Management of H. Pylori Infection
- Gram – rod
- Causes erosion of protective epithelial cells -> gastritis or peptic ulcer
H2 antagonist or PPI + Abx
- Metronidazole or amoxicillin/clarithromycin
- PPI + 2 or 3 antimicrobials is standard
- Ex: Ranitidine + Peptobismol + Clarithromycin + Amoxicillin 7-14 days
-Add bismuth if resistant H. pylori
- Ex: PPI + BMT (Bismuth + Metronidazole + tetracycline) 7days
Treatment for ZE Syndrome
- Gastrinoma of the duodenum or pancreas
-Elevated gastrin levels- Peptic/gastric ulcers
High dose PPI until resorting to surgery or chemotherapy for tumor removal
Umbilical cord prolapse
acute, life-threatening emergency for the fetus, in which a part of the umbilical cord lies between the antecedent part of the fetus (mostly head) and the pelvic wall, causing rupture of membranes
Epidemiology: rare (0.5% births)
Etiology: often seen in presentation anomalies (e.g., breech presentation, transverse fetal position), multiple pregnancy, long umbilical cord, or abnormal fetal movement (polyhydramnios, premature birth)
Clinical features: -
- an abrupt change from a previously normal CTG to one with fetal bradycardia or recurrent,
- severe decelerations,
- occuring after the rupture of membranes
Diagnostics: vaginal palpation → thick, pulsating cord is palpable
Treatment: Trendelenburg position; fetus is pushed back into the uterus; immediate tocolysis using β2-mimetics (e.g., fenoterol) → emergency cesarean section
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
- Abnormal synchronous APs of groups of neurons in various parts of brain
- Many casues (infection, fever, tumors, injury, lyte imbalance, etc)
- Therapy aimed to reduce excitability of neurons
Benzodiazepines (Clonazepam, Diazepam) - Diazepam used for status epilepticus
Barbiturates (Phenobarbital)- Benzos and Barbituates increase GABA channel - hyperpolarization of neurons
Gabapentin - Increases gaba release
Valproic acid - Increases GABA, also blocks Na+ and Ca2+ channels, and increase K+ conductance
2.Alter transmembrane flow of ions
Phenytoin- Blocks Na+ channels
Carbamazepine - Blocks Na+ channels and potentiates postsynaptic effect of GABA
Ethosuximde - Blocks Ca2+ channels
Iamotrigine - Blocks Na+ channels
3. Decrease glutamate excitatory tone
Glutamate antagonists have too many side effects and none are on the market as anticonvulstants yet
- Ankylosing spondylitis or AS, is a form of arthritis that primarily affects the spine, although other joints can become involved.
- It causes inflammation of the spinal joints (vertebrae) that can lead to severe, chronic pain and discomfort.
- Most people with AS have an antigen called HLA-B27
- Ankylosing spondylitis (AS) is a chronic, multisystem inflammatory disorder involving primarily the sacroiliac joints and the axial skeleton.
Key components of the patient history that suggest AS include the following:
• Insidious onset of low back pain - The most common symptom
• Onset of symptoms before age 40 years
• Presence of symptoms for more than 3 months
• Symptoms worse in the morning or with inactivity
• Improvement of symptoms with exercise
- AS can cause pain and inflammation in other parts of your body.
- Eyes. About 40% of people with AS have an eye problem called uveitis. It’s a painful inflammation that can blur your vision and make you sensitive to bright light.
- Heart valve. It’s not common, but AS can enlarge the aorta, the largest artery in your body. This can change the shape of the aortic valve, which can allow blood to leak back into your heart.
- Cancer. A large study found that people with AS are more likely to get certain types of cancers. They include bone and prostate cancers in men and colon cancer in women, as well as blood-related cancers in both sexes.
A glycogen storage disease (GSD, also glycogenosis and dextrinosis) is a metabolic disorder caused by enzyme deficiencies affecting either glycogen synthesis, glycogen breakdown or glycolysis (glucose breakdown), typically in muscles and/or liver cells. GSD has two classes of cause: genetic and acquired.
Mnemonic:VP CAM HT.– Very Poor Carbohydrate Affects Muscle and Hepatic Target.
Type 0 (Glycogen synthase deficiency)
There is hypoglycemia; hyperketonemia and early death.
Type I (Glucose-6-phosphatase deficiency)-Von Gierke’s disease
- most common autosomal recessive disease.
- characterized by severe hypoglycemia that coincides with metabolic acidosis,
- ketonemia and elevated lactate (due to excess glycolysis) and alanine
Type II (Lysosomal α1->4 and α1->6 Glucosidase deficiency)- Pompes disease
- It affects predominantly the heart and skeletal muscle, producing muscle weakness and cardiomegaly. Liver function is normal and patients do not have hypoglycemia. Two forms identified;
(1) infantile (pompes disease) that develop in first few months of life with weakness and respiratory difficulties and
(2) juvenile that is present in second or third decade of life with difficulty in walking.
Type III (Amylo-1,6-Glucosidase deficiency)-Forbe’s or Cori’s disease
- Deficiency of glycogen debranching enzyme results in storage of an abnormal form of glycogen (limit dextrinosis).
- Both liver and muscle are affected (type IIIA), producing hepatomegaly and muscle weakness. About 15% have only liver involvement (Type IIIB).
Differentiation from type I is by hyperglycemic response to galactose, low concentration of urate and lactate in blood, and elevated serum transaminases and creatinine kinase activities
- production of an abnormal form of unbranched glycogen in all tissue.
- Patients exhibit hepatospleenomegaly with ascites and liver failure.
- There is death from heart or liver failure before 5 years of age.
Type V (Muscle Phosphorylase deficiency)-McArdle’s disease
- Increased plasma creatine kinase activity at rest,
- failure of ischemic exercise to increase serum lactate concentrations while producing an exaggerated increase in ammonia,
- myoglobinuria and diminished activity of muscle phosphorylase establish the diagnosis.
- It manifest as hepatomegaly caused by increased deposits of normal glycogen in liver or in red or white blood cells.
Type VII (Muscle and erythrocyte phosphofructokinase deficiency)-Taruis’ disease
- Abnormal glycogen in muscle.
- Exercise intolerance, unresponsiveness to glucose administration, and hemolysis (caused by decreased glycolysis in RBC) are noted clinically,
- hyperbilirubinemia, pigmenturia and reticulocytosis.
Rheumatic fever occurs after a streptococcal infection (usually caused by Group A Beta-Hemolytic Strep (GABHS)).
It is an inflammatory condition that affects the joints, skin, heart and brain.
Major criteria are referred to as Jones criteria
J – Joint involvement which is usually migratory and inflammatory joint involvement that starts in the lower joints and ascends to upper joints
O – (“O” Looks like heart shape) – indicating that patients can develop myocarditis or inflammation of the heart
N – Nodules that are subcutaneous
E – Erythema marginatum which is a rash of ring-like lesions that can start in the trunk or arms. When joined with other rings, it can create a snake-like appearance
S – Sydenham chorea is a late feature which is characterized by jerky, uncontrollable, and purposeless movements resembling twitches
Minor criteria include
C – CRP Increased
A – Arthralgia
F – Fever
E – Elevated ESR
P – Prolonged PR Interval
A – Anamesis
L – Leukocytosis
Diagnosis of rheumatic fever is made after a strep infection (indicated by either throat cultures growing GABHS OR elevated anti-streptolysin O titers in the blood) and:
Two major criteria OR
One major criterion and two minor criteria
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
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.
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