Wednesday, May 29, 2013

Pathology Quiz

 Increased lipolysis of fat stores, which can result from starvation, diabetes mellitus, or corticosteroid use, is most likely to cause steatosis (fatty liver) through which one of the following mechanisms?

A.Decreased free fatty acid excretion from the liver leads to free fatty acid accumulation in hepatocytes 
 B.Excess NADH (high NADH/NAD ratio) causes excess production of lactate from pyruvate, which accumulates in hepatocytes 
 C.Increased free fatty acid delivery to the liver leads to triglyceride accumulation in hepatocytes 
 D.Inhibition of apoprotein synthesis by the liver leads to phospholipid accumulation in hepatocytes 
 E.Inhibition of HMG-CoA reductase activity leads to cholesterol accumulation in hepatocytes 

An adult patient presents with the sudden onset of massive diarrhea. Grossly, this individual’s stool has the appearance of “rice-water” because of the presence of flecks of mucus. Cultures of this patient’s stool grow Vibrio cholerae, a curved, gram-negative rod that secretes an enterotoxin consisting of a toxic A subunit and a binding B subunit. The cholera enterotoxin causes massive diarrhea by which of the following mechanisms?

 A.Inhibiting the conversion of Gi-GDP to Gi-GTP 
 B.Inhibiting the conversion of Gs-GTP to Gs-GDP 
 C.Stimulating the conversion of Gi-GDP to Gi-GTP 
 D.Stimulating the conversion of Gs-GDP to Gs-GTP 
 E.Stimulating the conversion of Gs-GTP to Gs-GDP 

A 24-year-old female presents with severe pain during menses (dysmenorrhea). To treat her symptoms, you advise her to take indomethacin in the hopes that it will reduce her pain by interfering with the production of which of the following
 D.Phospholipase A2 
 E.Prostaglandin F2 

A 23-year-old female presents with progressive bilateral loss of central vision. You obtain a detailed family history from this patient and produce the associated pedigree (dark circles or squares indicate affected individuals). Which of the following transmission patterns is most consistent with this patient’s family history? 

 A.Autosomal recessive 
 B.Autosomal dominant 
 C.X-linked recessive 
 D.X-linked dominant 

An 8-month-old male infant is admitted to the hospital because of a bacterial respiratory infection. The infant responds to appropriate antibiotic therapy, but is readmitted several weeks later because of severe otitis media. Over the next several months, the infant is admitted to the hospital multiple times for recurrent bacterial infections. Workup reveals extremely low serum antibody levels. The infant has no previous history of viral or fungal infections. Which of the following is the most likely diagnosis?

 A.Isolated IgA deficiency 
 B.Chronic granulomatous disease 
 C.DiGeorge’s syndrome 
 D.Wiskott-Aldrich syndrome 
 E.linked agammaglobulinemia of Bruton 

 A 35-year-old male living in a southern region of Africa presents with increasing abdominal pain and jaundice. He has worked as a farmer for many years, and sometimes his grain has become moldy. Physical examination reveals a large mass involving the right side of his liver, and a biopsy specimen from this mass confirms the diagnosis of liver cancer (hepatocellular carcinoma). The pathogenesis of this tumor involves which of the following substances?

 A.Aflatoxin B1 
 B.Direct-acting alkylating agents 
 C.Vinyl chloride 
 D.Azo dyes 

A 54-year-old male develops a thrombus in his left anterior descending coronary artery. The area of myocardium supplied by this vessel is irreversibly injured. The thrombus is destroyed by the infusion of streptokinase, which is a plasminogen activator, and the injured area is reperfused. The patient, however, develops an arrhythmia and dies. An electron microscopic (EM) picture taken of the irreversibly injured myocardium reveals the presence of large, dark, irregular amorphic densities within mitochondria, which are referred to as which of the following

 A.Apoptotic bodies 
 B.Flocculent densities 
 C.Myelin figures 
 D.Psammoma bodies 
 E.Russell bodies 

Histologic sections of an enlarged tonsil from a 9-year-old female reveal an increased number of reactive follicles containing germinal centers with proliferating B lymphocytes. Which one of the following terms best describes this pathologic process?
 A.B lymphocyte hypertrophy 
 B.Follicular dysplasia 
 C.Follicular hyperplasia 
 D.Germinal center atrophy 
 E.Germinal center metaplasia 

A 19-year-old female is being evaluated for recurrent facial edema, especially around her lips. She also has recurrent bouts of intense abdominal pain and cramps, sometimes associated with vomiting. Laboratory examination finds decreased C4, while levels of C3, decay-accelerating factor, and IgE are within normal limits. These findings are most likely to be associated with which of the following deficiencies?
 A. 2-integrins 
 B.C1 esterase inhibitor 
 C.Decay-accelerating factor 
 D.Complement components C3 and C5 
 E.NADPH oxidase 

Which one of the following laboratory findings is most consistent with an individual who is not taking any medication but has a familial deficiency of coagulation factor VII, assuming all other coagulation factors to be within normal limits? 

Answers & explanation

The answer is: C

Free fatty acids are normally taken up by the liver and esterified to triglyceride, converted to cholesterol, oxidized into ketone bodies, or incorporated into phospholipids that can be excreted from the liver as very-low-density lipoproteins (VLDLs). Abnormalities involving any of these normal metabolic pathways may lead to the accumulation of triglycerides within the hepatocytes. This accumulation of triglycerides is called fatty change or steatosis. Examples of abnormalities that produce hepatic steatosis include diseases that cause excess delivery of free fatty acids to the liver or diseases that cause impaired lipoprotein synthesis. Excess delivery of free fatty acids occurs in conditions that increase lipolysis of adipose tissue, such as starvation, diabetes mellitus, and corticosteroid use. Increased formation of triglycerides can result from alcohol use, as alcohol causes excess NADH formation (high NADH/NAD ratio), increases fatty acid synthesis, and decreases fatty acid oxidation. Impaired apoprotein synthesis occurs with carbon tetrachloride poisoning, phosphorous poisoning, and protein malnutrition. Inhibition of HMG-CoA reductase activity is the mechanism of lovastatin, which indirectly increases liver LDL receptors and increases LDL clearance from the blood.

The answer is: B

Many extracellular substances cause intracellular actions via second-messenger systems. These second messengers may bind to receptors that are located either on the surface of the cell or within the cell itself. Substances that react with intracellular receptors are lipid-soluble (lipophilic) molecules that can pass through the lipid plasma membrane. Examples of these lipophilic substances include thyroid hormones, steroid hormones, and the fat-soluble vitamins A and D. Once inside the cell these substances generally travel to the nucleus and bind to the hormone response element (HRE) of DNA.
Some substances that react with cell surface receptors bind to guanine-nucleotide regulatory proteins. These proteins, called G proteins, may be classified into four categories, namely Gs, Gi, Gt, and Gq. Two of these receptors, Gs and Gi, regulate the intracellular concentration of cyclic adenosine 5'-monophosphate (cAMP). In contrast, Gt regulates the intracytoplasmic levels of cyclic guanosine 5'-monophosphate (cGMP), and Gq regulates the intracytoplasmic levels of calcium ions. Gs and Gi regulate intracellular cAMP levels by their actions on adenyl cyclase, an enzyme located on the inner surface of the plasma membrane that catalyzes the formation of cAMP from ATP. The adenylate cyclase G protein complex is composed of the following components: the receptor, the catalytic enzyme (i.e., adenyl cyclase), and a coupling unit. The coupling unit consists of GTP-dependent regulatory proteins (G proteins), which may either be stimulatory (Gs) or inhibitory (Gi). When bound to GTP and active, Gs stimulates adenyl cyclase and increases cAMP levels. (Gs can be thought of as the “on switch.”) In contrast, when bound to GTP and active, Gi inhibits adenyl cyclase and decreases cAMP levels. (Gi can be thought of as the “off switch.”) It is important to note that cholera toxin and pertussis toxin both act by altering this adenyl cyclase pathway. Cholera toxin inhibits the conversion of Gs-GTP to Gs-GDP. In contrast, pertussis toxin inhibits the activation of Gi-GDP to Gi-GTP. Therefore, both cholera toxin and pertussis toxin prolong the functioning of adenyl cyclase and therefore increase intracellular cAMP, but their mechanisms are different. Cholera toxin keeps the “on switch” in the “on” position, while pertussis toxin keeps the “off switch” in the “off” position.

The answer is: E

Certain drugs are important in the control of acute inflammation because they inhibit portions of the metabolic pathways involving arachidonic acid. For example, corticosteroids induce the synthesis of lipocortins, a family of proteins that are inhibitors of phospholipase A2. They decrease the formation of arachidonic acid and its metabolites, prostaglandins and leukotrienes. Aspirin, indomethacin, and other nonsteroidal anti-inflammatory drugs (NSAIDs), in contrast, inhibit cyclooxygenase and therefore inhibit the synthesis of prostaglandins and thromboxanes. The prostaglandins have several important functions. For example, prostaglandin E2 (PGE2), produced within the anterior hypothalamus in response to interleukin 1 secretion from leukocytes, results in fever. Therefore aspirin can be used to treat fever by inhibiting PGE2 production. PGE2 is also a vasodilator that can keep a ductus arteriosus open. At birth, breathing decreases pulmonary resistance and reverses the flow of blood through the ductus arteriosus. The oxygenated blood flowing from the aorta into the ductus inhibits prostaglandin production and closes the ductus arteriosus. Therefore prostaglandin E2 can be given clinically to keep the ductus arteriosus open, while indomethacin can be used to close a patent ductus. Prostaglandin F2 (PGF2) causes uterine contractions, which can result in dysmenorrhea. Indomethacin can be used to treat dysmenorrhea by inhibiting the production of PGF2. Bradykinin is a nonapeptide that increases vascular permeability, contracts smooth muscle, dilates blood vessels, and causes pain. It is part of the kinin system and is formed from high-molecular-weight kininogen (HMWK). Histamine, a vasoactive amine that is stored in mast cells, basophils, and platelets, acts on H1 receptors to cause dilation of arterioles and increased vascular permeability of venules.

The answer is: E

Almost all genes occur on chromosomes within the nucleus. There are a few genes, however, that are located within the mitochondria. These mitochondrial genes are found on mitochondrial DNA (mtDNA). These genes are all of maternal origin, possibly because ova have mitochondria within the large amount of cytoplasm while sperm do not. This maternal origin means that mothers transmit all of the mtDNA to both male and female offspring, but only the daughters transmit it further. No transmission occurs through males. This mtDNA contains genes that mainly code for oxidative phosphorylation enzymes, such as NADH dehydrogenase, cytochrome c oxidase, and ATP synthase. Symptoms of deficiencies of these enzymes occur in organs that require large amounts of ATP, such as the brain, muscle, liver, and kidneys. The mtDNA of these patients may be composed of either a mixture of mutant and normal DNA (heteroplasm) or of mutant DNA entirely (homoplasmy). The severity of these diseases correlates with the amount of mutant mtDNA that is present. One disease associated with mitochondrial inheritance is Leber hereditary optic neuropathy (LHON), which is characterized by progressive bilateral loss of central vision and usually occurs between 15 and 35 years of age. Other examples of mitochondrial inheritance include mitochondrial myopathies, which are characterized by the presence in muscle of mitochondria having abnormal sizes and shapes. These abnormal mitochondria may result in the histologic appearance of the muscle as ragged red fibers. Electron microscopy reveals the presence within large mitochondria of rectangular crystals that have a “parking lot” appearance.

The answer is: E

In X-linked agammaglobulinemia of Bruton, B cells are absent but numbers and function of T cells are normal. This abnormality results from defective maturation of B lymphocytes beyond the pre-B stage. This maturation defect leads to decreased or absent numbers of plasma cells, and therefore immunoglobulin levels are markedly decreased. Male infants with Bruton’s disease begin having trouble with recurrent bacterial infections at about the age of 9 months, which is when maternal antibodies are no longer present in the affected infant. Therapy for Bruton’s disease consists primarily of IV gamma globulin. 
Isolated deficiency of IgA is probably the most common form of immunodeficiency. It is due to a block in the terminal differentiation of B lymphocytes. Most patients are asymptomatic, but some develop chronic sinopulmonary infections. Patients are prone to developing diarrhea (Giardia infection) and also have an increased incidence of autoimmune disease, such as Hashimoto’s thyroiditis. In patients with chronic granulomatous disease (CGD), the neutrophils and macrophages have deficient H2O2 production due to abnormalities involving the enzyme NADPH oxidase. These individuals have frequent infections that are caused by catalase-positive organisms, such as S. aureus, because the catalase produced by these organisms destroys the little hydrogen peroxide that is produced. DiGeorge’s syndrome is a T cell–deficiency disorder that results from hypoplasia of the thymus due to abnormal development of the third and fourth pharyngeal pouches. The parathyroid glands are also abnormal, and these individuals develop hypocalcemia and tetany. Congenital heart defects are also present. Wiskott-Aldrich syndrome is also an X-linked recessive disorder, but it is characterized by thrombocytopenia, eczema, and immune deficiency. The immune abnormalities are characterized by progressive loss of T cell function and decreased IgM. The other immunoglobulin levels are normal or increased. There are decreased numbers of lymphocytes in the peripheral blood and paracortical (T cell) areas of lymph nodes. Both cellular and humoral immunity are affected, and, because patients fail to produce antibodies to polysaccharides, they are vulnerable to infections with encapsulated organisms.

The answer is: A

Many chemicals are associated with an increased incidence of malignancy. These substances are called chemical carcinogens. Although there are direct-acting chemical carcinogens, such as the direct-acting alkylating agents that are used in chemotherapy, most organic carcinogens first require conversion to a more reactive compound. Polycyclic aromatic hydrocarbons, aromatic amines, and azo dyes must be metabolized by cytochrome P450–dependent mixed-function oxidases to active metabolites. Vinyl chloride is metabolized to an epoxide and is associated with angiosarcoma of the liver, not hepatocellular carcinoma. Azo dyes, such as butter yellow and scarlet red, are metabolized to active compounds that have induced hepatocellular cancer in rats, but no human cases have been reported.  -naphthylamine is an exception to the general rule involving cytochrome P450, as the hydrolysis of the nontoxic conjugate occurs in the urinary bladder by the urinary enzyme glucuronidase. In the past there has been an increase in bladder cancer in workers in the aniline dye and rubber industries who have been exposed to these compounds. Aflatoxin B1, a natural product of the fungus Aspergillus flavus, is metabolized to an epoxide. The fungus can grow on improperly stored peanuts and grains and is associated with the high incidence of hepatocellular carcinoma in some areas of Africa and the Far East. Hepatitis B virus is also highly associated with liver cancer in these regions

The answer is: B

With prolonged ischemia, certain cellular events occur that are not reversible, even with restoration of oxygen supply. These cellular changes are referred to as irreversible cellular injury. This type of injury is characterized by severe damage to mitochondria (vacuole formation), extensive damage to plasma membranes and nuclei, and rupture of lysosomes. Severe damage to mitochondria is characterized by the influx of calcium ions into the mitochondria and the subsequent formation of large, flocculent densities within the mitochondria. These flocculent densities are characteristically seen in irreversibly injured myocardial cells that undergo reperfusion soon after injury. Less severe changes in mitochondria, such as mitochondrial swelling, are seen with reversible injury. Cytochrome c released from damaged mitochondria can induce apoptosis, a process through which irreversibly injured cells can shrink and increase the eosinophilia of their cytoplasm. These shrunken apoptotic cells (apoptotic bodies) may be engulfed by adjacent cells or macrophages. Myelin figures are derived from plasma membranes and organelle membranes and can be seen with either reversible or irreversible injury. Psammoma bodies are small, laminated calcifications, while Russell bodies are round, eosinophilic aggregates of immunoglobulin.

The answer is: C

There are many adaptive mechanisms of cells to persistent stimuli. Hypertrophy is an increase in the size of cells. Examples of hypertrophy include enlarged skeletal muscle in response to repeated exercise or anabolic steroid use and enlarged cardiac muscle in response to volume overload or hypertension. In contrast to hypertrophy, hyperplasia is an increase in the number of cells. Hyperplasia may be the result of a physiologic response or a pathologic process. Examples of physiologic hyperplasia include the increased size of the female breast or uterus in response to hormones. Pathologic hyperplasia may be compensatory to some abnormal process, or it may be a purely abnormal process. Examples of compensatory pathologic hyperplasia include the regenerating liver, increased numbers of erythrocytes in response to chronic hypoxia, and increased numbers of lymphocytes within lymph nodes in response to bacterial infections [follicular (nodular) hyperplasia]. Examples of purely pathologic hyperplasia include abnormal enlargement of the endometrium (endometrial hyperplasia) and the prostate (benign prostatic hyperplasia). Atrophy is a decrease in the size and function of cells. Examples of atrophy include decreased size of limbs immobilized by a plaster cast or paralysis, or decreased size of organs affected by endocrine insufficiencies or decreased blood flow. Metaplasia is a term that describes the conversion of one histologic cell type to another. Examples of metaplasia include respiratory epithelium changing to stratified squamous epithelium (squamous metaplasia) in response to prolonged smoking, the normal glandular epithelium of the endocervix changing to stratified squamous epithelium (squamous metaplasia) in response to chronic inflammation, or the normal stratified squamous epithelium of the lower esophagus changing to gastric-type mucosa in response to chronic reflux. In contrast to metaplasia, dysplasia refers to disorganized growth and is characterized by the presence of atypical or dysplastic cells. Dysplasia can be seen in many organs, such as within the epidermis in response to sun damage (actinic keratosis), the respiratory tract, or the cervix (cervical dysplasia).

The answer is: B

Deficiencies of components of the complement system are associated with specific abnormalities. Patients with congenital deficiencies in the early components of the complement cascade have recurrent symptoms resembling those of systemic lupus erythematosus due to the deposition of immune complexes. Patients with deficiencies of the middle complement components (C3 and C5) are at risk for recurrent pyogenic infections, while those lacking terminal complement components (C6, C7, or C8, but not C9) are prone to developing recurrent infections with Neisseria species. A deficiency of decay-accelerating factor (DAF), which breaks down the C3 convertase complex, is seen in paroxysmal nocturnal hemoglobinuria (PNH), a disorder that is characterized by recurrent episodes of hemolysis of red cells because of the excessive intravascular activation of complement. Deficiencies of C1 esterase inhibitor result in recurrent angioedema, which refers to episodic nonpitting edema of soft tissue, such as the face. Severe abdominal pain and cramps, occasionally accompanied by vomiting, may be caused by edema of the gastrointestinal tract. To understand how a deficiency of C1 inhibitor can cause vascularly produced edema (angioedema), note that not only does C1 inhibitor inactivate C1, but it also inhibits other pathways, such as the conversion of prekallikrein to kallikrein and kininogen to bradykinin. A deficiency of C1 inhibitor also leads to excess production of C2, a product of C2 called C2 kinin, and bradykinin. It is the uncontrolled activation of bradykinin that produces the angioedema, as bradykinin increases vascular permeability, stimulates smooth muscle contraction, dilates blood vessels, and causes pain. In contrast, a defect involving  2-integrins is seen with leukocyte adhesion deficiency, while defects involving NADPH of leukocytes are characteristic of chronic granulomatous disease.

The answer is: A

The coagulation cascade involves the formation of fibrin through the intrinsic, extrinsic, and common pathways. The intrinsic pathway is initiated by contact of factor XII with several types of biologic surfaces. Activated XII (XIIa) initiates the formation of XIa and IXa. The extrinsic pathway is initiated by contact of tissue factor with factor VII. Activated factor VII acts together with IXa, VIIIa, and platelet factor 3 (PF-3), which is a phospholipid complex located on the surface of platelets, to produce activated factor X. This begins the common pathway, which continues with the interaction of Xa, Va, PF-3, and Ca++ to cleave prothrombin, forming thrombin, which in turn cleaves fibrinogen to form fibrin. 
Two laboratory tests that are used to evaluate the functioning of the coagulation cascade are prothrombin time (PT) and partial thromboplastin time (PTT). Abnormalities of the extrinsic pathway prolong (not shorten) the PT, while abnormalities of the intrinsic pathway prolong (not shorten) the PTT. Note that abnormalities of the common pathway prolong both the PT and the PTT. To illustrate, deficiencies of factor VII produce an abnormal (prolonged) PT with a normal PTT. Compare these results to each of the following: a normal PT with an abnormal PTT can be seen with deficiencies of factors XII, XI, IX, or VIII, while abnormal PT and PTT are seen with deficiencies of X, V, prothrombin, or fibrinogen.

I hope this quiz will help you! This is a start more yet to come !

Thursday, May 23, 2013

What is Basic Anatomy?

The definition of anatomy
Anatomy is a science dealing with morphology and structure of the body. 

Anatomy includes those structures that can be seen grossly (without the aid of magnification) and microscopically (with the aid of magnification). 

Typically, when used by itself, the term 'anatomy' tends to mean gross or macroscopic anatomy-that is, the study of structures that can be seen without using a microscopic. 

Microscopic anatomy, also called 'histology', is the study of cells and tissues using a microscope. 

The significance of studying anatomy

Anatomy forms the basis for the practice of medicine. 
Anatomy leads the physician towards an understanding of a patient's disease whether he or she is carrying out a physical examination or using the most advanced imaging techniques.
 Anatomy is also important for dentists, physical therapists, and all others involved in any aspect of patient treatment that begins with an analysis of clinical signs. 
The ability to interpret a clinical observation correctly is therefore the endpoint of a sound anatomical understanding. 

The classification of anatomy

By the different research methods, anatomy can be divided into micro-anatomy and macro-anatomy.
People recognize human body at different levels.

Whole body---organs(systems)---tissues---cells---cellular organs---ultramicrostructures---molecular

Presently, we study macro-anatomy. According to the different purposes, different research methods, macro-anatomy is divided into systematic anatomy and regional anatomy. 

The differences between systematic anatomy and regional anatomy are as follows: 

Locomotor system
Protection; support ; movement

Digestive system
To digest foods; to secrete enzymes and hormones( endocrine function  ; to   absorb the nutrient elements; to eliminate the useless residues

Respiratory system
To supply the blood with oxygen ; to get rid of excess dioxide; 

Urinary system
By eliminating the metabolic products to maintain the balance of substances in the body.

Reproductive system
Keeping maintenance of species.
secreting hormone

Circulatory system
Cardiovascular system to transport the substances with oxygen and nutrition.
Lymphatic system

The anatomical position

The body is upright,  legs together, and directed forwards
The palms are turned forward, with the thumbs laterally

 Anatomical planes
sagittal planes: Refers to any  longitudinal
planes that divide the human body into a right and a left part.

Coronal planes: Any vertical planes that divide the body into an anterior and a posterior part

Horizontal (transverse) planes: Any horizontal planes that divide the body into an upper and a lower part.They lie at right angles to both the sagittal and coronal planes.

Terms of direction

Introduction of locomotor system:
The formation of locomotor system, which comprise:

         There are 206 bones in the human body, which can be classified into a number of kinds according to their positions and shapes.

 The shape and classifications of bones

1- According to the position,all the bones can be classified into  four categories :

skull :                             29

bones of trunk:             51

bones of upper limb:   64

bones of lower limb:    62

The structures of bone

1- Periosteum which is a fibrous membrane, containing rich blood vessels and  nerves.
A. play an important role in regeneration of bones, having osteoblast. 
B. Provide nutrition for the development, growth and reconstruction  of bones
C. Containing receptor (accepting stimulate)
Parts: periosteum (except articular surface) / endosteum

2- Bony substance:
The physical properties of bone
      hard: bone removed organic materials; hard but fragile by  demonstration;
      flexible: bone removed inorganically material specimen, not hard, but flexible
The arrangement of bony substance
A- Compact substance: consist of regular compact bony plate
B- Sponge substance:   
      outer plate / diploĆ« / inner plate

The arrangement looks like a frame of a house.

Bone marrow
i) Which is located within medullary cavity and ‘network-eye’, divided into red and yellow bone marrow.
ii) 3-5y red bone marrow carrying out the function of blood-forming . For adult most of it become yellow bone marrow, but proximal end of humerus (femur), short bone, flat bone have life-long time red marrow.

outer plate / diploƫ / inner plate

The structure of bone

Bone is hard and flexible . It depends on its chemical components and arrangements.

Definition: The bones are connected together by means of fibrous, cartilaginous or osseous tissues at different parts of their surface. The connection is called articulation or joint.

1. The classification of articulations
i) Synarthrosis (immovable joints, direct joint)
    Definition: two or more separated bones are directly connected by fibrous , cartilaginous or osseous tissues.

Fibrous joints: 
a. sutures: skull
b. syndesmoses: ligmentum flava (yellow lig) { tibiofibular joint}
c. Gomphosis

a. synchondrosis: between sternum and 1st costal cartilage
 b. symphyses :     pubic symphysis


ii) Diarthrosis (movable articulations, synovial joints)  
Definition: the bones are connected by the joint capsule and ligaments. 

A- The essential (basical ) structures of synovial joint
 1. The articular surface: which is  a part of surface of bone covered by  hyaline cartilage.
 2. The articular capsule: it looks like a irregular sac, attaches the periphery of the articular surface and adjacent surface. Articular capsule include two parts: outer layer( fibrous layer ) and inner layer( synovial layer---produce synovial fluid)
 3. The articular cavity: it is a closed space enclosed by the synovial membrane and the articular cartilage. 

B. The accessory structures of the synovial joints
1. The ligment:
     intracapsular lig: it is inside the joint , surrounded by synovial membrane\
     extracapsular lig: which is outside the capsule
2. The articular disc (or cartilage): it is fibrocartilaginous, and divides the articular cavity    partially or completely into 2 parts.
3. The articular lip (labrum): it is a fibrocartilaginous ring, which can deepen the articular surface

C. The movement of joint

1. Flexion and extension: they are performed in the coronal axis. Flexion makes the angle between the adjacent bones decrease; extension increase the angle.
2. Adduction and abduction: which are performed in sagittal axis. Adduction means the movement toward the midline of the body; abduction means the movement apart from the midline.
3. Pronation and supination: in standard anatomical position, the pronation means the palm is turned backward; the supination means the palm is turned forward.
4. Rotation: the movement is performed in the vertical axis. A bone is moving around the vertical axis.
5. Circumduction: while the proximal end of a  bone remains relative stable, the distal end moves in a circle.

The movement of joint


  • Skeletal muscle: to move the skeleton
  • Cardiac muscle: to form the heart
  • Smooth muscle: to constitute viscera

Over 600 muscles in the body
Muscles are grouped by location:

  • Muscles of head.
  • Muscles of neck.
  • Muscles of thorax.
  • Muscles of.
  • Abdomen.
  • Muscles of upper limb.
  • Muscles of lower limb.

Naming the skeletal muscles by sereral criteria: 
1. location(brachialis); 
2. shape (trapezius);
3. direction of the muscle fibers(rectus,oblique); 
4. location ofattachments(brachioradialis); 
5.number of origins (biceps); 
6. action(flexor,extensor)

 The structures of muscles
I) Tendon and belly 

Belly: the fleshy part of a muscle

Tendon: the bundles consisting of connective tissue blending  
               with strong collagen

II)  The origin and insertion:
Origin: a fixed (less movable) attachment of a muscle

Insertion: a movable attachment of a muscle

Generally speaking, the origin is near the midline; the insertion is far from the midline. However, the origin and insertion may be exchanged each other. For example: pectoralis major m.

III) The relations of muscles to other structures

  • Most of muscles are attached to bones,
  • some of muscles are attached to skin, e.g; Platysma m. beneath the skin of neck
  • some of muscles are attached to organs. e.g; eyeball

IV) The shape of muscles

Because of functional differences, muscles have different shape.

The shape of muscles

IV)  The functional classification of muscles

Agonists ( prime movers ): the main muscles which contract to produce desired  movement
Antagonist: the muscles which act to oppose the action of  agonist

Agonist---contraction; antagonist---relax

Synergist: cooperation in a special action as a supporter
Fixator: fix proximal end of limbs in a special position.
               eg. Tightly making a fist


Fascia and tendinous sheath
1) Superficial fascia: lies under skin and covers the entire body containing a lot of fat / increase mobilityof skin; thermal insulation; a store of energy /contain cutaneous nerve, blood vessels and skin muscles 

2) Deep fascia: dense and inelastic
      membrane of collagenous fibers

Thursday, May 16, 2013


 Impairment of the capacity to think with normal
speed and clarity, associated with inattentiveness and disori-
entation. Delirium is a special example of an acute confu-
sional state in which impaired attention and reasoning are
associated with agitation, hallucinations, and in some cases,
tremor and convulsions.

 Inability to remain awake without external
stimulation; often associated with some degree of confusion.

 State in which only vigorous external stimulation
can arouse the patient; once aroused, responses remain
markedly impaired.

 Deep sleep-like state; patient cannot be aroused even
with vigorous or repeated external stimulation.

Causes of change in consciousness
1. With abnormal CT scan
• Hemispheric mass lesions that cross the midline or
impinge upon the brainstem.
• Brainstem lesions that directly affect the reticular forma-
• Subarachnoid hemorrhage.
2. With normal CT scan
• Inflammatory disorders, such as bacterial meningitis and
viral encephalitis.
• Exogenous toxins,such as sedative drugs,alcohols,opioids,
and carbon monoxide.
• Endogenous metabolic insults, such as global hypoxic-
ischemic insults, hypoglycemia, hyperammonemia, and
• Postictal state.
• Selective brainstem ischemia.

Diagnosis of cause of changes in consciousness:
Establishing a differential diagnosis for the cause of a patient’s change in
consciousness requires evaluation of the history preceding the
change,the physical examination,and the effectiveness of initial
empirical therapy.
Categories of cause of changes in consciousness
 Toxic and metabolic (e.g., opiate overdose, alcohol).
 Infectious (e.g.,meningitis,encephalitis,septic shock).
 Cerebrovascular (e.g.,stroke).
 Other (e.g.,seizures,neoplasms).

Role of history in diagnosis of changes in consciousness

  •  Preceding headache suggests meningitis,subarachnoid hemorrhage, or encephalitis.
  •  Preceding intoxication,confusion,or delirium suggests a diffuse process such as meningitis, endogenous metabolic insults, or exogenous toxins.
  •  Sudden onset of coma suggests brain stem infarct or hemorrhage (e.g., subarachnoid hemorrhage).

Role of physical examination in diagnosis of changes in
Localizing signs: Suggest focal lesion. 
> No localizing signs: Suggests encephalopathy as a result of
either an exogenous toxin or an endogenous metabolic
>  Important Structural versus Metabolic causes of COMA
 Asymmetrical or reflex functioning of the motor system indi-
cates a focal mass lesion. Changes in pupillary size and reflexes
are also useful in assessing the cause of coma.
 A unilaterally dilated nonreactive pupil suggests oculomotor
nerve (CN III) compression by an expanding hemispheric
> Pinpoint minimally reactive pupils suggests compromise of
the pontine tegmentum (e.g., in a pontine hemorrhage);
may also be seen in opiate intoxication. Small but reactive
pupils are a feature of many metabolic encephalopathies.
> Minimally reactive pupils in a mid or slightly dilated posi-
tion suggests a midbrain lesion.
> Bilaterally dilated, nonreactive pupils can be seen in cases of
damage to the midbrain tectum or in global ischemic brain
injury. It may also be caused by atropine and similar anti-
cholinergic agents.

Friday, May 10, 2013

How does HUNTINGTON CHOREA present? How to treat the disease?

Its autosomal dominant disorder characterized pathologically by degeneration of GABA-nergic neurons of caudate nucleus and clinically by chorea and dementia.

Clinical presentation

  • Involuntary writhing motions (i.e., choreiform) when pre-senting in adults during the fourth or fifth decades; seizures
  • and rigidity when presenting at a younger age.
  • Depression and cognitive impairment (i.e., dementia).
  • Patients often commit suicide because of the prognosis.


  •  Huntingtin gene on chromosome 4.
  •  Mutation is an increase in the number of CAG repeats in the huntingtin gene.
  • Transcription of the expanded CAG repeats results in the accumulation of excess numbers of polygluta-mine residues in the huntingtin protein. 
  • There is an inverse relationship between the number of CAG repeats and the age of onset of disease. 
  • The CAG repeats increase in number during spermatogenesis,which results in the disease presenting earlier in successive generations (referred to as anticipa-tion)

Clinical manifestation
i. The disease manifests between age 20-40 years.
ii.Chorea:sudden,unexpected and purposeless contractions of proximal muscles
iii. Changes in personality,marked tendency for suicide and dementia

Microscopic findings
Loss of medium spiny GABA-nergic neurons in the caudate and putamen,associated with gliosis

Genetic diagnosis possible but controversial

Antipsychotic drugs (e.g; haloperidol)

Friday, May 3, 2013

Beauty tips for healthy skin

Walnuts hold alpha-linolenic acid which is an omega-3 fat that helps lubricate the layer of skin that keeps it moist. Just a 1/2 ounce serving gives you all of your daily recommended serving of ALA. Studies show that eating walnuts around dinnertime can also help you get better beauty sleep!

Dark chocolate is high in flavonoids which can rejuvenate your complexion and give you smoother, softer, hydrated skin. It can also increase the blood flow to the brain for up to 2 hours after consuming. Some even suggest that may reduce the risk of dementia later in life.

Kiwi fruit contain high vitamin C levels that even out skin texture and fight damage and when scrubbed on the face, they act as tiny exfoliators. The best ways to use them? Slice them and apply or mash them into a paste that can be left on to improve your complexion.