Atopic Dermatitis (Eczema)
Type I (IgE) hypersensitivity inflammatory reaction 
Risk factors: Family history of atopy.   Exacerbated by scratching, stress
Epidemiology: Usually begins prior to 6m of age. 
(FACE): flexor surfaces get adults, children extensor)

Acute form
Pruritus. 
Appear erythematous, edematous with papules/plaques.
Scaling, weeping, and crusting  

Chronic form
Lichenification
painful fissures

Contact Dermatitis
Cell mediated reaction involving sensitized T lymphocytes. 
Etiology 
Irritant form: Chemical insult to skin. No previous sensitizing event. 
Allergic form is delayed-hypersensitivity reaction. Skin sensitized from initial exposure. During next exposure patient has reaction. 
Develop 24-96h post exposure
Pruritus
Acute present as vesicles with clear fluid on erythematous  edematous skin. 
Sub-acute is edema and papules

Stasis Dermatitis
Inflammatory skin disease that occurs on  lower extremities 
Extravasation of plasma proteins and RBC into subcutaneous tissues. Becomes brown in color due to hemosiderin deposits 
Results in interstitial fluid accumulation . Leads to reduced capillary blood flow 
Can progress to venous stasis ulcers and fibrosis
Found in 6-7% of elderly population

Diaper Dermatitis
Irritant dermatitis 
Cutaneous Candidiasis infection (C. Albicans )
Risks: areas where warmth and moisture lead to maceration of skin or mucous membranes 

Seborrheic Dermatitis
Skin rash that occurs in areas of high sebaceous gland concentration 
Cutaneous inflammation to dermis 
Etiology: Immune response to endogenous yeast Pityrosporum 
Triggered by seasonal changes, scratching, emotional stress, medications... 

Renal failure is defined as the cessation of kidney function with or without changes in urine volume
Anuria – UOP < 0.5 cc/kg/hour
Oliguria – UOP “more than 1 cc/kg/hour”

Acute Renal Failure - Definitions
70% Non-oliguric , 30% Oliguric
Non-oliguric associated with better prognosis and outcome
“Overall, the critical issue is maintenance of adequate urine output and prevention of further renal injury.”
Are we converting non-oliguric to oliguric with our hemofilters?

Pre-renal
Decrease in RBF constriction of afferent arteriole which serves to increase systemic blood pressure by reducing the “shunt” through the kidney, but does so at a cost of decreased RBF
At the same time, efferent arteriole constricts to attempt to maintain GFR
As GFR decreases, amount of filtrate decreases.  Urea is reabsorbed in the distal tubule, leading to increased tubular urea concentration and thus greater re-absorption of urea into the blood.
Creatinine cannot be reabsorbed, thus leading to a BUN/Cr ratio of > 20

Diagnosis
Ultrasound
Structural anomalies – polycystic, obstruction, etc.
ATN –
poor corticomedullary differentiation
Increased Doppler resistive index
(Systolic Peak – Diastolic peak) / systolic peak
Nuclear medicine scans
DMSA – Static - anatomy and scarring
DTPA/MAG3 – Dynamic – renal function, urinary excretion, and upper tract outflow

Overall, renal vasoconstriction is the major cause of the problems in ARF
Suggested ARF be replaced with vasomotor nephropathy
Insult to tubular epithelium causes release of vasoactive agents which cause the constriction
Angiotensin II, endothelin, NO, adenosine, prostaglandins, etc.

Renin Angiotensin Axis
Renin’s role in pathogenesis of ARF
Hyperplasia of JGA with increased renin granules seen in patients and experimental models of ARF
Increased plasma renin activity in ARF patients
Changing intra-renal renin content modifies degree of damage
Feed animals high salt diet (suppress renin production)  renal injury  less renal injury than those fed a low sodium diet..

Ankylosing Spondylitis

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Prevalence of Ankylosing Spondylitis
The estimated prevalence is 0.2% to 1.2%
Among adults with chronic low back pain:  prevalence is about 5%

Ankylosing spondylitis
Greek:  “ankylos” = bent
                 “spondylos” = spinal vertebra
Chronic inflammatory disease of axial skeleton causing back pain and progressive stiffness
Peak age 20-30 years
Three times more prevalent in men

Ankylosing spondylitis (AS) belongs to group of disorders that share a predilection to cause inflammation at  enthesis and an association with HLA-B27
Other members of spondyloarthritis (SpA) family:  reactive arthritis, psoriatic arthritis, arthritis associated with inflammatory bowel disease

Pathogenesis
Strong link between AS and HLA-B27
Relative Risk if 1st degree relative with AS:  16 to 94
Twin studies concordance of AS:  63% for identical twins
90% of risk estimated to be genetic
Only small percentage of HLA-B27 individuals in population suffer from a SpA (3-8% of Americans HLA-B27 positive), suggesting that other genetic and environmental factors may  play a role

History - Inflammatory back pain
Inflammatory back pain
Onset before age 40 years
Insidious onset
Improvement with exercise
No improvement with rest
Pain at night (with improvement upon arising)
Patient has a 25% probability of having ankylosing spondylitis if four of five of the above symptoms are present, assuming a 5% prevalence of AS among patients with chronic low back pain.

Exam
Schober test
Lateral spine flexion test
Chest expansion test

Schober’s test
Make a mark between two posterior superior iliac spines
Make another mark 10 cm above first mark
Have patient bend at waist
Distance between two marks normally if greater than 15 cm...

Aortic Valve Disease_Illustrative Cases

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Understand the use of echocardiography to assess aortic valve disease
Apply clinical guidelines to management of aortic valve disease

Selected Abnormalities of Aortic Valve
Aortic Stenosis
– Narrowing of the valve orifice
Aortic Regurgitation
– Incompetence of the valve
– Blood “leaks” from aorta to left ventricle in
ventricular diastole
Bicuspid Aortic Valve
Endocarditis

Why do aortic valves become stenotic?
Valvular Stenosis
– Bicuspid valve with calcification
– Age-related calcific aortic stenosis
– Rheumatic
– Rare causes: Congenital, Rheumatoid, Severe
atherosclerosis (Hyperlipidemia), alkaptonuria
Supravalvular Stenosis
Subvalvular Stenosis
– Discrete
– Hypertrophic Cardiomyopathy

Case 1
77 year old African American Male Referred for evaluation of murmur
Medical history: HTN
Asymptomatic, able to walk up and down stairs, shovel snow
BP 146/86
Crescendo/Descrescendo 3/6 systolic murmur at left lower sternal border

Pathphysiology of Aortic Stenosis
Previously felt to occur as a normal process of aging, related to mechnical stress on normal valve
Current theory involves inflammatory process with T lymphocyte and macrophage infiltration with lipid
accumulation, resulting in bone formation(calcification)

Case presentation
HPI: M is a 30 yo M  referred to endocrine surgery for a palpable thyroid nodule on physical exam by PMD. No dysphonia, dysphagia, odynophagia, change in voice. No smoking history. Recent cough for a few weeks. No fevers, chills, weight loss. No hx of radiation to neck
PMH: major depressive disorder, sleep apnea
Meds: desipramine, buproprion
PSH: left shoulder surgery 1996, pilonidal cyst excision 2000
All: NKDA
FHx: M: Hashimoto’s, F: benign goiter MAunt: hypothyroidism
SHx: no tobacco, social etoh, no drugs
PE
VS: unable to obtain (afebrile, normotensive)
Gen: NAD, healthy appearing
HEENT: palpable ~3 cm nodule in thyroid R lower lobe
CV: RRR, no murmurs
Pulm: CTA b/l, no wheezes
Abd: SNTND
Extr: 2+ DP pulses b/l

Case Presentation cont’d: US and FNA
US: Hypoechoic nodule in R lower lobe with punctate calcifications and some cystic degeneration measuring 2.9 x 3.0 x 3.4 cm sagittal. At the extreme R right lower pole, an adjacent hypoechoic nodule measured 1.2 x 1.6 x 1.4 cm sagittal with irregular margins. In the mid-R lobe, a cystic nodule measured 0.9 x 1.0 x 0.9 sagittal. A mid-L complex nodule with isoechoic solid elements measured 0.9 x 1.4 cm sagittal. A lower L hypoechoic nodule measured 0.7 cm

FNA: Positive for malignant cells. Papillary thyroid carcinoma. Foamy cells c/w cyst contents and/or cystic degeneration. Scant colloid. Rare nuclear grooves present. Rare intranuclear inclusions present.

1% of all new malignant disease
94% differentiated thyroid carcinoma
Derive from follicular epithelial cells
Papillary or follicular thyroid carcinoma
5% medullary thyroid carcinoma
Neuroendocrine tumors
1% anaplastic
Dedifferentiated thyroid carcinoma..

How to choose the sex of your baby

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The issues surrounding choosing the sex of a baby are controversial, to say the least. Those who are for gender selection feel that hereditary, gender-related diseases can be avoided,
as well as allowing for "family balancing." Those who are opposed to gender selection feel that it is not our place to take nature into our own hands

x-sperms, which are bigger,stronger,but slower
The y-sperms are smaller,weaker,but faster

Timing
Basal Body Temperature (BBT)
Cervical Mucus (CM)

2-4 days before suspected day of ovulation
Avoid intercourse at peak mucus level
Intercourse to coincide with ovulation (12 hours before ovulation) (use basal body temperature, cervical mucus)
Intercourse on day of definite temperature dip or if not sure of temperature dip, following morning after dip
Intercourse when shift from peak mucus to thicker, cloudier mucus occurs
Intercourse as close as possible to ovulation (before ovulation)
                         
The most important aspect of all is timing of intercourse during the monthly cycle
If you have sex 3 days or more before ovulation, the better your chances to conceive a girl, because the weaker y-sperms tend to die sooner and the x-sperms will be available in greater quantity whenever the egg is released.
The closer to ovulation you have sex, the better the chances to have a boy, because the y-sperms are faster and tend to get to the egg first.

Scrotal temperature
for a girl, the man is supposed to take a hot bath immediately before intercourse

caffeine One drug that may actually help you conceive a boy
Men and women shall avoid any high-caffeinated food or drink for long-term use.  
Coffee (a few cups of strong caffeinated coffee 30 minutes before intercourse For husband...

Nutritional Support in the ICU

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TPN vs. Enteral: Advantages?
Many prospective, randomized studies
TPN group had much higher infection rates
-    pneumonia, intraabdominal abscess, line sepsis

Potential Reasons for TPN Failure
TPN increases blood glucose if not strictly controlled
numerous studies now show hyperglycemia increases mortality and infectious complications

Does not contain glutamine

Why Enteral?
Preservation of villous architecture
may prevent translocation
role of translocation unclear in humans
good study in BMT patients

Ability to give glutamine
major fuel of enterocytes
major nitrogen transfer agent to viscera
in catabolic stress may be an essential AA

Refeeding Syndrome
In severely malnourished
Development of severe electrolyte abnormalities:
 phosphorous, potassium, magnesium
As muscle mass, cell mass, and ATP repleted:
 may reach critically low values, cardiac arrest

Consequences of Overfeeding
1.  Azotemia - patients > 65 years and patients given >      2g/kg protein are at risk.
2.  Fat-overload syndrome - recommended maximum is 1g lipid/kg/d.  Infuse IV lipid slowly over 16 - 24 hours.
3.  Hepatic steatosis - patients receiving high carbohydrate, very low fat TPN are at risk.
4.  Hypercapnia - makes weaning difficult.
5.  Hyperglycemia - increases risk of infection.  Glucose should not exceed 5 mg/kg/min (4 mg/kg/min for diabetics).
6.  Hypertonic dehydration - can be caused by high-protein formula with inadequate fluid provision.
7.  Hypertriglyceridemia - propofol, high TPN lipid loads, and sepsis increase the risk.  If the patient is hypertriglyceridemic, decrease lipid to an amount to prevent EFAD (500 cc 10% lipid twice weekly) and monitor.
8.  Metabolic acidosis - patients receiving low ratios of energy to nitrogen are at risk.      Acidosis can cause muscle catabolism and     negative nitrogen balance.
9.  Refeeding syndrome - common in malnourished patients or those held NPO prior to initiation of feeding.  Start feedings conservatively, advance gradually, and monitor Mg, Ph, and K closely


Intracranial Hypertension

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Monroe-Kellie Doctrine
Skull is a rigid structure (except in children with fontanels)
3 components:
Brain:  80% of total volume, tissues and interstitial fluid
Blood: 10% of total volume = venous and arterial
CSF: 10% of total volume
Vintracranial = Vbrain + VCSF + Vblood
An increase in one component occurs in the compression of another

Brain
80% of intracranial space = 80% water
Cell types
Neurons: Cell body, dendrites, axon, pre-synaptic terminal-neurotransmission
Astrocytes/Pericytes
Support the neurons & other glial cells by isolating blood vessels, sypnapses, cell bodies from external environment
Endothelial cells
Joined a tight junctions  form BBB
Oligodendrocytes
Myelin sheath around axons  propagates action potential  efficient transmission of information
Microglia
Phagocytes, antigen-presenting cells, secrete cytokines

CSF
10% of total volume
Choroid plexus > 70 % production
Transependymal movement fluid  from brain to ventricles ~30%
Average volume CSF in child is 90cc (150cc in adult)
Rate of production: 500cc/d
Rate production remains fairly constant
w/ increase ICP it is absorption that changes  (increase up to 3X via arachnoid villa)

Blood
10% of intracranial volume
Delivered to the brain via the Circle of Willis  course through subarachnoid space before entering brain
Veins & sinuses drain into jugular veins
Cerebral blood volume (CBV)
Contributes to ICP
Cerebral blood flow (CBF)
Delivers nutrients to the brain

Cerebral Edema
Vasogenic
Increased capillary permeability disruption BBB
Tumors/abscesses/hemorrhage/trauma/ infection
Neurons are not primarily injured
Cytotoxic
Swelling of the neurons & failure ATPase Na+ channels
Interstitial
Flow of transependymal fluid is impaired (increased CSF hydrostatic pressure..

Lymphatic Filariasis

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Disease manifestation range from
Acute-Filarial fever
Chronic-Lymphangitis, Lymphadenitis, Elephantiasis of genitals/legs/arms
Tropical Pulmonary Eosinophilia (TPE)
Filarial arthritis
Epididimoorchitis
Chyluria, etc.

Lymphatic Filariasis Diagnostic Methods
Lymphatic Filariasis can be diagnosed clinically and through laboratory techniques.

Clinically, diagnosis can be made on circumstantial evidence with support from antibody or other laboratory assays as most of the LF patients are amicrofilaraemic and in the absence of serological tests which is not specific other than CFA (ICT). In TPE, serum antibodies like IgG & IgE will be extremely high and the presence of IgG4 antibodies indicate active infection.

1. Demonstration of microfilarae in the peripheral blood
a. Thick blood smear: 2-3 drops of free flowing blood by finger prick method, stained with JSB-II
b. Membrane filtration method: 1-2 ml intravenous blood filtered through 3µm pore size membrane filter
c. DEC provocative test (2mg/Kg): After consuming DEC, mf enters into the peripheral blood in day time within 30 - 45 minutes.
2. Immuno Chromatographic Test (ICT): Antigen detection assay can be done by Card test and through ELISA. Circulating Filarial Antigen detection is regarded as “Gold Standard” for diagnosing Wuchereria bancrofti infection. Specificity is near complete, sensitivity is greater than all other parasite detection assays, will detect antigen in amicrofilaraemic as well as with clinical manifestations like lymphoedema, elephantiasis.
3. Quantitative Blood Count (QBC):
QBC will identify the microfilariae and will help in studying the morphology. Though quick it is not sensitive than blood smear examination.
4. Ultrasonography:
Ultrasonography using a 7.5 MHz or 10 MHz probe can locate and visualize the movements of living adult worms of W.b. in the scrotal lymphatics of asymptomatic males with microfilaraemia. The constant thrashing movements described as “Filaria dance sign” can be visualized.
5. Lymphoscintigraphy:
The structure and function of the lymphatics of the involved limbs can be assessed by lymphoscintigraphy after injecting radio-labelled albumin or dextran in the web space of the toes. The structural changes can be imaged using a Gamma camera. Lymphatic dilation & obstruction can be directly demonstrated even in early clinically asymptomatic stage of the disease.
6. X-ray Diagnosis:
X-ray are helpful in the diagnosis of Tropical pulmonary eosinophilia.
Picture will show interstial thickening, diffused nodular mottling.
7. Haematology : Increase in eosinophil count

Clinical Manifestations
Manifestations are 2 types
Lymphatic Filariasis (Presence of Adult worms)
Occult Filariasis (Immuno hyper responsiveness)..

Classification of malabsorption syndrome
Impaired intraluminal digestion
Intestinal malabsorption
Fermentation

In many cases  more factors elicit the malabsoprtion (e.g.bacterial overgrowth)

Malabsorption due to impaired intraluminal digestion
CF
Schwachman syndrome
Isolated lipase or colipase deficiency
Impaired bile acid synthesis
Bile duct atresia
Interrupted enterohepatic circulation
ileal resection
Crohn disease
Congenital malabsorption of bile acids
Congenitalis trypsinogen or enterokinase deficiency

Intestinal malabsorption
Coeliac disease
Sensitization to food proteins (cow’s milk, soya, rice, wheat)
Giardia infestation
Postenteritis syndrome
Immunodeficiency syndromes
Acrodermatitis enteropathica
Bacterial overgrowth
Crohn disease
Short bowel syndrome
Intestinal lymphangiectasia
Autoimmune enteropathy
Congenital microvillous atrophy
Selective transport defects

Symptoms of malabsorption
Chronic diarrhoea (longer than two weeks)
Slowened weight gain or weight loss
Abdominal distention
Decreased turgor
Vomiting
Anaemia (iron deficiencient or megaloblastic)
Oedema
Symptoms of secondary vitamin deficiencies (rickets, bleeding,  hemeralopia)

Suggested laboratory investigations
Blood test
Seum iron, transferrin, saturation, ferritin
Serum protein
Aminoacid chromatography
Immunoelectrophoresis
D-xylose loading test
alpha-1 antitrypsin content of stool
Serum bilirubin, bile acids
Serological tests (Antiendomysium, IgE antibodies against cow’s milk proteins)

Causes of villous atrophy
Postenteritis syndrome
Cow’s milk allergy
Soya allergy
Coeliac disease
Giardiasis
Immunodeficiency syndromes
Autoimmune enteropathy

Laparoscopic Inguinal Hernia Repair

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How common are they?
 ~ 700,000 inguinal hernia repairs performed in the US per year 
Types: Indirect  &   Direct -- separated by inf epigastric vessels

Open Inguinal Hernia Repairs
Bassini
McVay
Shouldice
Lichtenstein
Plug & patch

Lichtenstein Repair
Popularized the use of polypropylene mesh in primary hernia repairs
Mesh is laid over the undisturbed inguinal floor, posterior to the spermatic cord sutured to the shelving edge of the inguinal ligament, internal oblique fascia and the pubis

Laparoscopic Hernia Repair
When is laparoscopy appropriate?
Recurrent hernias - avoid a prev operated field
Bilateral hernias - one set of incisions better than two inguinal incisions; one mesh to cover both overlay bladder

Types of Laparoscopic Inguinal Hernia Repair
IPOM  (IntraPeritoneal On-lay Mesh) repair. A mesh is placed intra-abdominally covering the hernia defect and then secured to the abdominal wall. Very popular at the beginning of laparoscopic experience, it has since been abandoned.

TAPP   (Trans Abdominal Pre-Peritoneal) repair. With this technique, the pre-peritoneal space is accessed from the abdominal cavity and a mesh is then placed and secured. This is procedure of choice for recurrent inguinal hernias or in case of incarcerated bowel – visualized. 

TEP  (Totally ExtraPeritoneal) repair. The mesh is again placed in the retroperitoneal space, but in this case, the space is accesed without violating the abdominal cavity. This is probably the most physiological repair although technically more demanding.  The procedure of choice for bilateral inguinal hernia repairs


Infections of the CNS
Meningitis
Pachymeningitis:Epidural and subduralinfections
Leptomeningitis-Subarachnoid
Cerebral abscess-focal inflammation
Encephalitis-diffuse inflammation

Formation,circulation,function of CSF
Formation-500 ml/day
Ultrafilteration & secretion –choroid plexus, ependymal lining of ventricles
Circulation: ventricular system-foramina-subarachnoid space

Function of CSF
Protects, lubricates the brain
Provides nutrients, removes waste
90-150 ml adult
10-60 ml in newborn
Blood brain barrier –homeostasis;electrolytes
Urea,glucose ,protein,creatinine passively along concentration gradient

Normal CSF
Thin, colourless, clear fluid
Pressure 90-180mm WATER (10-100 neonates)
0-5 WBC’s /mm3 (neonates 0-30/ mm3 )
Lymphocytes & monocytes
Occasional ependymal or choroid plexus cells
Protein 15-45mg/dl
Glucose 50-80mg/dl
Chloride 113-130 mEq/L
Sterile

Pyogenic meningitis pathogenesis
Blood borne
Direct-sinuses,mastoid,middle ear,dural venous sinuses,direct trauma,fracture skull
Neonates:E Coli,Strep pneumoniae,
Adolescents: N Meningitides, H influenzae
Adults: N Meningitides, Strep pneumoniae type 3
Elderly :Listeria monocytogenes,strep pneumoniae type 3

Gross pathology
Pus in the subarachnoid space
Meningeal vessels engorged
Location-Pneumococcal-convexities
Tracks along vessels, ventriculitis
Microscopy
PMN in SA space,> meningial vessels
Thrombosis of superficial vessels &
Cerebral ischemic damage

Tubercular meningitis
Hematogenic spread
Gross:Thickening & opacity of leptomeniges
Basal meningitis, encasing cranial N’s
Discrete white granules on the meninges +/-
Microscopy-granulomas, lympho-plasmacytic infiltrate
Obliterative endarteritis..

Sexually Transmitted Infections

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The name of this group of diseases was changed from “venereal diseases” to “sexually transmitted diseases” or “STDs”
Now many persons call them “sexually transmitted infections or “STIs.”
A STI is an infection that is transmitted through sexually activity
Most neglected area of healthcare in developing countries (vaginitis, cervicitis and PID)
Major cause of infertility in both females and males

Importance of STDs
Account for up to 40% of gynecologic hospital admissions
Cofactor in HIV and HBV transmission
STDs are almost as common as malaria: 333 million new cases each year

The consequences of untreated STDs
Ectopic pregnancy (7-10 times increased risk in women with history of PID)
Increased risk of cervical cancer
Chronic abdominal pain (18% of females with a history of PID)

Infertility:
20-40% of males with untreated chlamydia and gonorrhea
55-85% of females with untreated PID
(8-20% of females with untreated gonorrhea develop PID)
Increased risk of HBV and HIV/AIDS transmission

Infants can:
Be infected at birth with blinding eye infections and pneumonia (chlamydia, genital herpes and gonorrhea)
Suffer central nervous system damage or die (syphilis or genital herpes) as a result of STDs

Bacterial STDs
Chlamydia
Most common STD
Females outnumber males 6 to 1
Cervix is site of infection
Most women are asymptomatic until the pain and fever from PID occur
If symptomatic - discharge, painful urination, lower abdominal pain, bleeding, fever and nausea
Complications include; cervicitis, infertility, chronic pain, salpingitis, ectopic pregnancies, stillbirths, reactive arthritis.
20-40% of women infected with chlamydia will develop PID (Pelvic Inflammatory Disease)
9% ectopic pregnancy
20% will become infertile
18% chronic pelvic pain

Gonorrhea
Females: gonococcal cervicitis_slight yellow-green discharge or vulvar irritation
Male:gonococcal urethritis_odorous cloudy discharge; urinary burning; swollen, tender lymph glands in groin

Mucus membranes affected include: cervix, anus, throat, eyes
Bacteria neisseria gonorrhea organism attacks cervix as first site of infection
Symptoms are thick discharge, burning urination, and severe menstrual or abdominal cramps
10 to 40 percent women develop PID
Untreated gonorrhea can result in arthritis, dermatitis, and tenosynivitis
Consequences:
FEMALE : PID with sterility; ectopic pregnancy, severe pelvic pain; infant conjunctivitis.
MALE: prostate abscesses with fever, difficult urination; gonococcal epididymitis with ? sterility...

The Limping Child

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Limp is defined as an uneven, jerky, or laborious gait, usually caused by pain, weakness, or deformity Limp can be caused by both benign and life-threatening conditions, the management varies from reassurance to major surgery depending upon the cause .

DIFFERENTIAL DIAGNOSIS 
Bone:
Fractures.
Legg-Calvé-Perthes.
Slipped capital femoral epiphysis.
Tumors.
Vasoocclusive crisis of sickle cell disease
Joints:
Transient synovitis
Septic arthritis
Acute rheumatic fever
Juvenile rheumatoid arthritis
Henoch-Schönlein purpura
Developmental dysplasia of the hip
Hemarthrosis: traumatic, hemophilia
Lyme disease
Systemic lupus erythematosis.

Soft tissue:
Viral myositis.
Intramuscular vaccination.
Cellulitis.
Myositis.

Neurological:
Cerebral palsy
Peripheral neuropathy
Meningitis.
Epidural abscess of the spine.

Vomiting in Children

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Vomiting is a symptom, presenting complaint in multitude of disorders
 Range from gastrointestinal pathology to disease in distant organ (otitis media or intracranial lesion)
In children, especially infants, must distinguish from regurgitation – effortless expulsion of gastric contents
Integrated response to noxious stimuli, coordinated by central nervous system

Centres responsible for vomiting
Vomiting centre
Nucleus solitarius and series of nuclei in brainstem medulla
Stimulation results in
 integrated motor responses involved in vomiting
 associated vasomotor activity (pallor, flushing), salivation, bulbar responses
Afferent input arises from
 posterior pharynx, GIT, brain

Chemoreceptor trigger zone
 Stimulated by humoral stimuli such as opiates, cytotoxins, ketones, ammonia
 Lies in area postrema – floor of 4th ventricle, outside blood-brain barrier
 Processes most of afferent input for the vomiting centre
Receptors and neurotransmitters involved   
 Dopamine (D2), histamine (H1), serotonin (5-HT3), vasopressin, substance P

Diagnostic evaluation
Before finding cause of vomiting, in any child should first
 Assess hydration status, attend to life-threatening complications
 Ascertain whether
  Bilious – suggests gastrointestinal obstruction
  Blood is present – diagnosis and management different
  If non-bilious and non-bloody, 2 important variables => temporal pattern and age of patient

Recurrent vomiting
Ongoing underlying pathology, therefore may be more worrying
Numerous causes
 GIT
  Infections – H. pylori, Giardia, oesophageal candidiasis
  Hepatitis, pancreatitis, partial intestinal obstruction
 Metabolic, neurologic, renal

Cyclic Vomiting Syndrome (CVS)
Paroxysmal, especially severe, recurrent vomiting disorder
Mysterious disorder, unknown aetiology, and pathophysiology
Substantial increase in interest and understanding of disease in past decade
Previously considered rare, may be 2nd only to GORD as cause of recurrent vomiting in children

Under-recognised
 No specific laboratory, radiographic or endoscopic markers for CVS
 Typically misdiagnosed for years – viral GE, food poisoning, GORD, psychogenic vomiting => leads to inappropriate therapy
  Surgery
  Psychiatric hospitalisation
  Very distressing to patients and families
Prevalence
Being diagnosed with increasing frequency, but actual prevalence remains unknown
0.04-2% among school-aged children
Overdiagnosed sometimes, and often underdiagnosed

The management of Uterine Leiomyomas

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The majority of fibroids are asymptomatic and will not require intervention or further investigations.
For the symptomatic fibroid, hysterectomy offers a definitive solution.
However, it is not the preferred solution for women who wish to preserve their uterus.
The predicted benefits of alternative therapies must be carefully weighed against the possible risks of these therapies.
In the properly selected woman with symptomatic fibroids,the result from the selected treatment should be an improvement in the quality of life.

Introduction
Uterine leiomyomas are the most common gynaecological tumours and are present in 30% of women of reproductive age.
The majority of uterine leiomyomas are asymptomatic and will not require therapy.
However,75% of hysterectomies are performed for menorrhagia with fibroids.

Clinical Features
The vast majority of leiomyomas are asymptomatic.
The most common symptom of uterine leiomyoma is abnormal uterine bleeding.
In published series of myomectomies , 30% of women suffered from menorrhagia.

The mechanism of fibroid-associated menorrhagia is unknown.
Vascular defects,
Submucous tumours, and
Impaired endometrial hemostasis
have been offered as possible explanations.

Pelvic pain is rare with fibroids and it usually signifies degeneration, torsion, or, possibly, associated adenomyosis.
Pelvic pressure, bowel dysfunction, and bladder symptoms such as urinary frequency and urgency may be present.

Urinary symptoms should be investigated prior to surgical management of fibroids to exclude other possible causes.

In the postmenopausal woman presenting with pain and fibroids, leiomyosarcoma should be considered.
Clinical examination is accurate with a uterine size of 12 weeks (correlating with a uterine weight of approximately 300 g) or larger.

Ultrasonography is helpful to assess the adnexa if these cannot be palpated separately with confidence.
Although reliable in measuring growth,routine ultrasound is not recommended as it rarely affects clinical management.
In women with large fibroids, diagnostic imaging will occasionally demonstrate hydronephrosis, the clinical significance of which is unknown.
Complete ureteric obstruction is extremely rare.
In women who present with abnormal uterine bleeding,it is important to exclude underlying endometrial pathology..

Introduction to Psoriasis

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Genetics and Pathogenesis
Psoriasis and the Immune System
 The major histocompatibility complex (MHC)
  Short arm of chromosome 6
 Histocompatibility Antigens (HLA)
  HLA-Cw6
  HLA-B13, -B17, -B37, -Bw16
 T-lymphocyte-mediated mechanism

Psoriasis as a Systemic Disease
Koebner Phenomenon
Elevated ESR
Increased uric acid levels → gout
Mild anemia
Elevated α2-macroglobulin
Elevated IgA levels
Increased quantities of Immune Complexes
Psoriatic arthropathy
Aggravation of psoriasis by systemic factors
Medication
Focal infections
Stress
Life-threatening forms of psoriasis

Clinical Variants of Psoriasis
Characteristic Lesion of Psoriasis
Sharply demarcated erythematous plaque with micaceous silvery white scale
 Histopathology
 Thickening of the epidermis
 Tortuous and dilated blood vessels
 Inflammatory infiltrate primarily of lymphocytes

Three Cardinal Signs of Psoriatic Lesions   
Plaque elevation
Erythema
Scale

Chronic Plaque Psoriasis
Most Common Variant
Plaques may be as large as 20 cm
Symmetrical disease
Sites of Predilection
 Elbows,Knees,Presacrum,Scalp,Hands and Feet..

Fever Clinical Pathophysiology

Posted by e-Medical PPT

Body Temperature
“Core Temperature”
Aortic blood temperature
Esophageal temperature
Tympanic membrane temperature

Normal Thermoregulation
Afferent Sensing
Cold receptors –> A delta fibers
Warm receptors –> C fibers
Integrated in spinal cord and CNS –> hypothalamus
Central Integration
20% each contribution from: skin, deep chest and abdomen, spinal cord, CNS, hypothalamus
Skin input predominates behavioral responses
Cold and warm response thresholds only 0.4º apart
Efferent Responses
Behavioral (clothing, adjusting environment)
Response to heat: sweat, cutaneous dilation
Response to cold: digital vasoconstriction
Nonshivering thermogenesis
Shivering

Endogenous Pyrogens
Interleukin–1 (alpha*, beta)
Interleukin–6
Interleukin–11
Tumor necrosis factor (alpha)
Interferon (alpha, beta, gamma)
Prostaglandin–E2
Platelet activating factor
Ciliary neurotropic factor (CNTF)
Oncostatin M
Cardiotropin–1
Leukemic inhibitory factor

Fever and Host Defense Enhancement
Neutrophil function
Enhanced migration
Enhanced superoxide production
Mononuclear function
Enhanced interferon production
Enhanced interferon tumor and viral activity
T–cell proliferation

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