bennet fracture

The Monteggia fracture is a fracture of the proximal third of the ulna with dislocation of the head of the radius. It is named after Giovanni Battista Monteggia.[1][2]

monteggia fracture

monteggia fracture - Google Search

vericause vein

vericose vein may develop due to

1.aterio venus fistula

2.previous DVT

3.

previous fracture tibia

4.familial predispose

DVT

heparine DVT theraputic dose is 1000u /hour ingusion

 waferrin 10mg stat to be given

leg elavated and stockings apply

lumber sympathectomy(L234) only improve the skin cerculation of foot.

it never improve claudication distance

increase intra abdominal and intrathoracic pressure cause defication and micturetion cause valsalva effect and ultimate syncope i  elderly patient,,

 call micturetion syncope

Watch "Trendelenburg -sign,test,operation,position,cannula" on YouTube

Watch "Varicose Vein Examination for Finals" on YouTube

The Trendelenburg Test or Brodie-Trendelenburg test is a test which can be carried out as part of a physical examination to determine the competency of the valves in the superficial and deep veins of the legs in patients with varicose veins.[1]

Procedure

With the patient in the supine position, the leg is flexed at the hip and raised above heart level. The veins will empty due to gravity or with the assistance of the examiner's hand squeezing blood towards the heart.

A tourniquet is then applied around the upper thigh to compress the superficial veins but not too tight as to occlude the deeper veins. The leg is then lowered by asking the patient to stand.

Normally the superficial saphenous vein will fill from below within 30-35 seconds as blood from the capillary beds reaches the veins; if the superficial veins fill more rapidly with the tourniquet in place there is valvular incompetence below the level of the tourniquet in the "deep" or "communicating" veins. After 20 seconds, if there has been no rapid filling, the tourniquet is released. If there is sudden filling at this point, it indicates that the deep and communicating veins are competent but the superficial veins are incompetent.[2]

The test is reported in two parts, the initial standing up of the patient (positive or negative based on rapid filling) and the second phase once the tourniquet is removed (positive or negative based upon rapid filling).

For example, a possible outcome of the test would be negative-positive meaning that the initial phase of the test was negative indicating competence in the deep and communicating veins and the second phase of the test was positive meaning that there is superficial vein incompetence.

The test can be repeated with the tourniquet at different levels to further pinpoint the level of valvular incompetence:

above the knee - to assess the mid-thigh perforators

below the knee - to assess incompetence between the short saphenous vein and the popliteal vein.[3]

Superficial veins of the leg normally empty into deep veins, however retrograde filling occurs when valves are incompetent, leading to varicose veins.

crohn dx

1.increase gall stone dx (bile salt absobtion ruduce  and increse sturation of body choleterol cause this)

2.increse renal calculi risk

3.50%chance of hving recurrence following sx for chronns dx

2/3 of gall bladder CA associate with gallstone

DIDA sacn use to assese the funtion of gallbladder .if isotope taken in to gall bladder js poor its due to acute cholysistitis

ancreatic pseudocysts (see the image below) are best defined as localized fluid collections that are rich in amylase and other pancreatic enzymes, that have a nonepithelialized wall consisting of fibrous and granulation tissue, and that usually appear several weeks after the onset of pancreatitis

retroperitoneal

not move with respirtion

lasge cyst xan see as epigastric mass

contain amylase more than lod amylase

can remove via percutineously

pancreatic psudocyst

Wednesday, January 13, 2016

4:54 PM

Cullen's sign is superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus. It is named for T gynecologist who first described the sign in ruptured ectopic pregnancy in 1916.  

also pancreatitis

Grey Turner's sign refers to bruising of the flanks, the part of the body between the last rib and the top of the hip. The bruising appears as a blue discoloration,[1] and is a sign of retroperitoneal hemorrhage, or bleeding behind the peritoneum, which is a lining of the abdominal cavity

turner sign

bile salt is suport to aborb fat in the jejunum .

bile salt reabsorb in distal ileum

intrinsic factor and vit B 12 aborb in distal ilium

iron, calcium,vit c and folic acid absorb in  proximal jejunum

dubble contrast barium anema.....visualize colon

Hereditary nonpolyposis colon cancer syndrome (HNPCC, Lynch syndrome) poses about a 40% lifetime risk for developing colorectal cancer; individuals with this syndrome are also at increased risk for urothelial cancer, endometrial cancer,

The approximate 5-year survival rate for colorectal cancer patients in the United States (all stages included) is 65%.[19] Survival is inversely related to stage: approximate 5-year survival rates are 95% for patients with stage I disease, 60% for those with stage III disease, and 10% for those with stage IV (metastatic) disease (see Staging).

The Dukes staging system is a classification system for colorectal cancer. This system is now mainly of historical interest as it has largely been replaced by the TNM staging system. It is not recommended for clinical practice.

The Dukes staging system is a classification system for colorectal cancer. This system is now mainly of historical interest as it has largely been replaced by the TNM staging system. It is not recommended for clinical practice.

Dukes A: invasion into but not through the bowel wall (90% 5 year survival)

Dukes B: invasion through the bowel wall but not involving lymph nodes (70% 5 year survival)

Dukes C:  involvement of lymph nodes (30% 5 year survival)

Dukes D: widespread metastases

Achalasia is a primary esophageal motility disorder characterized by the absence of esophageal peristalsis and impaired relaxation of the lower esophageal sphincter (LES) in response to swallowing.

acviored mientoric plexus degenaration,, (Hirshsprang is cogenital and affect other end)

cause funtinal obstrution of lower esophagial splincter

LES pressure  goes up.

air fluid level in the  xrays

no gastric air bubble in abdominal xray(air can not go through LES

)

increse risk of CA

harmacologic and other nonsurgical treatments include the following:

Administration of calcium channel blockers and nitrates decrease LES pressure (primarily in elderly patients who cannot undergo pneumatic dilatation or surgery)

Endoscopic intrasphincteric injection of botulinum toxin to block acetylcholine release at the level of the LES (mainly in elderly patients who are poor candidates for dilatation or surgery)

Surgical treatment includes the following:

Laparoscopic Heller myotomy, preferably with anterior (Dor; more common) or posterior (Toupet) partial fundoplication

Peroral endoscopic myotomy (POEM)

acalasia in xray

trigeminal nerve supply mucle of mastication(temporalis,masseter,pterygoids)

The internal auditory meatus (also meatus acusticus internus, internal acoustic meatus, internal auditory canal, internal acoustic canal, or IAC) is a canal within the petrous part of the temporal bone of the skull between the posterior cranial fossa and the inner ear.

Oral cholecystography is a procedure used to visualize the gallbladder by administering, by mouth, a radiopaque contrast agent that is excreted by the liver. This excreted material will collect in the gallbladder, where reabsorption of water concentrates the excreted contrast. Since only 10% of gallstones are radiopaque, the remaining 90% will appear as translucent on an opaque background in an abdominal X-ray. Current medical practice prefers ultrasound and CT over oral cholecystography. If needed, IV cholecystography and cholangiography may be done.

oral chol3cystography

Celiac disease, also known as celiac sprue or gluten-sensitive enteropathy, is a chronic disorder of the digestive tract that results in an inability to tolerate gliadin, the alcohol-soluble fraction of gluten. Gluten is a protein commonly found in wheat, rye, and barley.

When patients with celiac disease ingest gliadin, an immunologically mediated inflammatory response occurs that damages the mucosa of their intestines, resulting in maldigestion and malabsorption of food nutrients.(some web site say auto immune)

in lab can check immunglubulin

celeac disease associate with lymphoma

portal vein bile duct anatomy - Google Search

gallstone and ultrasound - Google Search

common bile duct diameter

A new sonographic technique for demonstration of the common bile duct is described in a prospective study of 200 patients. The mean diameter of the normal common duct was 4.1 mm. A common duct greater than 7 mm in diameter can be seen in (a) nonjaundiced patients with gallstones and/or pancreatitis, or (b) jaundiced patients with common duct obstruction by stone or tumor. A common duct greater than 11 mm in diameter is strongly suggestive of obstruction by stone or tumor.

The patient with intussusception is usually an infant, often one who has had an upper respiratory infection,

apex usually enlarge payers patches

associate with HSP

intersusseption

The hallmark physical findings in intussusception are a right hypochondrium sausage-shaped mass and emptiness in the right lower quadrant (Dance sign).

See Clinical Presentation for more detail.

Diagnosis

Imaging studies used in the diagnosis of intussusception include the following:

Radiography: Plain abdominal radiography reveals signs that suggest intussusception in only 60% of cases

Ultrasonography: Hallmarks of ultrasonography include the target and pseudokidney signs

Contrast enema: This is the traditional and most reliable way to make the diagnosis of intussusception in children

See Workup for more detail.

Management

Nonoperative reduction

Therapeutic enemas include the following:

Hydrostatic: With barium or water-soluble contrast

Pneumatic: With air insufflation; this is the treatment of choice in many institutions, and the risk of major complications with this technique is small

Surgical reduction

Hepatic encephalopathy is also described in patients without cirrhosis with either spontaneous or surgically created portosystemic shunts

It is theorized that neurotoxic substances, including ammonia and manganese, may gain entry into the brain in the setting of liver failure.

ammonia is detoxified in the liver by conversion to urea by the Krebs-Henseleit cycle.

Grading of the symptoms of hepatic encephalopathy is performed according to the so-called West Haven classification system, as follows[26] :

Grade 0 - Minimal hepatic encephalopathy (also known as CHE [27] and previously known subclinical hepatic encephalopathy); lack of detectable changes in personality or behavior; minimal changes in memory, concentration, intellectual function, and coordination; asterixis is absent.

Grade 1 - Trivial lack of awareness; shortened attention span; impaired addition or subtraction; hypersomnia, insomnia, or inversion of sleep pattern; euphoria, depression, or irritability; mild confusion; slowing of ability to perform mental tasks

Grade 2 - Lethargy or apathy; disorientation; inappropriate behavior; slurred speech; obvious asterixis; drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, and intermittent disorientation, usually regarding time

Grade 3 - Somnolent but can be aroused; unable to perform mental tasks; disorientation about time and place; marked confusion; amnesia; occasional fits of rage; present but incomprehensible speech

Grade 4 - Coma with or without response to painful stimuli

Classic EEG changes associated with hepatic encephalopathy are high-amplitude low-frequency waves and triphasic waves.

Medications: Drugs that act upon the central nervous system, such as opiates, benzodiazepines, antidepressants, and antipsychotic agents, may worsen hepatic encephalopathy.

Diuretic therapy: Decreased serum potassium levels and alkalosis may facilitate the conversion of NH4+ to NH3. At the author’s institution, diuretic-induced hypovolemia is the most common reason for patients with previously well-controlled hepatic encephalopathy to present to the emergency room with worsening mental function.

Avoid medications that depress central nervous system function, especially benzodiazepines. Patients with severe agitation and hepatic encephalopathy may receive haloperidol as a sedative. Treating patients who present with coexisting alcohol withdrawal and hepatic encephalopathy is particularly challenging. These patients may require therapy with benzodiazepines in conjunction with lactulose and other medical therapies for hepatic encephalopathy.

Lactulose appears to inhibit intestinal ammonia production by a number of mechanisms. The conversion of lactulose to lactic acid results in acidification of the gut lumen. This favors conversion of NH4+ to NH3 and the passage of NH3 from tissues into the lumen. Gut acidification inhibits ammoniagenic coliform bacteria, leading to increased levels of nonammoniagenic lactobacilli. Lactulose also works as a cathartic, reducing colonic bacterial load.

Initial lactulose dosing is 30 mL orally, daily or twice daily

tx for hepatic encephalopathi

Neomycin and other antibiotics, such as metronidazole, oral vancomycin, paromomycin, and oral quinolones, are administered in an effort to decrease the colonic concentration of ammoniagenic bacteria. Initial neomycin dosing is 250 mg orally 2-4 times a day. Doses as high as 4000 mg/d may be administered. Neomycin is usually reserved as a second-line agent, after initiation of treatment with lactulose. Long-term treatment with this oral aminoglycoside runs the risks of inducing ototoxicity and nephrotoxicity because of some systemic absorption.

Rifaximin (Xifaxan), a nonabsorbable derivative of rifampin, has been used in Europe

LOLA (Hepa-Merz) is available in Europe in both intravenous formulations and oral formulations. It is not available in the United States. LOLA is a stable salt of the 2 constituent amino acids. L-ornithine stimulates the urea cycle, with resulting loss of ammonia.

pernicious anaemia

noun

a deficiency in the production of red blood cells through a lack of vitamin B12.

The etiology of vitamin B12 deficiency is diverse and includes lack of intrinsic factor (IF), altered pH in the small intestine, and lack of absorption of B12 complexes in the terminal ileum. Vitamin B12 deficiency from any cause, as well as folic acid deficiency, can result in megaloblastic anemia.

Impaired IF production can occur in adults due to autoimmune destruction of parietal cells, which secrete IF. Gastrectomy can significantly reduce the production of IF.

The genetic defect in FAP is a germline mutation in the adenomatous polyposis coli (APC) gene.

FAP

familial adenomataus polyposis  is AUTOSOMAL dominant inherited disorder.

female to male ratio...1:1

rectum is not spared

100%malignant at age if 30 to 40

first apper at age of 10 to 15 year with pR bleeding, loose motion

associate with other cancers too

Endoscopic surveillance for FPC

Note the following:

Flexible sigmoidoscopy should be performed every 1-2 years starting at age 10-12 years in patients with FAP to document the onset of polyposis.

Sigmoidoscopic surveillance and ablation of any polyps in the retained rectum or ileal pouch should be performed every 3-6 months in patients with FAP who have undergone colonic (total or subtotal) resection. There is an increased risk for adenomas and carcinomas in the ileal pouch, as there is increased epithelial cell proliferation at this site as compared to the afferent ileal loop. [21, 22]

Once polyps are detected, colonoscopic surveillance is recommended to remove large polyps in patients who have not had an operation. This is important because surgery (colectomy) is usually deferred until an appropriate psychological age is reached (usually late teenaged years to early twenties). However, if the polyps have advanced histologic features, then early surgery is recommended.

Front- and side-view esophagogastroduodenoscopy should be performed every 1-3 years once the diagnosis is made and after surgical therapy. The front-view esophagogastroduodenoscopy allows for the detection of gastric and duodenal polyps. The side-view duodenoscope allows for the examination of the ampulla of Vater.

Capsule endoscopy is useful for the surveillance of jejunal-ileal polyps in selected patients but is not recommended for duodenal or ampullary surveillance. Some patients who are at high risk may benefit from screening with endoscopic ultrasound for periampullary and ampullary tumors. [

anal fisher typically  asso iate with anal tag

perianal fistula - Google Search

anal skin tag ,sentinal pile faecL soiling are common with anal fissuers

frmoral hernia pubic tubacal - Google Search

primary hyper parathyroidism is often asymtamatic and always disease of adult..itmay present S psycatric disorder

Gastrin is a peptide hormone that stimulates secretion of gastric acid (HCl) by the parietal cells of the stomach and aids in gastric motility. It is released by G cells in the pyloric antrum of the stomach, duodenum, and the pancreas.

Zollinger-Ellison syndrome (ZES) is caused by a non–beta islet cell, gastrin-secreting tumor of the pancreas that stimulates the acid-secreting cells of the stomach to maximal activity, with consequent gastrointestinal mucosal ulceration. ZES may occur sporadically or as part of an autosomal dominant familial syndrome, multiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the duodenum, the pancreas, and abdominal lymph nodes, but ectopic locations have also been described (eg, heart, ovary, gall bladder, liver, kidney).

HCL secrete by patital cella in stomac.paraital cells stimulated by gastrin which screte by G cells of stomac antram , deodinum and pancrese

zollinger Ellisonnsyndrome can be malignent

simple colloid goiter _= increase uptake iof Iodine131

nodule can be seen in later stage

if Tummour is more than 5 it is very signiticant

Screening mammography may be performed as early as 25 years old in patients with a very high lifetime risk of cancer (>20%). These include patients with the following:

Known mutation of the BRCA1 or BRCA2 gene.

Known mutation of PTEN or TP53 (Li-Fraumeni, Cowden, Bannayan-Riler-Ruvalcaba).

Untested first-degree relative of patient with one of the known gene mutations.

History of mantle radiation to the chest between the ages of 10 and 30 years.

Lifetime risk of breast cancer >20% based on models (Gail, Tyrer-Cuzick etc.)

recommended to do mamogram in evry 2 years all women  between 40 to 49 .

also 2yearly  mamogram  to be done up to 74 years

1.First, breast symmetry, size, general density, and glandular distribution are observed.

2.Next, a search for masses, densities, calcifications, architectural distortions, and associated findings is performed.

3. For masses, the shape, margins, and density are analyzed. The features of benign and malignant masses can be similar. Benign masses are often round or oval with circumscribed margins. Malignant lesions tend to have irregular, indistinct, or spiculated margins. Malignancies tend to have density greater than that of the normal breast tissue. The presence of very low density fat in a lesion often indicates benign findings such as oil cysts, lipomas, galactoceles, and hamartomas.

Calcifications can also be the first sign of cancer or a harmless process in the breast. Benign calcifications are usually larger than calcifications associated with malignancy. They are usually coarser, often round with smooth margins, and more easily seen. Benign calcifications tend to have specific shapes

Calcifications associated with malignancy are usually small (< 0.5 mm) and often require high-resolution magnification imaging with digital zooming for accurate assessment. They tend to have a pleomorphic or heterogeneous shape or a fine granular, fine linear, or branching (casting) shape.

The distribution of the calcification can provide clues to the underlying process and should be specified as grouped, clustered, linear, segmental, regional, or diffuse.

Special findings may be encountered, such as a linear density that might represent a duct filled with secretions or a reniform-shaped mass with a radiolucent center that is typical of an intramammary lymph node.

Associated findings are then taken into account. These include skin or nipple retraction, skin thickening (which may be focal or diffuse), trabecular thickening, skin lesions, axillary adenopathy, and architectural distortion.

screening of prostate cancer

The recommended age for starting screening is as follows:

50 years of age for men at average risk who have at least a 10-year life expectancy

40 or 45 years of age for African Americans and men who have had a first-degree relative diagnosed with prostate cancer before age 65 years

40 years of age for men with several first-degree relatives who had prostate cancer at an early age

No PSA level guarantees the absence of prostate cancer.

The risk of disease increases as the PSA level increases, from about 8% with a PSA level of 1 ng/mL to about 25% with a PSA level of 4-10 ng/mL

No PSA=100% no prostate cancer

Metastatic prostate cancer

Metastatic prostate cancer is rarely curable,

Paget's disease of bone is a chronic disorder that can result in enlarged and misshapen bones. Paget's is caused by the excessive breakdown and formation of bone, followed by disorganized bone remodeling. This causes affected bone to weaken, resulting in pain, misshapen bones, fractures and arthritis in the joints near the affected bones. Rarely, it can develop into a primary bone cancer known as Paget's sarcoma. Often Paget's disease is localized to only a few bones in the body. The pelvis, femur, and lower lumbar vertebrae are the most commonly affected bones.

The paired testicular arteries arise directly from the abdominal aorta and descend through the inguinal canal, while the scrotum and the rest of the external genitalia is supplied by the internal pudendal artery

also testis has colateral bld supply by cremasteric atery and atery yo ductjs deference

Lymphatic drainage of the testes follows the testicular arteries back to the paraaortic lymph nodes, while lymph from the scrotum drains to the inguinal lymph nodes.

testiculer seminoma (germ cell tumour)secreste serum  beta HCG and afa feto protein(tumour markers)

Seminomas account for one third of testicular germ cell tumors (GCTs), which are the most common malignancy in men aged 15-35 years

typical presentation in testicular seminoma is as follows:

A male aged 15-35 years presents with a painless testicular lump that has been noticeable for several days to months

Patients commonly have abnormal findings on semen analysis at presentation, and they may be subfertile

testiculer seminoma  treat with radical orchidectomy ,radiotherapy and chemo

causes for spleenomegaly

causes for massive spleenomegaly

Gaucher's disease or Gaucher disease (/ɡoʊˈʃeɪ/) (GD) is a genetic disease in which fatty substances (sphingolipids) accumulate in cells and certain organs. The disorder is characterized by bruising, fatigue, anemia, low blood platelets, and enlargement of the liver and spleen.  CAUSE TO MASSIVE SPLEENOMEGALY

sprue2

spruː/

noun

noun: tropical sprue

disease of the small intestine causing malabsorption of food, in particular:

a disease characterized by ulceration of the mouth and chronic enteritis, suffered by visitors to tropical regions from temperate countries.

another term for coeliac disease.

intrinsic factor need for absobtion of vit B 12 in illeum.astric resection may reduce intrisic factor and acuse to megalobalstic anemia where DNA repliaction affect

poosr intake of fplate associate with alcoholism, pregnacy and malignacy associate with megaloblastic aneamia

Hemophilia A is an X-linked, recessive disorder caused by deficiency of functional plasma clotting factor VIII (FVIII), which may be inherited or arise from spontaneous mutation. The development of inhibitory antibodies to FVIII can result in acquired hemophilia A or can complicate the treatment of genetic cases.

Hemophilia B, or Christmas disease, is an inherited, X-linked, recessive disorder that results in deficiency of functional plasma coagulation factor IX. Spontaneous mutation and acquired immunologic processes can result in this disorder as well. Hemophilia B constitutes about 20% of hemophilia cases, and about 50% of these cases have factor IX levels greater than 1%.

Normal values for FVIII assays are 50-150%. Values in hemophilia are as follows:

Mild: >5%

Moderate: 1-5%

Severe: < 1%

been based on either clinical bleeding symptoms or on plasma procoagulant levels; the latter are the most widely used criteria. Classification according to plasma procoagulant levels is as follows:

Severe hemophilia - FVIII level less than 1% of normal (< 0.01 IU/mL)

Moderate hemophilia - FVIII level 1-5% of normal (0.01-0.05 IU/mL)

Mild hemophilia - FVIII level more than 5% but less than 40% of normal (>0.05 to < 0.40 IU/mL)

Hemophilia C (deficiency of factor XI)

Even in severe deficiency of factor XI, the bleeding tendency is mild. Unlike the bleeding tendency in hemophilia A or hemophilia B

Mutations in the factor XI gene cause the congenital deficiency of factor XI clotting activity.[4] The inheritance pattern of factor XI is autosomal but not completely recessive, because heterozygotes may have bleeding.

orldwide incidence of hemophilia A is approximately 1 case per 5000 males,

urinary stone with uric acid and xanthen are radiolucent

PCKD may be associate with pancreatic cyst,liver cyst, berry aneurysem

Analgesic nephropathy is injury to the kidney caused by analgesic medications such as aspirin, phenacetin, and paracetamol. The term usually refers to damage induced by excessive use of combinations of these medications, especially combinations that include phenacetin.

associate with high tendancy to hv UTI,trancissional cell Ca, ureteric obtruction due to nrcrotic papile parts, calc7fication of papily, pyelonepritis

anti estrogen tamixifen most effective for menopose breat cancer patient  who is hving recurrents

both repiratory and metabolic alkalosis cause redution ne H.+

ion in bld.

renal tbuble  react and eceat K+

this cause hypokalemia

hydated cyst im the bone can cause pathalogical fracture

hydated dx bovenne dog feces valin vitgarai..not sheep feces

normal ratio to basal cela ca to squarmus cel ca 4 to 1..but immuno sipresa patients this will be reversed

strabismus

strəˈbɪzməs/

nounMEDICINE

abnormal alignment of the eyes; the condition of having a squint.

Bullous impetigo

Thursday, January 14, 2016

bullous impatigo

Image: Bullous impetigo in a 2-week-old baby. | Illustrated Textbook of…

often by staphylococcus aureus

treat with pemicillinase resistant penicillin

Image: A large (giant) congenital pigmented hairy naevus. Other smaller…

Melanocytic naevi (moles)

can cause malignat melanoma in later life

albinism cause refactory errors and visual disturbance and CA

Box 24.1 Causes of napkin rashes

CommonBare

Irritant (contact) dermatitis

Infantile seborrhoeic dermatitis

Candida infection

Atopic eczema

Acrodermatitis enteropathica (see p. 237)

Langerhans cell histiocytosis (see Fig. 21.18)

Wiskott–Aldrichsyndrome

common cause for napkin dermatitis

Irritant (contact) dermatitis

Infantile seborrhoeic dermatitis

Candida infection

Atopic eczema

infantale seborretic dermatitis

Thursday, January 14, 2016

5:49 PM

cause unknown

treat with aplication of salicilic acid with sulphur

later it can vconvert to eczema

Onset of atopic eczema is usually in the first year of life. It is, however, uncommon in the first 2 months,

Onset of atopic eczema is usually in the first year of life. It is, however, uncommon in the first 2 months, unlike infantile seborrhoeic dermatitis, which is relatively common at this age.

Capture Jan 14, 2016

Thursday, January 14, 2016

5:54 PM

eczema

1st 2 months  face and trunk

after that flexers of body

eczema treatment

sope shoud be avoid

emmollient shoud be apply

it contain

They include ointments such as one containing equal parts of white soft paraffin and liquid paraffin.

Molluscum contagiosum

ch24_figure_12

Figure 24.12 Molluscum contagiosum. Some of the pearly…

This is caused by a poxvirus. The lesions are small, skin-coloured, pearly papules with central umbilication (Fig. 24.12). They may be single but are usually multiple.

Image: Molluscum contagiosum. Some of the pearly lesions show…

Tinea capitis (scalp ringworm)

Annular scaling scalp lesion with patchy alopecia with broken hairs

Fungal hyphae on skin scrapings

Treated with topical or systemic antifungal

Treat the dog or cat, if infected

Image: Ringworm of the scalp showing hair loss & kerion.

Scabies is caused by an infestation with the eight-legged mite Sarcoptes scabiei

treatmet for scabies

permethin 5%

benzyl bensoate 25%

melathione  0.5%

all should apply below the neck 6 to 12 hours

Pediculosis capitis (head lice infestation) is the most common form of lice infestation in childre

allacia acreta

Image: Alopecia areata. Smooth well-defined patch of non-inflamed hair…

Stevens–Johnson syndrome, a severe bullous form of erythema multiforme also involving the mucous membranes (Fig. 24.21). The eye involvement may include conjunctivitis, corneal ulceration and uveitis, and ophthalmological assessment is required. I

hearing assement

Image | Illustrated Textbook of Paediatrics | Normal child development,…

At all ages, parental concern about hearing warrants further assessment.

Hearing test for children

1. Newborn

Evoked otoacoustic emission (EOAE) (Fig. 3.9a) – an earphone produces a sound which evokes an echo or emission from the ear if cochlear function is normal.

Auditory brainstem response (ABR) audiometry (Fig. 3.9b) – computer analysis of EEG waveforms evoked in response to a series of auditory stimuli

2. Distraction testing

7 to 9 months

3. Visual reinforcement audiometry

10 to 18 months

but can use upbto 3 years

4. Performance and speech discrimination testing

18 months to 4 years

5. Audiometry

more than 4 years

Tympanometry is an examination used to test the condition of the middle ear and mobility of the eardrum (tympanic membrane) and the conduction bones by creating variations of air pressure in the ear canal. Tympanometry is an objective test of middle-ear function.

Migraine with aura

Accounts for 10% of migrain

Torticollis (tilting of the head)

treatment  for migrain

Serotonin (5-HT1) agonists, e.g. sumatriptan

prophylactic agent for migrain

Pizotifen (5-HT antagonist) – can cause weight gain and sleepiness

Beta-blockers – propranolol; contraindicated in asthma.

Sodium channel blockers – valproate or topiramate.

tension type headache=constriction band

there is no sensory involment in GBS

seizure usually occurs early in a viral infection when the temperature is rising rapidly.

febrile seizer

The family should be taught the first aid management of seizures. If there is a history of prolonged seizures (>5 min), rescue therapy with rectal diazepam or buccal midazolam can be supplied.

Juvenile idiopathic arthritis (JIA) is the most common cause of chronic arthritis in children.

Friedreich's ataxia is an autosomal recessive inherited disease that causes progressive damage to the nervous system. It manifests in initial symptoms of poor coordination such as gait disturbance; it can also lead to scoliosis, heart disease and diabetes, but does not affect cognitive function. T

The ataxia of Friedreich's ataxia results from the degeneration of nervous tissue in the spinal cord, in particular sensory neurons essential (through connections with the cerebellum) for directing muscle movement of the arms and legs. The spinal cord becomes thinner and nerve cells lose some of their myelin sheath

Friedrich ataxia sign and symptoms

Muscle weakness in the arms and legs

Loss of coordination

Vision impairment

Hearing impairment

Slurred speech

Curvature of the spine (scoliosis)

High plantar arches (pes cavus deformity of the foot)

Diabetes (about 20% of people with Friedreich's ataxia develop carbohydrate intolerance and 10% develop diabetes mellitus)[6]

Heart disorders (e.g., atrial fibrillation, and resultant tachycardia (fast heart rate) and hypertrophic cardiomyopathy)

Juvenile idiopathic arthritis (JIA)/juvenile chronic arthritis

commonest chronic inflamatory Dx

It is defined as persistent joint swelling (of >6 weeks duration) presenting before 16 years of age in the absence of infection or any other defined cause.

. Its classification is clinical and based on the number of joints affected in the first 6 months, as polyarthritis (more than four joints) (Fig. 26.16) and oligoarthritis (up to and including four joints) or systemic (with fever and rash). Psoriatic arthritis and enthesitis are further subtypes. Subtyping is further classified according to the presence of rheumatoid factor and HLA B27 tissue type.

Complications

Chronic anterior uveitis

This is common but asymptomatic and can lead to severe visual impairment. Regular ophthalmological screening using a slit lamp is indicated, especially for children with oligoarticular disease.

some more complications are there

Image: Main clinical manifestations of Henoch–Schönlein purpura. (a)…

Henoch–Schönlein purpura

Henoch–Schönlein purpura is the combination of some of the following features:

Characteristic skin rash

Arthralgia

Periarticular oedema

Abdominal pain

Glomerulonephritis.

It usually occurs between the ages of 3 and 10 years, is twice as common in boys, peaks during the winter months and is often preceded by an upper respiratory infection

children often have a fever. The rash is the most obvious feature. It is symmetrically distributed over the buttocks, the extensor surfaces of the arms and legs, and the ankles. The trunk is spared unless lesions are induced by trauma. The rash may initially be urticarial, rapidly becoming maculopapular and purpuric,

Colicky abdominal pain occurs in many children and, if severe, can be treated with corticosteroids. Gastrointestinal petechiae can cause haematemesis and melaena. Intussusception can occur and can be particularly difficult to diagnose under these circumstances

Over 80% have microscopic or macroscopic haematuria or mild proteinuria

Adult-onset Still's disease (AOSD) is a rare systemic inflammatory disease characterized by the classic triad of persistent high spiking fevers, joint pain and a distinctive salmon-colored bumpy rash.

still,s dx

falt feet(pes planas) normal for 15%of developing choldrens..reasuarance enough

in toeing ....if less than 5 years manage by reasuarance

in toeing - Google Search

small VSD resolve spontaneously.but ASD wil not like that

Whooping cough (pertussis)

This is a highly contagious respiratory infection caused by Bordetella pertussis. It is endemic, with epidemics every 3–4 years. After a week of coryza (catarrhal phase), the child develops a characteristic paroxysmal or spasmodic cough followed by a characteristic inspiratory whoop (paroxysmal phase). The spasms of cough are often worse at night and may culminate in vomiting. During a paroxysm, the child goes red or blue in the face, and mucus flows from the nose and mouth. The whoop may be absent in infants, but apnoea is a feature at this age. Epistaxis and subconjunctival haemorrhages can occur after vigorous coughing. The paroxysmal phase lasts 3–6 weeks. The symptoms gradually decrease (convalescent phase) but may persist for many months. Complications of pertussis, such as pneumonia, convulsions and bronchiectasis, are uncommon, but there is still a significant mortality, particularly in infants. Infants who have not yet completed their primary vaccination at 4 months are particularly susceptible

The organism can be identified early in the disease from culture of a per-nasal swab, although PCR is more sensitive. Characteristically, there is a marked lymphocytosis (>15 × 109/L) on a blood count. Although erythromycin eradicates the organism, it decreases symptoms only if started during the catarrhal phase. Siblings, parents and school contacts may develop a similar cough, and close contacts should receive erythromycin prophylaxis

Bronchiolitis

Bronchiolitis is the commonest serious respiratory infection of infancy: 2–3% of all infants are admitted to hospital with the disease each year during annual winter epidemics; 90% are aged 1–9 months (bronchiolitis is rare after 1 year of age). Respiratory syncytial virus (RSV) is the pathogen in 80% of cases. The remainder are accounted for by human metapneumovirus, parainfluenza virus, rhinovirus, adenovirus, influenza virus, and Mycoplasma pneumoniae. Dual infection with RSV and human metapneumovirus is associated with severe bronchiolitis.

fine end inspiratory crackle is fx of bronchiolitis

acute upper airways obstruction (Box 16.1). They are characterised by:

Stridor, a rasping sound heard predominantly on inspiration

Hoarseness due to inflammation of the vocal cords

A barking cough like a sea lion

A variable degree of dyspnoea.

Bronchiolitis= 1  to 9 month  infants  ,commonly(80%) by RSV ,,. other by human meta pneumovirus, parainfluenza virus,rhinovirus, adenovirus,influenza virus, and mycoplasma pneumoniae

Croup= 6 month to 6 years, peak at 2nd year, commenest(95%) due to parainfluenza virus,

others due to influenza, metapneumovirus, and RSV

Acute epiglotitis= 1 year to 6 year,, due to H. influenza b

whooping cough(pertussis) = Bordatella pertussis

3 stages

1.caterrhal phase =about 1 week of coryza

2.paroxysmal phase = about 3 to 6 weeks  carasteristic with inspiratory whoop

3.convulsant phase

In pyloric stenosis, there is hypertrophy of the pyloric muscle causing gastric outlet obstruction. It presents at between 2 and 7 weeks of age, irrespective of gestational age. It is more common in boys (4 : 1), particularly first-borns, and there may be a family history, especially on the maternal side.

Clinical features are:

Vomiting, which increases in frequency and forcefulness over time, ultimately becoming projectile

Hunger after vomiting until dehydration leads to loss of interest in feeding

Intussusception describes the invagination of proximal bowel into a distal segment. It most commonly involves ileum passing into the caecum through the ileocaecal valve (Fig. 13.6a). Intussusception is the commonest cause of intestinal obstruction in infants after the neonatal period. Although it may occur at any age, the peak age of presentation is between 3 months and 2 years.

that viral infection leading to enlargement of Peyer’s patches may form the lead point of the intussusception. An identifiable lead point such as a Meckel diverticulum or polyp is more likely to be present in children over 2 years old. Intravenous fluid resuscitation is likely to be required immediately, as there is often pooling of fluid in the gut, which may lead to hypovolaemic shock.

An X-ray of the abdomen may show distended small

Meckel diverticulum

Around 2% of individuals have an ileal remnant of the vitello-intestinal duct, a Meckel diverticulum, which contains ectopic gastric mucosa or pancreatic tissue. Most are asymptomatic but they may present with severe rectal bleeding, which is classically neither bright red nor true melaena. Other forms of presentation include intussusception, volvulus around a band, or diverticulitis which mimics appendicitis. A technetium scan will demonstrate increased uptake by ectopic gastric mucosa in 70% of case

visual pathway - Google Search

Basic visual pathway

In cases of paracetamol overdose, the sulfate and glucuronide pathways become saturated, and more paracetamol is shunted to the cytochrome P450 system to produce NAPQI. As a result, hepatocellular supplies of glutathione become depleted, as the demand for glutathione is higher than its regeneration.[28] NAPQI therefore remains in its toxic form in the liver and reacts with cellular membrane molecules, resulting in widespread hepatocyte damage and death, leading to acute hepatic necrosis.[3][29] In animal studies, hepatic glutathione must be depleted to less than 70% of normal levels before hepatotoxicity occurs.[25]

pcm poisonin

A paracetamol level drawn in the first four hours after ingestion may underestimate the amount in the system because paracetamol may still be in the process of being absorbed from the gastrointestinal tract. Therefore, a serum level taken before 4 hours is not recommended.[1

pcm poisoing

Diagnosis

A person's history of taking paracetamol is somewhat accurate for the diagnosis.[30] The most effective way to diagnose poisoning is by obtaining a blood paracetamol level. A drug nomogram developed in 1975, called the Rumack-Matthew nomogram, estimates the risk of toxicity based on the serum concentration of paracetamol at a given number of hours after ingestion.[4] To determine the risk of potential hepatotoxicity, the paracetamol level is traced along the nomogram. Use of a timed serum paracetamol level plotted on the nomogram appears to be the best marker indicating the potential for liver injury.[1

pcm poisoning

Clinical or biochemical evidence of liver toxicity may develop in one to four days, although, in severe cases, it may be evident in 12 hours.[31] Right-upper-quadrant tenderness may be present and can aid in diagnosis. Laboratory studies may show evidence of hepatic necrosis with elevated AST, ALT, bilirubin, a

pcm poisoning

Paracetamol may be quantified in blood, plasma, or urine as a diagnostic tool in clinical poisoning situations or to aid in the medicolegal investigation of suspicious deaths. The concentration in serum after a typical dose of paracetamol usually peaks below 30 mg/l, which equals 200 µmol/L.[34] Levels of 30–300 mg/L (200-2000 µmol/L) are often observed in overdose patients. Postmortem blood levels have ranged from 50–400 mg/L in persons dying due to acute overdosage.

acetyl cystine for pcm poisoning

Intravenous acetylcysteine is given as a continuous infusion over 20 hours for a total dose 300 mg/kg. Recommended administration involves infusion of a 150 mg/kg loading dose over 15 to 60 minutes, followed by a 50 mg/kg infusion over four hours;

Acetylcysteine, also called N-acetylcysteine or NAC, works to reduce paracetamol toxicity by replenishing body stores of the antioxidant glutathione.

Cysteamine and methionine have also been used to prevent hepatotoxicity,[58][59] although studies show that both are associated with more adverse effects than acetylcysteine.[11] Additionally, acetylcysteine has been shown to be a more effective antidote, particularly in patients presenting greater than 8 hours post-ingestion.

Gastric decontamination

In adults, the initial treatment for paracetamol overdose is gastrointestinal decontamination. Paracetamol absorption from the gastrointestinal tract is complete within two hours under normal circumstances

What is Lamictal?

Lamictal (lamotrigine) is an anti-epileptic medication, also called an anticonvulsant.

Lamictal is used either alone or in combination with other medications to treat epileptic seizures in adults and children. Lamotrigine is also used to delay mood episodes in adults with bipolar disorder (manic depression).

A positive Pemberton's sign is indicative of superior vena cava syndrome (SVC), commonly the result of a mass in the mediastinum. Although the sign is most commonly described in patients with substernal goiters whe

carbimazole side effect

Whilst rashes and pruritus are common, these can often be treated with antihistamines without stopping the carbimazole. For those patients where sensitivity reactions can not be controlled, propylthiouracil may be used as an alternative; cross-sensitivity between these drugs is rare.

Its most serious rare side effect is bone marrow suppression causing neutropenia and agranulocytosis. This may occur at any stage during treatment and without warning; monitoring of white cell count is not useful. Patients are advised to immediately report symptoms of infection, such as sore throat or fever, so that a full blood count test may be arranged. If this confirms a low neutrophil count, discontinuation of the drug leads to recovery. However failure to report suggestive symptoms or delays in considering the possibility of immunosuppression and its testing, can lead to fatalities.

Catscratch disease (CSD), also known as catscratch fever or subacute regional lymphadenitis, is a bacterial infection affecting lymph nodes that drain the sites of inoculation. Bartonella henselae, a gram-negative rod, is considered the principal etiologic agent.[1, 2] CSD is one of the most common causes of chronic lymphadenopathy in children and adolescents.

Patients with CSD usually have a history of sustaining a scratch or bite from a cat (typically a kitten). The initial symptom is formation of a papule at the inoculation site, followed by solitary or regional lymphadenopathy within 1-2 weeks (see the images below). In most patients, the disease resolves spontaneously within 2-4 months.

emedicine.medscape.com/article/214100-images?imageOrder=2

pap smesr

Cervical intraepithelial neoplasia - Wikipedia, the free encyclopedia

Xenical (orlistat) blocks some of the fat that you eat, keeping it from being absorbed by your body.

Xenical is used to aid in weight loss, or to help reduce the risk of regaining weight already lost. This medicine must be used together with a reduced-calorie diet. Xenical is for use only in adults.