The proliferation and functioning of endometrial tissue outside of the uterine cavity
Incidence: - 15-30% of all premenopausal women, -mean age at presentation: 25-30 years
Etiology - unknown
- retrograde menstruation theory of Sampson
- Mullerian metaplasia theory of Meyer
- endometriosis results from the metaplastic transformation of peritoneal mesothelium under the influence of certain unidentified stimuli
- lymphatic spread theory of Halban
- surgical transplantation
- deficiency of immune surveillance
- age > 25 years
- family history
- obstructive anomalies of genital tract
Sites of Occurrence
ovaries most common location, 60% of patients have ovarian involvement
peritoneal surface of the cul-de-sac (uterosacral ligaments)
there may be little correlation between the extent of disease and symptomatology
pelvic pain - due to swelling and bleeding of ectopic endometrium, unilateral if due to endometrioma
dysmenorrhea (secondary) - worsens with age, suprapubic and back pain often precede menstrual flow (24-48 hours) and continue throughout and after flow
infertility - 30-40% of patients with endometriosis will be infertile, 15-30% of those who are infertile will have endometriosis
dyspareunia on deep penetration
premenstrual and postmenstrual spotting
bladder symptoms - frequency, dysuria, hematuria
bowel symptoms - direct and indirect involvement diarrhea, constipation, pain and hematochezia
truly a surgical diagnosis
history - cyclic symptoms - pelvic pain, dysmenorrhea, dyschezia
- tender nodularity of uterine ligaments and cul-de-sac
- fixed retroversion of uterus
- firm, fixed adnexal mass (endometrioma)
- dark blue or brownish-black implants (mulberry spots) on the uterosacral ligaments, cul-de-sac, or anywhere in the pelvis
- chocolate cysts in the ovaries (endometrioma)
- powder-burn lesions
- early white lesions and blebs
pseudopregnancy - cyclic estrogen-progesterone (OCP) or medroxyprogesterone (Provera)
pseudomenopause - danazol (Danocrine) = weak androgen, s/e: weight gain, fluid retention, acne, or hirsutism, leuprolide (Lupron) = GnRH agonist (suppresses pituitary GnRH)
s/e: hot flashes, vaginal dryness, reduced libido, and osteoporosis with prolonged use .these can only be used short term because of osteoporotic potential
- laparoscopic resection and lasering of implants
- lysis of adhesions
- use of electrocautery
- unilateral salpingo-oophorectomy
- uterine suspension
- rarely total pelvic clean-out
- follow-up with 3 months of medical treatment
1.cleft palate is best repaired
1) Soon after birth B
2) At one month
3) At 6-8 months
4) Between 12-18 months
Cleft lip repair should be done between 3-6 months of age.
2. Intra-osseous access for drugs and fluid administration is recommended for paediatric group up to the age of
1) <one year
2) <4 yeats
3) <6 years
4) Up to 12 years
3. Which of the following is a true statement regarding congenital diaphragmatic hernia (CDH)
1) Common on right side
2) Associated with pulmonary hypoplasia
3) Present with recurrent vomiting at birth
4) Baby benefited with bag mask ventilation
CHD is common on left side by which gastric contents herniate to thoracic cavity , Bag mask ventilation in these babies leads to gastric distension which may further compress the lungs and increase mediastinal shift.
a forcep is a metal device that enables gentle rotation and/or traction of the fetal head during vaginal delivery
Kielland: enables rotation and traction of the fetal head
Simpson: only enables traction of the fetal head
Barton: used for occiput transverse position of the fetal head
Piper: used to deliver the fetal head during breech delivery
Outlet: fetal head lies on the pelvic floor
Low: fetal head is below +2 station (not on the pelvic floor)
Mid: fetal head is below 0 station (not at +2 station)
High: fetal head is not engaged
Prolonged second stage of labor
Nonreassuring fetal heart rate
To avoid/assist maternal pushing efforts
Clinically adequate pelvic dimensions (see “Mechanics of childbirth”)
Full cervical dilation
Engagement of the fetal head
Knowledge of exact position and attitude of the fetal head
Emptied maternal bladder
No suspicion of fetal bleeding or bone mineralization disorders
Scalp injuries are less common
Cannot undergo decompression and “pop off”
Maternal: obstetric lacerations (cervix, vagina, uterus)
Fetal: head or soft-tissue trauma (e.g., scalp lacerations, injured ears), facial nerve palsy
- It include nitroglycerin (glyceryl trinitrate) or pentaerythritol tetranitrate, isosorbide dinitrate and isosorbide mononitrate.
- Liberation of NO
- Cause venodilation, decrease VR and ventricular filling pressure and wall tension; therefore decrease O2 consumption
- Problem with Tolerance – fix with intermittent administration (patch 12hrs on 12hrs off)
- Often offered sublingually or transdermally
- It include either cardioselectives such as acebutolol or metoprolol, or non-cardioselectives such as oxprenolol or sotalol.
- Reduce myocardial O2 demand by decreasing HR and contractility; blocking B1
- Contraindicated in variant angina, good for chronic prophylaxis of stable angina
Calcium Channel Blockers
-It include Class I agents (e.g., verapamil), Class II agents (e.g., amlodipine, nifedipine), or the Class III agent diltiazem.
- All existing CCBs block L-Type channels
- 1st Generation; 3 Classes: - Phenylalkalamines (ex: Verapamil) , - Benzothiazepinones (ex: Diltiazem) , - Dihydropyridines (ex: nifedipime)
- Less depressant activity on heart than the other
- Associated with reflex-tachycardia from baroreceptors
- Problem in pts with angina
Nifedipine is more a potent vasodilator and more effective in angina. It is in the class of dihydropyridines and does not affect refrectory period on SA node conduction.
L: Lungs - Atypical pneumonia.
Relatively nonproductive cough
Pleuritic or non pleuritic chest pain
Confluent or patchy infiltrates on x-ray
Random fact: Interstitial infiltrates aren’t seen often like in other atypical pneumonias.
E: Encephalon - Neurologic abnormalities.
Confusion or changes in mental status
G: Gastrointestinal symptoms.
ION: Na ion decreases.
Hyponatremia (serum sodium level of 131 meq/L)
Medications can interfere with folate metabolism, including:
anticonvulsant medications (such as phenytoin, primidone, carbamazepine or valproate)
metformin (sometimes prescribed to control blood sugar in type 2 diabetes)
methotrexate, an anti-cancer drug also used to control inflammation associated with Crohn disease, ulcerative colitis and rheumatoid arthritis.
sulfasalazine (used to control inflammation associated with Crohn disease, ulcerative colitis and rheumatoid arthritis)
triamterene (a diuretic)
birth control pills
Alport’s Sd (most cases): "hereditary nephritis", type IV collagen deficit, mutation of COL4A5 ("colaas" - alpha-5 chain, type 4 collagen), hearing loss, ocular abnormalities (lens & cornea), hematuria since childhood (gross, micro)
Charcot Marie Tooth: loss of motor & sensory innervation, distal weakness & sensory loss, wasting in the legs, decreased deep tendon reflexes, tremor, foot deformity with a high arch is common (pes cavus), legs look like inverted champagne bottles. Most accurate test: electromyography. No tx.
Focal Dermal Hypoplasia: skin abnormalities and a wide variety of defects in eyes; teeth; and skeletal, urinary, gastrointestinal, cardiovascular, and central nervous systems.
Fragile X Syndrome: CGG trinucleotid repeat, FMR 1 gene mutation, mental retardation, large ears and jaw, post-pubertal macro-orchidism (males), attention deficit disorder (females)
Hypophosphatemic rickets: infants may show growth retardation, widened joint spaces and flaring at the knees at age 1 (> boys), bowing of the weight-bearing long bones, young children-dentition absent or delayed, older children-multiple dental abscesses.
Incontinentia pigmenti: skin abnormalities (blister--> warts--> hyperpigmentation--> hypopigmentation), alopecia, hypodontia, cerebral atrophy, slow motor development, mental retardation, seizures, skeletal & structural anomalies. Letal >males.
Orofaciodigital Sd: OFD1 gene mutation, malformations of face, oral cavity, digits with polycystic kidney disease and variable involvement of the central nervous system.
RETT’s Sd: sporadic mutation of MECP2 gene, onset 2yo, acquired microcephaly, stopped development, motor & speech regression, autism-like behavior, self-mutilating behavior, inconsolable crying/screaming fits, emotional inversion, hypotonia, dystonia, chorea, bruxism, scholiosis, long QT
Alport’s Sd: "hereditary nephritis", type IV collagen deficiency, alternating thickening & thinning of GBM, COL4A5 mutation, hearing loss, ocular abnormalities (lens & cornea), hematuria (gross or micro) since childhood.
Bruton’s Agammaglobulinemia: btk gene defect, no mature B cells or plasma cells, low lymphoid tissue, hepatitis, enterovirus infxs, first 6 months protected by maternal ab (no symptoms)
Becker’s Muscular Dystrophy: altered dystrophin gene, later onset than Duchene's, slow progression, relatively normal life span, less severe, rare cardiac involvement.
Chronic Granulomatose Disease (CGD): NAPDH oxidase deficiency, recurrent catalase (+) infxs, nitroblue tetrazolium test negative (yellow)
Congenital Aqueductus Stenosis: MCC of congenital obstructive hydrocephalus.
Color blindness (red-green): can't distinguish shades of red and green (usually blue-green)
Duchene’s muscular Dystrophy: dystrophin gene mutation (Xp21), absent dystrophyn protein, MC & severe of muscular dystrophies, normal until 5yo, short life span (<30yo), progressive muscle weakness, calf pseudohypertrophy, <3 failure, arrythmias, respiratory insufficiency and infxs (decreased mucociliary clearence). Pneumonias CC of death.
Fabry’s Disease: alpha Galactosidase A, Ceramide trihexose accumulation, angiokeratomas, renal failure, peripheral neuropathy.
Glucose 6-P Dehydrogenase (G6PD) Deficiency: chronic hemolytic anemia, MCC of enzymatic deficiency HA, Heinz bodies, bite cells. Triggers are infections, drugs (antimalarial), fava beans
Hemophilia A & B: factor VIII & IX deficiency respectively. PTT prolongation.
Hunter Disease: iduronate sulfatase deficiency, heparan sulfate accumulation, no corneal clouding, aggressive behaviour.
Inherited Nephrogenic Diabetes Insipidus: V2 receptors in collecting duct don't respond to ADH.
Lesch-Nyhan Sd: HGPRT1 deficiency, spastic cerebral palsy, self-mutilation, hyperuricemia, oral crystals in diapers, early death.
Menkes Disease: ATP7A gene mutation (copper efflux protein), Cu+ is lysil oxidase cofactor, Cu+ accumulates in intestine & kidneys; deficient in other tissues = deficient collagen cross linking; steely 'kinky' hair, MR, arterial tortuosity, hypotonia.
Ornithine Transcarbamoylase Deficiency: urea cycle, orotic aciduria + hyperammonemia (no megaloblastic anemia), orotic acid accumulation, increased glutamine . Cerebral edema, lethargy, vomiting, hyperventilation, convulsions, coma, death.
SCID: IL-receptor, Gamma chain deficiency
Wiskott Aldrich Sd: combined partial B & T immunodeficiency, IgM deficiency, thrombocytopenia, eczema.
Thalassemias are a heterogeneous group of hereditary blood disorders characterized by faulty globin chain synthesis resulting in defective hemoglobin, which can lead to anemia
Thalassemia provides partial resistance against malaria.
- most commonly seen in people of Mediterranean descent
usually due to point mutations in promoter sequences or splicing sites
β-globin locus - short arm of chromosome 11
In a normal cell, the β-globin chains are coded by a total of two alleles . Thus, there are two forms of the disease.
Beta thalassemia minor (trait): one defective allele
Beta thalassemia major (Cooley's anemia): two defective alleles
Inefficient erythropoiesis → anemia
Beta thalassemia minor and major: faulty β-globin chain synthesis → ↓ β-chains→ ↑ γ-,δ-chains → ↑ HbF and ↑ HbA2
most commonly seen in people of Asian and African descent
usually due to deletion of at least one out of the four existing alleles
Inheritance pattern: autosomal recessive
In a normal cell, the α-globin chains are coded by a total of four alleles.
Thus, there are four forms of the disease. The severity of alpha thalassemia depends on the number of defective α-globin alleles.
- Silent carrier (minima form): one defective allele (-α/αα)
- Alpha thalassemia trait (minor form) -Two defective alleles ,Cis-deletion is common amongst Asian populations, whereas trans-deletions are more common in African populations
- Hemoglobin H disease: three defective alleles
- Hemoglobin Bart disease (major form): four defective alleles
Alpha thalassemia major (HbH disease) and Bart disease: faulty α-globin chain synthesis → ↓ α-chains → ↑ β-, γ-chains → ↑ HbH, ↑ Hb-Bart's
Chronic superficial glossitis
Chronic irritation -sharp tooth
Ulcer –most common
irregular margins evertededges
Induratedgrowth or mass
Usually age > 50 yrs
Sex both equally
Painless lump or ulcer on tongue
Ankyloglossia-immobility of tongue
Pain –involvement of nerve
Horsenessof voice & dysphagiain posterior 3rd tongue
Lump in neck
Site -common anterior 2/3 near edges
Ulcer papilliferoursor warty, lump fissure
Palpation of posterior 2/3 tongue
Examination of lymph node
Biopsy : margin or excision biopsy
Ultrasound deep LN
CT scan bone invasion & mets
MRI for oral cavity oropharynx