activity restriction to minimise sudden cardiac death
What is acromegaly
condition of cellular hyperplasia (increase in cell numbers)
Most common clinical manifestation :
- abnormal growth in hands and feet
- megaly : enlargement
- -acro : extremities
pathophysiology of acromegaly
leads to excessive growth
-bone, cartilage, soft tissues, organs
occurs after epiphyseal plate closure in the long bones
-acromegaly affects adults
