Histology III

GI Tract layers:

1. Mucosa (interact with food)

2. Submucosa (contain lymphoid, vessels)

3. Muscularis externa (SM, involuntary)

4. Adventitia (connective tissue)

Esophogus function:

move food

Stomach function:

chemical breakdown, release HCl, mucous

Small intestine:

nutrient absorption, microvilli (increase SA)

Large Intestine:

Mucous containing goblet cells, really only absorb water

Rectum:

chamber for holding stool

Hemorrhoids:

Can be internal (above pectinate line)

Can be external (below pectinate line)

Thrombosed hemorrhoid:

Painful blood clot, needs to be surgically removed

Exocrine (pancreas)

producst released into a duct

Secretin:

Acinar and duct cells to add water and HCO3 to create a buffer

Cholecystokinin:

Triggered by presence of fats, gastric acid, essential AA, release of bile

Endocrine:

Islet of Langerhans

Insulin and C-peptide realeased from:

Beta cells

Glucagon released from:

Alpha cells

Insulin:

Anabolic, help lower blood sugar by moving glucose out from blood stream

Glucagon:

Catabolic, release

What are the 3 types of muscles:

1. Skeletal

2. Cardiac

3. Smooth

Cardiac Muscle (Myocardium):

1. Striated

2. Intercalated discs (gap junctions - electricity for depolarization)

3. Involuntary

4. Can’t regrow

5. Can hypertrophy

What is the functional unit of cardiac muscle:

Cardiac myofibril

Skeletal Muscle:

1. Striated

2. Multinucleated

3. Voluntary

4. Limited regeneration

5. Can hypertrophy (workout)

6. Can atrophy (due to casts)

Smooth muscle:

1. No striation

2. Involuntary

3. No sacromere or troponin

4. Slower contraction

5. In GI, blood vessels

   1. Ca2+ mediated via calmodulin (2nd messenger)

Myofibril striated muscle:

1. Functional unit

2. Thin filaments

   1. Thick filaments

Thin filaments:

Actin, tropomyosin, tropnin

Thick filaments:

Myosin

How does a muscle fundamental unit contract:

Tropomyosin and troponin need to attach which opens binding site for actin must be uncovered for myosin to bind to actin, Ca2+ and ATP needed

Sarcolemma:

Where Ca2+ comes from to go into cell for contractionT

T Tubles:

Volt change for Ca2+ to enter

5 Muscle Proteins:

1. Thin filament: actin

2. Tropomyosin: form complex with troponin block myosin binding site until Ca2+ present

3. Thick filament: myosin, ATP dependent

4. Titin: stabilize actin filament and elasticity

Smooth and Skeletal Muscle contraction steps:

1. Muscle excitation

2. Rise in cytosolic Ca2+

3. Series of biochemical events/Physical reposition of troponin/tropomyosin

4. Phosphyloration of myosin/uncover cross bridge binding site

5. Bind of actin and myosin - cross bridge

6. Contraction

Differences between Smooth/Skeletal contraction for Ca2+:

1. Series of biochemical events/Physical reposition of troponin/tropomyosin

2. Phosphyloration of myosin/uncover cross bridge binding site

Why does rigor mortis happen:

1. Cells dying, Ca2+ dump in muscle, use up ATP for contraction = rigor mortis

2. Ca2+ used up, cannot upbridge

Clincial muscle biomakers:

1. Troponin: Subtype T/I (skeletal = C, cardiac = T/I only in myocardium) specific for cardiac muscle

2. Myoglobin: Released when muscle is damaged

3. Creatine Kinase: Released when muscle is damaged (MM - skeletal, MB - cardiac, BB - brain)

Myocardium also known as:

Cardiac muscle

Intercalated discs are only present in:

cardiac muscle

Inner most layer of myocardium/blood vessels:

Endocardium

Middle layer of myocardium/blood vessels:

Myocaridum

Arteries/Veins layers:

1. Outer: adventita

2. Middle: media (smooth muscle)

3. Inner: intima (semipermeable membrane)

Vasa vasorum:

Blood supply in arteries

Arterioles:

Regulate blood flow

Capillaries:

Gas exchange

How many valves do veins have/purpose(s):

1 way valve, prevent blood flow back

Stroke volume:

Amount of blood pumped out of LV during systole

Resistance = constant x (1/radius)

Poiseuilles law

What happens to the resistance if the radius of a vessel is small

High resistance

What happens to the resistance if the radius of a vessel is large

Low resistance

Heart rate:

number of times the heart beats in 1 minute

Cardiac Output:

Stroke volume x Heart rate

Peripheral Vascular Resistance:

Resistance against peripheral vasculature that heart pumps against

Blood pressure:

Cardiac output x peripheral vascular resistance

Hydrostatic Pressure:

Increase volume in vessel = increase pressure

(this will force fluid out of interstitiual space)

Oncotic pressure:

Proteins based - draw water in cardiovascular system.

No protein = fluid leak out

Edema:

Fluid moved out of vascular space and go into interstitial space (tissues)

Due to high hydrostatic or low oncotic

Pulmonary edema:

Fluid leave vascular and enter alveoli

Symptoms: SOB, paroxysmal nocturnal dyspnea

Polar cell:

Positive outside, negative inside cell

Depolarization:

Positive current move into cardiac myocytes

During depolarization what chemicals move into cell:

Na+ and Ca2+ move IN

Repolarization:

Positive current move out, negative move in

During repolarization what chemicals move:

K+ move OUT, Cl- move IN

What do P waves represent in an EKG:

sinus rhythm

HR between 60-99:

normal sinus rhythm

HR below 60bpm:

bradycardia

HR above 99bpm:

tachycardia

Upper respiratory tract functions:

1. filter

2. humidity

3. heat

How many lobes does the Righ lung have:

3

How many lobes does the Left lung have:

2

Lower respiratory tract contains:

1. Larynx

2. Trachea

3. R/L mainstem bronchus

Lower respiratory tract also known as:

conducting system

What epithelial layer is the inner layer of alveoli:

pseudostratisfied ciliated

What is the functional unit of the lung:

alveolus

Type 1 pneumocytes:

gas exchange

Type 2 pneumocytes:

produce surfactant (coat alveoli and allow it to stay open)

Respiratory Distress Syndrome (RDS)

Insufficient surfactant as newborn

How much “room air” do we breathe of O2?

21% FiO2

Atomspheric pressure=

760mmHg

How much O2 is in total atmospheric pressure:

21%

Alveolar-arterial gradient:

A: alveolar oxygen

a: oxygen in blood stream

Alveolar-arterial oxygen gradient:

PAO2 = (Patm - Ph2o)FiO2 - PACO2/0.8

Ventilation:

Getting air in and CO2 out

Perfusion:

O2 picked up by pulmonary capillaries, CO2 out of blood to be exhaled

Ventilation/Q (Perfusion) should be equal or slightly different:

Equal

Anatomic Dead Space:

Respiratory tract not directly participating in gas exchange

Problems with ventilation/perfusion can lead to:

Lower O2 levels in PaO2 (hypoxemia), higher CO2 levels PaO2 (hypercapnia)

What is the oxygen-hemoglobin dissociation curve:

Differences between what effects cause increase/decrease affinity of hemoglobin holding oxygen

What does a pulse oximetry measure:

How much O2 is bound to hemoglobin

Hypoxia:

Reduced O2 delivery to tissues

Hypoexmia:

low O2 in blood

Ischemia:

reduced blood flow to tissue

Types of Hypoxia:

1. Hypoxic hypoxia

2. Anemic hypoxia

3. Stagnant hypoxia

4. Histotoxic hypoxia

Hypoxic hypoxia:

Less O2 to breath in

Anemic hypoxia:

Not enough RBC to transport O2

Stagnant hypoxia:

heart cannot pump RBC throughout body

Histotoxic hypoxia:

cell poisoning