Part 13

Risk factors for what cancer? 

Life style factors responsible for 9/10 cases 

Obesity 

Alcohol 

Smoking 

Reflux causes metaplasia, dysplasia -> adenocarcinoma (Barret's, 1-5%) 

Most common type of cancer in the oesophagus (Barrets) 

Dysphagia 

Persistent indigestion / heartburn 

Weight loss 

Pain in throat or behind sternum 

Peristent cough 

Regurgitation of food 

T1 = mucosa / submucosa 

T2 = muscle involvement 

T3 = serosa involvement 

T4 = grown onto another body structure 

4a = pleura / pericardium / diaphragm 

4b =  trachea, vertebrae, aorta 

N1 = 1-2 nearby nodes 

N2 = 2-6 nearby nodes 

N3 = 7 or more 

You give neoadjuvant chemotherapy before surgery in what stages of oesophageal cancer 

Treatment for? 

Epirubicin, cisplatin, caecitabine (ECX) 

Epirubicin, oxaliplatin, caecitaibne (EOX)

Surgical treatment for cancer in the middle and lower third of the oesophagus? 

Laparotomy / laparoscopy to mobilise stomach, right thoracotomy to resect oesophagus (minimally invasive) 

Dysphagia 

Weight Loss 

Persistent indigestion (dyspepsia)

Feeling full despite eating a small quantity 

Sickness / vomitting 

Meleana / haematemesis 

Tiredness / breathlessness (Fe deficient anaemia) 

Roux-en-Y gastro jejunal anastomosis 

Billroth II gastrectomy: Gastro-jejunal anastomosis 

Oesophago-gastric anastomosis 

Total gastrectomy: oesophago-jejunal anastomosis 

What type of hypersensitivity is T1DM 

What HLA genes are involved in T1DM 

Found on chromosome 6 

Important in MHC molecules (which present antigens to our T cells) 

Polyphagia 

Polydipsia 

Glucosuria 

Polyuria 

Kussmaul respiration (deep / laboured breathing) 

Hyperkalaemia (In the blood) 

But low K+ stores in the cells 

High anion gap 

Symptoms= nausea, vomitting, mental status changes and severe -> cerebral oedema 

More common in T1DM 

Treatment for ?

Fluids - dehydration 

Insulin - to Lower blood glucose 

Electrolytes (K+) - 0.9% KCl

Bicarbonates 

^ all to help reverse the acidosis 

More common in T2DM 

Due to increased glucose in the blood, more water leaves the cells leading to increased urination and therefore total body dehydration 

Increased plasma osmolarity 

Symptoms = mental state changes (due to dehydration)

Complication of diabetes 

Fundscopy shows:

Cotton wool spots 

Flare haemorrhages 

Can result in blindness 

Anion gap metabolic acidosis 

Dehydration 

Acetone breathe 

Hyperkalaemia intially with hypokalaemia 

Ketones present in urine and ABG therefore pH <7.3 

Glucose >250mg/dL 

Gram stain reaction colours for: 

Gram +ve

Gram -ve 

Teichoic acid - structure

 Lipoteichioc acid - picked up by innate immune response 

Thick layer of peptidoglycan 

Survive well on drying 

Some produce spores 

Produce exotoxins 

Do not survive well on drying 

No spores 

Produce endotoxins in their cell wall 

Stain used to see 

Mycobacterium (gram +ve in structure but thick waxy layer of mycolic acids)

Alcohol and acid fast bacilli 

Uses heat to drive stain into cells, cannot rid of stain. Appear bright pink with a counter stain 

Neisseria meningitis - meningococcus 

Neisseria gonorrhoeae - Gonococcus 

Staphlococcus aureus 

Skin, soft tissue, wound 

Blood infection -> endocarditis 

Infection bone -> osteomyelitis and joints (septic arthritis) 

Pneumonia 

Toxic shock syndrome 

+ve coagulase reaction, can convert fibrin to fibrinogen 

Streptococci 

Normal flora in oral cavity, gut, genital tract 

Group A = Streptococcus pyogens

Sore throat, impetigo, cellulitis 

Group B = streptococcus agalactiae

Neonatal sepsis 

Also a Group C and D 

Streptococcus pneumoniae (alpha haemolytic on blood agar) 

Anaerobic spore forming = high mortality :

Clostridium specia - C. tetani, C botulinum, C. difficile

Aerobic spore formers 

Bacillus species - B. anthracis, B cereus (important cause of food poisoning) 

Non-spore forming 

Corynebacterium diptheria, listeria sp (blood stream, meningitis, neonatal sepsis) 

1 y/o child 

Flu like illness for 24hr 

Now droswy with rash 

MB report = turbid CSF, WCC = 450 (90% neutrophils, 10% monocytes), <5RBCs 

Gram stain shows multiple -ve diplococci 

Enterobacteriaceae - Facultative anaerobes:

Infections in UT and blood stream, bacterial food poisoning, intraabdominal infections such as appendicitis 

E-coli, klebsiella, proteus, salmonella 

Pseudomona aeruginosa - aerobe 

Blood stream and UTI; important cause of HCAI in I.c. patients 

Legionella

Environmental organism causing pneumonia 

Haemophillus influenza

A clinical response arising from a non-specific insult 

Including >2 of the following 

Temp >38 or < 36 

HR > 90bpm 

RR > 20 

WBC >12,000 or < 4000 

SIRS with a presumed or confirmed infectious cause 

Sepsis with > 1 sign of organ failure 

Cardiovascular (refractory hypotension) -> shock 

Renal 

Resp

Hepatic 

Haematologic 

CNS

Unexplained metabolic acidosis 

Can bring together T cells without needing an antigen presenting cell 

Therefore a much higher inflammation resposne 

Response to inflammation much higher and therefore can cause sepsis quicker 

Found in:

Group A strep 

Staph aureus TSTT-1

Causes of neonatal sepsis 

Management of? :

Fluids, DA, transfusion 

Resolution of precipitating problem 

Monitor:

Blood gases, Renal function 

CNS /GCS

LFTs 

Myocardial function

Give antimicrobials 

Co-amoxiclav (augmentin) and gentamicin 

Can add vancomycin 

Alternatives = 

Cefuroxime + metronidazole + gentamicin 

Ciprofloxacin + metronidazole + gentamicin 

Glucloxacillin + penicillin (amoxicillin) 

+/- gentamicin 

(consider adding clindamycine if group A strep or staph aureus TSS) 

Co-amoxiclav + doxycycline 

or 

Cerfuroxime + erthyromycin 

Penicillin 

or 

Cefrtiaxone 

Quinine 

Gentamicin + piperacillin + tazobactam (tazocin)