Pathophysiology final- TTU- Dr. Gollahon

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