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.
5-fluorouracil
Hydroxyurea
trimethoprim
sulfasalazine (used to control inflammation associated with Crohn disease, ulcerative colitis and rheumatoid arthritis)
triamterene (a diuretic)
birth control pills

Etiology

 - Complication of open abdominal surgery, especially when the bowel is frequently manipulated, with possible disruption of bowel anastomosis, inadvertent enterotomy, or small bowel injury.

 - Can occur as early as 8 days from initial laparotomy

 - Other causes: cancer, irradiation, IBD

Types

Enterocutaneous fistula: abnormal communication between the small or large bowel and the skin
Subtype enteroatmospheric fistula: abnormal communication between GI tract and the atmosphere, associated with high morbidity and mortality

Complications: sepsis, fluid and electrolyte abnormalities, malnutrition

Treatment

Conservative treatment and electrolyte repletion, antibiotics (in case of infections), nutritional support, control of fistula drainage (e.g., ostomy pouch), skin protection
Spontaneous closure occurs in roughly 70% of patients

Surgical Treatment : attempted 1–4 months after trial of conservative therapy if no signs of spontaneous closure

Lysis of adhesions
Resection of abnormal or diseased bowel
Reanastamosis of healthy bowel

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

 

Food Poisoning

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
Gram-positive bacterium
Some strains produce heat-stable enterotoxins that cause staphylococcal food poisoning.  
Transmission: ingestion of preformed toxins in contaminated food

Characteristics

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).

L: Lungs - Atypical pneumonia.
Relatively nonproductive cough
Dyspnea
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.
Headache
Confusion or changes in mental status
Encephalopathy

G: Gastrointestinal symptoms.
Abdominal pain
Nausea
Vomiting
Watery diarrhea

ION: Na ion decreases.
Hyponatremia (serum sodium level of 131 meq/L)

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

 

Constrictive Pericarditis

Etiology

- any cause of acute pericarditis may result in chronic pericarditis

Symptoms

- dyspnea, fatigue, palpitations
- abdominal pain

Signs

- general examination - mimics CHF (especially right-sided HF)
• ascites, hepatosplenomegaly, edema
- pulses: increased JVP, Kussmaul's sign (paradoxical increased in JVP with inspiration),
- Friedrich's sign (prominent “y” descent > “x” descent)
- pressures: BP normal to decreased, +/– pulsus paradoxus
- precordial examination: +/– pericardial knock (early diastolic sound)

Investigations

- 12 lead ECG: low voltage, flat T wave, +/– AF
- chest x-ray: pericardial calcification, effusions
- CT or MRI: pericardial thickening
- cardiac catheterization: equalization of RV and LV diastolic pressures, RVEDP > 1/3 of RV systolic pressure

Management

- medical: diuretics, salt restriction
- surgical: pericardiectomy

TYPES OF TRACHEOSTOMY TUBE

• A tracheostomy tube may be metallic or nonmetallic

Metallic Tracheostomy Tube

• Metallic tubes are formed from the alloy of silver, copper and phosphorus
• Example Jackson’s Tracheostomy tube.
• Has an inner and an outer tube.The inner tube is longer than the outer one so that secretions and crusts formed in it can be removed and the tube reinserted after cleaning without difficulty. However, they do not have a cuff and cannot produce an airtight seal.
• Advantages of a double lumen tracheostomy tube are easy to remove,clean and replace inner cannula.
• Inner cannula should be removed and cleaned as and when indicated for the first 3 days. Outer tube, unless blocked or displaced, should not be removed for 3-4 days to allow a track to be formed when tube placement will be easy.

Nonmetallic Tracheostomy Tube

• Can be of cuffed or noncuffed variety, e.g. rubber and PVC tubes.

Cuffed Tracheostomy Tubes

• Pediatric tubes do not have a cuff.
• 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).
• The cuff should be deflated every 2 hours for 5 mins to present pressure damage to the trachea.

Uncuffed Tracheostomy Tubes

• It is suitable for a patient who has returned to the ward from a prolonged stay in intensive care and requires physiotherapy and suction via trachea.
• This type of tube is not suitable for patients who are unable to swallow due to incompetent laryngeal reflexes, and aspiration of oral or gastric con­tents is likely to occur.
• An uncuffed tube is advantageous in that it allows the patient to breathe around it in the event of the tube becoming blocked. Patients can also speak with an uncuffed tube.

Important

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 .

• Example Jackson’s Tracheostomy tube.
• Advantages of a double lumen tracheostomy tube are easy to remove,clean and replace inner cannula.

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

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
- Treatment

High dose PPI until resorting to surgery or chemotherapy for tumor removal