Dropping TAGs

To drop TAG below 1.7 use

1. very low fat diet
2. diet of 6-12 capsules of fish oil
3. diabetic control (esp if bad)
4. meds: fibrates/fenofibrates/nicotinic acid

Guilty conscience

Hmm I know I'll pass med school. I know I'll make a good doctor given time. But I dont feel confident enough to excel in my current exams. And if I dont, the one overwhelming feeling I would have is guilt towards my parents...then I'll hear my mummy say "Its alright you tried your best". Strange how this guilt far weighs any guilt I have towards my own inadequecies. Gotta get in my head that God controls everything that I'm merely riding a roller coaster. Arh.....Funny how though people all think I know my stuff....work!

Case - AMI & complications

Mr T, is a 64 year old gentlemen admitted to hospital 5 days ago with a cough and SOB on a b/g of a recent AMI 6 weeks ago and subsequent pleural effusion with a background history of DM.

HOPC

He first developed dry Cough and SOB 5 weeks ago. Day 1 after being discharged from hospital for his AMI. He also had fevers, sweating. No sputum production, chest pains, palpitations at that time. 4 days later he went to his GP. Had a CXR done which showed left-sided pleural effusion. Then admitted to hospital and started on oral doxycycline and amoxicillin and observed. He was subsequently discharged with the following medication. He was feeling unwell throughout. 6 days ago in the evening he suddenly developed chest pains that radiated on the left side from the front to the back. He was unable to tell whether it was of a similar nature to his previous AMI pain. There was associated coughing and SOB, no sputum production. no palpitations, nausea, vomiting or sweating. Relieved by panadeine fort and GTN. 2 days later the GP sent him to the hospital where he was managed both for his respiratory and cardiac problems. For his respiratory, had his antibiotics switched to IV ceftriaxone, U/S of the chest and CXR showed resolution of the effusion. In terms of his cardia problems, put on a holter monitor that showed a tachycardia and an abnormal rhythm. He had DC cardioversion last night and he reports feeling well and he noticed better perfusion of his fingers and better skin tone.

Had a recent AMI 6 weeks ago during the evening with symptoms of vomiting, pain to his right shoulder tip, cheeks, chest, sweating and general sense of unwell. No meleana or fresh blood, he vomited only his food contents. His pain was 4/10 chest, 6/10 left cheek and 5/10 in his right shoulder tip. It was described as a dull aching pain. No agg/reliefing factors at that time. Unable to lie in bed and had to sit in his chair and slept fitfully the rest of the night. The next day he went to the GP who sent him to the ER and was diagnosed with a AMI with raised cardiac enzymes and ECG changes. He was subsequently investigated with an angiogram and a echocardiogram. 5 days post-admission he developed a sharp pain that radiated from his shoulder to the face with no other associated symptoms. It was an 8/10 in severity. Came on suddenly and was constantly there. He was diagnosed with pericarditis. Treated with morphine and oxygen. This pain subsided 48hrs later and he was discharged.

Medical history
CVD RF: No HT, no chol, smoked a pack a week for 3 years during his university days, drinks socially, has DM.

His type II diabetes was diagnosed 5-6 years ago on routine blood screen. Currently managed on diet and exercise control. He avoids sugary food, takes low fat and lean meat. Walks his dog 4 times a week/ 30min each time. Has lost 30kg from 134-104kg. After his recent admission to hospital his blood sugars were not well controlled and was put on insulin. currently on 3 times novorapid and one evening bolus of glargine. His current average blood glucose is 6mmol/L on insulin. No macro/microvascular complications of DM.

Non-active medical conditions: gall bladder removal, recently diagnosed carpel tunnel, hayfever and asthma when he was a kid, appendicitis.

Medications:
Novorapid, glargine, ceftriaxone, fruesemide, atenolol, atorvastatin, perindopril, aspirin, clopidogrel.

FH:
Father lung cancer, 79. Mother, diabetic.

Social: Live/family, support, depresion, financial, depression, exercise/drinking/diet/smoking, insight.

Physical examination:

Peter is a well-looking man, orientated in time/place. Not in any pain or respiratory distress.
V/S: HR 60bpm, regular. RR18bpm. BP110/70. Oxygen sats on room air was 94%. On general inspection. He had no supplemental oxygen, a venous cathether in the dorsum of this right hand. Scars??

On cardiac examination:
No pale palmar creases, no manifestations of IE. On inspection of his face, no central cyanosis or jaundice. JVP was not elevated. Carotid pulse felt normal. Apex beat was not displaced. No palpable heaves or thrills. Dual heart sounds with no murmers.

On respiratory examination:
No deviation of the trachea, No palpable LN. Chest expansion was equal and normal. Stony dullness to percussion on mid to lower region on his left side. On asculation, there was decreased breath sounds and decrease vocal resonance.

In summary, Mr T is a 64 y.o gentlemen who was admitted to hosptal 5 days ago with cough and SOB on a b/g of a recent AMI. The SOB began 3 weeks ago and was treated with IV ceftriaxone. His current physical examination findings are consistent with a left sided pleural effusion. His issues are.

1. managment of his pleural effusion - which requires organized follow up with the GPs + continued Antibiotics. CXR to monitor the current pleural effusion.

2. Managment of his MI - start him on ACS medication and continue to watch for SE. and monitor complications. Optimise the control of his risk factor particularly his diabetes.

Watery diarrhoea cryptosporidium

Peter is a 47 y.o man who presents with a 4 week history of watery diarrhoea on a b/g of renal transplantation for PCKD.

HOPC:
4 weeks ago, Mr P developed a sudden episode of watery diarrhoea that has not resolved over. He has 4 diarrhoeas 8-12 times a day. No blood, mucous seen in the stool. Volume of the fecal material is high. His normal bowel motion is 1/day. He also developed fevers, chills and rigors &abdominal cramps during day 1 and 2 but has not have any of this symptoms since then.

Other relevant negatives (considering he is immunocompromised)

• No LOW, night sweats, lack of appetite.
• No cough, sputum, SOB.
• No chest pain, palpitations.
• No symptoms of UTI but has noticed a low volume of urine output (10-15mL). Claims to be dehydrated.
• No fainting, dizziness, blackouts.
• No Neurological signs.

He presented to the GP on day 2 and was subsequently admitted to hospital last week and treated.

• I- flu vaccination is up to date
• Contact - works with children (prone to norovirus, adenovirus, rotovirus diarrhoea). Last worked? No other sick contacts.
• Travel - No travel. Any dubious food? Any stream water or tank water?
• O - irrelevant
• A- lives with a cat
• D- imunnosuppressive drugs + cardiac drugs.
• Sex - never ask.

Med Hx.

1. PCKD diagnosed during the 80's. Currently on 3rd transplant. First transplant lasted 4 days. His last transplant was in 94'. On immunosupressive drugs for it. Has 1 URT infection/ 2mths. and also occasional diarrhoea. Attributed to him working with children. Hospital admissions for complications?
2. Cardiac disease with triple bypass done? any symptoms? PND, orthopnea, pillows used, exercise tol?

Medication?

Family history?

Social history?

• Live with? Family, children?
• DALYs?
• Support?
• Finanacially stable?
• depressed?
• Smokes, drink?
• exercise
• diet

Osteomyelitis

Most common bug is SA treat with flucoxicllin.
Randomly, in radical prostectomy, most commonly by pseudomonas (10-20% ciprofluxacillin resistant).

Septic arthritis

Septic arthritis - acutely inflammed joint and may destroy within 24hrs. Treat empirically with antibiotics.

Signs/symptoms

• Swollen, red joint
• associated fevers, chills and rigors, consider localised symptoms.

DDX - OA, gout, haemarthrosis, less likely psoriatic arthritis, reactive arthritis.

Ix-

1. Imaging - x-rays may be normal, consider CT, U/S, MRI.
2. FBE, ESR, CRP - raised WCC, inflammation.
3. U&E and LFT for baseline.
4. Joint aspiriate - appearance: turbid,yellow, low viscosity, microscopy: raised WCC, neutrophils. Culture& sensitivty: for the organism + sensitivity. also for polarized light microscopy: crystals (negatively bifringement crystals for gout)

Mx-

1. Analgesia
2. Empirical antibiotics until culture is known. Flucloxacillin (as most common organism is SA. consider benzylpenicillin + gentamicin)
3. Consult microbiologist
4. Consider joint wash-out especially in prosthetic knee.
5. Seek/ treat underlying cause - immunosupression? focus of infection?

Other medication to consider

1. MSSA - 1st/2nd gen cephalosporin - cephazolin/cephalexin.
2. Gp D streptococci - (like GP A but affects immunocompromised patients). Ideal medication would be penicillin as you would prefer a narrow spectrum medication to avoid antibiotic resistance (unnecessay killing of gram negative) but ceftriazone for convinience - as it is once a day dose and lower risk of PICC line occlusion.
3. infected prosthetics - combination therapy with flucoxicillin + ciprofluoxacin or rifampicin. better chance of killing organism due to presence of biofilm. options: surgery to remove joint then IV antibiotics until aseptic then joint replacement takes 9 months or lifelong prophalaxis.
4. ???Culture negative - cipro, rifampicin(treat myco), fusedic acid.

PUO: investigations

PUO is defined as a temperature of >38.3 degrees for more than 3 weeks.

DDX think broadly from top to down.

1. Infection - abscesses
2. CTD/autoimmune
3. Malignancy
4. Drugs
5. Others; hypothalamic lesion, factitious fevers.

Ix:

1. FBC - raised WCC
2. U&E - ARF, pyelonephritis, baseline for antibiotic treatment
3. LFT - liver damage especially abscess
4. Haemolytic anemia - anemia, raised weiyong is smelly bilurubin, raised urobilinogen, raised LDH, reticulocytosis, direct antiglobulin test. Considering drug reaction?
5. Myeloma screen - serum plasma electrophoresis (paraprotein & monoclonal band), urine plasma electrophoresis (Bence Jones protein). beta2 microglobulin, Ig G, M, A levels
   
6. autoimmune - Rf, ANA, dsDNA, ENA, complement activity (C3, C4), ESR, CRP, GBM, ANCA(C & P), liver/kidney microsomal antibodies.
7. peripheral blood flow cytology
8. copper, ceruloplasmin.
9. ACE
10. septic workup. consider TB.
    
11. viral serology - HIV, HAV, Hbs Ag, HCV, others:flavivirs, mycoplasma, CMV, EBV, Q fever. CD4.
12. Imaging: CT brain, body, sinuses.
    

PUO- endocarditis

Intro:
Peter is a 80 y.o gentlemen who came to the hospital via ambulance due to an episode of uncontrollable rigors and SOB. This is in the setting of a previous pacemaker infection in October 2008.

HOPC

6 days ago, he had an episode of rigors that lasted about 20min. He was at home at that time and he started shaking uncontrollably with involved all of his limbs there was associated SOB, increase RR and feeling cold. No chest pains, palpitations. There was no associated neurological deficits- muscle weakness, numbness, visual changes. There was no LOC. During this episode he called the ambulance and was sent to the hospital. He recovered in the ambulance and was feeling tired but otherwise not confused. Prior to this episode he had two similar episodes while at home and while in hospital he developed a similar episode. The total number of attacks is 4.

Patient has no recent

· Fevers ( spiking (malaria), high swinging( abscesses), constant ( gen. bacterial/ neoplasia/CTD), intermittant fever (viral especially in paediatrics) ( (has chills and rigors)
· Fatigue, LOW(despite eating a lot), night sweats.
· Localised symptoms:
1. Cough, sputum(blood? Colour? Amt?), (SOB)
2. Chest pain, palpitations, PND, orthopnea, pillows used, peripheral odema (if HF)
3. urinary – freq, urgency, nocturia, dysuria, and incontinence
4. diarrhoea, constipation, abdominal pain, blood in stools
5. Neck stiffness, photophobia, Head ache
6. Arthralgia (backpain – epidural abscess), myalgia and skin rashes.
7. ear pain, face pain (sinusitis).
8. wounds/bites.

· Dentition
· Immunization – was up to date with both his pneumococcal and flu vaccine
· Contact – no contact with anyone that’s sick recently or anyone with TB
· Travel – gone to alice springs and NT but nothing too adventurous like swimming in rivers
· Occupation – purchasing manager
· Animals – No
· Drugs – later
· Sex- Nil.

Medical conditions

· Heart failure with AF was diagnosed in 2002. He presented with APO and was unable to sleep at night his wife had to send him in ED. A pace maker was then inserted in December 2002. Since then he does not complain of PND, orthopnea, uses 1 pillow, has occasional leg swelling well controlled by diuretics. His exercise tolerance is about 50m.
· October last year he noticed a rash on his skin overlying the pacemaker. Prior to this he developed a boil on his head when he bumped his head on the shower. His GP sent him to the hospital for further investigations and he was treated for a pacemaker infection with 1/12 of antibiotic treatment and the infection was presumed cleared.
· He had no other admissions for exacerbations for HF. His current HF meds are carvedilol, spironolactone, lasix.

Non-active medical conditions
· 2 hernia operations (1980)
· Right knee replacement (80’s)
· Backpain caused by lumber sacral spinal stenosis, which is getting worse recently. Still able to drive, no muscle weakness or numbness
· OSA(04’)- used to be on CPAP but doesn’t need to use it now.
· Bilateral varicose veins

CVD risk factors – HT, high cholesterol, No DM, smoked 16 pack/yrs and quit when he was 35.

Medications-
Carvedilol, spironolactome, lasix, lipitor, irbesatan, warfarin.
Was treated on ceftriaxone, flucoxicillin and vancomycin 3 days ago for empirical treatment of sepsis.

FH- NIL
Social – live, occupation, depression, financial, support, exercise, diet.

On physical examination

· Alert, well-orientated, no signs of fevers, rigors or sweats.
· V/S – 120/80 bp, 72 HR regular, sats 98%, temperature 37.7 at 0600hrs but previously afebrile.
· CVL in for 3 days – area of insetion not oedematous or red.
· Cannula on right arm.
· Pacemaker area not oedematous, no rash.

CVD exam – normal. Looking specifically for signs of IE – Janeway, oslers, splinter haemorrhage. Petechiae in the conjunctivae. Roth spots. Splenomegaly.

Resp- Normal

Abdomen – normal

Mx issues-
Identify source of infection – septic screen - sputum, stool, urine culture. CSF? CXR. Ideally 3 samples of bloods spaced at least 30min apart.
Empirical treatment for sepsis – antibiotics ( gentamycin+ ceftapine) + supportive therapy. This treatment does not cover for gram +ve -staphs aures, enterococci. [ use ampicillin or vancomysin], TB, PCP (co-trimaxazole, if allergic to sulphur meds use pentamidine), anaerobes(metronidazole). Consider fungal causes. If less sick ceftriaxone + stat dose of gentamycin is enough.

Treatment in type II diabetes.

1. Diet/weight/exercise control
2. Oral hypoglycemics - metformin is first line. Over time additional therapy is requried. add a 2nd drug, sulfonylureas. Beware thiazolidinediones ( especailly rosiglitazone - associated fluid retention. some studies show that it is associated with coronary artery disease)
3. Consider use of alpha-glucosidase inhibitors(acarbose), lipase inhibitors (orlistat) [ not good for weight loss but indicated for glycemic control], DPP-IV inhibitors (sitagliptan (Januvia)-oral [prevents incretin break down], GLP-1 receptor agonist(exenatide (byetta)-s/c [ increases incretin levels] This new class increases insulin secretion and decreases glucagon secretion. Lowers post-prandial sugar levels and keeps pre-prandial levels low.
4. once per day insulin is added to oral hypoglycemic therapy in patients with type 2 diabetes, either insulin NPH or detemir given at bedtime or insulin glargine given in the morning or at bedtime. Start low at 10 units and vary by 10-20% over 2-4 days.
5. Total daily dose of 1unit/BMI of insulin.
   
6. Consider pre-mixed insulin or NPH + a short acting. twice a day. Not recommended in type I diabetics.
7. More complex insulin regimens are recommended when needed. Similar to type I diabetes. (long-acting basal bolus in the night+ pre-meal short or rapid acting insulin)
8. Target of 4-6mmol pre-prandial and 4-7.7 post-prandial. HbA1C of 6-7% (reflects past 3 months glucose levels)
   

ALWAYS REMEMBER PATIENT EDUCATION! insulin injections, warnings on hypoglycemia - in relation to illnesses, missed doses, exercise, diet.

Types of insulin

Ultra-short acting: insulin aspart(novorapid), insulin lispro
Onset:15min Peak: 1hr duration: 4hrs

Short-acting: actrapid, hypurin neutral
Onset:30min Peak: 4hrs duration:8hrs

Intermediate: Protaphane, Humulin NPH, Hypurin Isophane (bovine), Hypurin Isophane (porcine) via SAS.
Onset:1.5hrs Peak: 8 hrs duration: 16hrs

Long-acting: glargine(constant output), detimir
Onset: 2hrs Peak: No peak Duration: 24hrs (less for detimir)

Mixed insulin: mixtard 70/30. novomix 70/30
Both contain a short-acting(30%) and a long-acting (70%), given twice a day.

http://www.betterhealth.vic.gov.au/BHCV2/bhcarticles.nsf/pages/Diabetes_insulin_choices?OpenDocument

Managment of mucositis post chemotherapy

Mucositis

Grade I - sore but can eat/ erythamatous mucosa
Grade II - modified diet/ patchy ulceration
Grade III - unable to maintain adequete hydration/ confluent ulceration
Grade IV - cannot eat or drink/ tumor necrosis and bleeding

Mx:

1. Symptomatic topical lignocaine mixed with mylanta (use when in pain or 30 min before meal)
2. diligent mouth care for anaerobes (Na bicarbonate)
3. nystatin fungal drop - candidiasis
4. nutritional status (inflammation of mucosa) - consider nasogastric feeding or total parenteral nutrition.
   

Febrile neutropenia

Definition: neutrophil count less than 0.5x 10^9/L or >38 degrees fever associated with neutrophils less than 1x 10^9/L with predicted to further drop.

DDX:

1. Drugs- post chemo(typically 10-14 days after chemotherapy), cytotoxic agents, carbimazole,sulfonamides.
2. Infection- viral or severe sepsis
3. Autoimmine- neutrophil antibodies (SLE, haemolytic anemia.)
4. hypersplenism - leukemias, felty's syndrome
5. bone marrow failure - Myeloproliferative, mylelofibrosis, malignant infiltration(myeloma), aplastic anemia, leukemia, infection(TB), drugs.
   

Examination: Paying attention to respiratory, abdominal (neutropenia colitis [typhlitits]), cardiac, pelvic(urinary). Look at mouth for mucositis and skin for rashes.

Treatment:

1. Initiated even if patient is afebrile but appears toxic. Assume septicemia.
2. Choice depends on local susceptibility. Cover for pseudomonas due to high morbidity and mortality.
3. Treat with broad spectrum Antibiotics - ceftazidime/cefepine( 4th generation - good pseudomonas cover + gram -ve), + timentin(ticarcillin+calvulanate acid)[ for gram +ve plus pseudomonas cover]. Austin protocol is ceftapine + gentamycin for more sick people and ceftriaxone + stat gentamycin for not so sick people. Note this this does not provide cover for staph aures, enterococci, TB, PCP, anaerobes.
4. Consider vancomycin for hospital acquired MRSA (rising due to increase presence of venous lines), serious shock, intravascular devices(PICC LINES ESPICALLY IN ONCOLOGY PATIENTS). This could result in the death of gut commensals and overpopulation of gut VRE which could lead to sepsis.
5. Treat routinely with anti-fungals(nilstat drop) and mouth washes to control ulcers and fungal mouth infections. Anti-virals if reactivation of VZV or HSV.
6. Consider barrier nursing and postive pressure room.
7. septic work up - blood (3 sets), sputum, urine, stool cultures. Swab also from any peripheral or central line. CXR
8. FBC, U&E, LFT, ABG ( decide if person is in hypoxic drive or not)
9. Continue until afebrile or neutrophil count recovers.
10. Failure to respond after 96 hrs consider fungal infections - candida or aspergillosus.(tx- amphotericin B or fluconazole)
11. Consider PCP, TB.
12. Granolocyte CSF- seek expert advice.
13. Education- food prep, hand washing, trauma to skin, oral hygiene, no live vaccines. If temp > 38 degrees go to ED.

---------------------
Always be aware of shock. Circulatory failure resulting in inadequete organ pefusion. bp <90.>

1. Call for arrest team
2. ABC ( high flow oxygen, consider bagging)
3. Initial work up - sats, glucose level, ECG, CXR, U&E (ARF?), LFT, FBE, CRP, ESR.
4. Septic workup and commence antibiotics (above) if suspected septic shock.
5. Need to correct for hypotension to maintain adequete organ perfusion.
6. IV access with 2 large bore for cystalloid infusion.
7. Consider inotropes(dobutamine) or vasopressors (dopamine, noreadrenalin) via central venous line to maintain a bp of >90mmHg, CVP 8-12mmHg, MAP>65.
8. Achieve a urine output of >0.5mL/kg/hr.
   

Oncology- colorectal cancer Part 2

Mangement:

Surgery of primary disease

• It is the mainstay for colorectal cancer. A segment of colon is removed with its blood supply and draining nodes excised. At least 5 cm margin of grossly negative colon is adequete and at least 12 LN for pathological evaluation.
• Obstructing tumors - primary resection. Consider intial decompression(proximal colostomy) or stent.
• Perforated colon cancer
• Rectal cancer - Local recurrence rates(less than 10%) using the total mesorectal excision(TME) [rectum is encised en bloc with the adjacent perirectal tissue for rectal cancers.
• A proportion of patients are suitable for metastatectomy after initial chemotherpay for liver mets. Radioablation shows promise.

Chemotherapy

• 5 fluorouracil or capecitabine therapy for patients with lymph node involvment increases 5-year survival from 64% to 71%. the addition of oxoliplatin improves survival.
• In metastatic cancer, 5 fluorouracil increases survival benefit from 6 to 12 months. The addition of oxaliplatin prolongs survival benefit to 18 months.

Biological therapy

• Anti-VEGF therapy(bevaciumab)
• anti-EGF(cetuximab)
  

Radiotherapy

• not routine.
  
• Adjuvant therapy
• neo-adjuvant therapy
• pallitive for local recurrence of rectal cancer.

Stage 0-1: surgery
Stage 2: + chemotherapy
Stage 3: +radiotherapy.
Stage 4:targetted therapy

Treating of symptoms

• Liver metastases- may cause pain. treat with NSAIDS or steriods. Hepatomegaly can cause squashed stomach syndrome lead to gastric fullness. treat with metoclopramide.
  
• perineal and pelvic pain- usually a neuropathic component to the pain. tenesmus. Requires intervention by palliative care doctors or anaesthetists.
  
• bowel obstruction-

1. Do a CT scan or barium enema to delineate the site of the obstruction and whether its multiple level to determine managment strategies
   
2. Surgical option involves putting a colonic stent via endoscopy or creating a stoma for for inoperable or recurrent cancers, low rectal cances. Multiple blocks are not amenable to surgicaltreatment
3. Medical treatment involves a syringe driver ad a mixture of analgesics, anti-emetics and anti-spasmodics.

• fistulae- between bowel and skin or bladder.
  
• rectal discharge and bleeding- refer to a oncologist as radiotherapy may help.
  
• hypoproteinaemia- common due to poor intake and por absorption. Lower limb odema
  
• poor apetite- treat with steriods.
  

Colorectal cancer- part 1. diagnosis and staging

What is the epidemiology of colorectal cancer?

Colorectal cancer is 2nd most common cause of cancer deaths. It is influenced by both enviromental and genetic factors There appears to be a 10 fold variation in incidence between developing and developed countries due to diet and genetic susceptibility. Accounts for 13% of new cancer diagnosis.

Risk factors?

1. Age is a major risk factor for sporadic CRC. It is a rare diagnosis before the age of 40, the incidence begins to increase significantly between the ages of 40 and 50, and age-specific incidence rates increase in each succeeding decade thereafter. The lifetime incidence of CRC in patients at average risk is about 5 percent, with 90 percent of cases occurring after age 50.
2. Genetics - Familial adenomatous polyposis (FAP) (accounts for less than 1% of cancers), Hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant syndrome, which is more common than FAP, and accounts for approximately 1 to 5 percent of all colonic adenocarcinomas.
3. Previous cancers-Patients with a personal history of CRC or adenomatous polyps are at risk for the development of a future large bowel cancer.
4. Inflammatory bowel disease — There is a well documented association between chronic ulcerative colitis and colonic neoplasia, with the extent and duration of disease being the primary determinants. Also Chrohn's disease, ureteric diversion to sigmoid colon.
5. Diabetes mellitus and insulin resistance — Increasing evidence suggests that diabetes mellitus is associated with an elevated risk of colon cancer. A meta-analysis of 15 studies (six case-control and nine cohort) including a total of 2,593,935 participants estimated that the risk of colorectal cancer among diabetics was approximately 30 percent higher than nondiabetics
6. Cholecystectomy
7. Alcohol
8. Obesity - 1.5 fold increase in getting cancer and increase risk of dying

Protective factors: diet high in fruits and vegetables, regular physical activity, the regular use of aspirin or nonsteroidal antiinflammatory drugs (NSAIDs), and hormone replacement therapy in postmenopausal women.

What is the clinical presentation of colorectal cancer?

Local and distant presentation

Local

• Rectum - tenesmus, PR bleeds, pain in the bottom.
• Descending colon - bowel obstruction, abdominal pain, changes in bowel habit (night diarrhoea is pathogenic)
  
• Ascending colon - IDA, abdominal pain.
  

Abdominal pain — 44 percent
Change in bowel habit(alternating between diarrhoea and constipation) — 43 percent
Hematochezia or melena — 40 percent
Weakness — 20 percent
Anemia without other gastrointestinal symptoms — 11 percent
Weight loss — 6 percent

Others: tenesmus, neuropathic pain syndrom(if sciatic or obturator nerve is affected), palpable abdominal mass, acute bowel obstruction. Diarrhoea in large bowel tends to be more watery than small bowel.

Approximately 20 percent of patients have distant metastatic disease at the time of presentation [1]. CRCs can spread by lymphatic and hematogenous dissemination, as well as by contiguous and transperitoneal routes. The most common metastatic sites are the regional lymph nodes, liver, lungs, and peritoneum, and patients may present with signs or symptoms referable to any of these areas.

What tests to order for diagnosis and managment?

Physical examination- remember to do PR exam. Abdo exam looking for palpable masses and looking for hepatamegaly.

• colonoscopy which can localise the lesion throughout the large bowel, collect a biopsy and even remove it. Consider air-contrast barium enema which flexible sigmoidoscopy but diagnostic yield is less than colonocscopy. In the 5 percent of people who we are unable to reach by colonoscopy(e.g. torturous intestines, blocked intestines)
• CT of the abdo, pelvis, chest. CT-demonstrate regional tumor extension, regional lymphatic and distant metastases, and tumor-related complications (eg, obstruction, perforation, fistula formation)
• PET scan for metabolically active cancers particulary nodal, peritoneal, liver involvment. When lesion is benign or malignant. To determine if localised metastic disease is resectable.
  
• General evaluation - FBC for microcytic anemia, Serum iron studies, liver function test-raised ALP has the most value ( in case of liver mets)
• liver ultrasound
• Tumor markers - carcinoembryonic antigen(CEA), carbohydrate antigen 19-9 are associated with colorectal cancer but they tend to have a lot of overlap with other beningn conditions like diverticultis, COPD, and other acute inflammatory states. Hence they are not recommended as a screening tool. However, they offer prognostic value. Raised levels are bad prognostic indicators. Failure of CEA to fall after the resection imply ongoing disease and a need for continual assessment.
• Genetic testing if family history

Rectal cancer: (additional)

• MRI- able to pick up more hepatic mets and good for rectal cancers as it can pick up characteristics other than size. Pre-op look for rectal cacner on nodal status and mesorectum involvment. If mesorectum is invaded and nodal involvment, recurrence rate is increased. Do pre-op radiotherapy and/or chemotherapy to reduce local recurrence but not metastatic disease.
• transrectal or endorectal ultrasound (EUS)-depth of transmural invasion and the presence of perirectal nodal involvement for rectal cancers. EUS-guided fine needle aspiration (FNA) biopsy improves the accuracy of N staging.

DDX of colonic mass?
Malignant lesions: Adenocarcinoma, Lymphoma, Carcinoid tumor, Kaposi's sarcoma, Prostate cancer
Benign lesions: Crohn's colitis, Diverticulitis, Endometriosis, Solitary rectal ulcer, Lipoma, Tuberculosis, Amebiasis, Cytomegalovirus, Fungal infection, Extrinsic lesion

Staging?

Once diagnosis of CRC is established, the local and distant extent of disease spread should be determined in order to provide a framework for discussing therapy and prognosis. Importantly to decide whether cancer is resectable, even consider whether metastatic cancer(liver/ lungs) is potentially amenable to surgery. Two types of staging exist for colorectal cancer

1.The Duke's classfication

A- beneath the muscularis mucosae B- through the muscularis mucosae

C- involves regional lymph nodes D- distant mets

2. TMN staging of the AJCC

Tumor and Nodal are determined on pathology of resected colon. Metastatic involvment is determined by CT scan.

-------

PROGNOSIS?

1. TMN staging - most important
   
2. histologic grade - well-differentiated (stage 1 or 2) have a better 5 year survival than with poorly differentiated (grade 3 or 4)
3. The anatomic location - rectal >transverse/descending>ascending
4. Clinical presentation - bowel obstruction or perforated bowel.
5. Genetics - chromosome loss of 18q.
   

ED-collapse

Why do people lose consciousness?

• People lose consciousness because either the O2 or nutrients supply to the brain is temporarily reduced.
• Thus, anything that interferes with O2 delivery to brain tissues will lead to syncope
1. Reduced blood flow
2. Altered brain metabolism (hypoglycaemia, hypoxia, CO2 narcosis, hypothermia)
3. Cerebral injury or pathology (head injury, intracranial bleeding, thrombosis, embolism, infection, swelling, tumour, fitting, etc…)

What are the causes of syncope?

Causes from the most common to least
1. Epileptic fits (incranial pathology?)
2. Postural hypotension
3. Vasovagal, micturation, cough.
4. Transient hypoglycaemia, electrolyte imbalance
5. Arrhythmias (typically high degree heart block)
6. Others include pulmonary embolism, transient blood loss, haemorrhage, infection



Scenario: Patients presents to the ED with a recent collapse. Take a history.

The attack!

1. When did this occur? What were you doing at that time?
2. Was there an actual LOC?
3. Was there an person present at that time when you were out?
4. How long was the attack? Was there any twitching, jerking, frothing, biting of tongue, blood? What colour was her face? (white or red means arrhythmia)
5. Was there incontinence?

Before the attack!

1. Did you feel any symptoms/warnings before the attack?
2. Was there any palpitations or chest pains? sweating, nausea?
3. Did you know what triggered it?
4. Can you prevent the attack?

After the attack!

1. Did you regain your conscious quickly?
2. Was there any muscle fatigue?
3. Confused or sleepy?
4. Did you hurt yourself?

Rule out ddx
• Cardiac – chest pain? Palpitations? Nausea, vomiting, sweating?
• Postural hypotension – Feel faint when you stand up suddenly?
• Sympathetics – Feel faint when you urinate, cough, emotional stress, exert yourself?
• Hypoglycemia - History of DM?
• Brain lesion – visual changes, speech disturbances, muscle weakness, balance disturbance, sensory changes.
• Brain – recent head trauma, nausea, vomiting?
• Infection – fever, chills, rigors? FUNDI. Cough, wheeze, sputum production. photophobia, neck stiffness, rashes
• Others – PE?

Background
• Increasing frequency? Once off event? Are they similar
• Patients concerns
• Medical hx - medication(e.g anti-hypertensives), medical conditions(heart problems, epilepsy)
• Family Hx - heart problems-arrhythmias, epilepsy
• Social History - living, marital status+kids, ADLs, occupation, financial status, diet, exercise

Newly diagnosed colorectal cancer

Patient: Mr C.R, 70 y.o. presents with newly diagnosed colorectal cancer in the setting of steriod treatment for his giant cell arteritis and repeated episodes of collapse.

HOPC:

He was diagnosed with colorectal cancer 2 weeks ago in the general ward. A CT scan showing a rectal cancer with mets to both the liver and lungs. A colonoscopy and biopsy was also done on him to confirm the diagnosis. (rememeber to ask!!) His symptoms of colorectal cancer are a 6 week history of fecal incontinence, blood in his stools and SOB. With regards to his fecal incontinence, this tends to come on particulary when he goes to the toilet to urinate and he would soil his pants. He therefore consciously sits on the toilet seat before urinating to prevent soiling his pants. (getting worse? agg/reliefing factors? concerns? previously had this problem?) His bowel motions are unchanged( know how many times?), no diarrhoea or constipation, no abdominal tenderness, bloating or vomiting or fatigue reported. His stools are solid although he reports occasional bright red blood in the stools(quantify?) or black coloured-stools. He also reports recent weight loss but is unable to quantify it for me. (still get the baseline). His SOB gradually came on over the last 6 weeks, previously fit and was not physically inhibited from SOB but now currently is only able to walk about 10m before feeling SOB. Exertion makes the SOB worse and rest makes it better. No chest pains, palpitations. No sputum, cough, fevers, rigors. No orthopnea, PND, lies flat when he sleeps.

Current treatment for his cancer is palliative chemotherapy which he started 3 days ago and during the course of the chemo he was feeling unwell and nauseated. Currently he is feeling well. (what chemo?)

Related medical hx:

He was diagnosed with GCA by a biopsy 6 weeks ago at the eye and ear hospital. His symptoms were bitemporal pain (U WANT TO KNOW MORE!). He was then started on high dose steriods(how much?) to prevent vision loss. As a result of his treatment, he developed steriod induced DM and is currently on novorapid sliding scale for it. He claims that it was the steriods that made him feel nauseasted and unwell. And that his symptoms coincided with the steriod treatment. Currently, his vision is still intact.

4 weeks ago, he had an episode of collapse due to muscle weakness. This happened in the morning when he got up to urinate and when he exited the toilet he actually collapsed with associated sweating. There was no other neurological deficit, no LOC, loss of vision, no speech impairment, confusion, abnormal muscle jerks. He was unable to get up and his wife called the ambulance, he slowly regained strength 2 hours later at the ED. He was drowsy but otherwise alert after the attack. There was no post-ictal confusion, residual neurological deficits such as sensory or muscle strength deficits. Before the attack there were no warning signs, no changes to his vision or feeling of impending doom or being unwell, no palpitations. Never reported having signs of a postural drop. he had never had an episode of collapse before this. Over his stay in hospital he had 3 more episodes of similar nature and currently goes to the toilet only under supervision. Increasing in frequency? Currently he is under specialist care for his collapse episodes and is having a 24hr bp monitor.

• spine operation + laminectomy done for an accident during work in 1983.
• double heart bypass in 1997. Since then he has not complain of anymore chest pains.
• He has a few broken ribs and bones as a result of his occupation.
• No HT, cholesterol, has smoked 10 pack years from age 18-28. No diabetes.

Medication: paracetomol, caltrate, cholecalciferol, pantoprazole, nilstat, pethidine, oxynorm, metoclopramide, novorapid.

Family Hx

• Father died at 70 due to lung cancer which he thought was due to his father's excessive smoking habits.

Social Hx

• Living - wife,66
• No problems with ADLs - previously very fit. Learnt to live healthily after the heart operation and the spine surgery
• Not depressed
• Financially stable
• Exercise - very often, mountain bikes daily to give out pamphlets and walks his dog often
• occupation-carpenter
• Diet- eats healthy lots of greens. Doesnt drink.

Physical exam: abdo, heart, lungs normal

In summary, Mr R is a 70 year old gentlemen with newly diagnosed colorectal cancer in the setting of steriod treatment for his GCA and unexplained episodes of collapse. His main issues are diagnosis and managment of his collapse, managment of his colorectal cancer along with symptomatic treatment for his SOB, blood in his stools and fecal incontinence, managment of the treatment for his GCA which involves altering the dose of steriods that balances between GCA disease activity and the development of steriod use complications such as steriod induced DM. And discharge planning for him such as a personal alarm, social support, occupational therapy and community help.

What are the differentials for his SOB?

1. pleural effusion - hypoalbuminaeima
2. lymphangitis carcinomatosis
3. PE-from hypercoaguable states.
4. infection
5. bronchial obstruction leading to collapsed lung
6. pericardial effusion
7. cardiac tamponade.

Consider concurrent illnesses: CCF, COPD.

What investigations would you order?

1. CXR
2. ABG
3. ECG(silent infarct)
4. CT(lymphangitis?)

What are your differentials for his episodes of collapse?

1. Micturation syncope - less likely due to no LOC
2. cardiogenic - arrhythmia? no palpitations?
3. neurogenic - brain mets causing seizures? no prodrome or post-ictal phase. ictus was also atypical.
4. postural hypotension - no history of dizziness when he changes posture
5. vasovagal, effort cough syncope to be considered
6. metabolic? (NO!!!)

ECOG performance status. If 2 or below we treat cancer, if 3-4 treating with chemo does not provide benefits to QOL. Some cytotoxics are reserved for 1. Extensive small cell carcinmoa is an exception, 6 weeks death without treatment. Cancers are very chemosensitive.

Differences between DM type 1 and type 2

1. Genetics- type 1 has only a 30% concordance between identical twins unlike type 2 which is 80%. HLA-DR3/DR4 are also associated with type 1.
2. Epidemiology- type 1- affects the young. consider late onset autoimmune diabetes(LADA). type 2- affects the middle age obese population. consider maturity onset disease of the young(MODY).
3. Presentation-

• Type 1 - polyuria, polydipsia, polyphagia, weight loss, nocturia, ketoacidosis(ketones on dipstick)
  
• Type 2- asymptomatic

4. Aetiolgy- type 1 - beta cell destruction. anti-islet cell Ab, anti-glutamic acid decarboxylase Ab type 2- insulin resistance. beta cell dysfunction.

Diagnosis of diabetes + relevant history questions.

Diagnosis is made by one of the following and must be confirmed on a subsequent day unless unequivocal hyperglycemia or metabolic decompensation.

1. random glucose of >11mmol/L
2. fasting glucose of >7.0mmol/L
3. OGTT>11mmol/L 2 hours after 75g of glucose after 3 days of fasting.

Diagnosis alogoritham

1. Do a random or fasting.
2. If <5.5, diabetes unlikely
   
3. If fasting 5.5-7.0, random 5.5-11.0 unequivocal, proceed to OGTT.
   
4. If F>7.0, R>11.0, diabetes likely
5. OGTT, between 7.8-11.0 impaired glucose tolerance, >11.0 diabetes likely.

Screen diabetes in pple >45 age.

CVD(AMI, stroke, PVD)
Hypertension
Obesity (>30kg/m2)
PCOS
Ethnic groups - aboroginal, torres strait, chinese (>35 age)

Physical examination for Myasthenia gravis

Introduction: MG is a neuromuscular autoimmune disease that attacks the nicotinic receptors. Increases muscle fatigue. less than 50, more common in women and associated with thymic dysplasia and autoimmune conditions. greather than 50 more common in men and associated and associated with thymic atrophy or tumor.

Presentation: extraocular, bulbar(swallowing, chewing), face, neck limb girdle, trunk are affected in that order.

1. Inspection: look for ptosis, squints, myasthenia snarl on smiling.
2. Test eye movements: ask for diplopia, test upward gaze for 30s to look for ptosis or failure to upward gaze.
3. Test proximal muscle strength: neck flexion, arm abd/add, hip flexion.
4. Test reflexes:normal
5. Test speech: gradual hypophonia, nasal escape as control of soft palate is lost.

Pleural fluid analysis

1. Clinical chemistry: protein, glucose, PH, LDH, amylase
2. cytology
3. bacteriology: Microscopy and culture, TB culture
4. Immunology: ANCA, RF, ANA, complement

Pleural effusion with liver cirrhosis

Patient: 40y.o. male with 2 weeks history of SOB on a history of genetically inherited liver cirrhosis.

DDX:
V - CCF, AMI
I - pneumonia, TB
T - pneumothorax
A - ANCA related vascultis (wegner's), SLE, RA etc.
M - hypoalbuminemia (in liver disease)
I-?
N - lung cancer, mesothioloma
C-?
D-e.g. decompensated HF?
E-COPD infective exacerbation


Examination:On respiratory exam, patient was breathing comfortably, He did not exhibit any signs of peripheral anemia, did not appear jaundiced or centrally cyanosed. His's trachea was not deviated. There appears to be reduced bilateral chest expansions. Stony dullness to percussion on the right lungs from the middle to lower zones. On ascultation, reduced breath sounds in the middle to lower zones of the right lung. Vocal fremitus was also reduced.

Ix: CXR, pleural fluid aspiration(for symptomatic relief) and analysis, Ultrasound(more for guidance), pleural biopsy only if pleural fluid analysis is inconclusive.

CXR:
A- airway
B-breathing
C- circulation
D-diaphragm
E- extra

This is an chest X-ray of a 40 y.o gentlemen. It is taken on adequete inspiration(look at 5 to 7 ribs anteriorly or 10 posteriorly), is not rotated(look at clavicle), of adequate exposure and appropriate position. A) Trachea is not deviated. B) right lungs showed 'white outs' of the lower to middle zones with blunting of the costophrenic angles and a upper concave border, C) cardiothoracic angle was normal, no cardiomegaly.

Comment on diaphragm if abnormal
Comment on mediatinum abnormal. (know that aortic knuckle, POT, left auricle, LV)

Diagnosis: Pleural effusion
DDX of pleural effusion:

• Transudate (<25g/l):> increase venous pressure(CCF, pericarditis, fluid overload), hypoproteinaemia( cirrhosis, nephrotic syndrome, malabsorption) , hypothyroidism or Meig's syndrome.
• Exudate (>25g/L): leakiness from blood vessels due to infection (TB, pneumonia), inflammation(SLE,RA) and malignancy. (bronchogenic lung tumors, mesothioloma, mets)

Mx:

1. Drainage (via diagnostic tap or intercostal drain)
2. fluid analysis
3. Manage underlying problem
4. Consider pleurodesis - break loculations allowing lung to reexpand to prevent lung collapse

Obstructive sleep apnoea

OSA definition: sleeps apnoeas caused by obstruction of the airway.

Clinical features: obese, middle age man who presents with snoring, daytime somnolence. Partner reports apnoeic episodes.

Ix: polysomnography

Mx:

1. weight reduction
2. CPAP ( gold standard)
3. Surgical procedures (uvulopalatopharyngoplasty, tonsilectomy)

UPPP: provides benefit for snoring in 80% at 5 years. provides benefit for OSA by 50% at 5 years. However, benefit after that is variable. UPPP are not indicated for OSA because removal of palate makes CPAP ineffective.

Laryngectomy

Laryngectomy defintion: Laryngectomy is the removal of the larynx. Patient breathes through a stoma. This is indicated for laryngeal cancer after using chemo or radiation therapy. A one way valve between the tracheal-osopheageal fistula(communications between two epithelial surfaces) is placed. Speech is generated via the vibration of the pharynx and articulation of the mouth and tongue.

Optic neuritis

Causes of optic neuritis: main cause is demyelination(MS), less common viral, vasculitis.

Clinical features:

1. rapid loss of vision - central scotoma with RAPD.
2. Pain on eye movements - stretching of the inflammed nerve fibre
3. Fundoscopy - optic disc can be normal or swollen. Optic atrophy develops months later.
4. vision usually improves in weeks.

Investigation:

1. MRI - to rule out MS.(plaques) Look for retrobulbar involvement or other brain plagues.

Papillodema

Definition of true paillodema: Swollen optic nerve head due to raised ICP caused by blockage to axoplasmic flow.

Causes of optic disc swelling:

1. Raised ICP (haematoma, hydrocephalus, tumors, brain swelling)
2. Failure of normal axoplasmic flow: mechanical compression, ischemia
3. Odema: retinal vein occulusion, inflammation
4. Cellular infiltrates: inflammation, neoplasia.

Clinical features:

1. Optic nerve dysfunction- early transient visual blurring. VA loss is late. field defects are variable. Can be a enlarged blind spot but commonly affects central vision. Colour vision(red-green defect) loss occur. RAPD may be present.
2. Underlying disease
3. Associated features (esp of raised ICP)

Investigations:

1. Fundoscopy: blurred optic disc and cup margins.
2. MRI: to investigate cause.

If untreated, optic atrophy(pale optic disc) results.

Chad2 criteria

CHAD2 score for warfarin use in AF.

C= Congestive Cardiac Failure(1 pt)
H= hypertension(1 pt)
A= age (>75) (1 pt)
D= diabetes(1 pt)
2= stroke(2 pt)

1 pt = use warfarin or aspirin
greater than 1 pt = warfarin