Gastroesophageal reflux disease(GERD)
Continues to be a challenge to diagnosis.
Classic symptoms– Only 60 %-- Heart-burn and regurgitation.
Achalasia, cholelithiasis, gastritis, peptic ulcer, coronary artery disease –  All mimic typical symptoms with GERD.
Atypical symptoms include chest pain, hoarseness, recurrent sorethroat, dental caries, bronchospasm, wheezing, chronic cough, recurrent chest infection.
Diagnosis include scintiscanning, barium radiography, acid-perfusion or Bernstein test, panendoscopy, present esophagitis.
The introduction of 24-hour esophageal pH monitoring provided a method to quantitate esophageal acid exposure.
Greatest sensitivity and specificity for diagnosis of gastroesophageal reflux –  As the gold standard test.

Three main cause of increase exposure of esophagus to refluxed gastric contents—
 (1) LES defective–  Most.
 (2) Inefficient esophageal clearance as low  peristaltic amplitudes or increase ineffective contractions.
 (3)Gastric abnormal–  Decrease gastric empting.
In early disease, the reflux episode occurred in upright position.
Bipositional reflux suggests more advanced disease and LES is severely impaired.
Pure supine reflux is rare.
Prolong reflux episodes suggest delayed esophageal clearance.

Bernstein test
Acid-perfusion test — Patient sitting with N-G tube 30 cm from nares, infusion normal saline 15 min, 0.1 N HCL at rate of 6 ml/min until symptoms produced.
The test is positive in two successive infusion periods acid induces pain and saline induces relief.
Specificity 89%, sensitivity is low because the pain induced by acid infusion does not correlate with the severity of esophagitis present.

Acid emptying test
Measeure the esophageal emptying capacity.
A bolus 15 ml of 0.1N HCl is introduced into esophagus 10 cm above the pH probe, patient repeat dry-swallows at 30-second intervals.
In normal–  Distal esophagus is cleared of acid within 10 swallows.
Prolonged clearance test indicates an impaired capacity of the esophagus to clear the irritant material.
Lacks sensitivity.

24-hour esophageal pH monitoring
Importance of—to detect an increased esophageal exposure to refluxed acidic gastric contents.
patient with severe symptoms are found mild degree esophagitis in endoscope frequently.
Mucosa injury was greatest in the exposure of pH 0-2.
Normal–  The gastric pH is 1-2, esophageal pH 4-7.
Continuously measured esophageal pH below 4–  Became the commonly used threshold of determing a reflux episode.
False negative—duodenogastric reflux.
Alkaline secretions neutralize gastric acid.
If suspected, a probe measures bilirubin.
Food in stomach can also neutralized gastric acid.
Probe malfunction or misplacement.
Medication use-- particularly proton pump inhibitors.

Liver Biopsies in Hepatitis C

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Hepatitis C
RNA Flaviviridae virus with 6 genotypes
– 75% type 1
– 15% type 2
– <5% type 3
Many subtypes and propensity to mutate lead to high rate of chronic infection
60-85% chronic HCV infection rate
20% of chronic infection develop cirrhosis in 10-20 years
Exacerbated by HIV co-infection
12,000 deaths annually in US

What the Clinician Needs?
How much active inflammation
How much injury of the liver has resulted in fibrosis
Is there any other disease

Grading Systems
Scheuer System
Grade: degree of inflammation, piecemeal or bridging necrosis
Grade 0:  no / minimal inflammation
Grade 1:  portal inflammation or lobular inflammation without necrosis
Grade 2:  mild periportal inflammation and piecemeal necrosis or focal hepatocellular necrosis
Grade 3:  moderate periportal inflammation and piecemeal necrosis or severe focal cell damage
Grade 4:  severe periportal inflammation and piecemeal necrosis or bridging necrosis

Stage: degree of fibrosis
Stage 0:  no fibrosis
Stage 1:  enlarged fibrotic portal tracts
Stage 2:  periportal fibrosis or portal to portal septa, without architectural distortion
Stage 3:  bridging fibrosis with architectural distortion, no obvious cirrhosis
Stage 4:  cirrhosis (probable or definite

Surgical Pathology Report
Chronic viral hepatitis C with mild activity and periportal fibrosis (Batts&Ludwig system)
   - Mild scattered steatosis
   - Mild stainable hepatocellular iron

What mimics chronic viral hepatitis with differential diagnosis of portal inflammation
Hepatitis C
Hepatitis B
Autoimmune hepatitis
Alpha-1-antitrypsin
PSC / PBC
Wilson’s disease
Hemochromatosis
Drug induced hepatitis

Cardiac Amyloidosis

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Amyloidosis
Rudolph Virchow in 1854 adopted the term "amyloid“ to refer to tissue deposits of material that stained in a similar manner to cellulose when exposed to iodine
Amyloidosis is a generic term that refers to the extracellular tissue deposition of fibrils composed of low molecular weight subunits (most of which are in the molecular weight range of 5 to 25 kD) of a variety of proteins.
At least 25 different human and eight different animal protein precursors of amyloid fibrils are now known
“Apple-green birefringence”

Many kinds of Amyloidosis
Primary (AL amyloidosis)
= plasma cell dyscrasia leading to overproduction of Immunoglobulin light chains
Clinical evidence of cardiac involvement occurs in up to 50 percent of patients
Secondary (AA amyloidosis)
Deposition of fragments of serum amyloid A protein, an acute phase reactant
Associated with chronic inflammatory disorders (eg RA).
Almost never produces clinically apparent heart disease (< 5%)
Senile systemic and Heritable amyloidosis 
= Transthyretin deposits
+ Cardiac involvement, but much slower time course than AL

Clinical Manifestations of AL amyloidosis
Nephrotic syndrome with or without renal insufficiency
Peripheral neuropathy, typically axonal, which can be associated with autonomic neuropathy. Carpal tunnel syndrome is commonly seen
Hepatomegaly, with elevated liver enzyme levels
Macroglossia
Purpura, characteristically elicited in a periorbital distribution (raccoon eyes) by a valsalva maneuver or minor trauma, is present in only a minority of patients, but is highly characteristic of AL amyloidosis

Cardiac exam findings
Elevation of the jugular venous pressure, sometimes with a low-volume pulse.
Right sided heart failure hepatomegaly and LE edema
A right-sided third heart sound is occasionally heard
 Fourth heart sound, which coincides with atrial systole, argues against the diagnosis since atrial infiltration causes atrial dysfunction
Amyloidosis rarely causes significant valve disease, but a murmur of tricuspid or mitral regurgitation is occasionally heard.

Echocardiography
Left ventricular wall thickening with evidence of diastolic dysfunction is the earliest echocardiographic abnormality,
In more advanced disease, wall thickening progresses resulting in a restrictive cardiomyopathy with a nondilated or small LV cavity, biatrial enlargement
Amyloid infiltration of the heart results in increased echogenicity.
 "granular, sparkling" appearance of the myocardium,  unusually high quality myocardial visualization
Only a minority of patients has this pattern 26% = low sensitivity

The diagnosis of cardiac amyloidosis is confirmed either by
demonstrating amyloid deposits on endomyocardial biopsy
or, in patients with appropriate cardiac findings, by demonstrating amyloid deposits on histologic examination of a biopsy from other tissues (eg, abdominal fat pad, rectum, or kidney).

COMMON GERIATRIC SKIN DISORDERS

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Common Geriatric Skin Disorders
Age-related changes in skin structure
Xerosis
Dermatitis
Purpura
Pruritis
Bullous Diseases
Dermatomyositis
Intertrigo
Acne Rosacea

Skin Changes with Age
Barrier properties - reduced due to:
 Decreased sweat and sebaceous activity
 Thinning of the epidermis and dermis
 Skin is dryer
Microvasculature - diminished blood flow
 Fewer vessels in the skin
 Disorganized and tortuous remaining vessels
Immunologic Function - decreases
 Acute inflammatory reactions are diminished.
 Contact allergy less severe.
Faulty Thermoregulation
 Heat loss through skin increases
Reduced Cellular Turnover
 Slower wound repair
 Slower desquamation

DERMATITIS
Despite decreased immune response, inflammation is very common in geriatric skin.
Eczematous dermatitis = general term  for erythematous, scaly skin.
May be generalized and non- specific in pattern
Eczema craquele´
Nummular eczema
Contact dermatitis

Contact Dermatitis
Irritant contact dermatitis is often caused by soaps, detergents, and other cleaners (like bleach) as well as formalin, latex, and certain antimicrobial skin ointments.
Allergic contact dermatitis include urushiol (a chemical in poison ivy, poison oak, and mango), nickel in hairpins, earrings, zippers, door handles, and ingredients in hair dyes, insecticides, fungicides, and rubber products.

PRURITIS
Pruritis without a dermatitis
a specific condition of itching with no preceding rash
causes include :
Malignancy (especially lymphomas)
 Thyroid disease
 Anemia, particularly iron deficiency
Renal or liver disease
Polycythemia vera

BULLOUS DISEASES
Paraneoplastic Pemphigus
Autoantibodies to epidermal adherence molecules
May develop in association with either malignant or benign tumors
Benign :  Castleman’s tumor, thymomas
Malignant:  Non-hodgkin’s lymphoma, adenocarcinomas, sarcomas

CERVICAL INCOMPETENCE

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It is premature painless diltation of endocervical canal in pregnancy It is estimated that cervical incompetence will complicate anywhere from 0.1% to 2% of all pregnancies
and is thought to be responsible for approximately 15% of habitual immature deliveries between 16 and 28 weeks of gestation
before onset of labour

The etiology
In most cases, the etiology is unknown
Known causes include Congenital weakness as  Mullerian abnormalities (cervical hypoplasia, in utero diethylstilbestrol [DES] exposure), traumatic abnormalities (prior surgical or obstetric trauma), and connective tissue abnormalities (Ehlers-Danlos syndrome).

Cervical Anatomy
Embryologically, the body and cervix of the uterus are derived from fusion and recanalization of the paramesonephric (Mullerian) ducts, a process that is complete by the 5th month of pregnancy.
Histologically, the cervix consists of fibrous connective tissue, muscle, and blood vessels. Muscular connective tissue constitutes approximately 15% of the cervical stroma, but is not uniformly distributed throughout the cervix, constituting approximately 30%, 18%, and 7% of the upper, mid, and lower thirds of the cervix, respectively (2).
 Conversely, the fibrous connective tissue content of the cervical stroma increases as one moves from the external os to the uterine corpus, and it this component that is believed to confer tensile strength to the cervix. Defects in tensile strength are thought to lead to premature cervical dilatation and pregnancy loss.

Despite many advances in modern obstetrics ,there remains much controversy regarding the diagnosis and treatment of cervical incompetence

Diagnosis
There is no precise method for diagnosing CI
Strongest evidence for diagnosis of CI is lack of any other causes for reccurrent pregnancy loss eg : chromosomal abnormalities,infection,endocrine disorders,immunologic disease)
    With history of consistent with condition. - Or + Pre-pregnancy physical findings
Ultrasonography is useful as adjunct to other diagnostic measures 

History of consistent with condition
Painless premature cervical diltation during pregnancy and before onset of labour
a sudden unexpected rupture of the membranes followed by painless expulsion of the fetus
Resulting in repeated  mid trimester spontaneous miscarriage or premature delivery

Ultrasonography is useful
Before cerclage – length of cervical canal , width of isthmus , funneling of upper part of cervical canal with protrusion of the membranes(when the cervical os (opening) is greater than 2.5 cm, or the length has shortened to less than 20 mm. Sometimes funneling is also seen )
After cerclage – determine exact site of cerclage,proximal cervical canal segment length above cerclage ,distal cervical canal segment length below cerclage,internal os diameter ,funneling if present  , and protrusion of membranes)

CERCLAGE  or encerclage
Suspected cervical incompetence remains the only acceptable indication for cervical cerclage. Indications can be classified as follows:
(1) Prophylactic (elective) cervical cerclage
(2) Asymptomatic women with sonographic evidence of cervical shortening and/or funneling may also benefit from cervical cerclage (often called urgent cerclage)
(3) Emergency (salvage) cervical cerclage
Cerclage should be delayed until after 14 weeks so that early miscarriage caused by other factors is possible. There is no consensus about how late in pregnancy

Shigella Infection

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Shigella Organisms Cause Bacillary Dysentery, A Disease That Has Been Recognized Since The Time Of Hippocrates.
Shigellosis Occurs World-wide. The Incidence In Developing Countries Is 20 Times Greater Than That In Industrialized Countries.
 >95% Of Shigella Infections Are Asymptomatic Hence The Actual Incidence May Be 20 Times Higher Than Is Reported.

The Shigella Bacillus
Shigella Species Are Aerobic, Non-motile, Glucose-fermenting, Gram-negative Rods.
It Is Highly Contagious, Causing Diarrhea After Ingestion Of As A Few As 180 Organisms.
Shigella Spreads By Fecal-oral Contact, Via Contaminated Water Or Food.

4 Species Of Shigella Are Identified, Namely:
 Shigella Dysenteriae
 Shigella Flexneri
 Shigella Sonnei
 Shigella Boydii

Pathology
Gross Pathology Consists Of Mucosal Edema, Erythema, Friability, Superficial Ulcers & Focal Mucosal Hemorrhage Involving The Rectosigmoid Junction Primarily.
Microscopic Pathology Consists Of Epithelial Cell Necrosis, Goblet Cell Depletion, Polymorph & Mononuclear Cell Infiltrates In Lamina Propria And Crypt Abscess Formation

Clinical Picture
Incubation Period Is From 12 To 48 Hours.
Symptoms Begin With Sudden Onset Of High-grade Fever, Abdominal Cramps & Watery Diarrhea
Subsequently The Diarrhea Became Mucoid, Of Small Volume & Mixed With Blood. This Is Accompanied By Abdominal Pain, Tenesmus & Urgency. Fecal Incontinence May Occur.
Physical Signs Are Those Of Dehydration Beside Fever, Lower Abdominal Tenderness & Normal Or Increased Bowel Sounds.

Gastrointestinal Risks
Rectal Prolapse
Toxic Mega Colon
Mild Hepatitis
Septicemia Particularly In Children With Pem

Neurological Complications
These Include:
Lethargy, Delirium, Meningismus & Seizures
Encephalopathy (rare & May Be Lethal)
Syndrome Of Inappropriate Adh Secretion
Febrile Seizures

Systemic Complications
Hemolytic Uremic Syndrome
Disseminated Intravascular Coagulation (dic)
Reiter Syndrome, Arthritis, Conjunctivitis & Urethritis
Myocarditis

Diagnostic Hysteroscopy

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Hysteroscopy is technically quite different from Laparoscopy and expertise with the laparoscopy is no guarantee of success with hysteroscopy.  
Co2 insufflators used for laparoscopy, should never be used for Hysteroscopy.
In laparoscopy the flow of Co2 is in litters, while in hysteroscopy  it is in ccs, with 100mm pressure to distend, uterine cavity. Patients have died in past due to wrong use of instruments. 

For hysteroscopy one is sitting on a low level stool while operation table Is to be raised, for the surgeon to be comfortable, as shown in picture.
For introduction of Hysteroscope with sheath, one  may need  occasionaly cervix to be dilated up to 7 Hegar. Be very gentle in dilating Cx.As any bleeding will interfere in your vision.
If you are using saline or ringer lactate, let  fluid  run from proximal end of scope, before you introduce it, in the cavity.

Once in uterine cavity, one should
pause momentarily until mucus bubbles have dissipated and vision is clear.

Diagnostic Hysteroscopy
To look into endocervix
To look Into uterine cavity
To look at endometrium
To look at tubal osteium

Indications of Diagno.Hysteroscopy
locate submucous myoma.
diagnose uterine septum.
locate & remove lost I.U.C.D.
locate Endometrial polyp.
locate uterine synechae.
detect endometrial cancer

With more and more use of carbon dioxide as a distending media and avabilty of sophisticated instrument like Hysterflator,Dignostic hysteroscopy has almost become an office procedure.which can be done without anesthesia or some times with local anesthesia.

It is most important to insure prevention of complications and their recognition, and  their management, if they occur.
Complication may occur due to
Instrumental  procedure
Distension  media.
Inadequate  visualization
Anesthetic  agent

Pits (Fistulas)
Commissural lip pits
– 12-20% of adults; 0.2-0.7% in children
– Males > Females
– Unilateral or bilateral
– Accentuated with age? or not developmental?
– Failure of processes to fuse
– Blind fistulas; sometimes saliva
– Infection can occur
– Associated with hearing loss, preauricular pits, rib
anomalies
– Combination with paramedian

Paramedian lip pits
– Blind ends
– Presence of salivary glands
– van derWoude syndrome (AD)
• Interferon regulatory factor 6 gene mutations (role in fusion of lip
and palate); chr 1 long arm
• Pits and cleft lip and/or cleft palate
• Mental retardation; dental malformations (hypodontia)
– Popliteal pterigium syndrome
• Same gene
• Popliteal webs
• Cleft lip and/or cleft palate
• Syngnathia (webs connecting upper & lower jaw)

Double Lip
Redundant fold
• Congenital (persistence of the pars glabrosa and
pars villosa) and acquired (trauma, habits)
• Ascher (Laffer-Ascher) syndrome
– Double lip
– Blepharochalasis (Fuchs 1896)
• Edema of the upper eyelid; vision interference
• Hyperplasia of lacrimal glands with prolapse of orbital fat
– Nontoxic thyroid enlargement (50%)
• DiffDx: angioedema, tumor

Leukoedema
• Diffuse grayish-white appearance of mucosa
• Blacks > Whites (racial pigmentation may make this
variation more prominent)
• Variation, not a disease
• More prominent in smokers, “poor” oral health
• Buccal mucosa extending to the lips
• Vagina, larynx
• Hyperplastic epithelium; intracellular edema
• No treatment
• DiffDx: Lichen planus, other leukoplakic lesions,
dentifrice stomatitis (chemical burn)

Microglossia
• Oromandibular-limb hypogenesis syndromes
– Hypodactyly
– Hypomelia
– Underdeveloped organs
– Some potential etiologic factors
• Lithium during pregnancy
• Chorionic villi sampling procedures

Tympanoplasty
Definition: operation involving tympanic membrane and evaluation of middle ear
Whereas myringoplasty is an operation of the tympanic membrane
Tympanoplasty can be accompanied with or without mastoidectomy

Types of Tympanoplasty
Type I: restoration of normal ME with intact ossicles
Type II: Ossicular chain partially destroyed but preserved ad continuity restored
Type III: TM lays on stapes suprastructure
Type IV: Round window protection with a small middle ear mobile footplate left exposed
Type V: Closed middle ear with round window protection; fenestra in the horizontal semicircular canal coveredby a skin graft.

Middle Ear Anatomy
Ossicles: Malleus, Incus, Stapes
Ligaments: sup malleolar ligament, stapedial tendon
Cochlearform process, pyramidal process

Technique
Evaluate TM and ME if perforation present
Create vascular strip
Incise postauricular incision for mastoidectomy
Mastoidectomy- identify lateral landmarks for drilling. Anterior boundary-post EAC, superior boundary- root of the zygoma, linea temporalis, inferior boundary- mastoid tip.  Drill medially and saucerize, delineating Tegmen superiorly, thinning post EAC anteriorly, Sigmoid sinus posteriorly, Horizontal SCC medially
Identify vertical segment of facial nerve between HSCC and digastric ridge
Open facial recess: boundaries are fossa incudus, facial nerve, chorda tympani
Visualization of incus, malleus in antrum, incus and stapes in facial recess.

Pelvic Adhesions

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Pelvic adhesions are considered to be post-inflammatory scar tissues that are formed after abdominal surgery, endometriosis and intra-abdominal infections. Adhesions may also be a severe and sometimes life-threatening complication. Although no universal nomenclature exists, they can be described as dense or flimsy, thick or  thin, opaque or trasluscent and vascular or avascular.

Epidemiology
3.5% of laparotomies is for adhesive intestinal obstruction.
0.9% of all admissions.
SCAR group - 1 in 3 post laparotomy pts are readmitted over 10 yrs.
 Mostly due to surgeries on ovaries and fallopian tubes in gynae and colon & rectum in gen surgery.

Pathophysiology.
Abnormal connective tissue attachments between tissues and organs( Internal scars).
Congenital or Acquired.
Trauma to the peritoneum-
                 Surgical or inflammatory.
                 Ischaemia.
                 Dessication or overheating.
                 Irritation from foreign materials.
                 Wound healing.

Risk Factors
Intrabdominal Infections: Pelviperitonitis.
                          Inflammatory pelvic disease.
                          Acute appendicitis.
                          Perihepatitis.
                          Others.
Abdominal Surgery.
Peritoneal Endometriosis.
Intraperitoneal tissue ischemia:
    Cauterization, Ligatures.
    Devascularization.
    Dryness of the serosa.

Some diagnostic considerations
Only a small percentage of patients with chronic pelvic pain have laparoscopically documented adhesions.
27% of patients without any remarkable history of adhesions present on laparoscopy.
Aproximately 50% of patients with 2 or more factors in their history really have adhesions.
An abnormal pelvic examination is useful in predicting the presence of adhesions in 74% of the cases.

Laparoscopic classification of pelvic adhesions
Stage I: Present around the fallopian tube, ovary or other area, but without impeding ovum capture.
 Stage II:  Present between the fallopian tube and the ovary or between these structures and other areas and may impede ovum capture.
Stage III:  Torsion or oclusion of the fallopian tube or complete blockage of ovum capture

Lipid-lowering drugs

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Atherosclerosis and lipoprotein metabolism
Atheromatous disease is ubiquitous and underlies the commonest causes
 of death (e.g. myocardial infarction) and disability (e.g. stroke) in  industrial
countries
Hypertension and dyslipidemia are ones of the most important risk factors, amenable to drug therapy
ATHEROMA is a focal disease of the intima of large and medium-sized arteries
Atherogenesis  involves several stages:
 endothelial dysfunction with altered PGI2 and NO synthesis
 monocyte attachment
 endothelial cells bind LDL
 oxidatively modified LDL is taken up by macrophages
 having taken up oxidised LDL, these macrophages (now foam cells) migrate subendothelially
 atheromatous plaque formation
 rupture of the plaque

LIPIDS, including CHOLESTEROL (CHO) and TRIGLYCERIDES (TG), are transported in the plasma as lipoproteins, of which there are four classes:
     - chylomicrons transport TG and CHO from the GIT to the tissues, where
     they are split by lipase, releasing free fatty acids.There are taken up in muscle and adipose  tissue. Chylomicron remnants are taken up in the liver
     - very low density lipoproteins (VLDL), which transport CHO and newly synthetised TG to the tissues, where TGs are removed as before, leaving:
    - low density lipoproteins (LDL) with a large component of CHO, some of which is taken up by the tissues and some by the liver, by endocytosis via specific
     LDL receptors
    - high density lipoproteins (HDL).which absorb CHO derived from  cell breakdown in tissues and transfer it to VLDL and LDL

There are two different pathways for exogenous and endogenous lipids:
THE  EXOGENOUS  PATHWAY: CHO + TG absorbed from the GIT are transported in the lymph and than  in the plasma as CHYLOMICRONS to capillaries in muscle and adipose tissues. Here the core TRIGL are hydrolysed by lipoprotein lipase, and the tissues take up the resulting FREE FATTY ACIDS
      CHO is liberated within the liver cells and may be stored, oxidised to bile aids or secreted in the bile unaltered
    Alternatively it may enter the endogenous pathway of lipid transpor in VLDL

THE  ENDOGENOUS  PATHWAY
CHO and newly synthetised TG are transported from the liver as VLDL to muscle and adipose tissue, there TG are hydrolysed and the resulting
      FATTY ACIDS enter the tissues
    The lipoprotein particles become smaller and ultimetaly become LDL ,
    which provides the source of CHO for incorporation into cell membranes, for synthesis of steroids, and bile acids
    Cells take up LDL by endocytosis via LDL receptors that recognise LDL apolipoproteins
    CHO can return to plasma from the tissues in HDL particles and the resulting cholesteryl esters are subsequently transferred to VLDL or LDL
        One species of LDL – lipoprotein - is associated with atherosclerosis (localised in atherosclerotic lesions). LDL can also activate platelets, constituting a further thrombogenic effect

Dyslipidemia
The normal range of plasma total CHO concentration < 6.5 mmol/L.
          There are smooth gradations of increased risk with
elevated LDL CHO conc, and with reduced HDL CHO conc.

Dyslipidemia can be primary or secondary.
 The primary forms are genetically determined
 Secondary forms are a consequence of other conditions such as diabetes mellitus, alcoholism, nephrotic sy,chronic renal  failure,  administration of drug

Ultrasonogram has become a routine imaging modality to diagnose congenital anomalies.
Hydronephrosis is one of the common anomaly detected in the fetus
Incidence of antenatally  detected  hydronephrosis 2 – 4 %
Antenatal diagnosis of hydronephrosis causes a significant distress to the parents during pregnancy.
Antenatal counseling is being done regularly these days.
It is important to know the natural history of the disease to give the parents an idea of what they can expect .
The existing literature on the outcome of antenatal hydronephrosis are unclear.

AIMS AND OBJECTIVES
To asses the outcome of antenatally diagnosed hydronephrosis in our series of patients.
To find out which children would require early surgical intervention, and who would require follow up evaluation.
To create a guideline for antenatal counseling based on our findings

Materials and methods
The study was conducted for 5 years from 2003 to 2008.
All the patients who were seen in our hospital with antenatally diagnosed hydronephrosis were included in  the study.

Materials and methods
The patients were followed up throughout the course of pregnancy and after birth.
Post natal evaluation included ultrasound (1-3 monthly)
Whenever indicated MCU, DTPA performed
Patients were followed from 1 to 4 years with a median follow up of 2.4 years.

Patient Groups
The patients were divided into two groups based on fetal USG,
Group I - Isolated unilateral hydronephrosis.
Group II – Hydroureter, bilateral involvement, bladder wall thickening.
The outcome between groups were compared.

Conclusions
Group 1: Isolated fetal hydronephrosis
Vast majority are minimal hydronephrosis which resolve spontaneously
Only 9% require surgery

Group II: Ureterohydronephrosis, Bilateral etc
55% required intervention
PUV, VUJ, Ureterocele etc

The parents of fetuses with isolated fetal hydronephrosis could be favorably counselled.

CC: 81 y.o. white male coming to ED after found in the bathroom.  + LOC, no amnesia.  Responsive on arrival.
C/o stroke like symptoms:headache,confusion,left sided weakness,unable to turn the head to the left side

PMHx:
HTN well controlled on Lisinopril and HCTZ
Type 2 DM well controlled by diet/exercise
Prostate cancer (on Megestrol)
Occasional CP (no AMI in the past)
COPD
PVD

PSHx:
Inguinal hernia repair
Umbilical hernia repair

Past Anesthesia Hx:
No complications with GA

Laboratory and studies report:
ECG: NSR~100 BPM, nonspecific S-T changes, no signs of acute ischaemia
ECHO: 19 July 2002: EF 74%, no ischaemic changes
Adenosine myocardial perfusion test: 19 July 2002: NSR, left axis anterior hemiblock, mild S-T changes. No evidence of ischaemia.  Normal test.

Intraoperative events:
Proximal aortic graft required resuturing
Episode of hypotension/clotted pump filter
Marked reduction in systolic function after weaning from bypass
Unresponsive to iv epi/norepinephrine, but responsive to intracardiac Epinephrine 1 mg
Blood gas revealed PaO2=45 mmHg
Delayed reinstitution of CPB/clotted oxygenator
Persistent lactic acidosis on bypass
Low urine output
Weaned from bypass, with persistent hypoxemia and lactic acidosis, and hematuria
Return to bypass for the 3rd time
Weaned from the bypass after 1 hour and 25 minutes
Blood clot removed from right atrium

Central Abdominal Pain, Mass and Distension
Foregut pain: Epigastrium.
Midgut pain: Peri-umbilical
Hindgut pain: Hypogastrium
Referred pain: Away from the anatomical location of the pathology but in a region that shares a common embryological origin.

SMALL BOWEL OBSTRUCTION
CLASSIFICATION
INTRALUMINAL
Foreign bodies,Barium inspissation (colon),Bezoar,Inspissated feces,Gallstone,Meconium (cystic fibrosis),Parasites,Other (e.g., swallowed objects, enteroliths),Intussusception (usually associated with tumor in adults),Polypoid, exophytic lesions
INTRAMURAL
Congenital (rare in adults)   Atresia, stricture, or stenosis,Intestinal duplication,  Meckel's diverticulum,Inflammatory process -Crohn disease,Diverticulitis,Chronic intestinal ischemia or postischemic stricture,Radiation enteritis,Medication induced (nonsteroidal antiinflammatory drugs, potassium chloride tablets) Neoplasms    Primary bowel (malignant or benign)    Secondary (metastases, especially melanoma),Traumatic (e.g., intramural hematoma of duodenum)
EXTRINSIC
Adhesions_Congenital(Ladd or Meckel's bands),Postoperative,Postinflammatory (after PID),Hernias,Volvulus,External mass effect,Abscess,Annular pancreas,Carcinomatosis,endometriosis,Pregnancy,Pancreatic pseudocyst

Mesenteric Arterial Embolism
50%: of cases. Due to:
Atrial fibrillation
Myocardial infarction
Arrhythmia
Intra-cardiac tumor such as atrial myxoma or a paradoxical embolus

Clinically:
Sudden and severe epigastric or mid-abdominal pain
Vomiting and explosive diarrhea
25% of patients have had previous embolic events
The abdominal examination may be normal initially with signs of acute abdomen later
Slight to moderate abdominal distension is common
Bowel sounds are highly variable
The classic presentation is severe abdominal pain that is out of proportion to minimal or absent physical signs
Peritoneal signs or blood in the stools are late ominous signs implying infarction

Melanoma

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Development Of Nevi
Melanocytes
 Dendritic, Neural Crest, Basal Cell Layer
 Synthesis Of Melanin
 1/10 To Keratinocytes
 Hyperplasia- Tanning/lentigines, Increased Ratio
Nevus Transformation
 Poorly Understood
 Dendritic- Rounded
 No Longer Lentigionous Pattern- Nests
Junctional Nevi
 Nests Along Dermal-epidermal Junction
Compound Nevi
 “invade” Dermis, First As Nests Then Cords And Single Cells
Dermal Nevi
 Junctional Component Lost

Dysplastic Nevi
Border Melanocytic Nevi And Malignant Melanoma
Clinical Resembles Malignant Melanoma
Lentiginous Compound Nevus, Prominent Bridging Across Rete Ridges
Aberrant In Inter-rete Spaces
Lamellar Fibrosis Of Papillary Dermis, Variable Lymphoid Response

Types Of Melanoma
Acral Lentiginous
Mucosal Melanoma
Superfical Spreading Melanoma
Lentigo Maligna Melanoma
Nodular Melanoma

Clinical Manifestations of Chronic HIV

Posted by e-Medical PPT

Common Clinical Manifestations of Chronic HIV Infection
Constitutional Symptoms
fever
weight loss/wasting
fatigue
Organ/System Specific
virtually all organ systems can be affected
Consider HIV testing for unexplained syndromes

Prophylaxis against Opportunistic Infections
Pneumocystis carinii pneumonia (PCP)
Toxoplasmosis gondii
Mycobacterium Avium Complex (MAC)
Cryptococcal Meningitis
CMV retinitis
Mycobacterium tuberculosis (TB)


PCP - Primary Prophylaxis
Initiate at CD4<200 or prior AIDS-defining illness
Consider desensitization if allergic reaction
up to 70% of patients can tolerate reinstitution of therapy

Toxoplasmic Encephalitis Primary Prophylaxis
Avoid contact with cat feces, raw or undercooked meat, esp. if IgG (-)
Initiate primary prophylaxis at CD4<100

MAC Primary Prophylaxis   
initiate at CD4<50; R/O dMAC first if symptomatic
survival benefit shown for clarithromycin
multiple interactions between rifabutin and antiretrovirals

Cytomegalovirus Primary Prophylaxis
Counseling and regular ophthalmological exams for patients with CD4<50
CMV(-) blood for patients who are CMV(-) at baseline

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