CP phys final

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48 Terms

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Peripheral venous disease (PVD)

varicose veins

dilated and twisted superficial vessels (causes weakened vessel walls)

commonly found in lower extremities

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How many people have PVD

10-20% of the population

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Who is more affected by PVD

women are affected 2-3 X more than men

often a genetic thing

older adults (due to sarcopenia)

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Where are varicose veins normally found

the inside of the leg because that’s where the saphenous vein is

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causes of PVD

intrinsic weakness of vessel walls

increased intraluminal pressure

congenital defects in venous valves (the valves fail to prevent retrograde flow which causes blood to build up and cause excess pressure or bulging)

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Primary PVD

originates in the superficial system due to factors like pregnancy (because of increased venous volume), prolonged standing (gravity is pulling the blood down and the vein has difficulty stopping it), and obesity

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Secondary PVD

occurs due to abnormalities in the deep venous system, deep vein thrombosis (DVT, blood flow is slowed and is more prone to clotting), and inflammation

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what is a concern with DVT

the thrombus can break loose and turn into an embolism

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Symptoms of PVD

many cases are asymptomatic

symptoms - dull ache, heaviness, or pressure sensations in the legs after prolonged standing

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Complications of PVD

superficial venous insufficiency - swelling and skin ulceration (usually around the ankle)

stasis of blood can lead to superficial vein thrombosis or rupture, causing a hematoma

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PVD diagnosis

physical exam and medical history

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Conservative treatment for PVD

the aim is to counterbalance increased venous hydrostatic pressure

elevation of legs while supine, avoid prolonged static standing (locking knees out slows blood flow, and moving around increases pressure and pushes the blood back up due to muscular contractions), wear compression stockings (TED hose)

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Advanced PVD treatment

symptomatic or venous insufficiency varicose veins may require advanced treatment

sclerotherapy - intravenous administration of chemical agents to fibrose varicose veins (causes the vein to become fibrotic/stiff and becomes non-functional)

thermal ablation - laser or radiofrequency catheters used to obliterate varicose viens

surgical therapy (vein stripping) - direct vein litigation and removal (for severe cases)

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Ventilation

filters, warms, and humidifies incoming air

air goes in and out

air goes to the alveoli (already body temp and cleaned by then)

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Nose

serves as an entry point for air into the respiratory system (along with the mouth)

during exercise, you cannot get enough air in through the nose

lined with respiratory epithelium

goblet cells - mucus producing cells that line the nasal passage

ciliated cells - have finger-like projections, the cilia move back and forth and prevent foreign substances from entering

filters, warms, and humidifies the inspired air

protects lung tissues from harmful particles and pathogens

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Pharynx

AKA throat

once air comes in through the nose or mouth, it enters the pharynx

nasopharynx - where the nasal passage meets the pharynx

oropharynx - where the oral cavity meets the pharynx

laryngopharynx - right above the trachea and esophagus

serves as a common pathway for both food and air

contains a flap of cartilage called the epiglottis (prevents food from entering the trachea during swollowing)

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Larynx

just below the pharynx

AKA voice box

during swallowing, the epiglottis protects the trachea against aspiration

during breathing, the larynx opens and closes

during voice production, the vocal cords vibrate as air passes through

the vestibular folds are another mechanism to keep foreign objects out

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Trachea

AKA windpipe

rigid tube with C shaped cartilage rings

the rings provide support and prevent collapse during inhalation

the C shaped rings allow for more flexibility and the ability to expand if needed

extends from the larynx and branches into the right and left main bronchi

inner lining is epithelium with goblet cells (warms, humidifies, and filters air)

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Bronchial tree

branching airways that conduct air into the lungs

right and left main, breaks into secondary, tertiary, bronchioles, terminal bronchioles, and respiratory bronchioles

as the tree branches, the cartilage rings get smaller and are eventually replaced by smooth muscle in the bronchioles

the bronchioles can vasodilate and vasoconstrict

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Alveoli

bronchiles → terminal bronchiole → respiratory bronchiole →alveoli

tiny, grape-like sacs at the terminal ends of the bronchial tree

surrounded by a network of pulmonary capillaries

estimated 300 million alveoli (same surface area as a tennis court)

lined with two types of pneumocytes

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Type 1 pneumocytes

flat shape that abuts the pulmonary capillary wall

optimizes gas diffusion between alveoli and pulmonary capillary

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Type 2 pneumocytes

produces surfactant which reduces surface tension

keeps alveolar walls from sticking together and prevents alveolar collapse

alveoli are surrounded by fluid and have a tendency to collapse (type 2 pneumocytes combat this)

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Pulmonary surfactant

production begins at 24 weeks gestation but isn’t adequate until 32 weeks

newborn surfactant deficiency (surfactant replacement therapy significantly increases survival)

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what’s one of the main issues in premature babies

lung development

they inject surfactant through a tube into the lungs

they also put the baby on oxygen and a ventilator since they do not have the muscle mass to breathe (sustained oxygen delivery can cause blindness)

most babies born before 34 weeks will not survive

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Lung anatomy

cone-shaped organs located in the thoracic cavity on either side of the mediastinum

rest on the diaphragm and extend to just above the clavicles

the right lung is larger (3 lobes) and the left lung is smaller (2 lobes) to accommodate the heart

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lung coverings

covered with a double-layered serous membrane called the pleura

visceral pleura adheres to the lung surface

parietal pleura lines the inner surface of the thoracic cavity

pleural cavity lies between the layers and contains pleural fluid (reduces friction during breathing)

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Blood supply in the lungs

the lungs receive blood from the bronchial circulation via the bronchial arteries

arises from branches of the descending thoracic aorta just distal to the left subclavian artery

courses posteriorly along the trachea and main bronchi to reach the lungs

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Resting pressures

gasses move from high pressure to low pressure

atmospheric pressure (Patm) = 760 mmHg

intrapleural pressure (Pip) = 754 mmHg (pressure in the intrapleural cavity)

intrapulmonary pressure (Palv) = 760 mmHg (pressure in the alveoli/lungs)

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Inspiration - muscular contraction

diaphragm contracts downwards and the external intercostal muscles contract (lifts the ribs up and out)

expands the volume of the thoracic cavity in vertical and lateral dimensions

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Inspiration - pressure changes

expansion of the thoracic cavity decreases Pip to 754 mmHg?

Palv decreases to 757 mmHg becoming lower than Patm

this creates a pressure gradient and air moves from the atm to the lungs

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Expiration - muscular relaxation

primarily a passive process relying on the relaxation of the diaphragm, external intercostals, and the elastic recoil of lung tissues

thoracic volume decreases

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Expiration - pressure changes

Pip = 755 mmHg

Palv = 763 mmHg

Patm = 760 mmHg

creates a pressure gradient of +3 and air moves from lungs to the atm

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Gas exchange and transport

available oxygen from the ambient air depends on two factors

concentration - oxygen = 20.93%, CO2 = 0.03%, nitrogen = 79.04%

pressure - relative to sea level (760 mmHg)

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Dalton’s law of partial pressure

total pressure of a gas mixture is equal to the sum of the partial pressure that each gas exerts independently

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ambient air

oxygen = 20.93% X 760

CO2 = 0.03% X 760

nitrogen = 79.04% X 760

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tracheal air

100% saturated air

760 - 47 = 713

oxygen = 20.93% X 713

CO2 = 0.03% X 713

nitrogen = 79.04% X 713

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alveolar air

100% saturated air

760 - 47 = 713

mixed with alveolar gases

oxygen = 14.5% X 713

CO2 = 5.5% X 713

nitrogen = 80% X 713

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Gas diffusion

gasses move from one area to another based on pressure (driving pressure, the greater the pressure the greater the force)

gas moves into a fluid based on the solubility

temperature and pressure dependent (faster at a warmer temp)

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solubility coefficients

ability of gasses to dissolve in a solution

oxygen = 2

CO2 = 57

nitrogen = 1.3

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Blood

men have 5.0-5.5 L (testosterone produces more RBC)

women have 4.5-5.0 L

Formed elements (45% of your blood)

  • RBC (99+% of the formed elements, transports O2)

  • buffycoat (<1%, WBC and platelets, sits between RBC and plasma)

plasma (55% of your blood)

  • 90% water

  • 10% solutes

hematocrit

  • fraction of RBC in blood

  • hematocrit/3 gives a pretty good estimate of hemoglobin levels

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Gas exchange between alveoli and blood

inspired air = PO2 - 159, PCO2 - 0.3

trachea = PO2 - 149, PCO2 - 0.3

alveoli = PO2 - 100, PCO2 - 40

venous blood = PO2 - 40 (O2 comes out of alveoli to venous blood), PCO2 - 46 (CO2 goes into alveoli)

arterial blood = PO2 - 100, PCO2 - 40

skeletal muscle = PO2 - 40, PCO2 - 46

systemic artery = PO2 - 100, PCO2 - 40

systemic vein = PO2 - 40, PCO2 - 46

pulmonary vein = PO2 - 100, PCO2 - 40

pulmonary artery = PO2 - 40, PCO2 - 46

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Oxygen transport

blood carries oxygen in two forms

dissolved

  • relatively poor solubility

  • 0.3 mL is dissolved per deciliter (100 mL)

  • 3 mL per liter

  • average blood volume = 5 L, so total dissolved = 15 mL

bound with hemoglobin

  • primary way to carry O2 in the blood

  • contains 4 iron containing subunits

    • can carry 4 oxygen at a time

  • males = 13.5-17 g/dL

  • women = 5-10% less

  • 1 g Hb can reveribly combine with 1.34 mL O2

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what does reversibly combine mean

at the lungs, Hb can load up with O2, and at the tissues it releases O2 (only releases however much is needed)

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Oxygen transport math stuff

it’s rare to have 100% Hb saturation (normally 97-98%)

concentration of Hb X 1.34 X Hb saturation, then add dissolved O2 to get the mL O2/dL

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Anemia and O2 transport

5% of women are anemic

anemia is low Hb, so people with anemia get less O2/dL

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Mt. Everest values

pH = 7.5

arterial PO2 = 25 mmHg

arterial PCO2 = 13.3 mmHg

alveolar PO2 = 30 mmHg

lactate = 2 mM

Hb = 19 g/dL

O2saturation = 50%

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Mt everest

10-11 months out of the yesr, it is physiologically impossible to climb

when at that altitude, you’re basically missing around 75% of normal arterial PO2

VO2 max is gonna be 25% of normal

28,000 feet is called the death zone

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why is the pH elevated at high altitudes

when you go to high altitudes, you hyperventilate and blow off more CO2

blowing off more CO2 decreases the acidity and pH begins to rise

carbonic anhydrase converts carbonic acid into CO2 and H2O (and the other way around)

diamox (acetazolamide) forces the kidneys to excrete bicarbonate which increases acidity and inhibits carbonic anhydrase

phange in pH can result in cerebral or pulmonary edema

EPO is a hormone released from the kidney in response to low O2 levels and it stimulates RBC formation