 Iron 

is absorbed in the duodenum.

 Vitamin B12 and bile salts are absorbed in the terminal ileum.
 Water and lipids are absorbed by passive diffusion throughout the
small intestine.
 Sodium Bicarbonate is absorbed by active transport
and glucose and amino acid co-transport.
 Fructose is absorbed by facilitated diffusion.
[edit]

DIF demonstrates in vivo deposits of antibodies and other immunoreactants, such as complement. DIF
usually shows immunoglobulin G (IgG) deposited on the surface of the keratinocytes in and around
lesions. IgG1 and IgG4 are the most common subclasses. Complement components such as C3 and
immunoglobulin M are present less frequently than IgG. DIF shows intercellular deposition throughout the
epidermis. This pattern of immunoreactants is not specific for pemphigus vulgaris and may be seen in
pemphigus vegetans, pemphigus foliaceus, and pemphigus erythematosus. The best location for DIF
testing is on normal perilesional skin. When DIF testing is performed on lesional skin, false-positive

results can be observed. DIF results are shown in the image below. 
Direct immunofluorescence showing intercellular immunoglobulin G throughout
 the 

Transtentorial herniation results in all except ?

A) Cheyne stokes respiration
B) Decebration
C) Ipsilateral hemiparesis
 D) Ipsilateral oculomotor paresis

Ans.: b. Decerebration.

Rather trantentorial herniation results in Decorticate posturing, with elbows,wrists and fingers flexed
and legs extended and internally rotated.

Explanation:

Spoiler! : 
In central herniation, (also called "transtentorial herniation") the
diencephalon and parts of the temporal lobes of both of the cerebral
hemispheres are squeezed through a notch in the tentorium cerebelli.
Transtentorial herniation can occur when the brain moves either up or
down across the tentorium, called ascending and descending
transtentorial herniation respectively; however descending herniation is
much more common.Downward herniation can stretch branches of the
basilar artery (pontine arteries), causing them to tear and bleed, known
as a Duret hemorrhage. The result is usually fatal. Radiographically,
downward herniation is characterized by obliteration of the suprasellar
cistern from temporal lobe herniation into the tentorial hiatus with
associated compression on the cerebral peduncles. Upwards herniation,
on the other hand, can be radiographically characterized by obliteration
of the quadrigeminal cistern. Intracranial hypotension syndrome has been
known to mimic downwards transtentorial herniation.
So, due to the prssure effects of the herniation, brainstem is depressed
leading to cheyne-stokes type of breathing (depression of respiratory
centre in the medulla) and also pyramidal fibres are pressed upon leading
to hemiparesis usually ipsilateral due to pressure on the alradt
decussated pyramidal fibres.
Physical
 Dermatomyositis is a disease that primarily affects the skin and the muscles but may affect other
organ systems.
 The characteristic, and possibly pathognomonic, cutaneous features of dermatomyositis include
heliotrope rash and Gottron papules. Several other cutaneous features, including malar erythema,
poikiloderma (ie, variegated telangiectasia, hyperpigmentation) in a photosensitive distribution,
violaceous erythema on the extensor surfaces, and periungual and cuticular changes, are characteristic
of dermatomyositis even though they are not pathognomonic.
 Muscle findings associated with dermatomyositis typically include proximal weakness and,
sometimes, tenderness. Other systemic features include joint swelling, changes associated
with Raynaud phenomenon, and abnormal cardiopulmonary examination findings.
 The heliotrope rash consists of a violaceous-to-dusky erythematous rash with or without edema in
a symmetrical distribution involving periorbital skin. Sometimes, this sign is subtle and may involve only
a mild discoloration along the eyelid margin. A heliotrope rash is rarely observed in other disorders;
 thus, its presence strongly suggests dermatomyositis. The heliotrope

flower from which the manifestation of dermatomyositis is named. Heliotrope rash in a

woman with dermatomyositis.
 The Gottron papules are found over bony prominences, particularly the metacarpophalangeal
joints, the proximal interphalangeal joints, and/or the distal interphalangeal joints. Papules may also be
found overlying the elbows, knees, and/or feet. The lesions consist of slightly elevated violaceous
papules and plaques. A slight scale and, occasionally, a thick psoriasiform scale may be present. These
lesions may resemble lesions of lupus erythematosus (LE), psoriasis, or lichen planus (LP).

Gottron papules and nailfold tela a ngiectasiare

present in this patient with dermatomyositis.
 Nailfold changes consist of periungual telangiectases and/or a characteristic cuticular change
with hypertrophy of the cuticle and small hemorrhagic infarcts with this hypertrophic area. Periungual
telangiectases may be apparent clinically or may be visible only on capillary microscopy.
 Poikiloderma may occur on exposed skin, such as the extensor surfaces of the arm, and may
appear in a V-shaped distribution over the anterior neck and upper chest and back (ie, shawl sign).

Dermatomyositis is often associated with a poikiloderma in a

photodistribution.
 With the exception of the heliotrope rash, the eruption of dermatomyositis is photodistributed and
photoexacerbated. Despite the prominent photodistribution of the rash, patients rarely report
 photosensitivity. These lesions on the dorsal hands demonstrate the
photodistribution of dermatomyositis. Note the sparing of the interdigital web spaces.
 Facial erythema may also occur in dermatomyositis. This change must be differentiated from
LE, rosacea, seborrheic dermatitis, and atopic dermatitis.
 Scalp involvement in dermatomyositis is relatively common and manifests as an erythematous-to-
violaceous psoriasiform dermatitis. Clinical distinction from seborrheic dermatitis or psoriasis is
occasionally difficult. Nonscarring alopecia may occur in some patients and often follows a flare of

systemic disease. A diffuse alopecia with a scaly scalp

dermatosis is common in patients with dermatomyositis.
 Dermatomyositis-sine myositis, also known as amyopathic dermatomyositis (ADM), is
characterized by typical cutaneous disease, no clinical evidence of muscle weakness, and normal
serum muscle enzyme levels for at least 2 years. Patients who have undergone disease-modifying
therapies such as corticosteroid or immunosuppressive agent treatment are not classified as having
ADM. Some patients with ADM have abnormal findings on ultrasonography, MRI, or muscle biopsy.
These patients have subclinical muscle involvement, but their condition may still be classified as ADM.
Because many patients with ADM are not evaluated beyond clinical and enzymatic studies, many
believe that ADM represents a systemic process that requires systemic therapies.
 Some cases of myositis resolve following therapy, but the skin disease remains an active
important feature of dermatomyositis. Although the skin disease is the major, and often only,
manifestation of dermatomyositis, these patients are not diagnosed with ADM. In addition, a small
subset of patients never develop myositis despite having prominent cutaneous changes. Rare
cutaneous manifestations of dermatomyositis include vesiculobullous erosive lesions and exfoliative
erythroderma. Biopsy tissue samples from these patients reveal an interface dermatitis (ie, inflammation
at the dermal-epidermal junction) similar to biopsy tissue samples from heliotrope rash, Gottron
papules, poikiloderma, or scalp lesions. These cutaneous manifestations may be more common in
patients with an associated malignancy.
 Various other cutaneous lesions that do not reflect the interface changes observed
histopathologically with the pathognomonic or characteristic lesions have been described in patients
with dermatomyositis or polymyositis. Panniculitis, urticaria, and hyperkeratosis of the palms (known as
mechanic's hands) are examples of these cutaneous lesions. Other findings include cutaneous
mucinosis, follicular hyperkeratosis, hyperpigmentation, ichthyosis, white plaques on the buccal
mucosa, cutaneous vasculitis, and flagellate erythema.
 Muscle disease of dermatomyositis manifests as proximal symmetrical muscle weakness.
Affected patients may have difficulty rising from a chair or squatting and raising themselves from this
position. In an effort to rise, some patients use other muscles that are not as affected. The careful
examiner may note this finding. Testing of the muscle strength is part of each assessment of the patient.
 Often, the extensor muscles of the arms are more affected than the flexors. Distal strength is almost
always maintained. Muscle tenderness is a variable finding.
 Calcinosis of the skin or muscle is unusual in adults with dermatomyositis but may occur in as
many as 40% of children or adolescents with the disease. Calcinosis cutis manifests as firm, yellow- or
flesh-colored nodules, often over bony prominences. Occasionally, the nodules extrude through the

surface of the skin, in which case secondary infection may occur.

Calcinosis caused by dermatomyositis (DM) in childhood can be observed in a patient who had active DM 15 years
before the time of this photograph.
 Joint swelling occurs in some patients with dermatomyositis. The small joints of the hands are
most frequently involved. The arthritis associated with dermatomyositis is not erosive or deforming.
 Patients with pulmonary disease may have abnormal breath sounds (crackles from interstitial
fibrosis or pneumonitis).
 Patients with an associated malignancy may have physical findings relevant to the affected
organs.
Previous

Immune complex disease

An immunologic category of diseases evoked by the deposition of antigen-antibody or antigen-antibody-
complement complexes on cell surfaces, with subsequent involvement of
breakdown products ofcomplement, platelets, and polymorphonuclear leukocytes, and development of vasculitis;
nephritis is common. Arthus phenomenon and serum sickness are classic examples, but many other disorders,
including most of the connective tissue diseases, may belong in this immunologic category; immune
complex diseases can also occur during a variety of diseases of known aetiology, such
as subacutebacterial endocarditis.
See: autoimmune disease.
Synonym: immune complex disorder, type III hypersensitivity reaction.

The coracoid process is a thick curved process attached by a broad

base to the upper part of the neck of the scapula; it runs at first upward
and medialward; then, becoming smaller, it changes its direction, and
projects forward and lateralward.
The ascending portion, flattened from before backward, presents in front
a smooth concave surface, across which the Subscapularis passes.
The horizontal portion is flattened from above downward; its upper
surface is convex and irregular, and gives attachment to the Pectoralis
minor; its under surface is smooth; its medial and lateral borders are
rough; the former gives attachment to the Pectoralis minor and the latter
to the coracoacromial ligament; the apex is embraced by the conjoined
tendon of origin of theCoracobrachialis and short head of the Biceps
brachii and gives attachment to the coracoclavicular fascia.
On the medial part of the root of the coracoid process is a rough
impression for the attachment of the conoid ligament; and running from it
obliquely forward and lateralward, on to the upper surface of the
horizontal portion, is an elevated ridge for the attachment of
the trapezoid ligament.
[edit]Clinical relevance
The coracoid process is palpable just below the lateral end of the
clavicle (collar bone). It is otherwise known as the "Surgeon's
Lighthouse" because it serves as a landmark to avoid neurovascular
damage.[citation needed] Major neurovascular structures enter the upper limb
medial to the coracoid process so surgical approaches to the shoulder
region always takes place lateral to the coracoid process.
[edit]

coracoid process
n 1882, Edward Hallaran Bennett, MD, described the fracture of the base of the first metacarpal that
bears his name. Bennett described the anatomic details of the fracture and suggested that early diagnosis
and treatment are imperative to prevent loss of function of this highly mobile joint. [1, 2, 3, 4, 5]

Images depicting Bennett fracture are shown below

he spondyloarthropathies (SpAs) are a family of related disorders that includes ankylosing spondylitis
(AS), reactive arthritis (ReA; also known as Reiter syndrome [RS]), psoriatic arthritis (PsA),
spondyloarthropathy associated with inflammatory bowel disease (IBD), undifferentiated
spondyloarthropathy (USpA), and, possibly, Whipple disease and Behçet disease. Ankylosing spondylitis,
which literally means "inflamed spine growing together," is the prototypical spondyloarthropathy.

The age of onset has a very wide range, with the peak onset at approximately age 50 years. The male-to-
female ratio is 1:3. The onset is usually insidious, and, even after years of active disease, sacroiliitis and
spondylitis are either absent or appear very mild on routine radiography.

Clinical manifestations of undifferentiated spondyloarthropathy include inflammatory back pain (90%),

buttock pain (80%), enthesitis (85%), peripheral arthritis (35%), dactylitis (17%), and fatigue (55%).

Extra-articular manifestations are uncommon, occurring in fewer than 10% of patients, and include acute
anterior uveitis (1-2%), oral ulcers, rash, nonspecific IBD, pleuritis, and pericarditis.
Findings of laboratory studies are generally unremarkable except for the presence of an elevated ESR or
C-reactive protein level (36%). HLA-B27 antigen is positive only in approximately 20-25% of patients.

These factors, especially the late age of onset, female predominance, and low HLA-B27 positivity,
suggest that Undifferentiated spondyloarthropathy is distinct from ankylosing spondylitis and the other
classic spondyloarthropathies.

The Anatomical Snuff-box

Boundaries (p. 582)

Anterior Abductor pollicis longus and extensor pollicis

brevis muscles

Posterior Extensor pollicis longus muscle

Proximal Styloid process of radius

Distal Base of 1st metacarpal bone and part of the trapezium

Floor Scaphoid and trapezium

Structures Crossing the Anatomical Snuff-box

1. Radial artery
2. Extensor carpi radialis longus and brevis.
3. Superficial branch of the radial nerve

 Primary amenorrhoea : When a girl has never experienced menarche and

menses, she is said to be suffering from primary amenorrhoea or primary lack
of menses. The cause is usually congenital, i.e. from birth, and can be due to
genetic or chromosomal abnormalities or due to a defect in the development
of thereproductive tract. Treatment of this condition is very difficult.
 Secondary amenorrhoea : When the patient has had at least one episode of
spontaneous menses before the loss of her periods, she is said to suffer from
secondary amenorrhoea. This is the commonest form of amenorrhoea. The
problem may lie in the hypothalamus and the pituitary, or the uterus or
 the ovary. Other endocrine glands like the thyroid, the pancreas and the
adrenal cortex also have a role to play in causing amenorrhoea.

Asherman's Syndrome is a condition in which there is formation of scar tissue (called

'adhesions' or 'synechia') inside the uterus, obliterating the endometrial cavity
partially or completely and preventing the occurance of normal menstrual periods

What are the causes of rectal bleeding?

Many diseases and conditions can cause rectal bleeding. Common causes
include:

anal fissures,

hemorrhoids,

cancers and polyps of the rectum and colon,

diverticulosis,

abnormal blood vessels (angiodysplasia),

ulcerative colitis,

ulcerative proctitis,

Crohn's colitis,

infectious colitis,

ischemic colitis, and

Meckel's diverticula.
Nitrous oxide ("laughing gas") is a stable, colourless gas used as an
inhalation anaesthetic. It is has a slightly sweet smell and taste. Unlike
ether, it isn't irritating to the mucous membranes. Unlike chloroform, it is
relatively safe, especially if used mixed with oxygen. Hypoxia as a result
of high doses of nitrous oxide needed when it's the sole anaesthetic agent
may trigger headache, dizziness, hypotension, cardiac arrhythmias,
anoxic brain damage, cerebral oedema and long-lasting neural deficits.
Chronic exposure to nitrous oxide can cause megaloblastic
erythropoiesis, neuron death and damage to the spinal cord.

Nitrous oxide is only weakly anaesthetic compared to chloroform and

ether. A 50/50 mixture of oxygen and nitrous oxide is used to induce
analgesia without loss of consciousness.

Nitrous oxide was first synthesised by Joseph Priestley in 1775. Its

potential as a surgical anaesthetic avant la lettre was glimpsed by Samuel
Latham Mitchill; and later by Humpry Davy before his attention wandered
elsewhere. In the modern era, controlled self-administration of nitrous
oxide using a demand-valve is common in a hospital setting. Nitrous oxide
is used in contemporary obstetrics, for changing painful dressings, as an
adjunct post-operative physiotherapy, and in emergency ambulances.

After the abortive demonstration of nitrous oxide anaesthesia in

Massachusetts by Horace Wells, Professor Charles Jackson advised William
Morton to use ether instead. In the 180s, Gardner Quincy Colton later
helped revive the use of nitrous oxide in dentistry.

Molecular weight: 44.02

Solubility in water - 1 litre of gas in 1.5 litre of water at 20°C and 2 atm.

Boiling point: -88.46°C (at atmospheric pressure)

Melting point: -90.81°C (at atmospheric pressure)

Density as a gas: 1.997 mg/cm3 at 0°C at atmospheric pressure

Vapour pressure: 4.93 pascals (at 20°C)

Relative molecular mass: 44.02

Viscosity: 1488.99 poise (at 27°C)

Specific gravity: 1.529 at 0°C, at atmospheric pressur

1. Anatomy

It is thicker and more membranous in character than the superficial fascia

of Camper, and contains a considerable quantity of orange elastic fibers.

It is loosely connected by areolar tissue to the aponeurosis of the

Obliquus externus abdominis, but in the middle line it is more intimately
adherent to the linea alba and to the symphysis pubis, and is prolonged
on to the dorsum of the penis, forming the fundiform ligament; above, it
is continuous with the superficial fascia over the rest of the trunk; below
and laterally, it blends with the fascia lata of the thigh a little below the
inguinal ligament; medially and below, it is continued over the penis and
spermatic cord to the scrotum, where it helps to form the dartos.

From the scrotum it may be traced backward into continuity with the
deep layer of the superficial fascia of the perineum (fascia of Colles).

In the female, it is continued into the labia majora and thence to the
fascia of Colles.

2. Eponym

It is named for Antonio Scarpe

The Tensor Fasciae Latae is a small muscle which attaches
inferiorly to the long thick strip of fascia, known at the
iliotibial band (ITB).

Origin

Anterior Iliac crest and ilium

Insertion

Lateral condyle of the tibia via the Iliotibial band

Actions

Flexion of the hip

Hip abduction

Innervation

Superior gluteal nerve

Daily uses

Keeping one foot in front of the other when walking

Example strengthening exercises

Standing hip abduction using a resistance band

Laying hip abduction using a resistance band

Example stretches

Outer hip stretch

Standing outer hip stretch

Related injuries

Iliotibial band friction syndrome (runners knee)

Related muscles

Gluteus medius, Gluteus minimus

Hypertriglyceridemia has many causes, including

familial and genetic syndromes, metabolic disease, and
drugs.

Genetic causes: Abnormalities of the enzyme pathway for chylomicron

metabolism are the best-characterized genetic causes of
hypertriglyceridemia. However, less clearly defined inheritable disorders
are more frequent causes of elevated triglycerides.

Type I hyperlipoproteinemia is the best-characterized genetic cause of

hypertriglyceridemia and is caused by a deficiency or defect in either the
enzyme LPL or its cofactor, apo C-II.

LPL hydrolyzes triglycerides in chylomicrons and VLDL, releasing free

fatty acids. The enzyme is found in the endothelial cells of capillaries and
can be released into the plasma by heparin. LPL is essential for the
metabolism of chylomicrons and VLDL, transforming them into their
respective remnants. Apo C-II, an apolipoprotein present in both
chylomicrons and VLDL, acts as a cofactor in the action of LPL.

The above pathway is affected by other genetic disorders, particularly

type 1 or type 2 diabetes, because LPL requires insulin for full activity.

Two triglyceride disorders are genetically controlled, but the mechanisms

are not clearly defined.

Familial combined hyperlipidemia is an autosomal dominant disorder

characterized by patients and their first-degree relatives who may have
either isolated triglyceride or LDL-c elevations or both. Diagnosis of the
disorder in a particular patient requires a family history of premature
coronary artery disease (CAD) in 1 or more first-degree relatives and a
family history for elevated triglycerides with or without elevated LDL-c
levels. The diagnosis is important for prognosis; 10-20% of patients with
premature CAD have familial combined hyperlipidemia.

Familial hypertriglyceridemia is also an autosomal dominant trait.[8]

These patients and their families have isolated triglyceride elevations and
may have an increased risk of premature coronary artery disease.

Metabolic causes[8]
Diabetes: Uncontrolled diabetes mellitus, both type 1 and type 2, is one
of the most common causes of hypertriglyceridemia, and it is often
severe in patients presenting with ketosis.

Patients with type 1 diabetes mellitus are insulin deficient, and LPL is
largely ineffective. Control of these patients' diabetes mellitus with
insulin will restore LPL function, reducing triglyceride levels and restoring
diabetes mellitus control.

In patients with uncontrolled type 2 diabetes mellitus and

hyperinsulinemia, triglycerides are elevated for several reasons. (1) LPL is
less effective in the insulin-resistant state. (2) Overproduction of VLDL by
the liver is common in patients with diabetes who are often overweight.
(3) Diabetes mellitus is one of the conditions that leads to incomplete
metabolism of VLDL, causing increased remnant VLDL or IDL observed in
dysbetalipoproteinemia (see Dysbetalipoproteinemia).

Obesity: Mild-to-moderate elevations in triglycerides are common in

obese patients, largely secondary to reduced efficacy of LPL and
overproduction of VLDL.

Hypothyroidism: It commonly causes LDL-c elevations but also may

lead to mixed hyperlipidemia or isolated triglyceride elevations. Reduced
hepatic lipase activity slows VLDL remnant catabolism. As with diabetes
mellitus, untreated hypothyroidism may cause dysbetalipoproteinemia in
patients with homozygous apolipoprotein E-2.

Nephrotic syndrome: It is thought to increase hepatic synthesis of

VLDL and also may slow catabolism of both LDL and VLDL. As in
hypothyroidism, elevated LDL-c levels are more common in this
condition, but mixed hyperlipidemia or isolated triglyceride elevations
may be observed. Higher levels of proteinuria are correlated with more
severe hyperlipidemia.

Drugs
High-dose thiazide diuretics or chlorthalidone

High-dose beta-adrenergic blocking agents, excluding those with intrinsic

sympathomimetic activity.

Unopposed oral estrogen replacement therapy

Oral contraceptives with high estrogen content

Tamoxifen

Glucocorticoids

Oral isotretinoin
Antiretroviral therapy (including some protease inhibitors, nonnucleoside
reverse transcriptase inhibitors)

Atypical antipsychotics

Other causes of hypertriglyceridemia

Alcohol: Excessive alcohol intake and high-carbohydrate diets (>60% of

caloric intake) are frequent causes of hypertriglyceridemia.

High-carbohydrate diets (>60% of caloric intake)

Acute pancreatitis: It may cause substantial elevations in triglycerides by

unknown mechanisms. However, much more frequently, severe
hypertriglyceridemia causes acute pancreatitis. In patients presenting
with acute pancreatitis and triglycerides greater than 1000 mg/dL, not
assuming that the triglycerides are the cause of the pancreatitis is
prudent. Other causes, such as common bile duct obstruction and
alcoholism, must be considered as possible etiologies.

Pregnancy: In patients with mildly-to-moderately elevated triglycerides in

the nonpregnant state, hypertriglyceridemia (sometimes severe) may
occur. Such patients should be monitored closely, particularly in the third
trimester. In fact, simply looking for laboratory notation of lipemic serum
in routine blood tests during pregnancy will avoid unexpected
complications resulting from unrecognized and untreated
hypertriglyceridemia during pregnancy.

Previous

Primary cardiac tumors are rare and occur in 1 per 1000 to 1 per 100,000
individuals inunselected autopsy series at tertiary care centers.1Among
these tumors,cardiac myxomasare the most common in adults,accounting
for nearly half of primary cardiac tumors. Formany years,the cellularity
of these lesions was controversial and some investigators
initiallyproposedthat they represented thrombus rather than neoplasia.
However,extensive analy-sis ultimately confirmed that these lesions
represented a primary neoplastic process.1,2Although the cell of origin
has yet to be isolated,they have been posited to arise from
asubendocardial cell,termed a “reserve”or “lepidic”cell. These tumors
usually exhibit atypical hypocellular appearance of small pyramidal or
stellate cells against a bland proteoglycan background. They may also
exhibit evidence of a wide variety of cellular lineages,including zones of
extramedullary hematopoiesis,acinar structures suggestive of
epithelialorganization,cells with electron microscopic features suggestive
of muscle,and a number ofimmunohistochemical markers consistent with
a remarkable range of cell types. Such his-tologic studies1-3suggest that
the cardiac reserve cell is pluripotent and,in the appropriategenetic and
biochemical milieu,may be a progenitor cell for a number of cardiac cells
in thehealthy and pathologic heart

The genus Clostridium consists of relatively large, Gram-positive, rod-

shaped bacteria in the Phylum Firmicutes (Clostridia is actually a Class in
the Phylum). All species form endospores and have a strictly fermentative
type of metabolism. Most clostridia will not grow under aerobic
conditions and vegetative cells are killed by exposure to O2, but their
spores are able to survive long periods of exposure to air.

Most of the clostridia are saprophytes, but a few are pathogenic for
humans, primarily Clostridium perfringens, C. difficile, C. tetani and C.
tetani. Those that are pathogens have primarily a saprophytic existence
in nature and, in a sense, are opportunistic pathogens. Clostridium tetani
and Clostridium botulinum produce the most potent biological toxins
known to affect humans. As pathogens of tetanus and food-borne
botulism, they owe their virulence almost entirely to their toxigenicity.
Other clostridia, however, are highly invasive under certain
circumstances.

lostridium perfringens, which produces a huge array of invasins and

exotoxins, causes wound and surgical infections that lead to gas
gangrene, in addition to severe uterine infections. Clostridial hemolysins
and extracellular enzymes such as proteases, lipases, collagenase and
hyaluronidase, contribute to the invasive process. Clostridium perfringens
also produces an enterotoxin and is an important cause of food poisoning.
Usually the organism is encountered in improperly sterilized (canned)
foods in which endospores have germinated.

AMINO ACID
Alanine A Ala

Very abundant, very versatile. More stiff than glycine, but small
enough to pose only small steric limits for the protein conformation. It
behaves fairly neutrally, can be located in both hydrophilic regions on the
protein outside and the hydrophobic areas inside.

Cysteine C Cys

The sulfur atom binds readily to heavy metal ions. Under oxidizing
conditions, two cysteines can join together in a disulfide bond to form
the amino acid cystine. When cystines are part of a protein, insulin for
example,this stabilises tertiary structure and makes the protein more
resistant to denaturation; disulphide bridges are therefore common in
proteins that have to function in harsh environments including digestive
enzymes (e.g., pepsin and chymotrypsin) and structural proteins (e.g.,
keratin). Disulphides are also found in peptides too small to hold a stable
shape on their own (eg. insulin).

Aspartic acid D Asp

Behaves similarly to glutamic acid. Carries a hydrophilic acidic group with

strong negative charge. Usually is located on the outer surface of the
protein, making it water-soluble. Binds to positively-charged molecules
and ions, often used in enzymes to fix the metal ion. When located inside
of the protein, aspartate and glutamate are usually paired with arginine
and lysine.

Glutamate E Glu

Behaves similar to aspartic acid. Has longer, slightly more flexible side
chain.

Phenylalanine F Phe

Essential for humans. Phenylalanine, tyrosine, and tryptophan contain

large rigid aromatic group on the side chain. These are the biggest amino
acids. Like isoleucine, leucine and valine, these are hydrophobic and tend
to orient towards the interior of the folded protein molecule.

Glycine G Gly

Because of the two hydrogen atoms at the α carbon, glycine is not

optically active. It is the smallest amino acid, rotates easily, adds
flexibility to the protein chain. It is able to fit into the tightest spaces,
e.g., the triple helix of collagen. As too much flexibility is usually not
desired, as a structural component it is less common than alanine.

Histidine H His

In even slightly acidic conditions protonation of the nitrogen occurs,

changing the properties of histidine and the polypeptide as a whole. It is
used by many proteins as a regulatory mechanism, changing the
conformation and behavior of the polypeptide in acidic regions such as
the late endosome or lysosome, enforcing conformation change in
enzymes. However only a few histidines are needed for this, so it is
comparatively scarce.

Isoleucine I Ile

Essential for humans. Isoleucine, leucine and valine have large aliphatic
hydrophobic side chains. Their molecules are rigid, and their mutual
hydrophobic interactions are important for the correct folding of roteins,
as these chains tend to be located inside of the protein molecule.
Lysine K Lys

Essential for humans. Behaves similarly to arginine. Contains a long

flexible side-chain with a positively-charged end. The flexibility of the
chain makes lysine and arginine suitable for binding to molecules with
many negative charges on their surfaces. E.g., DNA-binding proteins have
their active regions rich with arginine and lysine. The strong charge
makes these two amino acids prone to be located on the outer
hydrophilic surfaces of the proteins; when they are found inside, they are
usually paired with a corresponding negatively-charged amino acid, e.g.,
aspartate or glutamate.

Leucine L Leu

Essential for humans. Behaves similar to isoleucine and valine. See

isoleucine.

Methionine M Met

Essential for humans. Always the first amino acid to be incorporated into
a protein; sometimes removed after translation. Like cysteine, contains
sulfur, but with a methyl group instead of hydrogen. This methyl group
can be activated, and is used in many reactions where a new carbon atom
is being added to another molecule.

Asparagine N Asn

Similar to aspartic acid. Asn contains an amide group where Asp has a
carboxyl.Proline P Pro Contains an unusual ring to the N-end amine group,
which forces the CO-NH amide sequence into a fixed conformation. Can
disrupt protein folding structures like α helix or β sheet, forcing the
desired kink in the protein chain. Common in collagen, where it often
undergoes a posttranslational modification to hydroxyproline. Uncommon
elsewhere.

Glutamine Q GlnSimilar to glutamic acid. Gln contains an amide group

where Glu has a carboxyl. Used in proteins and as a storage for
ammonia.Arginine R Arg Functionally similar to lysine.
Serine S Ser

Serine and threonine have a short group ended with a hydroxyl group. Its
hydrogen is easy to remove, so serine and threonine often act as
hydrogen donors in enzymes. Both are very hydrophilic, therefore the
outer regions of soluble proteins tend to be rich with them.

Threonine T Thr

Essential for humans. Behaves similarly to serine.

Valine V Val

Essential for humans. Behaves similarly to isoleucine and leucine. See

isoleucine.

Tryptophan W Trp

Essential for humans. Behaves similarly to phenylalanine and tyrosine (see

phenylalanine). Precursor of serotonin.

Tyrosine Y Tyr

Behaves similarly to phenylalanine and tryptophan (see phenylalanine).

Precursor of melanin, epinephrine, and thyroid hormones.