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
Common pathogens attributed to food poisoning include Norovirus, Salmonella, Clostridium perfringens, Campylobacter jejuni, Staphylococcus aureus, and Escherichia coli.
Incubation periods depend on the cause, and range from a few hours to days. The clinical presentation associated with food poisoning varies, but typical symptoms include diarrhea, nausea, vomiting, and abdominal cramping.
Staphylococcal food poisoning
Pathogen: Staphylococcus aureus
Some strains produce heat-stable enterotoxins that cause staphylococcal food poisoning.
Transmission: ingestion of preformed toxins in contaminated food
Typically involves a short latency period; resolution of symptoms after 24–48 hours
Bacteria proliferate in inadequately refrigerated food (canned meats, mayonnaise/potato salad, custards).
Incubation period: 1–4 hours
Clinical findings: nausea, vomiting, abdominal discomfort, diarrhea
Bacillus cereus infection
Pathogen: Bacillus cereus, a heat-stable, spore-forming bacterium that produces two different enterotoxins
Transmission: The bacterium grows in heated food that cools down too slowly or is improperly refrigerated. Reheated rice is a common source of infection.
Incubation period and clinical findings
Enterotoxin I (emetic form): 30 min to 6 h after ingestion → nausea and vomiting
Enterotoxin II (diarrheal form): 6–15 h after ingestion → watery diarrhea for 24–48 h
Food poisoning from reheated rice - (B. cereus).
- The hallmark feature of rheumatoid arthritis is persistent symmetric polyarthritis (synovitis) of hands and feet.
- The spontaneous onset of excruciating pain, edema, and inflammation in the metatarsalphalangeal joint of the great toe (podagra) is highly suggestive of acute crystal-induced arthritis.
- Podagra is the initial joint manifestation in 50% of gout cases and is eventually involved in 90%.
- RA is a chronic autoimmune multisystem disease having inflammatory arthritis and systemic manifestation.
1. Women (30 to 50 years) are more commonly affected
2. HLA-DR 4 Q is a risk factor for RA.
3. Initial site of disease is synovial membrane
Initiation phase – It is due to non – specific inflammation
Amplification phase – Due to T cell activation
Chronic inflammatory phase – Due to cytokines IL – 1, TNF- alpha (AIPG 2009) and IL – 6
Four of seven criteria are required
1. Morning stiffness – lasting 1 hour before maximal improvement
2. Arthritis of 3 or more joint areas – 14 possible joint areas are right or left PIP MCP, wrist, elbow, knee, ankle and MTP joints
3. Arthritis of hand joints.
4. Symmetrical arthritis.
5. Rheumatoid nodules.
6. Positive Serum rheumatoid factor
7. Radiographic changes – including erosions or unequivocal bong decalcification localized in or most marked adjacent to the involved joint.
Most Common Site of Primary Bone Tumors
- Chondroblastoma (before physeal closure)
- Osteoclastom/Giant cell tumor (after physeal closure in adults)
- Articular osteochondroma
- Bone cyst
- Osteoclastoma (in children)
- Osteomyelitis mostly starts in metaphysis
- Round cell lesions: Ewing’s sarcoma/Multiple myeloma /Reticulum cell sarcoma
- Osteoid osteoma
Purines synthesis and metabolism
Purines are biologically synthesized as nucleotides and in particular as ribotides, i.e. bases attached to ribose 5-phosphate. Both adenine and guanine are derived from the nucleotide inosine monophosphate (IMP), which is the first compound in the pathway to have a completely formed purine ring system
The major site of purine synthesis is in the liver. Synthesis of the purine nucleotides begins with PRPP and leads to the first fully formed nucleotide, inosine 5'-monophosphate (IMP). This pathway is diagrammed below. The purine base without the attached ribose moiety is hypoxanthine.
Biosynthesis of purine and pyrimidine nucleotides requires carbon dioxide and the amide nitrogen of glutamine. Both use an amino acid nucleus – glycine in purine biosynthesis and aspartate in pyrimidine biosynthesis. Both use PRPP as the source of ribose 1-phosphate.
The end product of purine catabolism in man is uric acid.
Biosynthesis Of Pyrimidine Nucleotides
CO2 reacts with N of glutamine to form carbamoyl phosphate, which fuses with aspartate to form carbamoyl aspartate.
Carbamoyl aspartate on ring closure forms the first pyrimidine ring named OROTATE.
Orotate combines with PRPP to form OMP which is the first pyrimidine nucleotide.
OMP forms UMP which can be converted to CMP or dTMP
Each cavernous sinus is a large venous space situated in the middle cranial fossa on either side of the body of the sphenoid bone. Its interior is divided into a number of trabeculae or caverns. The floor of the sinus is formed by the endosteal dura mater. The lateral wall, roof and medial wall are formed by the meningeal dura mater.
Structures in the lateral wall of the sinus from above downwards:
Structures passing through the centre of the sinus:
Tributaries (incoming channels) of cavernous sinus
Draining channels (communications) of cavernous sinus
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
TYPES OF TRACHEOSTOMY TUBE
Metallic Tracheostomy Tube
Nonmetallic Tracheostomy Tube
Cuffed Tracheostomy Tubes
Uncuffed Tracheostomy Tubes
Nonmetallic Tracheostomy Tube - Cuffed tubes are used in situation where positive pressure ventilation is required, or when the airway is at risk from aspiration. (In unconscious patient or when patient is on respiration).
Metallic Tracheostomy Tube -Metallic tubes are formed from the alloy of silver, copper and phosphorus .
Amphotericin B: Naegleria fowleri, Leishmania donovani
Metronidazole: Giardia lamblia, Trichomona vaginalis, Entamoeba hystolytica
Bendazoles or Pyrantel Pamoate: Enterobius vermicularis, Ascaris lumbricoides, Ancylostoma duodenale, Necator americanus (ne M atodes)
Mebendazole: Toxocara canis
Albendazole: Strongyloides stercolaris, Toxocara canis, neurocysticercosis, Echinococcus granulosus.
Paziquantel: Taenia solium, Schistosoma, Diphylobotrium latum, Clonorchis (P latyhelminthes)
Pyrimethamine + Sulfadiazine: Toxoplasma gondii
Suramin: Trypanosma bruceii (blood borne)
Melarsoprol: Trypanosoma bruceii (CNS)
Nifurtimox or Benznidazole: Trypanosoma cruzi
Quinidine (IV): severe Plasmodium infx
Mefloquine or Atovaquone/Proguanil: Plasmodium resistant
Atovaquone + Azythromycin: Babesia
Diethylcarbamazine (DEC): Loa loa, Wucheria bancrofti
Ivermectin: Onchocerca volvulus, Strongyloides stercolaris
Sodium stibogluconate (Pentavalent Antimony): Leishmania donovani
Cloroquine: Plasmodium falciparum, Plasmodium malariae
Cloroquine + Primaquine: Plasmodium ovale, Plasmodium vivax
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