Eye histology

Lacrimal Gland

Anterior portion of the lens. The subcapsular epithelium secretes the lens capsule, which appears stained in red. The lens capsule is a thick basement membrane containing collagen type IV and laminin. Below the subcapsular epithelium, note the lens fibers, which are cells that have lost their nuclei and organelles, becoming thin, elongated, transparent structures

LENS:

The subcapsular epithelium secretes the lens capsule, which appears stained in red. The lens capsule is a thick basement membrane containing collagen type IV and laminin. Below the subcapsular epithelium, note the lens fibers, which are cells that have lost their nuclei and organelles, becoming thin, elongated, transparent.

subcapsular epithelium is single layer of cuboidal epithelial cells that is present only on the anterior surface of the lens.

CLINICAL:

When the lens becomes opaque, the condition is termed cataract, which may also be caused by excessive exposure to ultraviolet radiation. In diabetes mellitus, the high levels of glucose are believed to produce cataract.

Cartilage histology

Cartilage is characterized by an extracellular matrix enriched with glycosaminoglycans and proteoglycans, macromolecules that interact with collagen and elastic fibers.

FUNCTION OF CARTILAGE:

1:firm consistency of the extracellular matrix allows the tissue to bear mechanical stresses without permanent distortion.

2:support soft tissues.

3:Because it is smooth surfaced and resilient, cartilage is a shock-absorbing and sliding area for joints and facilitates bone movements.

4:Cartilage is also essential for the development and growth of long bones both before and after birth

As a consequence of various functional requirements, THREE forms of cartilage have evolved, depending on variations in matrix composition.

• HYALINE CARTILAGE
• ELASTIC CARTILAGE
• FIBROCARTILAGE

In all three forms, cartilage is AVASCULAR and is nourished by the diffusion of nutrients from capillaries in adjacent connective tissue (perichondrium) or by synovial fluid from joint cavities. In some instances, blood vessels traverse cartilage to nourish other tissues, but these vessels do not supply nutrients to the cartilage. As might be expected of cells in an avascular tissue, chondrocytes exhibit low metabolic activity. Cartilage has no lymphatic vessels or nerves.

HYALINE CARTILAGE

• Hyaline cartilage is the most common and best studied of the three forms. Fresh hyaline cartilage is BLUISH-WHITE and TRANSLUCENT. In the embryo, it serves as a temporary skeleton until it is gradually replaced by bone.
• In adult , hyaline cartilage is located in the
• articular surfaces of the movable joints,
• in the walls of larger respiratory passages (nose, larynx, trachea, bronchi),
• in the ventral ends of ribs, where they articulate with the sternum,
• and in the epiphyseal plate, where it is responsible for the longitudinal growth of bone .
• Hyaline cartilage contains primarily TYPE II COLLAGEN .

ELASTIC CARTILAGE

Elastic cartilage is found in the auricle of the ear, the walls of the external auditory canals, the auditory (eustachian) tubes, the epiglottis, and the cuneiform cartilage in the larynx.

Elastic cartilage is essentially identical to hyaline cartilage except that it contains an abundant network of fine elastic fibers in addition to collagen type II fibrils. Fresh elastic cartilage has a yellowish color owing to the presence of elastin in the elastic fibers. .

FIBROCARTILAGE

• Fibrocartilage is a tissue intermediate between dense connective tissue and hyaline cartilage. It is found in intervertebral disks, in attachments of certain ligaments to the cartilaginous surface of bones, and in the symphysis pubis. Fibrocartilage is always associated with dense connective tissue.
• it is rich in Collagen type I.

As we know connective tissue contain

1: Cells

2:Ground substance

3:Fibers

In Cartilage also the arrangement is same .

Photomicrograph of HYALINE CARTILAGE. Chondrocytes are located in matrix lacunae, and most belong to isogenous groups. The upper and lower parts of the figure show the perichondrium stained pink. Note the gradual differentiation of cells from the perichondrium into chondrocytes.

Photo-micrograph of elastic cartilage, stained for elastic fibers. Cells are not stained.

Photomicrograph of FIBROCARTILAGE. Note the rows of chondrocytes separated by collagen fibers. Fibrocartilage is frequently found in the insertion of tendons on the epiphyseal hyaline cartilage.

PERICHONDRIUM

Except in the articular cartilage of joints, all hyaline cartilage is covered by a layer of dense connective tissue, the perichondrium, which is essential for the growth and maintenance of cartilage. It is rich in COLLAGEN TYPE I fibers and contains numerous FIBROBLASTS. Although cells in the INNER LAYER of the perichondrium resemble fibroblasts, they are CHONDROBLASTS and easily differentiate into chondrocytes.

REGULATION OF RESPIRATION

PONTO MEDULLARY RESPIRATORY CENTERS

ALL ARE PAIRED & INTERCONNECTED

RESPIRATORY CENTERS:-

PNEUMOTAXIC CENTER:

• Location: Upper Pons
• Absence causes APNEUSTIC BREATHING (Esp when the vagi are cut)
• Curtails inspiratory activity & thus can increase the rate of respiration

APNEUSTIC CENTER:

• Location: Lower Pons
• Stimulates the Inspiratory Center and increases Inspiration
• Gets feed back from Vagi & other Centers.

RESPIRATORY CONTROL ORGANIZATION:MODERN CONCEPT

• All the respiratory centers are termed as the BULBOPONTINE RESPIRATORY NEURONAL COMPLEX
• There is an inspiratory ramp generator called Respiratory Control Pattern Generator: Pre Bottzinger Complex
• The Inspiratory Off switch(IOS) is fine tuned by PTC & the chemoreceptor drive.
• Both Neural & Chemical controls are well coordinated.

PERIPHERAL INFLUENCES ON RESPIRATORY CONTROL

LUNG OR PULMONARY RECEPTORS:

• Receptors in and around the lungs.

CHEMORECEPTORS

• Peripheral Chemoreceptors
• Central Chemoreceptors.

PERIPHERAL INFLUENCES

• The four influences from the lungs are:
• Pulmonary stretch receptors
• Lung irritant receptors
• J receptors
• Proprioceptors
• Along with the chemoreceptors, these receptors send information to the respiratory centers.

HERING BREUER(HB) REFLEX

• It is a ‘Volume’ reflex.
• Receptors are located in between the smooth muscles of the small airways.
• These receptors are unmyelinated nerve endings.
• They are stimulated by the change of shape of the Airways.

• Excessive deflation of the lungs causes Inspiration.
• This reflex prevents Atelectasis.
• Atelectasis is the collapse of the lungs.
• This reflex also opens up collapsed portions of the lung.

CHEMICAL CONTROL:THE THREE MAIN ‘CHEMICALS’

OXYGEN

PO2 levels in blood.

CARBON DIOXIDE:

PCO2 levels in blood.

HYDROGEN ION:

Concentration in blood.

CO2 & [H+] act centrally while the Oxygen levels act on the peripheral chemoreceptors.

RESPIRATORY CHEMORECEPTORS

• CENTRAL:
• CHEMORECEPTOR ZONE:
• BILATERAL
• LOCATED IN THE MEDULLA
• JUST BENEATH IT’S VENTRAL SURFACE
• HIGHLY SENSITIVE TO PCO2 AND [H+]
• FUNCTIONS BY STIMULATING THE RESPIRATORY CENTERS:
• DRG,VRG & PTC.

CENTRAL CHEMORECEPTORS

• PRIMARY STIMULUS:
• [H+]
• PERHAPS THE ONLY IMPORTANT DIRECT STIMULUS FOR THE CENTRAL CHEMORECEPTOR CELLS (MEDULLARY CHEMORECEPTORS)
• But these ions do not cross the Blood Brain Barrier
• So, the blood PCO2 level has more effect as CO2 readily crosses the BBB.

STIMULATION BY CARBONDIOXIDE

• Is not direct.
• Even the indirect effect of CO2 is most potent. Why?
• Because CO2 easily crosses the BBB.
• Once it is across the BBB,
• CO2 + H2O -- H2CO3 -- H+ + HCO3-
• These increased H+ ions in the brain stimulate the medullary chemoreceptors.

QUANTITATIVE EFFECT OF H+ IONS

• The stimulatory effect of H+ ions increases in the first few hours.
• It then decreases in the next 1 to 2 days.
• It comes down to about 1/5th the initial effect.
• This is due to Renal readjustment of [H+] in the circulating blood.
• The kidneys increase blood HCO3.
• This bicarbonate binds with the free H+ ions in the blood & decreases their concentration.
• Bicarbonate also diffuses slowly past the BBB and decreases the H+ ions in the brain.
• Therefore the effect of H+ ions is:
• POTENT: Acutely
• WEAK : Chronically.

EFFECT OF CO2

• Change in PCO2 between 35 to 75mmHg causes peak increase in alveolar ventilation.
• 
  
• Change in the normal range causes less than tenth of change in alveolar ventilation.

EFFECT OF OXYGEN

• The partial pressure of Oxygen has no effect on the medullary chemoreceptors.
• 
  
• It only has an effect on the peripheral chemoreceptors.

PERIPHERAL CHEMORECEPTORS

• There are two pairs of chemoreceptors:
• Aortic Bodies: located at the arch of aorta.
• Carotid bodies: located at the branching of the common carotid arteries.
• Their functions are:
• To detect changes in the PO2
• To transmit nervous signals to the Respiratory Centers.
• These bodies have two types of special cells called glomus cells.
• The type 2 glomus cells have special ion channels sensitive to PO2.
• They fire the nerve endings and send signals via:
• Aortic bodies: Vagi.
• Carotid bodies: Hering nerve & Glossopharyngeal nerve.
• Both these bodies receive their own special blood supply through minute arteries, directly from the trunk.
• Their blood flow is roughly 20 times their own weight.
• THEY ARE ALL THE TIME EXPOSED ONLY TO ARTERIAL BLOOD.
• Decreased PO2 stimulates these chemoreceptors strongly.

ARTERIAL PO2 & IMPULSES IN AORTIC BODY

Decreased PO2 especially between 60 and 30mm Hg strongly stimulates the carotid bodies.

This is the range wherein the Hb saturation decreases

EFFECT OF PO2

• When PCO2 & [H+] are kept constantly normal,
• There is no effect if the PO2 is >100mmHg
• If it falls below 100mmHg, ventilation doubles upto 60 mmHg.
• It increases upto 5 times at very low PO2 levels

CO2 & H+

• They also stimulate the peripheral chemoreceptors.
• But their effects on the central or medullary chemoreceptors are more powerful.
• PCO2 stimulates the peripheral chemoreceptors 5 times as rapidly as it stimulates the central ones.
• So this is responsible for the rapid response to CO2 at the onset of exercise.

What is the difference between NSTEMI and STEMI?

Acute coronary syndromes (ACS) are divided into:

1. STEMI - ST Elevation MI - the classical MI

2. NSTEMI - Non-ST Elevation MI.

3. UA - Unstable Angina

STEMI is when there is a transmural infarction of the myocardium - which just means that the entire thickness of the myocardium has undergone necrosis - resulting in ST elevation. Usually due to a complete block of a coronary artery (occlusive thrombus). This requires the use of thrombolytics like Streptokinase to lyse the thrombus. Evidence has proven that it is very effective and not as risky (Benefits > Risk)

UA or NSTEMI is when there is a partial dynamic block to coronary arteries (non-occlusive thrombus). There will be no ST elevation or Q waves on ECG, as transmural infarction is not seen. The main difference between NSTEMI and unstable angina is that in NSTEMI the severity of ischemia is sufficient to cause cardiac enzyme elevation.

Why is streptokinase not used in treating UA/ NSTEMI?

In patients with UA/NSTEMI, plaque stabilization to prevent progression of the disease is required. While fibrinolytics like Streptokinase benefit patients with STEMI, they may increase risk of bleeding complications for those with NSTEMI. This is also based on evidence - no benefit, more risk.

Summary:

1. STEMI - occlusive thrombus - ST elevation (and Q waves) - Cardiac Enzyme elevation - Fibrinolytics beneficial

2. NSTEMI - non-occlusive thrombus - NO ST/Q - Cardiac Enzyme elevation present - Fibrinolytics not beneficial

3. UA - non-occlusive thrombus - NO ST/Q - Cardiac Enzyme elevation absent - Fibrinolytics not beneficial

DYSPNEA & ABNORMAL TYPES OF RESPIRATION

RESPIRATORY INSUFFICIENCY

Narcosis, other pharmacologic influences,

hypoxia, and pathologic processes ->

reduce excitability of respiratory neurons

-> respiratory failure

• Narcotic drugs & respiratory depression:

Leads to reduced PaO2 & increased PaCO2.

Carries best prognosis & amenable to Rx.

Narcotic drugs also diminish metabolism.

Complications of narcotic poisoning-

1.Asphyxia

2.Microbial infections

3.Circulatory depression

4.Renal functional derangements

5.Hypo or hyperthermia

6.Consequences of therapeutic measures

• Asphyxia- depression of PaO2 and elevation of PaCO2; assisted ventilation.
• Circulatory depression- due to central vasomotor depression, hypoxemia, and direct narcotic effects on blood vessels; blood supply of brain is maintained due to hypercapnia induced cerebral vasodilatation; support of circulation.
• Hypothermia- due to reduced metabolism & deranged heat regulating mechanisms; hyperthermia in case of infections
• Renal impairment- due to hypotension
• Respiratory insufficiency due to pulmonary pathologies:

(i) Pulmonary Emphysema

(ii) Pneumonia

(iii) Atelectasis

(iv) Asthma

(v) Tuberculosis

Pulmonary Emphysema

• Excessive air in lungs
• Causes- chronic infections, chronic smoking.
• Physiologic abnormalities-

1.Increased airway resistance

2.Destruction of alveolar walls - reduced diffusing capacity - increased PaCO2 & reduced PaO2

3.Reduced alveolar capillaries - pulmonary hypertension - right heart failure

Pneumonia

• Inflammatory condition of respiratory membrane
• Alveoli are filled with fluid and blood cells
• Most common- bacterial- pnemococcal
• Reduction in total available area for gas exchange
• Decreased VA/Q
• Hypoxemia and hypercapnia

Atelectasis

• Collapse of alveoli / lobe / lung
• Causes- (i) Airway obstruction and (ii) lack of surfactant
• Hyaline Membrane Disease is fatal

Asthma

• Airway hyper-responsiveness
• Allergic hypersensitivity- pollen
• Older people- pollution
• Histamine, SRS-A, ecf, bradykinin are released from mast cells
• Localized edema in walls of airways and spasm of bronchiolar smooth muscles
• Reduced PEFR and FEV1
• Increase in FRC and RV

Tuberculosis

• Mycobacterium tuberculosis
• Tubercle- due to walling off of infection
• Cavitation- in untreated cases
• Fibrosis- in late stages

1.Reduced VC

2.Reduced surface area and increased thickness of respiratory membrane

3.Abnormal VA/Q

Apnea

• Cessation of breathing (generally temporary)

1.Reduction in stimulus to respiratory centre

2.Active inhibition of respiratory neurons- prolongation of Hering-Breuer reflex

3.Decreased ability of respiratory neurons to react to stimuli- narcotics

Dyspnea

• Labored, distressful breathing with conscious effort
• Factors leading to dyspnea -

1.Abnormality of respiratory gases in body fluids

2.Amount work to be performed by respiratory muscles

3.State of mind

Disorders of rhythm

• Cheyne-Stokes respiration:
• Periodic breathing
• Seen in congestive heart failure, uremia, brain disease and sleep.
• Prolongation of circulation time
• Increased sensitivity to CO2