Pathophysiology final- TTU- Dr. Gollahon

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arterial BP (common BP)

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1

arterial BP (common BP)

120 mm Hg

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BP from aorta to capillary network

120 to 35

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capillary Hydrostatic BP

18-35 mm Hg

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Venous Pressure

18 mm Hg

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circulatory pressure

overall pressure from circulatory system

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circulation

occurs when circulatory pressure is greater than cardiovascular pressure

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difference in pressure

about 100 mm Hg (from 18 - 120)

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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

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what happens once the blood reaches the capillaries

the systolic and diastolic pressure drop drastically and the velocity decreases

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peripheral resistance

resistance pressure from the cardiovascular system

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Total Peripheral Resistance

1. Vascular resistance

2. blood viscosity

3. turbulence

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Vascular resistance

friction created by diameter of vessel

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note the changes in velocity and pressure

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brain areas and corresponding function

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blood viscosity

friction created by the thickness of the blood from the components and their interactions

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turbulence

friction created by eddies and swirls that cause high flow rates, irregular surfaces, and sudden changes in diameter that disrupt uniform flow

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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

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The organs that regulate blood pressure

1) Heart (volume rate/velocity)

2) Kidneys (renin/vasoconstriction)

3) blood vessels (vasoconstriction)

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goal of BP regulation

meet OXYGEN requirements remove CO2 and WASTE

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Sodium

- primary ECF CATION (+)

- regulates OSMOTIC FORCES (water)

- roles in acid-base balance, chemical reactions, membrane transport

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Chloride

- primary ECF ANION (-)

- provides electroneutrality (neutral substance charge)

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RAAS

Renin- Aldosterone- Angiotensin System

aldosterone- sodium (and H2O) reabsorption angiotensin- promotes aldosterone secretion Renin- vasoconstriction

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Natriuretic Peptides

hormones that cause sodium excretion by kidneys

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ANP

Atrial Natriuretic peptides- secreted by atria

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BNP

Brain Natriuretic peptides- secreted by brain

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Chemoreceptor Reflexes

response system to changes in the chemicals in blood or CSF

1) CO2

2) Oxygen

3) pH levels

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Carotid Body chemoreceptors

in neck near carotid sinus

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Aortic Body Chemoreceptors

near Aortic Arch

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Baroreceptor Reflexes

response system to cardiovascular regulation, and cardiac output and peripheral resistance (how much blood is being pumped and at what pressure)

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Baroreceptor locations

- carotid sinus

- aortic sinus

- wall of right atrium

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What is caused by Body Fluid Imbalance

Primarily High BP which can lead to:

1) Cardiovascular Disease (CVD)

2) Obesity

3) Arteriosclerosis

4) Stress

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BP increase during exercise

- Skeletal Muscle

- Heart

- Skin

- Total output

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BP decrease during exercise

- Kidney

- Abdomen

- Misc.

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BP the same during exercise

Brain

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hypertension

consistently high BP

- systolic >140 or

- diastolic >90

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Diagnosing Hypertension

  • 70 million people UNdiagnosed

  • must have high BP readings months apart (different doctor visits)

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Etiology Primary Hypertension

- Idiopathic

- may be genetic or environmental

- 92-95% all hypertension patients have primary

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Hypertension Mediating Factors

- Sympathetic Nervous System (SNS)

- RAAS

- Natriuretic Peptides

- RAAS-blocking

Drugs:

ACE, Renin, ARB, and Aldosterone inhibitors

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Malignant Hypertension

Rapidly progressive Hypertension

  • Diastolic > 140 causes organ damage due to high pressure tearing organs

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Complicated Hypertension

-Chronic hypertensive damage to blood vessels and tissues - leads to target organ damage (heart, kidney, brain, and eyes)

-Myocardial hypertrophy

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Hypertension Pathophysiology

Genetic and Environmental vulnerabilities - cause neurohormonal dysfunction in SNS, RAAS, and Natriuretic peptides

- promotes inflammation

- creates insulin RESISTANCE

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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

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How do nerves fire?

100%, all-or-none response

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white matter is...

myelinated faster at transmitting signals

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gray matter is...

NOT myelinated slower at transmitting signals

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synapse

space between synaptic pre and post-synaptic terminals

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organs that send stimuli

CNS

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stimuli-responding organs

- cardiac muscle

- skeletal muscle

- smooth muscle

- glands

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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

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Myelin basics

- made by schwann cell

- wrap around axon to keep electrical charges concentrated around axon

- makes for faster action potential

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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

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Neural Activity is Multi-modal (multiple means of working): CHEMICAL

neurotransmitters (ligands) bind to receptors

ex. dopamine, serotonin, norepinephrine

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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

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Neural Activity is Multi-modal (multiple means of working): MECHANICAL

pressure on membranes or membrane distortion causes depolarization

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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

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Nerve impulse Stimulation and Inhibition is always...

on the Postsynaptic Membrane

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Stimulatory impulse

excitatory, when the ligand binds to receptor, it causes ions to enter and depolarize cell

ex. norepinephrine

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Inhibitory impulse

ligand binds to receptor and keep membrane potential below -70mV, repressing impulse

ex. GABA

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Informal categories of Neural Disorders

- Purely neural- problem in brain/cerebrum

- Somatosensory and somatomotor- faulty connection in nerves throughout body and signals

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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

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Structural damage

Physical damage to brain

ex. concussion, blunt force trauma to brain

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Non-structural damage

neurotransmitter or neuron connection problems ex. drugs inhibit action potential reaching the the next postsynaptic terminal

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Somatosensory and Somatomotor Disorders

faulty connection between Incoming Signals Outgoing signals or the ability to correctly interpret said signals

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Cerebrum areas and function

study the different areas and their functions

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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

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Nonstructural causes for confusion and coma is very history based

some examples:

- drugs

- cerebral ischemia

- hyperglycemia

- hypoglycemia

- hypoxia

- seizure

- hypothyroidism

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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

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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

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ALS

upper and lower motor neuron dysfunction

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Parkinson

dopamine control and motor system dysfunction

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Ischemic stroke

large areas of brain stop function or die

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Hemiplegic gaits

arm and leg on one side of body are affected

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spastic or diplegic gaits

both arms or both legs are affected, often spazzing

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neuropathic gait

foot movement is weakened causing foot drop, looks like foot is pointing

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myopathic gait

described as waddling, weakness in pelvic muscles that would keep pelvis horizontal during walk, pelvis droops on one side

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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

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choreiform gait

irregular, jerky movements in all extremities

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sensory gait

feet sensory fails to detect when foot has made contact with ground, patient slams foot into ground to sense it.

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Cerebellar Ataxia gait

wide gait, clumsy movements, patients body swings from side-to-side as they walk

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Cerebellar Ataxia presentation

cerebellum and connections are affected

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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)

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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

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Infections Overview

leading causes of death GLOBALLY

- significant morbidity and mortality

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susceptible populations

- elderly

- very young

- immunocompromised

- disenfranchised

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Vector

someone or something that carries the disease and can pass on to others

includes animals, people, objects, and food

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Zoonotic hosts

animals carrying infectious agents and even amplifying it

ex. rats and the black plague, mosquitos and malaria

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communicability

ability to spread from one individual to others

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Infectivity

ability for pathogen to invade and multiply in host

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Pathogenicity

ability of infectious agent to produce disease

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Virulence

capacity of pathogen to cause severe disease

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colonization

microorganisms outcompete normal flora and multiply

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Toxigenicity

ability of microbe to produce soluble toxins or endotoxins

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Normal Flora

microorganism in the body, don't cause harm, and can even prevent infection

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Overt Infection

an infection that shows obvious signs in patient

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Covert Infection

an infection that is not obvious in a patient, may be hard to diagnose

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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)

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Infection Severity

Asymptomatic to Life-threatening

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Course (rapidity) of infections

1) acute (rapid, onset)

2) subacute (in the middle)

3) Chronic (long, drawn out)

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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

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