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arterial BP (common BP)
120 mm Hg
BP from aorta to capillary network
120 to 35
capillary Hydrostatic BP
18-35 mm Hg
Venous Pressure
18 mm Hg
circulatory pressure
overall pressure from circulatory system
circulation
occurs when circulatory pressure is greater than cardiovascular pressure
difference in pressure
about 100 mm Hg (from 18 - 120)
trend in arterial tissue different than venous tissue
arteries have high elastic tissue composition because they rely on pressure rather than a series of valves like the veins
what happens once the blood reaches the capillaries
the systolic and diastolic pressure drop drastically and the velocity decreases
peripheral resistance
resistance pressure from the cardiovascular system
Total Peripheral Resistance
1. Vascular resistance
2. blood viscosity
3. turbulence
Vascular resistance
friction created by diameter of vessel
note the changes in velocity and pressure
brain areas and corresponding function
blood viscosity
friction created by the thickness of the blood from the components and their interactions
turbulence
friction created by eddies and swirls that cause high flow rates, irregular surfaces, and sudden changes in diameter that disrupt uniform flow
Total Body Water (TBW)
A. Intracellular fluid
B. extracellular fluid
1-interstitial fluid
2-intravascular fluid
3-lymph, synovial, intestinal, pleural, peritoneal, pericardial, intraocular fluids
4-CSF, sweat, urine
The organs that regulate blood pressure
1) Heart (volume rate/velocity)
2) Kidneys (renin/vasoconstriction)
3) blood vessels (vasoconstriction)
goal of BP regulation
meet OXYGEN requirements remove CO2 and WASTE
Sodium
- primary ECF CATION (+)
- regulates OSMOTIC FORCES (water)
- roles in acid-base balance, chemical reactions, membrane transport
Chloride
- primary ECF ANION (-)
- provides electroneutrality (neutral substance charge)
RAAS
Renin- Aldosterone- Angiotensin System
aldosterone- sodium (and H2O) reabsorption angiotensin- promotes aldosterone secretion Renin- vasoconstriction
Natriuretic Peptides
hormones that cause sodium excretion by kidneys
ANP
Atrial Natriuretic peptides- secreted by atria
BNP
Brain Natriuretic peptides- secreted by brain
Chemoreceptor Reflexes
response system to changes in the chemicals in blood or CSF
1) CO2
2) Oxygen
3) pH levels
Carotid Body chemoreceptors
in neck near carotid sinus
Aortic Body Chemoreceptors
near Aortic Arch
Baroreceptor Reflexes
response system to cardiovascular regulation, and cardiac output and peripheral resistance (how much blood is being pumped and at what pressure)
Baroreceptor locations
- carotid sinus
- aortic sinus
- wall of right atrium
What is caused by Body Fluid Imbalance
Primarily High BP which can lead to:
1) Cardiovascular Disease (CVD)
2) Obesity
3) Arteriosclerosis
4) Stress
BP increase during exercise
- Skeletal Muscle
- Heart
- Skin
- Total output
BP decrease during exercise
- Kidney
- Abdomen
- Misc.
BP the same during exercise
Brain
hypertension
consistently high BP
- systolic >140 or
- diastolic >90
Diagnosing Hypertension
70 million people UNdiagnosed
must have high BP readings months apart (different doctor visits)
Etiology Primary Hypertension
- Idiopathic
- may be genetic or environmental
- 92-95% all hypertension patients have primary
Hypertension Mediating Factors
- Sympathetic Nervous System (SNS)
- RAAS
- Natriuretic Peptides
- RAAS-blocking
Drugs:
ACE, Renin, ARB, and Aldosterone inhibitors
Malignant Hypertension
Rapidly progressive Hypertension
Diastolic > 140 causes organ damage due to high pressure tearing organs
Complicated Hypertension
-Chronic hypertensive damage to blood vessels and tissues - leads to target organ damage (heart, kidney, brain, and eyes)
-Myocardial hypertrophy
Hypertension Pathophysiology
Genetic and Environmental vulnerabilities - cause neurohormonal dysfunction in SNS, RAAS, and Natriuretic peptides
- promotes inflammation
- creates insulin RESISTANCE
Secondary hypertension
-caused by systemic disease (infects entire body)
-raises peripheral or
-resistance or cardiac output
could be renal vascular or parenchymal disease, tumors, or drugs
How do nerves fire?
100%, all-or-none response
white matter is...
myelinated faster at transmitting signals
gray matter is...
NOT myelinated slower at transmitting signals
synapse
space between synaptic pre and post-synaptic terminals
organs that send stimuli
CNS
stimuli-responding organs
- cardiac muscle
- skeletal muscle
- smooth muscle
- glands
membrane potential recap
- Na OUTSIDE cell
- more positive outside cell
- K INSIDE cell
- less positive inside cell
membrane potential = -70mV
- action potential stimulus causes channels to open, Na IN, K OUT, inside cell becomes MORE POSITIVE, reaches point to send action potential to next cell
Myelin basics
- made by schwann cell
- wrap around axon to keep electrical charges concentrated around axon
- makes for faster action potential
neurotransmitter facts and drug influence
- Na initiates depolarization
- Ca stimulates neurotransmitter release
- imbalance in these chemicals messes up neural function
- drugs can either intervene on the Pre-synaptic or Post-synaptic terminals to work
Neural Activity is Multi-modal (multiple means of working): CHEMICAL
neurotransmitters (ligands) bind to receptors
ex. dopamine, serotonin, norepinephrine
Neural Activity is Multi-modal (multiple means of working): ELECTRICAL
ion charges can encourage or inhibit activity down an axon
ex. Na/K activity in axon encourage
Cl inhibits activity
Neural Activity is Multi-modal (multiple means of working): MECHANICAL
pressure on membranes or membrane distortion causes depolarization
Neural Activity is Multi-modal (multiple means of working)
1)chemical
2)electrical
3)mechanical
multiple places were neurons can go wrong and be modified
Nerve impulse Stimulation and Inhibition is always...
on the Postsynaptic Membrane
Stimulatory impulse
excitatory, when the ligand binds to receptor, it causes ions to enter and depolarize cell
ex. norepinephrine
Inhibitory impulse
ligand binds to receptor and keep membrane potential below -70mV, repressing impulse
ex. GABA
Informal categories of Neural Disorders
- Purely neural- problem in brain/cerebrum
- Somatosensory and somatomotor- faulty connection in nerves throughout body and signals
Purely Neural Disorders
cerebrum is affected
1) Trauma- Traumatic Brain Injury (TBI)
affects memory and emotions
2) Aneurysms- Stroke
affects Broca (speech) Area 4 (motor) Wernicke (understanding speech)
3) Consciousness, Cognition, Awareness- trauma, medication, drugs
can be structural or non-structural
Structural damage
Physical damage to brain
ex. concussion, blunt force trauma to brain
Non-structural damage
neurotransmitter or neuron connection problems ex. drugs inhibit action potential reaching the the next postsynaptic terminal
Somatosensory and Somatomotor Disorders
faulty connection between Incoming Signals Outgoing signals or the ability to correctly interpret said signals
Cerebrum areas and function
study the different areas and their functions
Brain herniation
swelling on brain that is placing pressure on a certain section of brain, causing inflammation, cell damage, and/or loss of function in said area
how the brain is being compressed determines what brain functions are influenced/inhibited
Nonstructural causes for confusion and coma is very history based
some examples:
- drugs
- cerebral ischemia
- hyperglycemia
- hypoglycemia
- hypoxia
- seizure
- hypothyroidism
Pathophysiology of Neural disorders
Purely Neural v. Somatosensory/motor
Degenerative changes:
only somatosensory/motor, mostly changes (irreversible damage) in myelin
metabolic imbalances
BOTH
structure changes
BOTH
cancers
BOTH
Inflammation
BOTH
Pathophysiology of Selected Neural Disorders Continued
can be hyperactive(seizure) or under active (post stroke)
functional disorders- what body/brain function affected is dependent upon which NEURAL NETWORK is affected
ALS- upper and lower motor
Parkinson-dopaminergic (dopamine release), motor system
Ischemic stroke- large areas of brain
Gaits- very different from each other, very informative
ALS
upper and lower motor neuron dysfunction
Parkinson
dopamine control and motor system dysfunction
Ischemic stroke
large areas of brain stop function or die
Hemiplegic gaits
arm and leg on one side of body are affected
spastic or diplegic gaits
both arms or both legs are affected, often spazzing
neuropathic gait
foot movement is weakened causing foot drop, looks like foot is pointing
myopathic gait
described as waddling, weakness in pelvic muscles that would keep pelvis horizontal during walk, pelvis droops on one side
parkinsonian gait
severe muscle rigidity, patient remains in hunched over posture, takes small steps, struggles to initiate steps
Parkinson posture- stooped head, small steps, tuck hands at sides, hunched over
choreiform gait
irregular, jerky movements in all extremities
sensory gait
feet sensory fails to detect when foot has made contact with ground, patient slams foot into ground to sense it.
Cerebellar Ataxia gait
wide gait, clumsy movements, patients body swings from side-to-side as they walk
Cerebellar Ataxia presentation
cerebellum and connections are affected
Cerebellar Ataxia clinical features
-ataxic gait
-truncal gait (needs arms for support)
-Dysmetria (no smooth coordination, cant do finger to nose touch)
-limb ataxia (uncoordinated limb tremor, slows movement down to compensate)
-vertigo (spinning dizziness)
-static and kinetic tremors (shaking when still or moving)
- cerebellar dysarthria (slurred speech)
-Nystagmus and ocular dysmetria (shaking eyes, eyes unable to focus)
Infectious Disease Pathogenesis
dependent on:
1) human host
2) which infectious agent
3) exogenous or endogenous environmental factors
KEY FACTOR-
how susceptible the patient is to disease
Infections Overview
leading causes of death GLOBALLY
- significant morbidity and mortality
susceptible populations
- elderly
- very young
- immunocompromised
- disenfranchised
Vector
someone or something that carries the disease and can pass on to others
includes animals, people, objects, and food
Zoonotic hosts
animals carrying infectious agents and even amplifying it
ex. rats and the black plague, mosquitos and malaria
communicability
ability to spread from one individual to others
Infectivity
ability for pathogen to invade and multiply in host
Pathogenicity
ability of infectious agent to produce disease
Virulence
capacity of pathogen to cause severe disease
colonization
microorganisms outcompete normal flora and multiply
Toxigenicity
ability of microbe to produce soluble toxins or endotoxins
Normal Flora
microorganism in the body, don't cause harm, and can even prevent infection
Overt Infection
an infection that shows obvious signs in patient
Covert Infection
an infection that is not obvious in a patient, may be hard to diagnose
Overt infection: steps of causative agent (pathogen that causes illness)
1) encounter host
2) enter host
3) multiply and spread at entry site
4) cause tissue injury in host
- directly (cytotoxin) indirectly (inflammation response from body)
Infection Severity
Asymptomatic to Life-threatening
Course (rapidity) of infections
1) acute (rapid, onset)
2) subacute (in the middle)
3) Chronic (long, drawn out)
Infection Outcomes
1) Resolve (recovery)
2) Chronic Infection
- active (parasitic)
- prolonged asymptomatic excretion of agent (agent is being produced in body for period without patient knowing)
- latency of agent within host (sleeps for a time then awakes)
3) Death of Host