Total Topics :1155

- The forehead is formed by the smooth, broad, convex plate of bone called the frontal squama.
- In foetal skulls, the halves of the frontal squama are divided by a metopic suture.
- In most people, the halves of the frontal bone begin to fuse during infancy and the suture between is usually not visible after 6 years of age.
- The frontal bone forms the thin roof of the orbits (eye sockets).
- Just superior to and parallel with each supraorbital margin is a bony ridge, the superciliary arch, which overlies the frontal sinus. This arch is more pronounced in males.
- Between these arches there is a gently, rounded, medial elevation called the gabella; this term derives from the Latin word glabellus meaning smooth and hairless. In most people, the skin over the gabella is hairless.
-The slight prominences of the forehead on each side, superior to the superciliary arches, are called frontal eminences (tubers).
- The supraorbital foramen (occasionally a notch), which transmits the supraorbital vessels and nerve is located in the medial part of the supraorbital margin.
- The frontal bone articulates with the two parietal bones at the coronal suture.
-It also articulates with the nasal bones at the frontonasal suture. At the point where this suture crosses the internasal suture in the medial plane, there is an anthropological landmark called the nasion . The depression is located at the root of the nose, where it joins the cranium.
- The frontal bone also articulates with the zygomatic, lacrimal, ethmoid, and sphenoid bones.
In about 8% of adult skulls, a remnant of the inferior part of the metopic (interfrontal) suture is visible. It may be mistaken in radiographs for a fracture line by inexperienced observers.
- The superciliary arches are relatively sharp ridges of bone and a blow to them may lacerate the skin and cause bleeding.
- Bruising of the skin over a superciliary arch causes tissue fluid and blood to accumulate in the surrounding connective tissue, which gravitates into the upper eyelid and around the eye. This results in swelling and a "black eye".
- Compression of the supraorbital nerve as it emerges from its foramen causes considerable pain, a fact that may be used by anaesthesiologists and anaesthetists to determine the depth of anaesthesia and by physicians attempting to arouse a moribund patient.


Graded Contractions and Muscle Metabolism

The muscle twitch is a single response to a single stimulus. Muscle twitches vary in length according to the type of muscle cells involved. .


Fast twitch muscles such as those which move the eyeball have twitches which reach maximum contraction in 3 to 5 ms (milliseconds).  [superior eye] and [lateral eye] These muscles were mentioned earlier as also having small numbers of cells in their motor units for precise control.

The cells in slow twitch muscles like the postural muscles (e.g. back muscles, soleus) have twitches which reach maximum tension in 40 ms or so.

 The muscles which exhibit most of our body movements have intermediate twitch lengths of 10 to 20 ms.

The latent period, the period of a few ms encompassing the chemical and physical events preceding actual contraction.

This is not the same as the absolute refractory period, the even briefer period when the sarcolemma is depolarized and cannot be stimulated. The relative refractory period occurs after this when the sarcolemma is briefly hyperpolarized and requires a greater than normal stimulus

Following the latent period is the contraction phase in which the shortening of the sarcomeres and cells occurs. Then comes the relaxation phase, a longer period because it is passive, the result of recoil due to the series elastic elements of the muscle.

We do not use the muscle twitch as part of our normal muscle responses. Instead we use graded contractions, contractions of whole muscles which can vary in terms of their strength and degree of contraction. In fact, even relaxed muscles are constantly being stimulated to produce muscle tone, the minimal graded contraction possible.

Muscles exhibit graded contractions in two ways:

1) Quantal Summation or Recruitment - this refers to increasing the number of cells contracting. This is done experimentally by increasing the voltage used to stimulate a muscle, thus reaching the thresholds of more and more cells. In the human body quantal summation is accomplished by the nervous system, stimulating increasing numbers of cells or motor units to increase the force of contraction.

2) Wave Summation ( frequency summation) and Tetanization- this results from stimulating a muscle cell before it has relaxed from a previous stimulus. This is possible because the contraction and relaxation phases are much longer than the refractory period. This causes the contractions to build on one another producing a wave pattern or, if the stimuli are high frequency, a sustained contraction called tetany or tetanus. (The term tetanus is also used for an illness caused by a bacterial toxin which causes contracture of the skeletal muscles.) This form of tetanus is perfectly normal and in fact is the way you maintain a sustained contraction.

Treppe is not a way muscles exhibit graded contractions. It is a warmup phenomenon in which when muscle cells are initially stimulated when cold, they will exhibit gradually increasing responses until they have warmed up. The phenomenon is due to the increasing efficiency of the ion gates as they are repeatedly stimulated. Treppe can be differentiated from quantal summation because the strength of stimulus remains the same in treppe, but increases in quantal summation

Length-Tension Relationship: Another way in which the tension of a muscle can vary is due to the length-tension relationship. This relationship expresses the characteristic that within about 10% the resting length of the muscle, the tension the muscle exerts is maximum. At lengths above or below this optimum length the tension decreases.



1. Composition

a. Inorganic (70%)—calcium hydroxyapatite crystals.

b. Organic (30%)—water and type I collagen.


2. Types of dentin

a. Primary dentin

(1) Dentin formed during tooth development, before completion of root formation.

It constitutes the majority of dentin found in a tooth.

(2) It consists of a normal organization of dentinal tubules.

(3) Circumpulpal dentin

(a) The layer of primary dentin that surrounds the pulp chamber.  It is formed after the mantle dentin.

(b) Its collagen fibers are parallel to the DEJ.

b. Secondary dentin

(1) Dentin formed after root formation is complete.

(2) Is deposited unevenly around the pulp chamber, forming along the layer of dentin closest to the pulp.

It therefore contributes to the decrease in the size of the pulp chamber as one ages.

(3) It consists of a normal, or slightly less regular, organization of dentinal tubules. However,

as compared to primary dentin, it is deposited at a slower rate.

(4) Although the dentinal tubules in secondary dentin can be continuous with those in primary

dentin, there is usually a tubular angle change between the two layers.


c. Tertiary (reparative, reactive) dentin

(1) Dentin that is formed in localized areas in response to trauma or other stimuli such as caries, tooth wear, or dental work.

(2) Its consistency and organization vary. It has no defined dentinal tubule pattern


d. Mantle dentin

(1) The outermost layer of dentin
(2) Is the first layer of dentin laid down by odontoblasts adjacent to the DEJ.

(3) Is slightly less mineralized than primary dentin.

(4) Has collagen fibers that are perpendicular to the DEJ.

(5) Dentinal tubules branch abundantly in this area.


e. Sclerotic (transparent) dentin

(1) Describes dentinal tubules that have become occluded with calcified material .

(2) Occurs when the odontoblastic processes retreat, filling the dentinal tubule with calcium phosphate crystals.

(3) Occurs with aging.

f. Dead tracts

(1) When odontoblasts die, they leave behind empty dentinal tubules, or dead tracts.

(2) Occurs with aging or trauma.

(3) Empty tubules are potential paths for bacterial invasion.

3. Structural characteristics and microscopic features:

a. Dentinal tubules

(1) Tubules extend from the DEJ to the pulp chamber.

(2) The tubules taper peripherally (i.e., their diameters are wider as they get closer to the pulp). Since the tubules are distanced farther apart at the periphery, the density of tubules is greater closer to the pulp.

(3) Each tubule contains an odontoblastic process or Tomes’ fiber.

Odontoblastic processes are characterized by the presence of a network of microtubules, with

Occasional mitochondria and vesicles present.

Note: the odontoblast’s cell body remains in the pulp chamber.

(4) Coronal tubules follow an S-shaped path, which may result from the crowding of  odontoblasts as they migrate toward the pulp during dentin formation.


b. Peritubular dentin (intratubular dentin)

(1) Is deposited on the walls of the dentinal tubule, which affects (i.e., narrows)the diameter of the tubule .

(2) It differs from intertubular dentin by lacking a collagenous fibrous matrix. It is also more mineralized than intertubular dentin.

c. Intertubular dentin

(1) The main part of dentin, which fills the space between dentinal tubules

 (2) Is mineralized and contains a collagenous matrix.

d. Interglobular dentin

(1) Areas of hypomineralized or unmineralized dentin caused by the failure of globules or calcospherites to fuse uniformly with mature dentin.


(2) Dentinal tubules are left undisturbed as they pass through interglobular dentin; however,

No peritubular dentin is present.

(3) Interglobular dentin is found in the:

(a) Crown—just beneath the mantle dentin.

(b) Root—beneath the dentinocemental junction, giving the root the appearance of a granular

layer (of Tomes).


e. Incremental lines

(1) Dentin is deposited at a daily rate of approximately 4 microns.

(2) As dentin is laid down, small differences in collagen fiber orientation result in the formation of incremental lines.

(3) Called imbrication lines of von Ebner.

(a) Every 5 days, or about every 20 µm, the changes in collagen fiber orientation appear more

accentuated. This results in a darker staining line, known as the imbrication line of von


(b) These lines are similar to the lines of Retzius seen in enamel.


f. Contour lines of Owen

(1) An optical phenomenon that occurs when the secondary curvatures of adjacent dentinal tubules coincide, resulting in the appearance of lines known as contour lines of Owen.

(2) Contour lines of Owen may also refer to lines that appear similar to those just described; however, these lines result from disturbances in mineralization.


g. Granular layer of Tomes

(1) A granular or spotty-appearing band that can be observed on the root surface adjacent to the dentinocemental junction, just beneath the cementum.



An acute, contagious disease caused by Corynebacterium diphtheriae, characterized by the formation of a fibrinous pseudomembrane, usually on the respiratory mucosa, and by myocardial and neural tissue damage secondary to an exotoxin.

Cutaneous diphtheria (infection of the skin) can occur when any disruption of the integument is colonized by C. diphtheriae. Lacerations, abrasions, ulcers, burns, and other wounds are potential reservoirs of the organism. Skin carriage of C. diphtheriae is also a silent reservoir of infection.


C. diphtheriae may produce exotoxins lethal to the adjacent host cells. Occasionally, the primary site is the skin or mucosa elsewhere. The exotoxin, carried by the blood, also damages cells in distant organs, creating pathologic lesions in the respiratory passages, oropharynx, myocardium, nervous system, and kidneys.


The myocardium may show fatty degeneration or fibrosis. Degenerative changes in cranial or peripheral nerves occur chiefly in the motor fibers

In severe cases, anterior horn cells and anterior and posterior nerve roots may show damage proportional to the duration of infection before antitoxin is given. The kidneys may show a reversible interstitial nephritis with extensive cellular infiltration.

The diphtheria bacillus first destroys a layer of superficial epithelium, usually in patches, and the resulting exudate coagulates to form a grayish pseudomembrane containing bacteria, fibrin, leukocytes, and necrotic epithelial cells. However, the areas of bacterial multiplication and toxin absorption are wider and deeper than indicated by the size of the membrane formed in the wake of the spreading infection.


Congenital anomalies 

1. Meckel's diverticulum (a true diverticulum) is due to persistence of the omphalomesenteric vitelline duct. 
2. Atresia is a congenital absence of a region of bowel, leaving a blind pouch or solid fibrous cord. 
3. Stenosis refers to a narrowing of any region of the gastrointestinal tract, which may cause obstruction. 
4. Duodenal diverticula are areas of congenital weakness permitting saccular enlargement. The duodenum is the most common region of the small bowel to contain diverticula. 
5. Diverticula of jejunum and ileum are herniations of mucosa and submucosa at points where the mesenteric vessels and nerves enter. 


1. Bacterial enterocolitis
may be caused by the ingestion of preformed bacterial toxins, producing symptoms ranging from severe but transient nausea, vomiting, and diarrhea (Staphylococcus aureus toxin) to lethal paralysis (Clostridium botulinum toxin). Ingestion of toxigenic bacteria with colonization of the gut (e.g., Vibrio cholera, toxigenic E. coli, various species of Campylobacter jejuni, Shigella, salmonel
Yersinia, and many others) is another potential cause. 

2. Nonbacterial gastroenterocolitis
a. Viral 
(1) Rotavirus (children)
(2) Parvovirus (adults) 
b. Fungal-Candida 
c. Parasitic 
(1 ) Entamoeba histolytica 
(2) Giardia lamblia 

3. In HIV patients. Causes of infectious diarrhea in HIV patients include Cryptosporidium, Microsporidia, isospora belli, CMV, and M. avium-intracellulare. 

C. Malabsorption is defined as impaired intestinal absorption of dietary constituents. 
Clinical features include diarrhea,steatorrhea, weakness, lassitude, and weight loss. Steatorrhea results in deficiency of fat-soluble vitamins (A, D, E, K) and calcium. 

1. Celiac sprue
a. Etiology. Celiac sprue (nontropical sprue or gluten enteropathy) is caused by an allergic, immunologic, or toxic reaction to the gliadin component of gluten. There is a genetic predisposition. 

– Steatorrhea, abdominal distention, flatulence, fatigue, and weight loss

– Iron and vitamin deficiency
– Risk of lymphoma (T-cell type)

Extraintestinal manifestation:
– Dermatitis herpetiformis (a pruritic papulovesicular rash with IgA deposits at the dermoepidermal junction) 

2. Tropical sprue

Etiology. Tropical sprue is of unknown etiology, but may be  caused by enterotoxigenic E. coli. 

3. Disaccharidase deficiency is due to a deficiency of brush border enzymes. Lactase deficiency is most common. 

4. Diverticulosis Coli

- Acquired colonic diverticula are present in nearly half of the population over the age of 50
- Diverticula are associated with low-fiber, low-residue diets
- Etiology is most likely high intraluminal pressure required for propulsion of hard, small stools
- Complications include hemorrhage, acute diverticulitis, perforation, fistula formation 

Obstructive lesions

Hernias cause 15% of small intestinal obstruction. They are due to a protrusion of a serosa-lined sac through a weakness in the wall of the peritoneal cavity. They occur most commonly at the inguinal and femoral canals, at the umbilicus, and with scars. They may lead to entrapment, incarceration, and strangulation of the bowel. 

Tumors of the small bowel account for only 5% of gastrointestinal tumors. 

Benign tumors in descending order of frequency include:
leiomyomas, lipomas, adenomas (polyps), angiomas, and fibromas. Adenomatous polyps are most common in the stomach and duodenum and may be single or multiple, sessile or pedunculated. The larger the polyp, the greater the incidence of malignant transformation. 

Malignant tumors, in descending order of frequency, include: endocrine cell tumors, lymphomas, adenocarcinomas, and leiomyosarcomas. 

Idiopathic Inflammatory Bowel Disease (IBD)

- Chronic, relapsing, idiopathic inflamamtory disease of the GI tract
Crohn’s Disease
– Transmural granulomatous disease affecting any portion of the GI tract
Ulcerative Colitis
– Superficial, non-granulomatous inflammatory disease restricted to the colon

Ulcerative Colitis
- Bloody mucoid diarrhea, rarely toxic megacolon
- Can begin at any age, peaks at 20-25 years
- Annual incidence of ~10 per 100,000 in US
- Negligible risk of cancer in the first 10 years, but 1% per year risk of cancer thereafter
- Good response to total colectomy if medical therapy fails

- Normal serosa
- Bowel normal thickness
- Continuous disease
- Confluent mucosal ulceration
- Pseudopolyp formation

- Crypt distortion + shortening
- Paneth cell metaplasia
- Diffuse mucosal inflammation
- Crypt abscesses
- Mucin depletion
- Mucosal ulceration

Crohn’s Disease

- Variable and elusive clinical presentation with diarrhea, pain, weight loss, anorexia, fever
- Can begin at any age, peaks at 15-25 years
- Annual incidence of ~3 per 100,000 in US
- Many GI complications and extracolonic manifestations
- Risk of cancer less than in UC
- Poor response to surgery 

Fat wrapping
Thickened bowel wall
Skip Lesions
Stricture formation
Cobblestoned mucosa

- Cryptitis and crypt abscesses
- Transmural inflammation
- Lymphoid aggregates +/- granulomas
- “Crohn’s rosary”
- Fissuring
- Neuromuscular hyperplasia