Vitamin is required in the production of rhodopsin

Results in Night Blindness

The visual pigment used in low light levels.

Requires vitamin A for production.

1. emmetropia (normal refraction)
2. presbyopia
3. hyperopia = hypermetropia
4. myopia
5. astigmatism
6. cataract

Normal refraction

"Old eye"

Natural elasticity of the eye is reduced, ability to focus on near items reduces

Reading glasses

A convex lens:

to increase the power of the eye and focus near-objects on retina

"Farsightedness"

Caused by eyeball being to short

Light rays focus behind the retina

A convex lens:

to increase the power of the eye

"Nearsightedness"

Caused by the eyeball being too long

Light rays focus in front of the retina

A concave lens:

to decrease the power of the eye

Irregular curvature of the eye

Vertical lines can be focused, horizontal lines can not

loss of lens transparency... becomes opaque

requires lens removal corrective surgery

only two of the color rods

1. protanopes
2. deuteranopes
3. tritanopes

Dichromat:  Green and blue, insensitive to red

Confuse:  Red, yellows, greens

dichromat: can see blue and red

confuse:  reds, yellows, greens

Match all colors to red and green

Can not see blue

blood pressure falls when standing up causing a dizzy spell.

impaired baroreceptor reflex

often associated with shy-drager syndrome

hardening of the arteries

loss of elasticity in the arteries

caused by buildup of calcium

a chronic disease involving the deposition of plaques containing lipids and cholesterol in the coronary,carotid, and aorto-femoral vascular beds

causes Coronary Artery Disease (CAD)

1.  Primary (aka essential) Hypertension:

S₁ problem

A-V valves do not close properly

blood regurgitates into atrium during ventricular systol

S₂ problems

semilunar valves do not close properly

blood regurgitates into ventricles during ventricular diastole

narrowing of the aortic valve or aorta

increases afterload

similar to effect of an increase in total peripheral resistance

1. Sinus node (S-A node)
2. Atria
3. A-V nodal (junctional)
4. A-V block and bundle branch black
5. Ventricles

1. Sinus tachycardia
2. Sinus bradycardia

an elevation in heart rate observed at rest

caused by an increased rate of depolarization and repolarization of the sinus node

rhythm is normal, but rate is greater than 100 bpm

Slow heart rate

caused by a decreased rate of depolarization/repolarization of the sinus node

heart rate below 60 bpm

**may be normal for an athlete

atrial arrhythmia

caused by waves of depolarization circling around the bands of atrial muscle fibers

atria may beat 250-300 bpm

A-V Nodal Arrhythmias

Also, how is the ECG affected?

occurs when parts of the A-V node take over the pacemaker duties of the S-A node

rate of A-V node is lower than S-A node, so ventricles beat at rate of 40-60 bpm

P-wave is altered: lost into QRS complex or inverted

Intermittent block

Some QRS are dropped

For example:  every second atrial beat may fail to get through the ventricles, therefore the atrial rate will be twice the ventricular rate

Complete heart block

Atria and ventricles beat independently of each other (no relationship between P-waves and QRS)

conduction delay or block in the bundle branches (usually conduction delay)

one ventricle may depolarize somewhat later than the other = broadened QRS complex, maybe two R waves

splitting between S1 and S2 sounds

Generate wide and bizarre QRS complexes that do not have a preceding P-wave.

Caused by ectopic focus in one of the ventricles.

small region of the ventricular myocardium that decides to depolarize all on its own

caused by inflammatory disease, lack of blood, or drugs

An ectcopic focus generates a depolarizing stimulus during the T-Wave  that causes circular waves of depolarization that pass repeatedly around the ventricular walls

ventricles beat 250-350 contractions/min

pumping efficiency is very poor b/c ventricles do not have time to filly and empty properly

Ventricular Fibrillation

Lethal

electrical record rapid and achotic, myocardium contracts at random w/o coordination

heart no longer pumps blood

dead

1. Increased venous hydrostatic pressure
2. Reduced plasma osmotic pressure
3. Increased interstitial fluid osmotic pressure
4. Blocked lymphatics

Discuss causes of Edema:

Increased venous hydrostatic pressure

Causes

• standing for a long time
• failing heart

Discuss causes of Edema:

Reduced plasma osmotic pressure

Causes:

• malnutrition
• liver disease

Discuss causes of Edema:

Increased interstitial fluid osmotic pressure

Causes:

• buildup of proteins in the interstitial space

Discuss causes of Edema:

Blocked lymphatics

Causes:

• surgery
• tumor
• parasitic infection

parasitic inflammation of lymphatics

associated with Blocked lymphatics edema

Fluid accumulation in the lungs

Could be caused by failure of the left ventricle:

right ventricle continues to pump blood into the lungs but the left cannot pump it away at the same rate.  rise in pressure in pulmonary veins/capillaries

Can cause death

Hemorrhage

Reduction in blood volume

occurs when the heart demands more oxygen than the coronary circulation is able to supply.

Influenced by inadequate supply (blood clot, thromboembolism, athersclerosis, it) or excessive demand 

Heart Attack

interruption or reduction of coronary blood supply to the myocardium is so severe and long-lasting that function can no longer be sustained

the ischemic cardiac muscle cells that make up the affected myocardium become injured then die

1. Hemorrhage (loss of blood)
2. Severe burns (loss of plasma)
3. Vomiting (loss of fluid and electrolytes)
4. Diarrhea (loss of fluid and electrolytes)

Major myocardial infarction

infarction of more than 40% of the myocardium

--> Decreased cardiac output --> decreased coronary flow --> myocardial ischemia --> reduced pumping efficiency -->

the structure or function of the heart impairs its ability to supply sufficient blood flow to meet the body's needs

symptoms:  edema (especially in lungs)

thickening of the left myocardium of the left ventricle

increases the afterload that the heart has to contract against

caused by aortic stenosis, aortic insufficiency, or hypertension

Sympathetic

Parasympathetic

Enteric

• excites skeletal muscles
• Voluntary
• neurotransmitter: acetylcholine

1. cardiac muscle
2. smooth muscle
3. glands

"brain in the gut"

many neurons located in the gastrointestinal tract.

one of it's neurotransmitters is serotonin

ganglion

postganglionic 

"Fight or Flight"

1. Pupil dilation
2. Heart rate and force of contraction increase
3. Blood vessels in skin and viscera contract
4. Dilation of bronchioles: faster movement of air into lungs
5. Blood vessels in skeletal muscles dilate
6. Liver glycogen converted to glucose
7. Epinepherine and norepinephrine are secreted by adrenal medulla
8. "Non-essential" activities are inhibited (digestive)

"Rest and Digest"

1. Eye pupil constricted
2. Increased motility of stomach
3. Decreased rate of heart
4. Lungs constricted
5. Penis erection

ANS: Sympathetic Branch

Form synapses with: (3)

1. Paravertebral ganglia
2. Collateral ganglia
3. Adrenal Medulla

Sympathetic branch

form a chain on both sides of the vertebral column

Collateral ganglia

(3 type)

1. Superior mesenteric
2. Inferior mesenteric
3. Ciliac

Adrenal Medulla

(Sympathetic branch of ANS)

• Preganglionic fibers make synaptic contact with neurosecretory cells (in adrenal medulla)
• Cells secrete epinephrine (adrenalin) norepinephrine into the bloodstream and are carried to all tissues in the body

Fill out the Chart:

[image]

A.  Cholinergic

B.  Adrenergic

C.  Nicotinic receptors

D.  Alpha- or Beta- adrenergic receptors

A.  Cholinergic

B.  Cholinergic

C.  Nicotinic

D.  Muscarinic

• Color vision
• bright light
• high visual acuity

• dim light
• no color vision
• low visual acuity

Neurons:

• rods, cones 
• bipolar cells
• horizontal cells
• amacrine cells

1. regulating the passage of nutrients from the choroidal blood into the retina
2. metabolizing vitamin A
3. removing fragments of membranes that have been shed by photoreceptors 

sodium ions

depolarized

Increase in sodium permeability

Depolarization of the membrane

1. CN VIII and the spiral ganglion -->
2. cochlear nucleus in the medulla -->
3. medial geniculate nucleus in the thalamus -->
4. primary auditory area of the cerebral cortex

1. CN VIII -->
2. Vestibular ganglion -->
3. Vestibular nucleus in the medulla -->
4. outputs to the cerebellum
5. and vestibulospinal tract

1. Preload
2. Afterload
3. Heart Rate
4. Myocardial Contractility

A.  S1, Mitral Valve closing

B.  Aortic Semilunar Valve opens

C.  S2,  Aortic Semilunar Valve closes

D.  Mitral Valve opens

A.  12 mm Mercury

B.  65 mm Mercury

C.  125 mm Mercury

Much lower than left heart

Systolic right ventricular pressure:  30 mm Hg

Mean right atrial pressure:  7 mm Hg

1. norepinephrine and epinephrine acting via beta-adrenergic receptors in cardiac muscle cells in the ventricular myocardium
2. increased extracellular calcium
3. cardiotonic drugs such as digitalis, which increase intracellular calcium

Cardiac action potential = 250 msec

Nerve action potential = 2 msec

A cardiac muscle action potential has a very pronounced PLATEAU at PHASE 2

A nerve action potential does not

• Phase 0
• Phase 1
• Phase 2
• Phase 3
• Phase 4

• Phase 0:  opening of voltage-gated Sodium channels
• Phase 1:  closing of voltage-gated Sodium channels
• Phase 2:  opening of slow, voltage-gated calcium channels;  causes decrease in potassium permeability
• Phase 3:  closing of the slow calcium channels; increase of potassium permeability

increase the inward calcium current

enhances cardiac contractily

Epinephrine and Norepinephrine

released at sympathetic nerve terminals or from adrenal medulla during sympathetic activation

increase inward calcium current, enhances cardiac contractility

drugs that block the action of catecholamines on the heart

bind to and block β-adrenergic receptors

1. used to moderate the effect of acceleration and increased contractility on the heart
2. decreases the strain on the heart by diminishing frequency and severity of anginal attacks