Makpats

Cardiovascular System | Cardiology - Makpats

2020-09-21T12:09:00.014+05:30

Cardiovascular System

The cardiovascular system is often referred to as the vascular or circulatory systems. One of the most crucial organs necessary for maintaining life is the human heart. It resembles a clenched first in size and is essentially a muscle. Throughout a person's lifetime, the human heart beats and pumps nearly 200 million litres of blood. Over the course of a person's lifetime, the heart beats around 2.5 billion times, making it one of the strongest and busiest muscles in the body.

Position of heart in human body

The human heart is situated behind and slightly to the left of the sternum, between the lungs (breastbone).
The left side of the chest contains two-thirds of the heart, with the right side holding the remaining third in balance.

Structure of the human heart

The human heart is about the size of a human first and is divided into four chambers, namely two ventricles and two atria.
The ventricles are the chambers that pump blood and atrium are the chambers that receive blood.
Among which both right atrium and ventricle mark up the “right heart” and the left atrium and ventricle mark up the “left heart”.
The structure of the heart also houses the biggest artery in the body the aorta.
The right and the left region of the heart are separated by a wall of muscle called the septum.
The right ventricle pumps the blood to the lungs for re-oxygenation through the pulmonary arteries.
The right semilunar valves close and prevent the blood from flowing back into the heart.
Then, the oxygenated blood is received by the left atrium from the lungs via the pulmonary veins.

External structure of the heart

Pericardium

The human heart is situated to the left of the chest and is enclosed within a fluid-filled cavity known as the pericardial cavity.
The walls and lining of the pericardial cavity are made up of a membrane known as the pericardium.
The pericardium is a fibrous membrane found as an external covering around the heart.'
It protects the heart by producing a serous fluid, which serves to lubricate the heart and prevent friction between the surrounding organs.
Apart from the lubrication, the pericardium also helps by holding the heart in its position and by maintaining a hollow space for the heart to expand itself when it is full.

The pericardium has two exclusive layers.

Visceral Layer: It directly covers the outside of the heart.
Parietal Layer: It forms a sac around the outer region of the heart that contains the fluid in the pericardial cavity.

Internal Structure of the heart

Internal Structure of the heart contains chamber and values that control the flow of blood.

Chamber of the heart

there are 4 (four) chamber of heart

1. Left atrium

2. Right atrium

3. Left ventricle

4. Right ventricle

Atria: atria are thin less muscular walk and smaller than ventricle these are the blood-receiving chamber that are fed by the large veins.
Ventricles: ventricles are larger and more muscular chambers responsible for pimping and pushing blood out to the circulation. These are connected to larger arteries that deliver blood for circulation.

The right ventricle and right atrium are comparatively smaller than the left chamber.

The walls consist of fewer muscle compared to the left portion and the size difference is based on their function.

The blood origination from the right ride flows through the pulmonary circulation, while blood arising from the left chamber is pumped throughout the body

Valves

Valves are flops of fibrous tissues located in the cardiac chamber blur the veins
They ensure that the blood from flows in a single direction.
Flaps also prevent the blood from flowing backward
Based on their function, values are of types.

Atrioventricular valves: atrioventricular valves are between ventricles and atria the value between the right ventricle and right atrium is the tricuspid value, and the one which is found between the left ventricle and left atrium is known as the mitral value.

Semilunar valves: semilunar valves are located between the left ventricle and aorta. It is also found between the pulmonary artery and right ventricle.

Blood Vessels

The blood vessels typically comprise of the following:

Veins: veins supply deoxygenated blood to the heart via inferior and superior vena cava, and it eventually drains into the right atrium.
Capillaries: capillaries are tiny, tube-like vessels, which form a network between the arteries to veins.
Arteries: arteries are muscular – walled tubes mainly involved in supplying oxygenated blood away from the heart in all other parts of the body. Aorta is the largest of the arteries, and it branches off into various smaller arteries throughout the body.

Structure of the heart wall

The heart wall is made up of 3 layers, namely

1. Epicardium: epicardium is the outermost layer of the heart.

It is composed of a thin-layers the outer section.

2. Myocardium: this is a layer of muscle tissue, and it constitutes the middle layer wall of the hear.

It contributes to the thickness and responsible for the pumping action.

3. Endocardium: It is the innermost layer that lines the inner Peart chambers and covers the heart values.

Furthermore, it prevents the blood from sticking to the inner walls, thereby preventing potentially total blood clots.

Hyper of circulation

1. Pulmonary circulation: pulmonary circulation is a portion of circulation responsible for carrying deoxygenated blood away from the heart, to the lungs and them brings oxygenated blood back to the heart.

2. Systemic circulation: systemic circulation is another portion of circulation where the oxygenated blood is pumped from the heart to every organ and tissue in the body, them back again to the heart.

3. Coronary circulation: coronary circulation is an essential portion of the circulation, where oxygenated blood is supplied to the heart. This is important, as the heart is responsible for supplying Blood throughout the body. The circulation system plays a vital role in supplying oxygen, nutrients and removing carbon dioxide and other waster from the body.

The function of heart

The function of the heart in any organism is to maintain a constant flow of blood throughout the body.
This replenishes oxygen and circulation nutrients among the cells and tissues.

✔ Following are the main functions of the heart:

One of the primary function of human heart is to pump blood throughout the body.
Blood delivers oxygen, hormones, glucose and other components to various heart.
The heart also ensures that adequate blood pressure is maintained in the body

The Aorta

the aorta is the largest artery of the body which carries the oxygenated blood from the left ventricle and supplies it to all the parts of the body.

The aorta initially is one inch wide in diameter.
The aorta is classifies as a large elastic artery.

It can be divided into 4 section:

1. The ascending aorta

2. The aortic arch

3. The thoracic (descending) aorta.

4. The abdominal aorta.

The first 3 parts are confined to the thoracic cavity and together create the thoracic aorta.

Common Carotid Artery: The common carotid artery is a paired structure that supplies blood to the head and neck.
Subclavian Artery: Paired major arteries of the upper thorax, below clavicle. The receive blood from the aortic arch.
Axillary Artery: Large blood vessel that conveys oxygenated blood to the lateral aspect of the thorax, the axilla (armpit) and the upper limb.
Brachial Artery: Major blood vessel of the (upper) arm.
Superficial Palmar Arch: The superficial and deep palmar arches (serve as a network of arteries inside the palm).
Femoral Artery: Large artery in the thigh and the main arterial supply to the thigh and leg.
Internal iliac Artery: Runs downward along the lateral wall of the pelvis.
Inferior Vena cava (IVC): Large vein that carries the deoxygenated blood from the lower and middle body into the right atrium of the heart. Its walls are rigid and it has valves so the blood does not flow down via gravity.
Hepatic Portal Vein: Blood vessel that carries blood from the gastrointestinal tract, gallbladder, pancreas and spleen to the liver. This blood contains nutrients and toxins extracted from digested contents.
Portosystemic Anastomoses: The importance is to provide alternative routes of circulation when there is a blockage in the liver or portal vein. These routes ensure that venous blood from gastrointestinal tract still reaches the heart through inferior vena cava (IVC) without going through the liver.
Great Saphenous Vein (GSV)/ Long Saphenous Vein: A large, subcutaneous, superficial vein of the leg. It is the longest vein in the body, running along the length of the lower limb, returning blood form foot, leg and thigh to the deep femoral vein at the femoral triangle.
Dural Venous Sinuses: The spaces between the endosteal and meningeal layers of the dura. They contain venous blood that originates for the most part from the brain or cranial cavity.

Peripheral Pulse

It refers to the palpation of the high-pressure wave of blood moving away from the heart through vessels in the extremities following systolic ejection.

Palpation occurs at various locations of the upper and lower extremities including the radial, brachial, femoral, popliteal, posterior tibial and dorsalis pedis arteries.

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What is Cartilage? Anatomy - Makpats

2020-08-10T09:17:00.016+05:30

What is Cartilage?

Cartilage is a precursor to bone. Cartilage is a connective tissue composed of cells (chondrocytes) and fibres embedded in a firm, gel like matrix which is rich in a mucopolysaccharide. It is much more elastic than bone.

General Features of Cartilage

1. It has no blood vessels or lymphatics. The nutrition of cells diffuses through the matrix.

2. It has no nerves. It is therefore, insensitive.

3. Cartilage is surrounded by a fibrous membrane, called Perichondrium.

4. When cartilage calcifies, the chondrocytes die and the cartilage is replaced by bone like tissue.

Comparison Between Bone and Cartilage

BONE	CARTILAGE
It is hard	It is firm (soft)
Matrix has inflexible material called ossein	Matrix has flexible material called Chondroitin
Calcium salt are present in bone	Calcium salts are not present
It has rich nerve supply. it is vascular in nature	It doesn't have nerve supply. it is Avascular in nature.
Bone marrow is present	Bone marrow is absent
Growth is only by surface deposition	Growth is both by surface or within surface deposition

Types of Cartilage

Three Types of Cartilage:

1. Hyaline Cartilage

2. Fibro Cartilage

3. Elastic Cartilage

1. Hyaline Cartilage: This type of cartilage has very thin fibers having same refractive index as the matrix of the cartilage and thus these fibers are not seen.

- Hyaline cartilage is the articular cartilage of the long bones, sternum, ribs etc.

- Its colour is bluish white and it is flexible.

2. Fibro Cartilage: This type of cartilage has numerous white fibers.

- It is present in the symphysis pubis, and sternoclavicular joint etc.

- Its colour is glistening white and the appearance is opaque.

- In the intervertebral disks, and in articular meniscs.

3. Elastic Cartilage: This type of cartilage has numerous yellow elastic fibers.

- It is present in the ear pinna, external auditory meatus, Eustachian tubes, and epiglottis etc.

- Its colour is yellowish and the appearance is opaque.

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What is Anatomy and Physiology? Makpats

2020-06-29T19:22:00.015+05:30

Introduction to the study of anatomy and physiology

Definition: Anatomy is the science which deal with the structure of the human body.

Sub division of Anatomy:

1. Cadaveric Anatomy: It is studies on dead embalmed bodies usually with the naked eye. These can be done by two approaches.

a) Regional Anatomy: The bodies study in parts like the apperlimb, lower limb, thorax, abdomen, head and neck and brain.

b) Systemic Anatomy: The bodies study in systems like the skeleton(Osteology), muscular system(Myology), vascular system(Angiology), Nervous system(Neurology), and Respiratory system, Digestive system, Urogenital system and Endocrine system.

2. Riving Anatomy: It is study by inspection, palpation, endoscopy, radiography, electromyography etc.histology

3. Embryology: the study of the origin and development of organism It is the study of the prenatal development changes in an individual.

4. Histology: It is the study of structures with the use of microscope.

5. Surface Anatomy: Also called Superficial anatomy and Visual anatomy. it is the study of the external features of the body of an animal.

6. Radiographic and Imaging Anatomy: It is the study of the bones and deeper organs by radiography, by ultrasound and computerised tomographic scans (CT Scans).

7. Comparative Anatomy: It is the study of anatomy of the other animals to explain the changes in form, structure and function of different part of body.

8. Physical Anatomy: It deals with the external features and measurement of different races and groups of peoples and with the study of the prehistoric remains. It comprises a head, neck, trunk (which includes the thorax and abdomen), arms and hands, legs and feet.

9. Applied Anatomy: It deals with the application of the anatomical knowledge to the medical and surgical practice.

10. Experimental Anatomy: It is the study of the factors which influence and determine the forms, structure and function of different parts of body.

11. Genetics Anatomy: It deals with the study of information present in the chromosomes.

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What Is A Cell? Structure, Type, Function - Makpats

2020-06-27T20:11:00.008+05:30

What is a cell?

Robert Hook(1665), an English scientist, He described the cork as composed of small spaces surrounded by firm wall and gave the name cells. after that In 1831 Robert Brown discovered the nucleus in the cell. therefore it is concluded that cell is a structural and functional unit of all living organism.

Cell and Its Organelle

Cells are the basic unit of life

1. All organisms are made up of one or more cells and the products of those cells.

2. All cells carry out life activities (require energy growth, have a limited size.)

3. New cells arise only from other living cells by the process of cell division.

Despite their difference, they often share certain structures, these are referred to as organelles.

CELL STRUCTURE

Three main components of any plant/ animal cells.

1. Plasma Membrane / Cell Membrane:

Structure: A lipid membrane layer composed of proteins and carbohydrates. It is fluid like.

Functions: The cell membrane separates the cell from its external environment. It protects the cell and provides stability.

In order to transport materials, proteins are found embedded within the plasma membrane.

Carbohydrates are attached to proteins and lipids on the outer lipid layer.

2. Cytoplasm:

Structure: The jelly like structure composed of mainly water and found between the cell membrane and nucleus. The cytoplasm makes up most of the body of a cell and is constantly streaming (flowing)

Function: Organelles are found here and substances like salts may be dissolved in the cytoplasm.

3. Nucleus:

Structure: The largest organelle in the cell. It is dark and round, and is surrounded by a double membrane called the nuclear envelope / membrane. The nucleus contains genetic information (DNA) on special strands called chromosomes.

Functions: The nucleus is the “control centre” of the cell for cell metabolism and reproduction.

Organelles are found in both plant and animal cells

1. Endoplasmic Reticulum (ER): ER is made of Cisternae. The ER is a network of membranous canals filled with fluid. They Carly materials throughout the cell. The ER is the “Transport System” of the cell.

There are two types of ER.

a. Rough ER: It is lined with ribosomes and is rough in appearance.

b. Smooth ER: It is contains no ribosomes and is smooth in appearance.

2. Ribosomes: Ribosomes are small particles which are found individually in the cytoplasm and also line the membranes of the rough ER. Ribosome produce protein. They could be thought of as “factories” in the cell.

3. Golgi Body / Apparatus: Golgi bodies are stacks of flattened membranous stacks. It temporarily stores protein which can them leave the cell via vesicles pinching off from the Golgi.

4. Lysosomes: Lysosomes are small sac-like structure surrounded by a single membrane and containing strong digestive enzymes which when released can break down worn out organelles or food. The lysosome is also known as a suicide sac.

5. Mitochondria: The mitochondria are round “tube-like” organelles that are surrounded by a double membrane with inner membrane being highly folded.

The mitochondria are often referred to as the “powerhouse” of the cell.
These mitochondria release food energy from food molecules to be used by the cell
This process is called respiration.
Some cell (muscle cells) require more energy than other cells and so would have many more mitochondria.

6. Vacuoles: They are fluid filled organelles enclosed by a membrane. They can store material such as food, water, sugar, minerals and waste products.

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Human Body System - Human Anatomy | Makpats

2020-06-27T19:47:00.008+05:30

Systems of body

1. Integumentary System: It includes skin and structure such as nails, hairs, sweat and sebaceous gland.

2. Skeletal System: It includes all 206 bones of body, they are associated cartilage and the joints of body.

3. Muscular System: It specifically refers to the skeletal muscles tissue and tendons. They participate in bringing about movement maintaining posture and produces heat. read more...

4. Circulatory System: It includes the heart, blood and blood vessels. It transport oxygen and nutrients to tissues and removes waste nutrients. Read more...

5. Lymphatic System: It includes lymph, lymph vessels and organs like spleen and lymph nodes containing lymphatic tissue. It cleans and return tissue fluid to the blood.

6. Nervous System: It includes brain, nervous and sense organ. It controls internal functions of body and responds to stimuli.

7. Endocrine System: It includes all hormones producing glands and cells such as pituitary gland, thyroid gland and pancreas. read more...

8. Respiratory System: It includes the lungs and a series of associated organs such as pharynx, larynx (voice box), trachea and bronchial tubes(bronchi).

9. Digestive System: It is a long tubular structure called as gastro intestinal tract. It includes mouth, salivary gland, oesophagus, stomach, small intestine and large intestine. Organs associated with digestive system are gall bladder, liver and pancreas.

10. Urinary System/ Excretory System: It includes the kidneys, urinary bladder and urethra that together produce, store and remove urine.

11. Immune System: It consist of several organs as well as WBC’s in the blood and lymph. It includes lymph nodes, blood vessels, bone marrow and WBC’s.

12. Reproduction System: It includes testis, epididymis, urethra, vas deference, seminal vesical, prostrate and pennies in males. In females it includes ovaries, fallopian tubes, uterus and vagina.

What Are Glands? The Anatomy and Function - Makpats

2020-06-25T19:40:00.011+05:30

GLANDS

· Definition: Epithelia are a group of tissues derived from all 3 embryonic germ layers, which are involved in absorption, secretion, selective diffusion and physical protection.

Epithelia primarily involved in secretion are arranged into structures known as glands.

Types of glands:

1. Exocrine

2. Endocrine

1. Exocrine Gland:

It release their secretions onto an epithelia surface via a duct. It consists of 2 main parts.

(i) Secretory unit (ii) A duct

- On the bases of shape, types of secretory unit of gland, types of exocrine glands are:

a. Tube shaped is referred as tubular.

b. Spherical shaped is referred as alveolar or acinar.

c. Both tubular and alveolar tubuloalveolor.

- On the basis of branched or unbranched duct, types of exocrine glands are:

a. An unbranched duct is known as simple. (Ex: Sweat gland)

b. Branched duct is known as compound. (Ex: Pancreas)

Classification by Function: On the basis of their function exocrine glands are of 3 types

1. Serous Glands: Produce Serous fluid, a watery substance containing enzymes.

2. Mucous Glands: Involved in the production of mucus, a viscid (sticky) glycoprotein.

3. Mixed Glands: Comprised of both the above glands, secrete a mixed substance containing both serous fluid and mucus.

2. Endocrine Glands:

1. Endocrine glands release their secretory products directly into the bloodstream, rather than via a duct.

2. These glands are surrounded by a strong connective tissue capsule, which has fibrous extensions known as trabeculae.

These trabeculae provide internal support and give the gland a lobular appearance. Endocrine glands release secretions known as hormones, which travel via the bloodstream to reach their target cells, where they elicit functional changes.

The glands that make up the human of Endocrine system include:

1. Hypothalamus

2. Pitutary gland

3. Thyroid

4. Parathyroid

5. Adrenal gland

6. Pineal gland

7. Reproductive gland (which include Overies and testes)

8. Pancrease

1. Hypothalamus is the part of the human brain. located superior and anterior to the brain stem and inferior to the thalamus. the hypothalamus contains special cells called Neurosecretory cells (neuron that secrete hormone).

Thyrotropin-releasing hormone (TRH)
Groeth hormone-releasing hormone (GHRH)
Growth hormone inhibiting hormone (GHIH)
Gonadotropin-releasing hormone (GnRH)
Corticotropin-releasing hormone (CRH)
Oxytocin
Anti-diuretic hormone (ADH)

2. Pitutary gland also known is hypophysis, is a small pea-size lump of tissue connected to the inferior portion of the brain. many blood vessels surrounded the PG to carry the hormone. Situated in a small depression in the sphenoid bone called Sella turcica.

The PG is made of 2 structure: The posterior PG and Anterior PG

Posterior Pitutary secrete 2 hormone.

Oxytocin triggers uterine contractions during childbirth and the release of milk during breastfeeding.
Anti-Diuretic hormone(ADH) prevent water loss in the body by increasing the re-uptake of water in the kidneys and reducing blood flow to sweat glands.

Anterior Pitutary secrete 6 hormone.

Thyroid stimulating hormone(TSH), that stimulate the thyroid gland that produce the thyroxine(T4) and then triiodothyronin(T3) which stimulate metabolism of almostr every tissue in the body.
Follicle stimulating hormone(FSH), stimulates the follicle cells of the gonands to produce gametes-Ova in female and sperm in male.
Adrenocorticotropic hormone(ACTH), stimulate the adrenal cortex, the outer paert of the adrenal gland, to produce its hormone.
Luteinizing hormone(LH), stimulate the gonads to produce the sex hormones- estrogens in females and testosterone in males.
Human growth hormone(HGH), affects many target cells throughout the body by stimulating their growth, repair and reproduction.

Anatomy of a Joints | Anatomy - Makpats

2020-06-25T18:58:00.007+05:30

JOINTS

Joint is a junction between two or more bones or cartilage.

It is a device to permit movements.

Classification of Joints:

1. Structural classification

a. Fibrous joints

i. Sutures

ii. Syndesmosis

iii. Gomphosis

b. Cartilaginous joints

i. Primary cartilaginous joints

ii. Secondary cartilaginous joints

c. Synovial joints

i. Ball and socket

ii. Saddle

iii. Condylar

iv. Ellipsoid

v. Hinge

vi. Pivot

vii. Plane

2. Functional classification

a. Synarthroses (immovable)

b. Amphiarthroses (slightly movable)

c. Diarthroses (freely movable)

3. Regional classification

a. Skull type (immovable)

b. Vertebral type (slightly movable)

c. Limb type (freely movable)

4. According to No. of Articulating Bones

a. Simple joint: When only 2 bones are joint.

b. Compound joint: When more than 2 bones are joint.

c. Complex joint: When joint cavity is divided by an intra articular disc.

Synovial Joints

Synovial joints are most evolved and so most mobile type of joints.

Classification of synovial joint and their movement

1. Plane or Gliding type: Gliding movement (wrist and ankle)

2. Uniaxial joints:

a. Hinge joint: flexion and extension (ankle, elbow)

b. Pivot joint: Rotation only (head and neck)

3. Biaxial joints:

a. Condylar joint: flexion, extension, adjunct rotation/ wrist.

b. Ellipsoid joint: flexion, extension, abduction, adduction and circumduction (wrist).

4. Multiaxial joints:

a. Saddle joint: flexion, extension, abduction, adduction and conjunct rotation (joint of thumb).

b. Ball and socket joint: flexion, extension, abduction, adduction, circumduction (hip and shoulder joint).

Mechanical axis of bone: The mechanical axis of a bone is the straight line connecting the joint centre points of the proximal and distal joints.

Movement and Mechanism of joints:

1. Angular Movement:

i. Flexion: Decreasing the angle between bone or 2 parts.

ii. Extension: Increasing the angle between 2 bones or 2 parts.

iii. Abduction: Moving the part away from the midline.

iv. Adduction: Bringing the part towards the midline.

2. Rotating Movements:

i. Rotation: Rotating along the vertical axis.

ii. Circumduction: Moving the part round in a circle so that the whole part inscribes a cone when a flexion, abduction, extension and adduction occur in sequence the movement is called as the circumduction.

3. Gliding: One part slides on another.

Limitation of Movement:

1. Reflex contraction of antagonistic muscles.

2. Due to stimulation mechanoreceptors in articular tissue.

3. Ligaments get taut.

4. Approximation of soft parts.

Disorders of Joints:

1. Arthritis: They are of two types

i. Rheumatoid Arthritis: It is an inflammatory systemic disease resulting in thickened synovial membranes of small joints of the hands.

- Due to chronic inflammatory process there is erosion of bones leading to deformity of the finger.

ii. Osteoarthritis: It is degenerative condition of large weight bearing joints.

- The articular cartilage wears out, degenerates and there is formation of peripheral osteophytes.

- The patients feel lot of pain due to rubbing of bones together during movements of joints.

2. Spondylitis: The degenerative change may occur in the cervical spine, leading to narrowed intervertebral foramen, causing pressure on the spinal nerve.

- This condition is known as spondylitis.

Neuropathic joints: Neuropathic joint disease (NJD), is a particularly severe form of osteoarthritis.

- It is recognized by severe joint damage in the context of relatively little pain in the presence of neuropathy and associated with characteristic radiographic changes in well-established disease.

Patients with diabetes are at particular risk of NJD.

How many bones in human body? Anatomy - Makpats

2020-06-25T16:15:00.006+05:30

BONES

Bone is one-third connective tissue. It includes all 206 bones of body.

It is impregnated with calcium salts which constitute the remaining two-thirds part.

Functions of Bones:

1. Give shape and support to the body, and resist any forms of stress.

2. Provide surface for the attachment of muscles, tendons, ligaments etc.

3. Serve as levers for muscular actions.

4. The skull, vertebral column and thoracic cage protect brain, spinal cord and thoracic and some abdominal viscera, respectively.

5. Bone marrow manufactures blood cells.

6. Stores 97% of the body calcium and phosphorus.

7. Contains reticuloendothelial cells which are phagocytic in nature and take part in immune responses of the body.

8. Larger paranasal air sinuses. Ex. Ethmoidal sinuses affect the timbre of voice.

Classification of Bones:

A. Types of bone on the basis of shape.

1. Long bones

Ex: humerus, radius, ulna.

2. Short bones

Ex: tarsals, carpals.

3. Flat bones

Ex: sternum, ribs.

4. Irregular bones

Ex: vertebrae, facial bones.

5. Sesamoid bones

Ex: patellae.

6. Accessory bones

Ex: cervical ribs.

B. Types on the basis of development.

1. Membrane bone (Ex: frontal bone)

i. Cartilaginous bones

Ex: femur.

ii. Membrano- cartilaginous bones

Ex: clavicle.

2. Somatic bones (Ex: most of the bones are somatic)

i. Visceral bone

Ex: hyoid bone.

C. Types on the basis of regional.

1. Axial skeleton

Ex: includes skull, vertebral column and thoracic cage.

2. Appendicular skeleton

Ex: upper and lower limb.

D. Types on the basis of structural.

1. Compact bone

2. Cancellous or Spongy bone

Parts of a young growing bone.

1. Epiphysis

2. Diaphysis

3. Metaphysis

4. Epiphyseal plates

1. Epiphysis: The ends and tips of a bone which ossify from secondary centres are called Epiphysis.

2. Diaphysis: It is the elongated shaft of a long bone which ossifies from a primary centres of ossification.

3. Metaphysis: The epiphyseal ends of a diaphysis are called metaphysis.

4. Epiphyseal Plates: It separates epiphysis from metaphysis.

Types of Muscle Tissue | Anatomy - Makpats

2020-06-22T20:03:00.001+05:30

MUSCLE

Definition: Muscles is a contractile tissue which brings about movements. It can be regarded as motors of the body.

Types of Muscles.

1. Skeletal Muscles

2. Smooth Muscles

3. Cardiac Muscles

1. Skeletal Muscles: Skeletal Muscles are those which attach to bones and have the main function of contracting to facilitate movement of our skeletons.

- They are also sometime known as striated muscles due to their appearance.

- The cause of this ‘stripy’ appearance is the bands o actin and myosin which from the sarcomere, found within the myofibrils.

- Skeletal muscles are also sometime called voluntary muscles because we have direct control through nervous impulses from our brains sending messages to the muscle.

- Contractions can vary to produce powerful, fast movements or small precision actions.

- Skeletal muscles also have the ability to stretch or contract and still return to their original shape.

2. Smooth Muscle: Smooth muscle is also sometimes known as involuntary muscle due to our inability to control its movements, or unstriated as it does not have the stripy appearance of skeletal muscle.

- Smooth muscle is found in the walls of hollow organs such as the stomach, oesophagus, bronchi and in the walls of blood vessels.

- This muscle type is stimulated by involuntary neurogenic impulses and has slow, rhythmical contractions used in controlling internal organs.

- For Example, moving food along the oesophagus or constricting blood vessel during vasoconstriction.

3. Cardiac Muscle (Heart Muscle): This type of muscle is found solely in the walls of the heart.

- It has similarities with skeletal muscles in that it is striated and with smooth muscles in that its contractions are not under conscious control.

- However, this type of muscle is highly specialized.

- It is under the control of the autonomic nervous system, however, even without a nervous input contraction can occur due to cells called pacemaker cells.

- Cardiac muscle is highly resistant to fatigue due to the presence of a large number of mitochondria, myoglobin and a good blood supply allowing continuous aerobic metabolism.

Diuretics: Symptom-Drugs-Dose-MOA-Side Effects | Makpats

2020-02-27T21:22:00.005+05:30

Diuretics

All diuretics increase the excretion of water from bodies. Alternatively, an antidiuretic is an agent or drug which reduces the excretion of water in urine.

CLASSIFICATION

1. High efficacy diuretics (Inhibitors of Na+- K+-2Cl¯ cotransport)
Sulphamoyl derivatives: Furosemide, Bumetanide, Torasemide

2. Medium efficacy diuretics (Inhibitors of Na+-Cl¯ symport)
(A) Benzothiadiazines (thiazides):

Hydrochlorothiazide, Benzthiazide,

Hydroflumethiazide, Bendroflumethiazide
(B) Thiazide like (related heterocyclics):

Chlorthalidone,
Metolazone,
Xipamide,
Indapamide,
Clopamide

3. Weak or adjunctive diuretics
(A) Carbonic anhydrase inhibitors: Acetazolamide
(B) Potassium sparing diuretics:
(ⅰ) Aldosterone antagonist:
Spironolactone, Eplerenone

(ⅱ) Inhibitors of renal epithelial Na+ channel:
Triamterene, Amiloride
(C) Osmotic diuretics:
Mannitol, Isosorbide, Glycerol

MECHANISM OF ACTION

1. HIGH CEILING (LOOP) DIURETICS (Inhibitors of Na+ -K+ -2Cl¯ Cotransport)

Furosemide (Frusemide) Prototype drug: Its maximal natriuretic effect is much greater than that of other classes.

The diuretic response goes on increasing with increasing dose: upto 10 L of urine may be produced in a day. It is active even in patients with relatively severe renal failure.

The onset of action is prompt (i.v. 2–5 min., i.m. 10–20 min., oral 20–40 min.) and duration short (3–6 hours).

The major site of action is the thick AscLH (therefore called loop diuretics) where furosemide inhibits Na+- K+-2Cl¯ cotransport.

The corticomedullary osmotic gradient is abolished and positive as well as negative free water clearance is blocked. K+ excretion is increased mainly due to high Na+ load reaching DT. However, at equinatriuretic doses, K+ loss is less than that with thiazides.

Furosemide has weak CAse inhibitory action; increases HCO3 ¯ excretion as well; urinary pH may rise but the predominant urinary anion is Cl¯ . Therefore, acidosis does not develop.

furosemide causes acute changes in renal and systemic haemodynamics.

After 5 min of i.v. injection, renal blood flow is transiently increased and there is redistribution of blood flow from outer to midcortical zone; g.f.r. generally remains unaltered due to compensatory mechanisms despite increased renal blood flow.

Intravenous furosemide causes prompt increase in systemic venous capacitance and decreases left ventricular filling pressure, even before the saluretic response is apparent.

Furosemide increases Ca2+ excretion as well as Mg2+ excretion by abolishing transepithelial potential difference in the thick AscLH which drives reabsorption of these divalent cations.

Molecular mechanism of action: A glycoprotein with 12 membrane spanning domains has been found to function as the Na+ -K+ -2Cl¯ cotransporter in many epithelia performing secretory/absorbing function, including AscLH.

Recently, distinct absorptive and secretory isoforms of Na+-K+-2Cl¯ cotransporter have been isolated. The former is exclusively expressed at the luminal membrane of thick AscLH—furosemide attaches to the Cl¯ binding site of this protein to inhibit its transport function. The secretory form is expressed on the basolateral membrane of most glandular and epithelial cells.

Pharmacokinetics:

Furosemide is rapidly absorbed orally but bioavailability is about 60%.

Lipid-solubility is low, and it is highly bound to plasma proteins.

Some excretion in bile and directly in intestine also occurs.

Plasma t½ averages 1–2 hour.

Dose:

Usually 20–80 mg once daily in the morning.

In renal insufficiency, upto 200 mg 6 hourly has been given by i.m./i.v. route.

In pulmonary edema 40–80 mg may be given i.v.

Bumetanide: It is similar to furosemide in all respects, but is 40 times more potent. It induces very rapid diuresis and is highly effective in pulmonary edema.

the site of action, ceiling effect, renal haemodynamic changes and duration of action are similar to furosemide.

Hyperuricaemia, K+ loss, glucose intolerance and ototoxicity are claimed to be less marked, but it may rarely cause myopathy.

Bumetanide is more lipid-soluble.

oral bioavailability is 80–100%.

Bumetanide is extensively bound to plasma proteins, partly metabolized and partly excreted unchanged in urine.

Plasma t½ ~60 min.

Dose: 1–5 mg oral OD in the morning, 2–4 mg i.m./i.v., (max. 15 mg/day in renal failure).

Torasemide (Torsemide): Another high ceiling diuretic with properties similar to furosemide, but 3 times more potent.

Oral absorption is more rapid and more complete.

The elimination t½ (3.5 hours) and duration of action (4–8 hours) are longer.

Torasemide has been used in edema and in hypertension.

Dose: 2.5–5 mg OD in hypertension; 5–20 mg/day in edema; upto 100 mg BD in renal failure.

Use of high ceiling diuretics:

1. Edema

2. Acute pulmonary edema (acute LVF, following MI)

3. Cerebral edema

4. Hypertension

Hypercalcaemia of malignancy

2. Medium efficacy diuretics (Inhibitors of Na+-Cl¯ symport):

Chlorothiazide was synthesized as a CAse inhibitor variant which (unlike acetazolamide) produced urine that was rich in Cl¯ , and diuresis occurred in alkalosis as well as acidosis.

Here they inhibit Na+–Cl¯ symport at the luminal membrane.

Positive free water clearance is reduced, because tubular fluid is not maximally diluted (very dilute urine cannot be passed in theabsence of ADH), but negative free water clearance (in the presence of ADH) is not affected.

This strengthens the view that the site of action is in between thick AscLH and late DT. These drugs gain access to their site of action via organic acid secretory pathway in PT and then along the tubular fluid to the early DT, where they bind to specific receptors located on the luminal membrane. Like the Na+-K+-2Cl¯ cotransporter, the Na+-Cl¯ symporter is also a glycoprotein with 12 membrane spanning domains that binds thiazides but not furosemide or any other class of diuretics.

However, it may confer some proximal tubular action to the compounds, and accounts for the increase in HCO3 ¯ and PO4 3¯ excretion.

Under thiazide action, increased amount of Na+ is presented to the distal nephron, more of it exchanges with K+ ® urinary K+ excretion is increased in parallel to the natriuretic response. The maximal diuresis induced by different agents falls in a narrow range; though potency (reflected in daily dose) differs markedly.

Nevertheless, they are moderately efficacious diuretics, because nearly 90% of the glomerular filtrate has already been reabsorbed before it reaches their site of action.

Chlorthalidone: It is a particularly long acting compound with a t½ 40–50 hours, used exclusively as antihypertensive.

Metolazone: It has marked additive action when combined with furosemide.

Metolazone has been used mainly for edema (5–10 mg/day, rarely 20 mg), and occasionally for hypertension (2.5–5 mg/day).

Xipamide: It is used both as antihypertensive (10–20 mg/ day) and for treatment of edema (40 mg/day, max. 80 mg/day).

Indapamide: it is highly lipid soluble

Pharmacokinetics:

well absorbed orally.

There are no injectable preparations of these drugs.

Their action starts within 1 hour.

The elimination t½ of hydrochlorothiazide is 3–6 hours, but action persists longer (6–12 hours).

Uses:

1. Edema

2. Hypertension

3. Diabetes insipidus

4. Hypercalciuria

3. Weak or adjunctive diuretics

(A) Carbonic anhydrase inhibitors:

Carbonic anhydrase (CAse) is an enzyme which catalyses the reversible reaction H2O + CO2 ↔ H2CO3. Carbonic acid spontaneously ionizes H2CO3 ↔H+ + HCO3 ¯.

Carbonic anhydrase thus functions in CO2 and HCO3 ¯ transport and in H+ ion secretion. The enzyme is present in renal tubular cell (especially PT) gastric mucosa, exocrine pancreas, ciliary body of eye, brain and RBC. In these tissues a gross excess of CAse is present, more than 99% inhibition is required to produce effects.

Acetazolamide: It is a sulfonamide derivative which noncompetitively but reversibly inhibits CAse (type II) in PT cells resulting in slowing of hydration of CO2 ® decreased availability of H+ to exchange with luminal Na+ through the Na+-H+ antiporter.

Inhibition of brush border CAse (type IV) retards dehydration of H2CO3 in the tubular fluid so that less CO2 diffuses back into the cells. The net effect is inhibition of HCO3 ¯ (and accompanying Na+) reabsorption in PT. However, the resulting alkaline diuresis is only mild, because part of the Na+ (but not HCO3 ¯ ) rejected in the PT is reabsorbed at the high capacity AscLH.

Though H+ is secreted at this site by a H+ -ATPase, it is generated in the cell by CAse mediated reaction.

When CAse inhibitors are given, the distal Na+ exchange takes place only with K+ which is lost in excess.

The extrarenal actions of acetazolamide are:

(i) Lowering of intraocular tension due to decreased formation of aqueous humour (aqueous is rich in HCO3 ¯ ).

(ii) Decreased gastric HCl and pancreatic NaHCO3 secretion: This action requires very high doses—not significant at clinically used doses.

(iii) Raised level of CO2 in brain and lowering of pH ® sedation and elevation of seizure threshold. (iv) Alteration of CO2 transport in lungs and tissues. These actions are masked by compensatory mechanisms.

Pharmacokinetics

Acetazolamide is well absorbed orally and excreted unchanged in urine. Action of a single dose lasts 8–12 hours.

Uses:

1. Glaucoma

2. To alkalinise urine

3. Epilepsy

4. Acute mountain sickness

5. Periodic paralysis

Dose: 250 mg OD–BD

Adverse effects:

fever, rashes, Acidosis, hypokalaemia, drowsiness, paresthesias, fatigue, abdominal discomfort.

(B) POTASSIUM SPARING DIURETICS

Aldosterone antagonists and renal epithelial Na+ channel inhibitors indirectly conserve K+ while inducing mild natriuresis, and are called ‘potassium sparing diuretics’.

(ⅰ) Aldosterone antagonist:

Spironolactone It is a steroid, chemically related to the mineralocorticoid aldosterone.

Aldosterone acts by combining with an intracellular mineralocorticoid receptor (MR) ® induces the formation of ‘aldosterone-induced proteins’ (AIPs).

Spironolactone acts from the interstitial side of the tubular cell, combines with MR and inhibits the formation of AIPs in a competitive manner.

It has no effect on Na+ and K+ transport in the absence of aldosterone, while under normal circumstances, it increases Na+ and decreases K+ excretion.

Pharmacokinetics

The oral bioavailability is 75%.

completely metabolized in liver.

The t½ of spironolactone is 1–2 hours.

Dose: 25–50 mg BD–QID; max 400 mg/day

Use:

1. To counteract K+ loss due to thiazide and loop diuretics

2. Edema

3. Hypertension

Adverse effects:

Drowsiness

Ataxia

mental confusion

epigastric distress

loose motions

Eplerenone It is a newer and more selective aldosterone antagonist.

it particularly suitable for longterm use in the therapy of hypertension

side effects are like spironolactone.

Pharmacokinetics:

well absorbed orally.

inactivated in liver by CYP3A4.

excreted in urine (2/3rd) as well as faeces (1/3rd).

The t½ is 4–6 hours.

Dose: 25–50 mg BD

(ⅱ) Inhibitors of renal epithelial Na+ channel

Triamterene and amiloride are two nonsteroidal organic bases with identical actions. Their most important effect is to decrease K+ excretion, particularly when it is high due to large K+ intake or use of a diuretic that enhances K+ loss. This is accompanied by a small increase in Na+ excretion. The excess urinary Na+ is matched by Cl¯ and variable amounts of HCO3 ¯ ; urine is slightly alkalinized.

Mechanism of action

The luminal membrane of late DT and CD cells expresses a distinct ‘renal epithelial’ or ‘amiloride sensitive’ Na+ channel through which Na+ enters the cell down its electrochemical gradient which is generated by Na+K+ ATPase operating at the basolateral membrane.

This Na+ entry partially depolarizes the luminal membrane creating a –15 mV transepithelial potential difference which promotes secretion of K+ into the lumen through K+ channels.

Though there is no direct coupling between Na+ and K+ channels, more the delivery of Na+ to the distal nephron—greater is its entry through the Na+ channel—luminal membrane is depolarized to a greater extent—driving force for K+ secretion is augmented. As such, all diuretics acting proximally promote K+ secretion.

The intercalated cells in CD possess an ATP driven H+ pump which secretes H+ ions into the lumen. This pump is facilitated by the lumen negative potential. Amiloride, by reducing the lumen negative potential, decreases H+ ion secretion as well and predisposes to acidosis. Thus, amiloride conserves both K+ and H+ while marginally increasing Na+ excretion.

Triamterene:

Pharmacokinetics:

It is incompletely absorbed orally.

largely metabolized in liver.

excreted in urine.

Plasma t½ is 4 hours.

Side effects:

nausea, dizziness, muscle cramps and rise in blood urea.

Dose: 50–100 mg daily

Amiloride It is 10 times more potent than triamterene

Pharmacokinetics:

Only ¼ of an oral dose is absorbed.

It is not bound to plasma proteins and not metabolized.

The t½ (20 hours) and duration of action are longer than triamterene.

side effects:

nausea, diarrhoea and headache.

(C) OSMOTIC DIURETICS

Mannitol

It is minimally metabolized in the body; freely filtered at the glomerulus and undergoes limited reabsorption: therefore excellently suited to be used as osmotic diuretic.

Mannitol appears to limit tubular water and electrolyte reabsorption in a variety of ways:

1. Retains water isoosmotically in PT—dilutes luminal fluid which opposes NaCl reabsorption.

2. Inhibits transport processes in the thick AscLH by an unknown mechanism.Quantitatively this appears to be the largest contributor to the diuresis.

3. Expands extracellular fluid volume (because it does not enter cells, mannitol draws water from the intracellular compartment)— increases g.f.r. and inhibits renin release.

4. Increases renal blood flow, especially to the medulla—medullary hypertonicity is reduced (due to washing off)—corticomedullary osmotic gradient is dissipated—passive salt reabsorption is reduced. Though the primary action of mannitol is to increase urinary volume, excretion of all cations (Na+, K+ , Ca2+, Mg2+) and anions (Cl¯ , HCO3 ¯ , PO4 3¯ ) is also enhanced.

Pharmacokinetics

Mannitol is not absorbed orally.

has to be given i.v. as 10–20% solution.

It is excreted with a t½ of 0.5–1.5 hour.

Uses

1. Increased intracranial or intraocular tension

2. To maintain urine flow in impending acute renal failure

3. To counteract low osmolality of plasma/e.c.f. due to rapid haemodialysis or peritoneal dialysis (dialysis disequilibrium).

side effect

headache

Nausea and vomiting may occur; hypersensitivity reactions are rare.

Isosorbide and glycerol These are orally active osmotic diuretics which may be used to reduce intraocular or intracranial tension.

Intravenous glycerol can cause haemolysis.

Dose: 0.5–1.5 g/kg as oral solution

Anti-hyperlipidemic: Symptom-Drug-Dose-MOA-Side Effect

2020-02-23T21:30:00.001+05:30

Anti-hyperlipidemic

Hypolipidemic agents, cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are called lipid-lowering drugs.

SYMPTOMS:

Hyperlipidaemia doesn't cause any symptoms. Consult a doctor for medical advice

CLASSIFICATION

1. HMG CoA reductase Ingibitors

Lovastatin

Simvastatin

Metastatin

Pravastatin

Fluvastatin

Atorvastatin

Pitavastatin

Rosuvastatin

2. Fibric accid derivatives

Clofibrate

Fenofibrate

Gemfibrozil

Ciprofibrate

Benzaffibrate

Fluvastatin

3. Bile acid sequestrants

Cholestyramine

Colestipol

4. Pyridine derivative

Nicotinic acid (NIACIN)

Nicotinamide

5. Cholesterol absorption inhibitors

Ezetimibe

6. PCSK9 inhibitors
Evolocumab
Alirocumab

7. Omega-3 fatty acids
Docosahexaenoic acid(DHA)
Eicosapentaenoic acid(EPA)

MECHANISM OF ACTION

1. HMG CoA Reductase Ingibitors

Liver cell where HMG-CoA reductase enzyme converts HMG-CoA into mevalonic acid which is a cholesterol precursor. So inhibiting this enzyme statins effectively reduce concentration of cholesterol within the liver cell. Liver cells sense the reduced level of cholesterol production and begin to compensate by synthesizing more LDL receptors which in turn bind and internalize LDL that is circulating in in the blood. additionally low intracellular cholesterol level lead to decrease secretion of VLD which also contributes in lowering of triglyceride level.

DOSE:

Lovastatin: 20 mg orally OD with the evening, Maintenance dose: 10 to 80 mg orally OD

SIDE EFFECTS:

pain in your stomach area

nausea

heartburn

constipation

headache

muscle pain

memory loss/forgetfulness

2. Fibric acid derivatives

Fibrates work primarily by activating nuclear transcription receptor called peroxisome proliferator-activated receptor-𝛼(PPAR_alpha). PPAR-𝛼 if found in metabolically active tissue such as liver and adipose tissue. The bind of fibrates to PPAR-𝛼 induces activation and inhibition of certain genes that code for proteins involved in lipid metabolism.

The main effects induced by fibrates is increased expression of lipoprotein lipase which in turn increase the removal triglycerides from circulation and their breakdown to fatty acid. furthermore fibrates decrease expression of protein called APO-CⅢ which inhibits lipoprotein lipase activity and lastly fibrates also increase APO-AⅠ and APO-AⅡ which are major component of HDL, thus leading to increase in it's concentration.

Dose:

Clofibrate: 500 mg orally QID

Fenofibrate: Maximum dose: 1 tablet or capsule orally once a day

Lipofen (capsules): 150 mg, Fenoglide (tablet): 120 mg

Fluvastatin: 40 mg orally OD or BD

SIDE EFFECTS:

headache

nausea

vomiting

rash

constipation

diarrhea

muscle pain

3. Bile acid sequestrants

Bile acids are produced in the liver, stored in the gallbladder and they are excreated into the gut where they facilitate digestion and absorption of lipid.

Bile acid sequestrants serve as an ion exchange resins that bind negatively charged bile acids and salts in the small intestine. the formation of this insoluble complex prevents the reabsorption of bile acids and thus leads to their excretion. this is in turn creates increase demand for their production.

since bile acids are made from cholesterol, liver cells increase their number of LDL receptors to bring in more LDL cholesterol in order to meet this new demand. so the end result is decrease levels of circulating LDL

DOSE:

Cholestyraminen

Initial dose: 4 g orally OD or BD

Maintenance dose: 8 to 16 g orally

Colestipol:

Initial dose: 4 g orally OD or BD

Maintenance dose: 8 to 16 g orally

SIDE EFFECTS:

Constipation

Diarrhea

Gas

Stomach pain

Nausea

Vomiting

4. Pyridine derivative

Nicotinic acid(NIACIN):

Nicotinic acid works on adipose tissue, where it inhibits enzyme called hormone-sensitive lipase which is responsible for breakdown of triglycerides to free fatty acid.

by reducing level of free fatty acid available for transport to the liver, nicotinic acid effectively decrease hepatic VLDL synthesis which in turn leads to decrease level of LDL

DOSE:

Children: Between 1-16 mg daily, depending on Age

Men: 14 mg daily

Women (pregnant): 18 mg daily

Women (breastfeeding): 17 mg daily

Maximum daily intake for adults of all ages: 35 mg daily

SIDE EFFECTS:

Skin Flushing

redness and itching occurs on the face, neck, chest, and back

rash

nausea

vomiting

5. Cholesterol absorption inhibitors

Ezetimibe

Free cholesterol that comes either from bile or dietary sources, first binds to protein abbreviated NPC1L1 which is located in the plasma membrane of cells known as enterocytes that line the intestinal walls. this binding then triggers endocytosis which utilizes protein complex called AP2 that works on the cell membrane to internalize the cholesterol cargo upon endocytosis the cholesterl is released and the NPC1L1 returns back to the plasma membrane.

The cholesterol absorption inhibitor binds to NPC1L1 and inhibit it's ability to interact with clathrin AP2 complex that is necessary for endocytosis. this leads to decrease delivery of intestinal cholesterol to the liver which is turn cause decrease in hepatic cholesterol level and ultimately increased clearance of LDLcholesterol from the circulation.

DOSE:

Ezetimibe: 10 mg orally OD

SIDE EFFECTS:
Abdominal fullness

Black tarry stool

Darkened urine

Blood in urine or stool

Skin rash

vomiting

6. PCSK9 inhibitors

Evolocumab

Alirocumab

PCSK9 is an abbreviated name of enzyme circulating in the blood that binds to LDL receptors on the surface of liver cells and promotes their degradation in other word the activity of PCSK9 reduces the removal of LDL from the circulation.

PCSK9 inhibitors are monoclonal antibodiesthat binds and inactivate PCSK9. In the absence of PCSK9 there is more LDL receptor available to bind and clear LDL from the circulation leading to decreased level of of LDL cholesterol.

DOSE:

Evolocumab: 140 mg/ml subcutaneously every 2 week OR 420 mg/3.5ml subcutaneously Once a month.

Alirocumab:

Initial dose: 75 mg/ml subcutaneously every 2 week

Maximum dose: 150 mg/ml subcutaneously every 2 week

SIDE EFFECTS:

fever

rash

nausea

neurocognitive problem

7. Omega-3 fatty acids

Omega-3 fatty acids are used primarily for their Triglyceride lowering effects which are thought to be caused by inhibiting of VLDL and triglyceride synthesis in the liver.

DOSE:

(high enough doses there appears to be some increased risk of bleeding)

SIDE EFFECTS:

Abdominal pain

nausea

diarrhea

Official Site: Makpats.com

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Anti-arrhythmic: Symptom-Treatment-Drug-Dose-MOA-Side Effect

2020-02-23T14:40:00.000+05:30

Anti-arrhythmic

These are drugs used to prevent or treat irregularities of cardiac rhythm.

Symptoms

A fluttering in your chest

Anxiety.

Fatigue.

Sweating.

dizziness
Palpitation

CLASSIFICATION

[CLASS-1] : Na+ channel blocker [agents interfere with the sodium (Na⁺) channel]

A.Minimal phase 'O' depressors [shorten repolarization]

Lidocaine

Phenytoin

Mexiletine

Tocainide

B.Moderate phase 'O' depressors [prolong repoarization]

Quinidine

procainamide

disopyramide

moricizine

C. Marked phase 'O' depressors [No effect on repolarization]

Encainide

Flecainide

idecainide

lorcainide

[CLASS-2] : 𝛃-adrenoreceptor blocker [agents are anti-sympathetic nervous system agents]

propranolol

acebutolol

Esmolol

[CLASS-3] : K+ channel blocker [agents affect potassium (K⁺) efflux]

Amiodarone

Bretylium

sotalol

[CLASS-4] : Ca++ channel blockers [agents affect calcium channels and the AV node]

Verapamil

Diltiazem

MECHANISM OF ACTION

[CLASS-1] : Na+ channel blocker [agents interfere with the sodium (Na⁺) channel] :

Class-1(A):
(Na⁺) channel block (intermediate association/dissociation) and K+ channel blocking effect; affects QRS complex

Class-1A prolong the action potential and has intermediate effect on the 0 phase of depolarization

Class-1(B):

Na⁺ channel block (fast association/dissociation); can prolong QRS complex in overdose

class 1b shorten the action potential of myocardial cell and has weak effect on intiation of phase 0 of depolarization

Class-1(C):

Na⁺ channel block (slow association/dissociation) has no effect on action potential and has the strongest effect on the initiation phase 0 of depolarization

DOSE:

* Lidocaine: given only by iv route: 50-100 mg bolus followed by 20-40 mg every 10 20 min or 1-3 mg/min infusion.

* Quinidine: PRONESTYL 250 mg tab., I g/10 ml inj.

* Propafenone: 150 mg BD- 300 mg TDS

ADVERSE EFFECTS:

1(A) Lidocaine: CNS effects

2(B) Quinidine: cinchonism

3(C) Flecainide: Blurred vision, nausea

[CLASS-2] : 𝛃-adrenoreceptor blocker

Their mechanism in Arrhythmia is primarily cardiac beta blockage and reduction in cAMP,which resulting in both sodium and calcium currents and the suppression of abnormal Pacemakers.

DOSE:

* Esmolol: MINIBLOCK 100 mg/10 ml, Short acting, Route-iv.

* Propranolol: 40-80 mg 2-4 times a day.

[CLASS-3] : K+ channel blocker

They cause prolongation of the action potential duration by blockage of potassium channel that are responsible for the repolarization of the action potential.

AP prolongation result in effective refractory period and reduce the ability of the heart to respond to rapid ectropic beat

DOSE:

* Amiodarone: orally 400-600 mg/day for few weeks

* Sotalol: SOTALAR-40 mg tab, SOTAGARD-40. 80 mg tabs.

ADVERSE EFFECTS:

Fall in BP, bradycardia and myocardial depression occurs on i.v. injection.

Nausea, gastrointestinal upset may attend oral medication

[CLASS-4] : Ca++ channel blockers

Cardiac effect:

* Verapamil blocks both activated and inactivated L-type calcium channel.

-AV node conduction time and effective refractory period are prolonged.

-Slow the SA node by its direct action.

DOSE:

* Verapamil: 60 to 120 mg TDS

CALAPTIN 40, 80 mg tab; 120, 240 mg SR tab, 5 mg/2 ml inj.

*Diltiazem: The direct cardiac actions of diltiazem are similar to those of verapamil

For rapid control of ventricular rate in AF or AFI, i. v. diltiazem is preferred over verapamil, because it can be more easily titrated to the target heart rate, causes less hypotension or myocardial depression and can be used even in the presence of mild-to-moderate CHF.

DOSE:

DILZEM 30, 60. 90 mg tabs, 25 mg/5 ml inj.

Anti-anginal:Symptom-Treatment-Drug-Dose-MOA-Side Effect

2020-02-23T11:20:00.001+05:30

Anti-anginal

An antianginal is a drug used in the treatment of angina pectoris, a symptom of ischaemic heart disease.

Drugs used are nitrates, beta blockers, or calcium channel blockers.

Symptoms:

Chest pain

Pain in your arms, neck, jaw

Nausea

Fatigue

Shortness of breath

Sweating

Dizziness

CLASSIFICATION:

Nitrates:

Short acting: Glyceryl trinitrate and Isosorbide dinitrate (sublingual).

Long acting: isosorbide dinitrate and isosorbide mononitrate.

𝛃-Blocker:

Cardioselectives such as acebutolol or metoprolol

Non-cardioselectives such as Oxprenolol or Sotalol

Calcium channel Blocker:

Verapamil, Diltiazem, Amlodipin

Potassium channel opener:

Nicorandil

Other anti anginal drugs:

Trimetazidine, Ranolazine, Jvabradine, Dipyridamole

Mechanism of action (MOA)

Nitrates:

Nitrates

↓

Formation of nitrogen oxide(NO)

↓

Activate Guanylate cyclase

↓

↑cGMP

↓

Activate protein kinase

↓

Dephosphorylation of light chain myosin

↓

Relaxation of actin myosin

↓

Smooth muscle relaxation

↓

Vasodilation

Uses:

Angina pectoris,

Acute coronary syndromes,

Biliary Colic

Myocardial infarction(MI),

Esophageal spasm,

Cyanide poisoning

Side Effects:

Headache

tachycardia

𝛃-Blocker:

The Beta adrenergic blockers decrease the oxygen demands of the myocardium by blocking 𝛃1 receptors, Resulting in decreased heart rate,Contractility, Cardiac output(CO) and blood pressure.

Side effects:

fatigue, weight gain

shortness of breath

dizziness

headache

upset stomach.

Calcium channel blocker:

There are 2 main calcium channels:

T-type calcium channel blocker:

In the heart pacemaker cells which control the heart rate, there are T-type calcium channel. Calcium activity in the pacemaker cells cause the heart to pump faster and increasing the BP.

By using the T-type calcium channel blockers it will block calcium activity. And thus decrease heart rate, decrease cardiac output and then decrease blood pressure.

L-type calcium channel blocker:

It is found on smooth muscle cells.

Blood vessel which contain smooth muscles, L-type calcium channels allow influx of calcium into the muscle filaments which will cause contraction and this will increase BP. by using L-type calcium channel blocker block calcium channel. thus smooth muscle will relax and decrease BP.

Dose:

Verapamil: 40-160 mg TDS oral, 5 mg by slow i.v. injection.

(Interactions: Verapamil should not be given with 13 blockers)

(It should not be used along with other cardiac depressants like quinidine and disopyramide)

Adverse effects:

Constipation

Bradycardia

nausea

Diltiazem:

It is somewhat less potent vasodilator than nifedi pine and verapamil.

Dose: 30- 60 mg TDS-QID oral; DILZEM, 30, 60 mg tabs.

Adverse effect:

Similar to verapamil

Amlodipin:

Dose: 5- 10 mg OD

Felodipine:

Dose: 5- 10 mg OD, max. 10 rng BD.

Nitrendipine:

Dose: 5- 20 mg OD; NITREPI . CARDff 10, 20 mg tabs.

Potassium channel opener:

Nicorandil:

Potassium Channel Opener

↓

Open KATP

↓

Enhance Kᐩ efflux

↓

Membrane Hyperpolarization

↓

↓ Ca ᐩᐩ entry

↓

Reduced intracellular Calcium

↓

Smooth muscle Relaxation

These are the drugs that activate (open) ATP sensitive potassium channel in vascular smooth muscle. Opening of these channels, hyperpolarizes the smooth muscle, which closes voltage-gated calcium channel and decrease intracellular calcium, leading to muscle relaxation and vasodilatation, Decreasing vascular resistance and decrease blood pressure.

Dose: 5-20 mg BO

Side effects:

flushing

palpitation

weakness

headache

dizziness

nausea and vomiting

Other anti anginal drugs:

Trimetazidine:
Dose: 20mg TDS

Ranolazine:
Dose: 0.5-1 g BD

Hypertension:Symptom-Treatment-Drug-Dose-MOA-Side Effect

2020-02-05T11:01:00.002+05:30

Hypertension is another name for High blood pressure (HBP).➤Usually hypertension is defined as blood pressure above 140/90.

SYMPTOMS:High blood pressure is called the “silent killer” because it often has no warning signs or symptoms.The only way to know if your bool pressure is high is through regular checkups.

If your blood pressure is extremely high, there may be certain symptoms to look out for,including:

High blood pressure brain symptoms:

1. Headaches

2. Blurred vision

3. dizziness

4. Nausea and vomiting

High blood pressure and heart symptoms:

1. Chest pain

2. Shortness of breath

TREATMENT :
Treating high blood pressure can take a multi-pronged approach including diet changes, medication, and exercise.

· High blood pressure drug:

These medication work in a variety of way to lower blood pressure.

1. ACE (Angiotensin Converting Enzyme) Inhibitors

2. Angiotensin || Receptor Blockers

3. α(Alpha)-Adrenergic Blockers

4. β(Beta)-Adrenergic Blockers

5. α + β Adrenergic Blockers

6. Calcium Channel Blockers

7. Diuretics (Water Pills)

8. Direct Renin Inhibitor

9. Central Sympatholytics

10. Vasodilators

CLASSIFICATION

1. ACE (Angiotensin Converting Enzymes) Inhibitors: ( ~PRIL )

Captopril

Enalapril

Lisinopril

Ramipril

Perindopril

Fosinopril

2. Angiotensin-II Receptor Blockers: (~SARTAN )

Losartan

Valsartan

Telmisartan

Candesartan

Irbesartan

3. Alpha(α) Adrenergic Blockers:

Prazosin

Terazosin

Doxazosin

Pentolamine

Phenoxybenzamine

4. Beta(β) Adrenergic Blockers:(~OLOL )

Atenolol

Propranolol

Metoprolol

Timolol

5. α + β Adrenergic Blockers:

Labetalol

Carvedilol

6. Calcium channel Blocker: ( ~DIPIN )

Nifedipin

Nimodipin

Nicardipin

Amlodipin

Felodipin

Lacidipin

Verapamil

Diltiazem

7. Diuretics:

Thiazides: Hydrochlorthiazide

Chlorthiazide

Chlorthalidone

Indapamide

High ceiling: Furosemide, etc.

Potassium(K⁺)Sparing:
Spironolactone
Amiloride

8. Direct Renin Inhibitor:

Aliskiren

9. Central Sympatholytics:

Clonidine

Methyldopa

10. Vasodilators:

Arteriolar: Hydralazine

Minoxidil

Diazoxide

Arteriolar + Venous: Sodium nitroprusside

· [NOTE: Adrenergic neuron blockers (Reserpine, Guanethidine, etc.) and Ganglionic blockers (Pentolinium, etc.) are only of historical Importance, though reserpine is still marketed.]

MECHANISM OF ACTION (MOA):
1. ACE (Angiotensin Converting Enzyme) Inhibitors:

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The liver produces molecules called Angiotensinogen when there is a decrease in blood pressure in the arteries

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The kidney will detect this and then produce a molecule called Renin

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Renin enters into circulation and is responsible for converting Angiotensinogen into Angiotensin-I

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Angiotensin-I will then circulate around the body and get in contact with a membrane-bound enzyme called ACE or Angiotensin converting enzyme which mainly resides in the lung tissues

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ACE(angiotensin converting enzyme) converts Angiotensin-I to Angiotensin-II

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Angiotensin-II Important regulator of blood pressure

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Angiotensin-II binds on to angiotensin-II receptors on many different types of cells around the body and depending on what cell angiotensin binds to it’s effect on the body differs so essentially it will result in an increase in blood pressure

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Effect of Angiotensin-II includes:

-Increasing sympathetic activity

-Vasoconstriction

-Stimulating the release of aldosterone

These effects all of them will lead t an increase in blood pressure

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ACE inhibitor ( ~Pril) is inhibits ACE(Angiotensin converting enzyme) so it inhibit the conversion of Angiotensin-I to Angiotensin-II

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Because of less Angiotensin-II means that decrease blood pressure.

· Dose:

Enalapril: 2.5-10 mg/day

(used alone they control hypertension in ~50% patients, and addition of a diuretic/ β-blocker extends efficacy to ~90%.)

· Side effects:

Dry cough

headache

Nausea/Vomiting

Diarrhoea

Angioedema

Rash

· Contraindications:

Pregnancy

Chronic cough

Asthma

Kidney disease

Allergy

2. Angiotensin-II Receptor Blockers:

As the name suggests the mechanism of action,

it blocks the binding of Angiotensin-II to its receptor

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so it will decrease the activity of Angiotensin-II

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decrease in blood pressure

(see figure no:01)

·
Dose:

Losartan: 50 mg/day

(Addition of 12.5 gm/day hydrochlorothiazide further enhances the fall in BP.)

·
Side effect:

Headache

Nausea

Diarrhoea

Backpain

· Contraindication:

Pregnancy

Allergy

3. Alpha(α) Adrenergic Blockers:

*Aim is to work on the vessel epithelial cells. Surrounding the lumen of blood vessel is the endothelial cells and the smooth muscle cells.

· Smooth muscle cells contract = narrow lumen = increase BP.

(figure:02)

The smooth muscle cells that surround the vessels have alpha-I receptors(α_IR)

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These receptor react to nor-adrenaline/adrenaline(NA/A) produced by the nerve fibers

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Noradrenaline will bind to the alpha-I receptor(α_IR)

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This will cause or stimulate contraction of smooth muscle cell

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Vessel to become more smaller = narrow the lumen

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This will lead to an increase blood pressure

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alpha-I receptor(α_IR) Blockers, they block alpha-I receptors(α_IR) and inhibits the adrenergic activity leading to the decrease in blood pressure.

(alpha-I receptor(α_IR) Blockers also have role in decreasing total cholesterol in the boy)

· Dose:

Prazosin GITS 2.5 mg, 5 mg tabs ; Prazopress 1,2mg tabs.

· Side effect:

Hypotension

4. Beta(β) Adrenergic Blockers:

Beta-receptor is everywhere in the body. β-blockers block beta-receptors which is important for sympathetic activity.

(i) The heart have cells called Pacemaker cells(they directly control the heart rate).

Pacemaker cells have receptors on them the beta-I receptor(β_IR).

Adrenergic neurons target these pacemaker cells and release NA/A which will bind on to beta-I receptor(β_IR)

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It’ll stimulate the pacemaker cells to fire more rapidly

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Increase the heart rate = increase cardiac output (CO)

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Increase in blood pressure.

Beta-blockers block the sympathetic function on the heart by blocking the beta-I receptor(β_IR) ↓

Decrease heart rate = decrease cardiac output

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Decrease blood pressure

(figure:03)

(ii) cardiac muscle cells are the cells which contract and help eject blood out and these heart muscle cells also contain beta-I receptor(β_IR).

NA/A released by adrenergic cells

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The sympathetic nervous system can stimulate the beta-I receptor(β_IR) of cardiac muscle cells

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Cause the chronic muscle cells to contract

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Contraction the heart is able to increase cardiac output(CO)

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increase blood pressure

Beta-blockers block the sympathetic function on the heart by blocking the beta-I receptor(β_IR),

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decrease Myocardial contraction = decrease cardiac output(CO)

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Decrease blood pressure

·
Side effect:

Bradycardia

Fatigue

Hypotension

Bronchoconstriction

·
Contraindication:

Obstructive lung disease

PVD(peripheral vascular disease)

5. α + β Adrenergic Blockers:

It is a combined α and β blocker

· Acts faster than pure β blocker

Drugs:

*Labetalol: it has been used i.v. for rapid BP reduction in hyperadrenergic states, cheese reaction, clonidine withdrawal, eclampsia, etc.

*Carvedilol: This nonselective β+ weak selective α₁blocker produces vasodilation and has additional antioxidant/free radial scavenging properties. Carvedilol is a frequently selected drug for long term treatment of congestive heart failure(CHF).

6. Calcium channel Blocker(CCBs):

· Calcium channels are important channels in our body that allow the movement of calcium in and out of cells or cellular organelles.

· There are two main calcium channels:
(i) T-type calcium channel blocker
(ii) L-type calcium channel blocker

T-type calcium channel blocker:

In the heart pacemaker cells which control the heart rate, there are T-type calcium channel. Calcium activity in the pacemaker cells cause the heart to pump faster and increasing the BP.

By using the T-type calcium channel blockers it will block calcium activity. And thus decrease heart rate, decrease cardiac output and then decrease blood pressure.

L-type calcium channel blocker:

It is found on smooth muscle cells.

· Side effect of Dihydropyridine:

Headache

Dizziness

Palpitation

· Contraindication:

Congestive heart failure

7. DIURETICS:

Diuretics works on the kidney. The functional unit of kidney are called nephrons. There are millions of nephrons in the kidney where diuretics work.

Mechanism of action of diuretics is to increase urine output, decrease fluid overload and this will decrease BP.

There are 3 types of diuretics:
(i) Loop diuretics
(ii)Thiazide diuretics
(iii) K⁺sparing diuretics

· (1)Loop diuretics:

In the loop of henle in the ascending part there is channel which transports one sodium molecules, two chloride molecules and one potassium from the nephron back into circulation back into the blood vessel.

When sodium is reabsorbed in the blood, water follows loop diuretics inhibit the transport are transported by inhibiting the movement of chloride ions which will disrupt the whole transport so don’t get sodium moving into the blood vessel therefore don’t get water following and result in decrease in BP.

· (2) Thiazide diuretics:

Thiazide diuretics work on the distal part of the nephron.

Transporter which reabsorb sodium and chloride together, this will then draw water back into the blood which will increase the blood pressure in the body. Thiazide diuretics block this transporter and block sodium reabsorption and result in decrease in BP.

Side effect of loop and thiazide diuretics:

Hyperglycemia, hypokalemia, hyperuricemia, hypotension

· (3)K⁺sparing diuretics:

It is also work on the distil part of the nephron.

Transporter which is reabsorb sodium but secretes potassium.

Potassium sparing diuretics inhibit the transporter and decrease the reabsorption of sodium which means decrease the reabsorption of water which subsequently decrease BP.

Side effect of K⁺sparing diuretics:

Hyperkalemia, gynaecomastia.

8. DIRECT RENIN INHIBITORS:

· Aliskiren the only available member of the latest class of RAS inhibitors which act by blocking catalytic activity of renin and inhibiting production of Ang-I and Ang-II.

· Aliskiren is an equally effective antihypertensive as ACE inhibitors.

9. CENTRAL SYMPATHOLYTICS:

*Clonidine is imidazoline derivative having complex actions. Clonidine is a partial agonist with high affinity and high intrinsic activity at α₂ receptors, especially α_2Asubtype in brainstem. The major haemodynamic effect result from stimulation of α_2Areceptors present mainly postjunctionally in medulla (vasomotor centre). This decrease sympathetic out-flow → fall in BP and bradycardia.

On chronic administration of clonidine decrease cardiac output contributes more to the fall in BP.

Dose:Start with 100 µg OD or BD,

Max. 300 µg TDS, orally or i.m.

CATAPRES 150 µg tab, ARKAMIN 100 µg tab.

Side effect:

sedation

mental depression

disturbed sleep

dryness of mouth

constipation.

*Methyldopa acts on central α₂receptors to decrease efferent sympathetic activity.it may be acting on a different population of neurones in the vasomotor centre than clonidine.

In large doses, methyldopa inhibits the enzyme dopa decarboxylase in brain and periphery → reduce NA synthesis and form the false transmitter methyl-NA in periphery as well. These mechanisms were considered to be responsible for the antihypertensive effect.

Dose: 0.25-0.5 g BD-QID oral.

Side effect:

Sedation

Reduce mental capacity

Dryness of mouth

Weight gain

Hepatitis

Fever

Rash

10. VASODILATORS:

· * Hydralazine:

Vasodilation:

Opens K+ channels and relaxes the smooth muscles of arteries.

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This leads to decrease in peripheral vascular resistances.

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Decrease in arterial blood pressure.

Dose: 40 mg/d to 200 mg/d

Contraindication:

Ischemic heart disease

Side effect:

CNS: headache, dizziness

CVS: palpitation, flushing, angina

GIT: Nausea

SKIN: sweating, skin rashes.

*Minoxidil:

Opens k⁺ channels in smooth muscles of arteries.

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Hyperpolarization of smooth muscles leading to dilation of blood vessels.

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Decrease in peripheral vascular resistance.

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Decrease in blood pressure

Dose: 5-40 mg/d in single or divided doses.

Side effects:

CNS: headache

CVS: tachycardia, palpitation, angina

SKIN: sweating, flushing

RENAL: edema.

*DIAZOXIDE:

It is an effective and relatively long-acting parenteral vasodilator.

Opening k⁺ channel in the smooth muscles of arteries thus relaxing them.

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This decreases peripheral vascular resistance.

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Decreased arterial blood pressure.

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Relax sympathetic system stimulation.

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Dose: Started with low doses about 50 to 150mg.

Dose of 150mg should be increased after every 5 min until BP is lowered.

Contraindication:

Diabetes mellitus

Congestive cardiac failure.

Side effect:

CVS: angina

ENDO: hyperglycemia

RENAL: edema.

*SODIUM NITROPRUSSIDE:

It is poisonous if given orally because of hydrolysis into cyanide.

It dilates both arteries and venous vessels.

Its action is due to nitrous oxide.

· Side effect:

BLOOD: methemoglobinemia

THIOCYNATE POISONING: weakness, psychosis, muscle spasms

ENDO: delayed hypothyroidism

CYANIDE TOXICITY: arrhythmias

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