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Year 3 > CPC's - medical > Flashcards

CPC's - medical Flashcards

1
Q

How do you examine a pathology pot?

A
  • ORGAN:
    • Hollow/Solid
    • Presentation/ anatomic features
  • DIMENSIONS:
    • Size of organ
    • Size of lesion (if present)
  • DISTRIBUTION OF ABNORMALITY: Diffuse/multiple/solitary
  • SIZE/SHAPE/BORDER/ANATOMICAL BOUNDARIES OF LIASION
  • CUT SURFACE OF LESION:
    • Homogenous/ Heterogenous
    • Colour
    • Solid/ cystic/ texture?
    • Border: demarcated/spiculated/defined
    • Haemorrhage/necrosis
    • Exophytic (growth outwards) or endophytic (growth inwards)
  • DDx:
    • NEOPLASTIC vs NON-NEOPLASTIC
      • Neoplastic: beign or malignant
      • Non-neoplastic: Infectious/inflammatory/deposit/ harmatomas/congential
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2
Q

How do you describe a lump?

12 points

A
  1. Size
  2. Site
  3. Shape
  4. Surface
  5. Margin/edges
  6. Tenderness
  7. Composition
    1. Consistency
    2. Fluctuation (fluid-filled)
    3. Fluid thrill
    4. Transillumination
    5. Resonance
    6. Pulsatility
  8. Reducibility
  9. Mobility/fixation of lump and its tissue layer
  10. Overlying skin
  11. Regional lymph nodes
  12. Other:
    1. Muscle wasating
    2. Joint movement
    3. Gait
    4. General physical examination
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3
Q

What are the possible causes of “black diarrhoea”?

A
  • Blood
  • Iron
  • Food colouring
  • Beetroot
  • Licorice
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4
Q

What further information would you seek from the history in a patient with vomiting and diarrhoea?

A

Diarrhoea:

  • Colour (is it melaena?)
    • Tar-like
    • Bright red - fresh blood (more likely to be a lower GI bleed)
    • Green - iron
  • Nature:
    • Watery
    • How much
  • Frequency of motions: did all of them contain blood?
  • Volume
  • Smell

Vomiting

  • Nature - Haematemesis
  • Did it precede the diarrhoea?
  • Frequency?
  • Quantity
  • Smell
  • Faecal-like material

Associated symptoms:

  • Has it been asscoiated with “indigestion”/dyspepsia (and waht does the patient mean by indigestion?)
  • Nausea
  • Syncope
  • ‘ligh-headed’ or ‘giddy-ness’
  • Related to anaemia - dyspnoea/ Angina
  • Pain - SOCRATES

Medications:

  • What medications are they currently on?
  • Is there regular use of NSAIDs or aspirin
  • Anticoagulants?

Past medical / surgical Hx:

  • Prior GI bleeding
  • Previour GU disease
    • previous diagnosis of peptic ulcer
    • FHx of peptic ulcers
  • Underlying medical disorder - especially liver disease
  • Previous surgery
  • Brusing
  • Change in bowel habits
  • Weight loss/anorexia
  • History of oropharyngeal disease

Social Hx: Alcohol and smoking

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5
Q

What are the differentials for upper GI bleeding?

A

Anatomical approach - oesophagus to anus:

  • Mallory Weiss tear
  • Varices
  • Erosive oesophagitis
  • Peptic ulcer disease
  • Gastroduodenal erosins
  • Malignancy (can occur anywhere)
  • Crohn’s disease
  • Infectious gastroenteritis
  • Angiodysplastic lesions

Things going to kill the patient:

  • Bleeding or perforation peptic ulcer
  • Varices
  • Multiple blood transfusion
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6
Q

What investigations would you perform in a patient with upper GI bleed?

A

Blood tests:

  • FBC:
    • Hb: may be slightly decreased or normal, depending on how long the bleeding has been going on.
    • Hct: may not reflect blood loss accurately if taken soon after the onset og bleeding (as with Hb)
    • Platelets: rise with bleeding, but could be an indication of another underyling disease contributing to/or causing GI bleed.
  • UECs: in upper GI bleeding, expect a high urea with a normal creatinine → unless there is underlying renal impairment.
  • LFTs: to ascertain underyling liver disease.
  • Coags: is there underlying bleeding disorder
  • Group and hold: incase transfusion is needed
  • gastroscopy: gold standard in upper GI bleeds.

Imaging:

  • Chest x-ray
  • arteriography and embolisation
  • Tc-labelled red blood cell tag

ECG

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7
Q

How do you manage a patient actuely with upper GI bleeding?

A

Stabilise the patient first:

  • IV fluids

After patient is stabilised:

  • Consider need for transfusion - group and hold
  • Anaglesia (only is patient is in pain)
  • IV antibiotics if peritonitis is thought to be an issue (perforation)
  • Correct any coagulation deficiencies

Urgent endoscopy.

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8
Q

What is Helicobacter pylori and how does it cause gastric ulceration (as would be described to a patient)?

A
  • H. Pylori is a bug/bacteria that sits in the stomach and causes inflammation of the lining of the stomach. In a certain percentage of people, this leads to an ulcer.
  • H. Pylori is present in about 50% of the world’s population.
    • 20% of the developed world is infected
    • over 70% of the developing work is infected
  • Can be detected by urea breath test
  • H. Pylori coverts urea to ammonium hydroxide (through its urease), which provides it with an alkaline environment in which to live → makes it resistant to acidic stomach contents.
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9
Q

How do you manage a patient who has GI bleeding due to a peptic ulcer caused by H. Pylori?

A

Treat symptoms, the disease and prevent complications.

  • Immediate treatment:
    • Stop bleeding:
      • Injection - adrenaline/ ‘glue’/ alcohol
      • Diathermy
      • IV PPI
  • Intermediate treatment:
    • PPI and two antibiotics - ‘triple therapy’
      • Esomeprazole 20mg orally, twice daily for 7 days PLUS amoxycillin 1 g orally, twice daily for 7 days PLUS claritheromycin 500 mg orally, twice daily for 7 days
  • Long term treatment:
    • After 6 weeks review patient to determine if H. Pylori has been eradicated.
      • Urea breath test
    • If infection still present need to check antibiotic resistant, move to ‘quadruple therapy’
      • PPI twice daily for 7 to 14 days PLUS colloidal bismuth subcitrate 120 mg orally, 4 times daily for 7 to 14 days PLUS tetracycline 500 mg orally, 4 times daily for 7 to 14 days PLUS metronidazole 400 mg orally, 3 times daily for 7 to 14 days.
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10
Q

What is portal hypertension and how does it cause oesophageal varices?

A

Portal hypertension occurs as a result of increased resistance to blood flow through the portal system. It can occur under the following cicrumstances:

  • Prehepatic:
    • Obstructive thrombosis
    • massive splenomegaly shunting blood into the splenic vein
  • Hepatic:
    • Cirrhosis
    • Infections such as milliary TB or schistosoomiasis
    • Sarcoidosis
  • Posthepatic:
    • Righ sided heart failure
    • Contrictive pericarditis
    • Hepatic vein outflow obstruction

The rise in portal system pressure causes bypasses to develop wherever the systemic and portal circulation share common capillary bed.
Oesophagogastric varices develop in 65% of patients with advanced cirrhosis. Most commonly seen in alcoholic cirrhosis.

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11
Q

What are complications associatd with chronic gastric ulceration?

A
  • Bleeding
  • Perforation
  • Obstruction from oedema or scarring
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12
Q

What Hx would you get from a person who presents with increased weight gain and ankle swelling?

A
  • SOCRATES:
    • Chest pain?
    • Fatigue?
    • Bruising eaily?
    • Jaundice?
    • Cough with sputum/haemoptysis
  • PMHx: medical/surgical/medications/allergies
  • FHx: cardiac disease, renal, diabetes. autoimmune disease.
  • POSH: recent travel, sexual Hx, pregancy?/ drinking, smoking, drug use
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13
Q

What are the DDx for ankle oedema?

A
  • Renal disease:
    • Glomerulonephritis:
      • Nephrotic syndrome
      • Acute nephritic syndrome
    • Chronic renal failure
  • Cardio disease:
    • Congestive heart failure
    • Pericardial effusion, constrictive pericarditis, restrictive cardiomyopathy
    • Local venous disease: DVT, chronic venous insufficiency
  • Hepatic disease:
    • Cirrhosis
  • Pulmonary: Cor pulmonale, pulmonary hypertension
  • Lymph obstruction
  • Sepsis
  • Pregnancy
  • Hypothyroidism/myxoedema
  • Iatrogenic: medicine-induced oedema
  • Sleep apnoea
  • Idiopathic
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14
Q

Describe the pathophysiology of oedema.

A

Oedema - palpable swelling produced by expansion of the interstitial fluid volume.

Two basic steps:

  • An alternation in capillary haemodynamics that favours the movement og fluid from the vascular space into the interstitium.
  • The renal retention of dietary sodium and water, thereby expanding the extracellular fluid volume.
    • This can be as a result of primary renal sodium retention
    • Can be as a result of an appropriate response to a decrease in the effectuve circulating volume

The development of oedema requires a relatively large alternation in one or more of the Starling’s forces in a direction that fabours an increase in net filtration:

  • Elevation in capillary hydralic pressure
  • Reduced plasma oncotic pressure
  • Ehnaced capillary premeability
  • Lymphatic obstruction

Nephrotic syndrome oedema:

The oedema that results from nephrotic syndrome is not due to decreased plasma onctoic pressure alone, but rather is the result of an interplay of increased capillaruy hydraulic pressure (renal retention of Na and water) and decreased plasma oncotic pressure.

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15
Q

What tests would you order for a patient with suspected nephrotic syndrome and what would you expect to see in the results?

A
  • Dipstick test.
  • Urinalysis MCS and 24 hour protein:
    • Nephrotic syndrome (minial change disease): Proteinuria >3.5gmd/24 hrs, lipiduria, negative culture
  • UEC:
    • Looking for potassium abnormalities, but not expecting to find any in this case.
    • Evidence of renal disease → raised creatinine or urea
  • LFTs: looking for evidence of cirrhosis or other liver disease (cause of oedema)
  • Albumin: low albumin due to either renal disease (most likely) or liver disease.
  • Coags: need to make sure these are normal before a renal biopsy can be done.
    • High risk thrombo-embolism especially in membranous nephropathy
  • Lipid profile:
    • There are abnormal lipids in nephrotic syndrome, including minimal change disease.
    • Cardiovascular disease risk factor
  • FBC: anaemia and platelets
  • ECG and CXR: to rule out any acute cardiac problems and pulmonary oedema
  • Renal biopsy: Definitive diagnosis
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16
Q

How would you manage a patient initial as a GP with oedema due to nephrotic syndrome?

A
  • Initial treatment:
    • Commence diuretic to treat the oedema: Thiazide + K+ sparing diuretic (spironolatone, amiloride)
    • Over investigations
  • Refer to renal outpatient clinic
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17
Q

What is the definition of nephrOtic syndrome?

A

Proteinuria (≥3.5 g/day), generalised oedema, hypoalbuminaemia, and hyperlipidemia. Approximately one-third of all cases result from systemic disases such as DM, SLE, or amyloidosis.

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18
Q

What is the definition of nephrItic syndrome?

A

A disorder of glomerular inflammation, also called glomerulonephritis. Proteinuria may be present but is usually <1.5 g/day.

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19
Q

What investigations should a renal physician order in a patient with ?nephrotic syndrome and low albumin?

A
  • Urine and serum electrophoretogram - myeloma
  • Lupus/Autoimmune screen
  • Renal U/S - one or two kidneys, check size, abormality such as Horseshoe kidney
  • Renal Biopsy - essential for diagnosis minimal change disease in adults (common in children).
    • H&E, immunofluoresence, electron microscopy
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20
Q

What are the risks and benefits of a renal biopsy?

A
  • Risks:
    • Renal infarct: damaging more of an already vulnerable kidney
    • Bleeding
    • Not enough tissue to make a diagnosis (need 20-30 glomeruli)
    • If focal disease, then biopsy wont be sensitive a test (could miss the diseased part)
  • Benefits:
    • Necessary for the definitive diagnosis
    • Helps guide treatment
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21
Q

What does this show?

A

This is a normal glomerulus. In minimal change disease the biopsy on light microscopy appears normal.

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22
Q

What disease process is occuring in this electron microscopy image?

A

his is minimal change disease (MCD) which is characterized by effacement of the epithelial cell (podocyte) foot processes and loss of the normal charge barrier such that albumin selectively leaks out and proteinuria ensues. By light microscopy, the glomerulus is normal with MCD. In this electron micrograph, the capillary loop in the lower half contains two electron dense RBC’s. Fenestrated endothelium is present, and the basement membrane is normal. However, overlying epithelial cell foot processes are effaced (giving the appearance of fusion) and run together.

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23
Q

How does the kidney prevent proteinuria? What are the filtration mechanisms?

A
  • Epithelial foot processes (podocytes) and split membrane
  • Ionic barrier - basement membrane and fenestrated endothelial cells negatively charged and repel large molecules such as Albumin with like charge
  • Normal basement membrane 300 nm - in minimal change disease the BM is normal, but thickened in membranous nephropathy secondary to immune complex deposition.
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24
Q

Minimal change disease causes 90% of nephrotic syndrome in children <10 years, 50% in those >10 years, but only 15% in adults. What is the aetiology of MCD in adults and children?

A
  • Idiopathic - most
  • Drugs - NSAIDs, Abx, bisphosphonates, 5-ASA (IBD drugs)
  • Neoplasia especially haematological (Hogkin’s)
  • Post-infective: TB, HIV, syphilia, mycoplasma, Hep C
  • Atopy
  • Other glomerular disease
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25
Q

What are other causes, besides minimal change disease, that cause nephrotic syndrome?

A
  • Primary glomerular nephropathies 70%
    • Membranous -33%
    • Focal segmental glomerulosclerosis - 33%
    • MCD - 15%
  • Secondary to systemic disease with glomerular involvement:
    • SLE
    • DM
    • Amyloidosis - increasing age
    • Other: Goodpastures, Wegener’s
  • Hereditary:
    • Alports syndrome - initially thin membrane thickening later
    • Thin membrane disease
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26
Q

How do you treat minimal change disease?

A
  • Prednisone: 90% of children respond in 2 weeks, adults longer
  • If relapses: other immunosupressive Tx are used in addition to steroids:
    • Cyclophosphanide
    • Calcineurin inhibitors
    • Mycophenolate mofetil
    • Azithioprine
    • Rituximab
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27
Q

What are the possible complications from minimal change disease?

A
  • Acute renal failure
  • Incomplete remission - a reduction of proteinuria, but not a complete return to baseline filtration
  • Frequent recurrences: a relapsing and remitting picture
  • The risks of associated with immunosupression
  • If resistant to steroids consider other histology
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28
Q

What is the difference between nephritic and nephrotic syndrome that you would see on O/E?

A
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29
Q

What is the difference between an exudate and a transudate?

A
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30
Q

Know the relationship between diabetes and renal disease. What are the possible pathological findings that one can see in a kindey from a diabetic person?

A

Diabetic nephropathy occurs as a result of both diabetic macro and microvascular diseases. Renal failure is seconad only to myocardial infarction as a cause of death. Three lesions are encountered:

  • Glomerular lesions:
    • Capillary basement mebrane thickening
    • Diffuse measangial sclerosis
    • Nodular glomerulosclerosis
  • Hyaline arteriosclerosis of both afferent and efferent arterioles.
  • Papillary necrosis.
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31
Q

What are the DDx for chest pain?

(At least 15)

A
  • Things that kill patients: MI, PE, RAAA, Bleeding (shock)
  • Most likely: MI
  • Cardiac: Angina, MI, pericarditis, myocarditis, tamponade
  • Pulmonary: Pleurisy, PE, pneumonia, viral pleuritis, spontaneous pneumothorax, pleural effusion
  • Gastro: GORD, PU, oesophageal spasm, acute cholecystitis, pancreatitis, gastritis
  • MSK: Costochondritis
  • Psycho: Aniexty or panic disorder.
  • Other: Hypoglycaemia, anaemia
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32
Q

What Hx would you want from a patient who has chest pain?

A
  • SOCRATES
  • Associated features:
    • Heavy weight in chest
    • radiation to arm, back or jaw
    • SOB
    • Dizziness, palpitations, syncope
    • Diaphoresis, nausea and vomiting
  • PMHx:
    • GI bleeding, ulcers, GORD, haematemesis
    • Previous angina or chest pain
    • Recent surgery
    • Any recent illness or fever?
  • FHx:
    • cardiovascular disease, stroke, MI, peripheral vascular disease.
  • POSH: smoking/ drinking, recent travel
  • Medications.
  • Weight/BMI/ glycaemic control
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33
Q

Describe what the heart sounds represent?

A
  • 1st sound: closing mitral and tricuspid valves.
  • 2nd: closure aortic valve
  • 3rd: rapid ventricular filling, early distole
    • When arising from the LV, it is best audible at the apex with the patient in left lateral decubitus position with breath held at end expiration. When it is of RV origin, S3 is best audible at the left lower sternal border or the xiphoid with the patient in supine position.
  • 4th: late distolic/early systolic - forceful atrial ejection
    • When of LV origin, S4 is best heard at the apex with the patient in the left lateral decubitus position at end expiration. When of RV origin, it is heard best at the left lower sternal border. Maneuvers that increase the preload increase the intensity of S4 by increasing the separation of S4 from S1. Left-sided S4 is also augmented by increased afterload as can happen with hand grip.
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34
Q

If a patient presents to you at the GP clinic with chest pain how would you manage them?

A
  • Call an ambulance
  • Monitor vital signs
  • ECG
  • Sublingual nitrate - spray or tablet, titrate to effect
  • Aspirin
  • O2
  • Consider morphine
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35
Q

When a patient with chest pain presents to ED what investigations do you order?

If they are having an MI what would you expect to see in the results?

A
  • FBC: normal
  • UEC: normal
  • Blood glucose: elevated expected result in diabetic patient under stress
  • LFT: normal or elevated transaminase; elevated lactic dehydrogenase indicates cell dealth but is very non-specific.
  • Troponin: elevated - within 6 hours of onset, remain elevated for approx 14 days
  • CK-MB: elevated - within 4 hours of onset, peak at 18-24 hours, normalise within 3-4days
  • CXR: may be initially normal, may show early signs of heart failure (slight enlargement, prominent vessles, early oedema)
  • ECG: ST elevation or depression
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36
Q

Which ECG leads correlate to which areas of the heart?

A
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37
Q

Which ECG leads correlate with which coronary artery?

A
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38
Q

Describe the histology of an atherosclerotic plaque?

A
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39
Q

Describe the morphological changes that occur to the heart after MI?

A
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40
Q

How do you manage a patient who presents to ED with MI?

A
  • ECG
  • IV access
    • Bloods for FBC, UEC, glucose, lipids, cardiac enzymes
  • O2
  • Aspirin 300mg (unless already given by GP or paramedics
  • Morphine 5-10mg IV + anti-emetic
  • Clexane
  • B-blocker
  • CCU admission
    • Percutaneous coronary intervention (angioplasty)
    • NO PCI available fibrinolysis/thrombolysis
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41
Q

What are the possible complications of MI?

A
  • Death
  • Arrhythmis/heartblock/pacemaker
  • Heart failure
  • Thromboembolism
  • Pericarditis
  • Dresslers syndrome
  • Stroke
  • Rupture of ventriuclar aneurysm/mitral vavle chordae
  • Infection: UTI, pneumonia, phlebitis
  • Recurrent angina
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42
Q

Who forms part of the multidisciplinary team in the management of MI?

A
  • Cardiologist
  • Haematologist
  • Intensivist
  • Physio
  • Diet and exercise counsellor
  • GP
  • Cardiac rehab
  • Nurses
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43
Q

What are the modifable and non modifiable risk factors for coronary artery disease?

A

Modifiable:

  • Weight
  • Hyperlipidaemia
  • HTN
  • Diet
  • Diabetes
  • Chronic renal disease
  • Obstructive sleep apnoea
  • Inactivity
  • Smoking
  • Psychosocial/stress
  • Medications

Non-modifiable:

  • FHx of CHD or hyperlipidaemia
  • Genetics
  • Age
  • Sex
  • Previous MI
  • Diabetes
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44
Q

What are the secondary preventions that can be used to reduce the risk of further MI?

A
  • Life rehab
  • Rx:
    • Statins
    • Anti-coagulant
    • Ace inhibitors
    • B-blockers
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45
Q

What are the DDx for SOB?

A
  • Things that kill: Asthma, MI, PE
  • Pulmonary: COPD, pneumonia, bronchospasm, pneumothorax, tumour, pulmonary oedema, pleural effusion.
  • Cardiac: CHF, cardiogenic shock
  • Haematological: Anaemia
  • Psych: Anxiety, panic attack
  • Renal: acidosis
  • Gastro: pancreatitis, ascites
  • Systemic: Sepsis, anaphylaxis, adverse drug reaction
  • Endo: thryoid disease, obesity, cushings syndrome
  • Neuro: myasthenia gravis, Guillain-barre syndrome, phrenic nerve palsy
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46
Q

What information would you want from the Hx of a patient with SOB?

A
  • SOCRATES
  • Associated symptoms:
    • cough, haemoptysis, chest pain, sweating, fever, dizziness, fever, syncope, nausea, vomiting, abdominal pain, calf pain
  • Exacerbating/relieving factors:
    • Better or worse positions
    • any medications tried
  • PMHx: Asthma, cardiac conditions, diabetes, Hx cancer, recent illness or surgery.
  • Medications
  • POSH: smoker, contraception use, pregnancy
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47
Q

What is the Wells Criteria?

A
  • Clinical signs and symptoms of DVT: +3
  • PE is most liekly diagnosis, or equally likely: +3
  • Heart rate >100: +1.5
  • Immobilisation at least 3 days or surgery in last 4 weeks: +1.5
  • Previous objectively diagnosed PE or DVT: +1.5
  • Hameoptysis: +1
  • Malignancy treated within last 6 months, or palliative care: +1

Low risk <2

Moderate risk 2-6

High risk >6

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48
Q

What investigations would you order for a suspected PE? What would you expect to see in these results?

A
  • ABG: respiratory alkalosis, hypoxaemia, low PoCO2, low PaO2
  • FBC: normal
  • UEC: normal
  • D-dimer: elevated
  • Cardiac enzyme: normal
  • ECG: right heart strain
  • CXR: might show areas of collapse; wedge shaped areas of infarction may be visible after 12 hours in smaller emboli
  • CTPA: visualise embolus in pulmonary vessels
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49
Q

What does an elevated D-dimer mean?

A

D-dimer indicates recent fibrinolysis and may be raised in infarction and malignancy, as well as in patients who have recently undergone surgery. It has a good negative predicitve value in patients with a low pre-test probability (sensitive, but not specific)

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50
Q

How do you manage a patient acute with PE?

A
  • O2
  • IV access
  • Morphine
  • IV low molecular weight heparin or unfractionated heparin
  • Consider thrombolysis
  • CTPA
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51
Q

What strategies can be used to prevent pulmonary embolism?

A
  • Prevention of DVT
  • Early mobilisation after surgery
  • Surgical compression stockings
  • Calf compressors
  • Prophylactic use of anticoagulants such as low molecular weight heparin (clexane)
  • Early recognition and treatment of DVT
  • IVC filters in appropriate patients
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52
Q

What are the risk factors for a pulmonary embolus?

(12 points)

A
  • Previous thrombo-embolism (either DVT or PE)
  • Known DVT, especially of proximal vessels
  • increasing age
  • Female sex
  • Recent surgery
  • Major trauma
  • Malignancy
  • Obesity
  • Immobility
  • Thrombophilias:
    • Factor V Leiden
    • Protein C and S deficiencies
    • Anti-thrombin 3 deficiency
    • 20210 A gene mutation
    • Anti-phospholipid antibodies
  • OCP
  • Pregnancy or recent childbirth (higher if caesarean delivary)
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53
Q

What further information would you like from patient who present with overweight and slightly breathless?

A
  • Any current illness?
  • PMHx: cardio, HTN, hyperlipidaemia, diabetes, imparied glucose tolerance, gout, renal disease, obstructive sleep apnoea, weight Hx, arthritis.
  • Lifestyle issues: exercise history/tolerance, occupation, stress levels, diet, smoking, alcohol
  • Drug Hx: medications
  • FHx: especially cardiovascular disease, obesity, type II diabetes, obstructive sleep apnoea
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54
Q

What physical exams would you perform on a patient who is obese and slightly breathless?

A
  • General physical exam (including blood pressure, waist circumference, height, weight). SPecific examinations:
    • Cardio
    • Resp
    • Abdo
    • MSK
    • Dipstick - protein/glycosuria
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55
Q

What is the diagnostic criteria for metabolic syndrome?

A

Any three of the following:

  • Waist circumference: >102 cm (males, >88 cm (females)
  • Triglycerides: ≥1.7mmol/L or drug treatment for elevated triglycerides
  • High density lipoprotiens: <1mmol/L (males, <1.3mmol/L (females)
  • Blood pressure: ≥135/≥85 mmHg
  • Fasting glucose: ≥5.6mmol/L or drug treatment for elevated blood glucose levels.
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56
Q

Describe the pathophysiology of metabolic syndrome?

A
  • Adipose tissue storing large quantities of lipid releases substances that reduce the response of tissue to insulin and affect glucose and fattry acid utilisation in the peripheries
  • The hormonal activities of adipose tissue results in insulin resistance.
  • Insulin resistance is the main mechanism involved in metabolic syndrome, as it predisposes to type II diabetes and cardiovascular disese
  • Other effects of adiopocyte cytokines include mediating blood vessel inflammation, effects on lipid profile, hypertension and vascular endothelial dysfunction.
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57
Q

What investigations would you order in a patient with suspected metabolic syndrome and what would you expect to see in the results?

A
  • FBC: normal
  • UEC: Normal
  • LFTs: Elevated ALT, AST, GTT and AlkP, normal bilirubin and albumin.
  • Urinalysis: ± protein
  • Triglycerides and total cholesterol: total cholesterol and triglycerides elevated.
  • High density lipoproteins: low
  • Glucose tolerance test: impaired GTT or diabetes.
  • HbA1c: high
  • CXR: normal
  • ECG: may be normal or show ischemic changes
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58
Q

How do you manage metabolic syndrome?

A

Treat the underlying causes intensively.

  • Diet: with reduced intake of simple sugars, saturated fats, cholesterol and transfats, and increase intake of fruits, vegetables and whole grains. The aim is for 7-10% bodyweight loss over 6-12 months. Consider a referral to a dietician for more detalied advice if weight loss is inadequate.
  • Physical activity: 60-90 minutes per day can produce modest weight reduction, but 30 mins per day provides significant health benefits.
  • Pharmaceutical or weifght loss aids: not first line treatment but may be useful if conservative treatment does not work.

Treat cardivascular disease risk factors:

  • Lipids: statinsor fibrates
  • HTN: ACE inhibitors or angiotension 2 inhibitors
  • DM: treat if present
  • Smoking cessation
  • Regular monitoring: blood glucose, BP, lipids.
59
Q

What monitoring tests are important in metabolic syndrome?

A
  • Fasting blood glucose levels/ HbA1c
  • TG’s, HDL, LDL
  • BP, weight and waist circumference
  • LFT
  • UEC
  • Uric acid level (if gout is present)
60
Q

What diseases have an increased risk of developing becuase of metabolic syndrome?

A
  • cardiovascular
  • DM
  • Non-alcoholic fatty liver disease (which can progress to fibrosis and cirrhosis)
  • Hyperuricaemia and gout
  • Obstructive sleep apnoea
  • Chronic renal disese
  • Female patients are susceptible to PCOS
  • Malignancy: Colorectal, oesophageal and kidney. In females breast and endometrial are also increased.
61
Q

How do you manage a patient with diabetes?

A
  • Diabetic education about diabetes and self-monitoring of blood glucose levels
  • Hypoglycaemia agents: Metform/Thioglitazone, add sulfonylurea or sitagliptin if not controlled with metformin
  • Regular physical examination to detect complications:
    • Vision, visual acuity, visual fields, fundoscopy
    • Cardiovascular system exam
    • Orthostatic blood pressure
    • Diabetic foot examination
    • Neurological exam of teh upper and lower limb
  • HbA1c, UEC and microalbuminuria (protein:creatinine ratio) to regular monitoring
  • Consider referral to podiatrist for assessment of/advise about footwear and foot care.
62
Q

What are the diagnositc criteria for overweight/obesity?

A
  • BMI >25 and <30 for overweight
  • BMI 30 - 34.9 obesity class I
  • BMI 35-39.9 obesity class II
  • BMI ≥ 40 obesity class III
63
Q

What further information would you want from a patient who presents with increased bowel motions over 3 months?

A
  • HOPC:
    • What bowel motions are normal for this patient?
    • Define what is happening now.
    • Is it related to eating?
    • How many stools per day?
    • Blood or mucus in stool?
    • Any pain on defaecation?
    • Any feeling of incomplete evacuation?
    • Abdo pain? SOCRATES
    • Nocturnal diarrhoea?
    • Weight loss?
    • Aggravating/alleviating factors?
    • Night sweats?
  • PMHx: new/existing medications
  • Social: recent travel, infection, chnage in diet/dietary triggers, smoking/alcohol
  • FHx: of IBD, coelic disease, other malabsorption disease, IBS
64
Q

What are the DDx for increased frequency of bowel motions for 3 months?

A
  • IBS
  • IBD
  • Coelic disease
  • Lactose intolerance
  • Diet related ie excessive use sugar free gums/sweets
  • Laxative use/abuse
  • Congenital sucrase-isomaltase deficiniency
  • Hyperthyroidism
  • Alcohol abuse
65
Q

What are the Rome Criteris for IBS?

A

IBS can be diagnosed based on at least 12 weeks, which need not be consecutive, of the preceding 12 months there was abdominal discomfort or pain that had two out of three of these features:

  • Relived with defaecation; and/or
  • Onset associated with change in frequency of stool; and/or
  • Onset associated with a change in form (appearance) of stool.

Symptoms that cumulatively support the diagnosis of IBS:

  • Abnormal stool frequency
  • Abnormal stool form
  • Abnormal stool passage
  • Bloating or feeling of abdominal distention

Supportive symptoms of IBS:

  • Fewer than three bowel movements a week
  • More than three bowel movements a day
  • Hard of lumpy stool
  • Loose or watery stools
  • Straining during a bowel movement
  • Urgency
  • Feeling of incomplete bowel movement
  • Abdominal fullness, bloating or swelling
66
Q

What investigations would you oder for a patient who presents with diarrhoea, containing blood with diffuse abdo and rectal pain?

?IBD

A
  • FBC: Anaemia, leucytosis, elevated platelets
  • UEC: Normal
  • CRP: Elevated
  • LFTs: Normal unless bile duct involed
  • ESR: Elevated
  • AXR: normal
  • Colonoscopy: Colitis
67
Q

What red flags would you want to rule out for IBS, that may suggest more serious disease?

A
  • Fever
  • Tachycardia
  • Weight loss
  • Pallor
  • Night sweats
  • Nocturnal diarrhoea
  • Some diffuse abdo tenderness
  • Rectal exam showing blood on glove
68
Q

What are the macro and microscopic differences between UC and Crohns disease?

A
69
Q

What are the clinical differences between UC and Crohns disease?

A
70
Q

What pathology is occuring in this small intestine?

A

This is another example of Crohn disease involving the small intestine. Here, the mucosal surface demonstrates an irregular nodular appearance with hyperemia and focal ulceration. The distribution of bowel involvement with Crohn disease is irregular with more normal intervening “skip” areas.

71
Q

What pathology is occuring here?

A

Microscopically, Crohn disease is characterized by transmural inflammation. Here, inflammatory cells (the bluish infiltrates) extend from mucosa through submucosa and muscularis and appear as nodular infiltrates on the serosal surface adjacent to fat. Note the granulomatous inflammation.

72
Q

What pathology is occuring in this large intestine?

A

This gross appearance is characteristic for ulcerative colitis. The most intense inflammation begins at the lower right in the sigmoid colon and extends upward and around to the ascending colon. At the lower left is the ileocecal valve with a portion of terminal ileum that is not involved. Inflammation with ulcerative colitis tends to be continuous along the mucosal surface and tends to begin in the rectum.

73
Q

What pathology is ocuring microscopically in this large intestine?

A

Microscopically, the inflammation of ulcerative colitis is confined primarily to the mucosa. Here, the mucosa is eroded by an inflammatory process with ulceration that undermines surrounding mucosa. The resulting ulceration often has a flask shape (Erlenmeyer flask…triggering flashbacks to organic chemistry).

74
Q

What apthology is occuring in this microscopic image of the large intestine?

A

On microscopic examination at higher magnification, the intense inflammation of the mucosa is seen. The colonic mucosal epithelium demonstrates loss of goblet cells. The shape of the crypts is distorted. An exudate is present over the surface. Both acute and chronic inflammatory cells are present.

75
Q

What pathology is occuring in this microscopic picture of the small intestine?

A

On microscopic examination at high magnification the granulomatous nature of the inflammation of Crohn disease is demonstrated here with epithelioid cells, giant cells, and many lymphocytes. Special stains for organisms are negative.

The clinical manifestations of CD are variable and can include diarrhea, fever, and pain, as well as extraintestinal manifestations of arthritis, uveitis, erythema nodosum, and ankylosing spondylitis.

76
Q

What test results would help confirm inflammatory bowel disease?

A
  • FBC: worsening anaemia, leucocytosis and neutrophilia
  • ESR & CRP: Elevated
  • LFTs: hypoalbuminaemia
  • UEC: dehydration, electrolyte loss
  • Faecal calprotectin level: elevated
77
Q

How do you manage severe fulminant UC?

A
  • Admission to hospital
  • Rescusciatiton: IV fluids
  • Bowel rest with clear fluids only
  • High dose IV steroids
  • Cyclosporine (IV or PO) - check cholesterol - if low risk of seizure.
  • Biologicals (infliximab) if no improvement/steroid resistant
  • Pain relief
  • Antibiotics
  • Exclude infectious cause
  • Surgical review - colectomy if not better in 72 hours
78
Q

How is UC and Crohns controlled short term and long term?

A
79
Q

What are the complication of UC?

A
  • Severe bleeding
  • A hole in the colon (perforated colon)
  • Severe dehydration
  • Liver disease (rare)
  • Bone loss (osteoporosis)
  • Inflammation of your skin, joints and eyes, and sores in the lining of your mouth
  • An increased risk of colon cancer
  • A rapidly swelling colon (toxic megacolon)
  • Increased risk of blood clots in veins and arteries
80
Q

What are some of the extra intestinal features of UC?

A
  • Aphthous ulcers of the mouth
  • Ophthalmic
    • Iritis or uveitis
    • Episcleritis
  • MSK:
    • Seronegative arthritis, which can be large joint oligoarthritis, or may affect many small joints of the hands and feet.
    • Ankylosing spondylitis
    • Sacroiliitis
  • Cutaneous:
    • Erythema nodosum
    • Pyoderma gangrenosum
  • DVT and PE
  • Autoimmune haemolytic anaemia
  • Clubbing
  • Primary sclerosing cholangitis
81
Q

What are some of the extra intestinal features of Crohns?

A

Similar to those of UC.

  • Uveitis
  • Episcleritis
  • Seronegatove spondylarthropathy
  • Ankylosing spondylitis
  • Sacroilitis
  • Erythema nodosum
  • Pyoderma gangrenosum
  • DVT and PE
  • Autoimmune haemolytic anaemia
  • Clubbing
82
Q

What are the long term complications of IBD? are these associated with the treatment or the disease itself?

A
  • UC has increased risk of developing adenocarcinoma of the bowel
  • Steroid use increases risk of osteoporosis, infection, diabetes
  • Immunosuppressive and biologicals increase risk of infection and other malignancies e.g. skin cancers
83
Q

How do patients with IBD prevent the long term complications?

A
  • Patients using steroids need to take calcium and Vit D supplementation
  • Immunosuppressed patient need to be vaccinated
  • Regular monitoring of blood sugar and lipids for long term use of steroids
  • regular colonoscopy 10 years after diagnosis of IBD
84
Q

Before placing someone on immunosuppressive treatment what addition tests need to be performed?

A

Screening for infectious diseases: TB, HIV, HBV, HCV, CMV

85
Q

What are the DDx for temporary facial paralysis?

A
  • TIA
  • Stroke
  • Bell’s palsy
  • Seizure
  • Migraine auras
86
Q

What further information would you want from a patient who you suspect to have had a TIA?

A
  • SOCRATES: weakness
    • Associated pain, tingling, numbness
    • Witnesses
    • Other neurological symptoms: confusion, LOCm visual deficits, hearing/speech problems, tinnitus, vertigo, imblance, nausea.
    • Recent memory changes
    • Recent illness
    • Recent palpitations
  • PMHx:
    • Cardiovascular disease: MI, peripheral vascular disease, HTN, dysrythmia, previous stroke, dyslipidaemia, DM, thrombophilia/thromboembolic disease
  • FHx: TIA, stroke, cardiovascular disease, HTN, dyslipidaemia, DM
  • Social: smoking, alcohol, home situation, occupation, diet, physical activity, recent travel
  • Medications
  • Allergies
87
Q

What physical exam would you perform on a patient with suspected TIA?

A
  • Vital signs
  • Residual deficits: craniel nerves, upper limb and lower limb neuro exam
  • Cardiovascular exam
88
Q

Define TIA?

A

Transient ischaemic attack is defines as “a clinical syndrome characterised by an acute loss of focal cerebral or monocular function with symptoms lasting less than 24 hours and which is thought to be due to inadequate cerebral or ocular blood supply as a result of low blood flow, arterial thrombosis or embolism associated with diseases of the arteries, heart or blood”.

It is important to note that this syndrome is often associated with radiological evidence of mild cerebral infarction - especially on MRI diffusion-weighted images.

Resolution is necessary for this label to be used. A cerebral ischaemic event which has not yet reolved and which has not yet been present for 24 hours is a stroke, NOT a TIA, though it remains possible it will turn into a TIA.

89
Q

What investigations would you perform in a patient with suspected TIA and what results would you expect?

A
  • FBC: Rule out polycythaemia, infection, vasculitis, thrombophilia.
  • Coags: Rule out hypercoagulable states
  • UEC: Normal
  • Blood glucose: Normal or elevated. Rule out diabetes
  • LFTs: Normal or elevated
  • CRP: Rule out vasculitis
  • Lipid profile: Normal or elevated. Rule out dyslipidaemia
  • ESR: Rule out vasculitis
  • ECG: AF
  • Transoesophageal echo: Rule out thrombus in left atrium
  • Carotid US: Check for atheromatous plaques and thrombus formation
  • CT/MRI brain: nomral or infarct
90
Q

Define what symptoms will represent where a stroke may have occured?

A
91
Q

How do you manage a patient who is diagnosed with TIA?

A
  • Investigations
  • Identify risk factors and then treat
  • Once bleeding excluded:
    • Aspiring (75 mg) daily
    • Heparin and warfarin: due to AF. Cease heparin anf aspirin once INR is between 2-3 seconds.
  • Monitor and treat HTN: target ≤140/80 mmHg or ≤130/80 mmHg with diabetes or kidney disease.
    • ACE inhibitors if possible
  • Treat dyslipidaemia:
    • Statin
  • Non-pharmacological:
    • Diet
    • Exercise
    • Lifestyle issues advice
  • Neurological referral
  • Consider vascular surgical opinion (re carotid disease)
  • Regular review
92
Q

What are the criteria used for carotid endarterectomy?

A

Endarterectomy is normally considered if the patients has a symptomatic carotid stenosis of at least 70%, or a very tight asymptomatic stenosis ~95%.

93
Q

What is the difference between a transient loss of vision in the left eye vs transient loss of vision in the left hemifield? How might this be differentitated on Hx?

A

Transient loss of vision in left eye: most likely amaurosis fugas (TIA of the retina.

Ischaemia of the retina or optic nerve due to:

  • Emboli, clot or cholesterol
  • Choroidal or retinal vascualr spasm (especially younger patients)
  • Severe occlusive carotid disease
  • Aortic dissection
  • Hyperviscosity, e.g. polycythemia vera, leukemia
  • Arteritis (temporal)
  • Increased intracranial pressure (more transient, bilateral)

Left hemifield transient vision loss: most likely TIA or migraine

  • Others: retinal migraine, conversion disorder
  • Others (rare): papilloedema
  • Causes that would NOT resolve in 15 mins: inflammation of eye, rential detachment, central retinal vein occlusion, central retinal artery occlusion, optic neuropathy, optic nerve compression, optic neuritis.
94
Q

What physical exam and investigations would you order in someone who presents with behavioural changes?

A

Physical exam:

  • Vital signs
  • Testing of visual acuity and visual fields and full neuro exam
  • Fundoscopy
  • Dementia screen: MMSE, activities of daily living scale
  • Depression screen: geriatric depression scale

Investigations:

  • Vitamin 12 and folate: rule out vitamin deficiency as a cause of demetia
  • TSH, T3, T4: rule out endocrine causes of dementia
  • Syphilis serology: rule out tertiary syphilis
  • Carotid US: for stenosis
95
Q

What are the modifiable and non-modifiable risk factors for stroke?

A

Non-modifiable:

  • Age
  • Gender
  • race/ethnicity
  • FHx

Modifiable (see table)

96
Q

Define dementia.

A

A disorder that is characterised by impairment of memory and at least one other cognitive domain (aphasia, apraxia, agnosia, executive function) that represents a decline from previous level of function and is severe enough to interfere with daily function and independence.

97
Q

What are the different types of dementia?

A
98
Q

How does vascular dementia differentiate from Alzheimer’s dementia?

A

The main difference between the two types of dementia are that vascular dementia is characterised by:

  • Previous stroke
  • Hx of TIAs
  • Heart disease
  • HTN
  • DM
99
Q

What is the ABCD2 score and how is it utilised clinically?

A

The ABCD2 score is a clinical prediction rule used to determine the risk for stroke in the days following a transient ischemic attack.

100
Q

What are the DDx for SOB and cough?

A
  • Respiratory: Post viral/bacterial cough, pneumonia, acute bronchitis, asthma - poor control, PE
  • Trauma: rib fracture/soft tissue damage, pneumothorax
  • Cardiac: Pulmonary oedema, CHF (unlikely)
  • Renal failure (unlikely)
  • Foreign body in airway (unlikely)
101
Q

What further infromation would you like from a patient who has SOB and cough?

A
  • HOPC:
    • SOCRATES
    • When were you last well? What was the first thing you noted wrong?
    • Nocturnal symptoms, orthopnoea
    • Chest pain - pleuritic, ischaemic
    • Other symptoms: Fever, shivering, chills, nausea/vomiting, fatigue, mental state change
  • PMHx:
    • Recent acute illness (especially resp)
    • Chronic respiratory illness (e.g. asthma, bronchitis, COPD, cystic fibrosis, allergies, TB)
    • CVS and thromboembolic disease
    • Chronic illness causing immunosuppression or managed with immunosuppressant medication (DM, HIV)
    • Previous hospital admissions
  • FHx:
    • Chronic respiratory illness
    • Early onset cardiac disease
    • Early onset renal disease
    • Allergic disease
  • Drug and allergy Hx:
    • Any current medications
    • Any allergies
  • POSHx:
    • Occupational exposures
    • Sick contacts
    • Smoking Hx
    • Alcohol Hx
102
Q

What investigations would you order for a patient who you suspect has pneumonia? what would you expect to see in the results?

A
  • FBC: leukocytosis - bacterial, lymphocytosis - viral
  • UEC: normal to evidence early renal failure and dehydration, raised urea and creatinine.
  • ESR & CRP: elevated
  • Blood culture: 15% chance if septic in hospital pre-treatment
  • Sputum MCS and gram stain
  • Nasal swab and PCR: ?swine flu
  • PCR/serology: for viruses and legionella
  • CXR: radiological features of pneumonia-
    • Opacities, air bronchograms, silhouette sign, pleural effusion and fluid level.
  • CT: chest pathology
  • ECG: to exclude MI and PE
103
Q

How do you assess if a patient needs to be admitted to hospital with pneumonia?

A

Can use either:

  • Pneumonia severity index (PSI)
  • Curb65:
    • Confusion, Urea>7mmol/L, RR>30, BP systolic <90, age >65.
    • Score 0-5: 0-1 Home, 2-3 admit, 3-5 ICU
104
Q

How do you manage a patient with pneumonia?

A
  • O2 till sats are >90%
  • Monitoring vitals
  • IV access and fluid rescus
  • IV Abx
  • ?ICU - CURB65
105
Q

Define community acquired pneumonia and healthcare associated pneumonia, how they are related to the organisms involved?

A
  • Community acquired pneumonia develops in the outpatient setting, or in the first 48 hours after admission to hospital.
  • Hospital pneumonia (nosocomial) develops at least 48 hours after a patient is admitted to hospital and is acquired in the health care system
  • Healthcare associated pneumonia is a third category that is aquired in other health care facilities, e.g. nursing home, dialysis clinic or within 90 days of discharge from an acute o chronic care facility.

Organisms: see table

*

106
Q

What are the predisposing factor of the bacteria and the host that allows for infection?

A

Bacterial:

  • Virulence
  • Inoculant size
  • Effects on cilia/mucus - C pn, M pn, Influ virus
  • TB and legionella resist phagocytosis
  • S pneumonia and Neisseria M capsular

Host:

  • Extremes of age
  • Altered consciousness
  • Immunosuppression including drugs: DM, CRF, malnutrition, alcohol
  • Recent influenza - beware Staph aureus
  • Smoking
  • Chronic lung disease - COPD, bronchitis, bronchiectasis, cystic fibrosis, previous pneumonia
  • Pulmonary oedma
  • Inherited cilia dysfunction
  • Mechanical obstruction
107
Q

What Abx are used to treat, community, hospital and healthcare aquired pneumonias?

A
  • Community: Macrolide or Doxycycline or amoxicillin. If co-morbidity respiratory Fluoroquinolones (RF)
  • Hospital: Mox or beta-lactm (Cef) plus Respiratory fluoroquinolone or pen allergy RF + aztreonam
  • ICU: cef + Azithromicin or same + aminoglycoside for pseudomonas piperacillin/merepenem + cipro or levoflocacin
108
Q

What are the four pathological stages of the inflammatory response in bacterial lobar pneumonia? What are the macro and microscopic apearances?

A
  • Congestion:
    • macro: vascular engorgement, red, boggy lung that is heavy.
    • Micro: intra-alveolar fluid often containing large numbers of bacteria, but few neutrophils
  • Red hepatisation:
    • Macro: affected lung region has liver-like consitency; red, airless and firm
    • Micro: Alveolar spaces filled with a confluent exudate containing abundant neutrophils, fibrin and erythrocytes
  • Grey hepatisation:
    • Macro: Dry, greyish brown surface
    • Micro: the exudate still contains fibrin and neutrophils, but the erythrocytes are degraded.
  • Resolution:
    • Macro: Alveolar spaces filled with semifluid debris that is progressively expectorated, engulfed by macrophages, resobred or organised
    • Micro: Macrophages engulf exudate, organisation of exudate occurs
109
Q

What are the possible complications of pneumonia?

A
  • Respiratory failure → Death
  • Pleural effusion
  • Empyema
  • Pulmonary abscess (often post-aspiration and gram -ve)
  • Necrotizing pneumonia
  • Bronchiectasis
  • Local destruction of lung parenchyma with fibrosis/organisation ?pleural adhesions
  • Adult respiratory distress syndrome
  • Ventilator dependence
  • Cavitation
  • Superinfection
110
Q

What are the DDx of a painful knee?

A

Inflammatory:

  • Rheumatoid arthritis
  • SLE
  • Infectious - arbovirus e.g. Ross river virus
  • Sjogren’s syndrome
  • Adult Still’s disease
  • Reactive arthritis (Reiter syndrome) mainly larger joints
  • Enteropathic IBD

Non-inflammatory: osteoarthritis, trauma, RSI

111
Q

What further information would you seek from a patient with a sore knee?

A
  • SOCRATES for joint
    • Extra-articular symptoms:
      • Eyes: scleritis and episcleritis
      • Sicca syndrome (dry mouth and eyes)
      • Skin - rash
      • Respiratory
      • Tensosynovitis, nodules
    • Associated symptoms: fever, weight loss, fatigue, carpal tunnel syndrome, trigger finger, Raynaud’s syndrome.
    • Precipitation features
    • Preceding illness, e.g. viral, bites, GIT genitourinary
  • PMHx:
    • Anything like this before?
    • Past injuries?
    • Autoimmune conditions?
    • Medical or surgical conditions
  • FHx:
    • Rheumatoid arthritis
    • Autoimmune disease
  • SHx:
    • Home situation, family, stairs
    • What job? Ability to work?
    • Smoking/alcohol consumption, diet, exercise
    • Travel - ?mosquitoes
    • Medications
    • Allergies
112
Q

What examinations would you perform on a patient with a sore knee?

A
  • Vital signs
  • MSK:
    • Assess the symptomatic joints (inflammation), wasting, deformity, and function
    • Screen all the other joints
    • Check for extra-articular signs - eyes, skin, nodules, luns (basal fibrosis), heart sounds
113
Q

What investigations would you order on a patient with sore knee? what would you expect to see in a patient with ?Rheumatoid arthritis?

A
  • FBC: Anaemia may be present (normocytic normochromic). The platelets rise with active disease.
  • ESR: elevated in proportion to the activity of the inflammatory process
  • CRP: Elevated in proportion to the activity of the inflammatory process.
  • UEC: confirm no renal impairment
  • LFTs: checking for poretinura, nephrotic syndrome (long-standing disease)
  • RF: is presenting in approx 70% of cases at low titre
  • Antinuclear antibodies: ANA present in 30% of cases at low titre
  • Anti-CCP: new cases, similar to RF, indicated aggresive disease and guides prognosis
  • ENA, d/s DNA: To help with exlcusion of SLE
  • Xray of affected joints: aim to establish a baseling. Only soft tissue swelling is seen in early disease.
  • Nerve conduction studies: carpal tunnel syndrome
  • Joint aspiration: Opalescent fluid with high protein and neutrophils count.
114
Q

How is disease activity assessed for joint disease?

A

Based on the following factors:

  • Number of joints involved
  • inflammatory markers
  • Functional assessment (often questionnaire)
  • RF or ACCP not good marker of flares or progress
  • Albumin and anaemia
  • Xray changes - erosions

Mild disease: <6 inflamed joints, no extraarticular disease and no evidence of erosins or cartilahe loss on plain radiographs.

Moderate disease: between 6 and 20 inflammed joints + inflammatory markers and erosions.

Severe disease: >20 inflamed joints, increased ESR and/or serum CRP and one or more of the following:

  • Anaemia of chronic disease
  • hypoalbuminaemia
  • RF positive and/or Anti-CCP antibodies
  • Joint radiographs demonstrating rapid appearance of bony erosions and loss of cartilage
  • Extra-articular disease
115
Q

What are the characteristics changes of RA?

A
  • Synovitis, swelling MCP, PIP and wrist.
  • Muscle wasting and ulnar deviation
  • Rheumatoid nodules
  • Early periarticular erosions
  • Deviation, sublacation, periarticular osteoporosis, joint destruction.
  • Swan neck or Boutonniere deformity
  • Bow string sign - prominent extensor tendons
  • Extensor tendon rupture (rare) usually thumb, little or ring finger
  • Early loss of wrist extension
  • Volar subluxation and radial drift of the carpus
116
Q

What is rheumatoid arthritis?

A

RA is a multi-system disease with articular synovitis as the inital presentation.

The aetiology and pathogenesis remains unclear, but there is acute and chronic inflammation in the synovium, associated with aproliferative and destructive progress in joint tissues. Much of the joint damage that ultimately results in disability begins early in the course of the disease. This is what needs urgent treatment to limit disability.

117
Q

Describe the articular changes in RA?

A

RA causes a broad spectrum of morphologic alternations

The synovium becomes oedematous, thickened and hyperplastic and there is:

  • A dense perivascular inflammatory infiltrates composed of lymphoid aggregates (mostly CD4+ helper T cells), B cells, plasma cells, dendritic cells and macrophages
  • Increased vascularity due to vasodilatation and angiogenesis
  • Aggregation of organising fibrin covering portions of the synovium and floating in the joint space as rice bodies
  • Accumulation of neutrophils in the synovial fluid
  • Osteoclastic activity in the underlying bone
  • Pannus formation(mass of synoviumand synovial stroma consisting of inflammatory cells, granulation tissue, and synovial fibroblasts), which grows over hte articular cartilage and causes its erosion.
118
Q

How do you treat a patient with RA?

A

Non-pharmalogical:

  • Rest (for active arthritis)
  • Exercise (to maintain joint range)
  • Physical therapy and occupational therapy
  • Nutrition and dietary therapy
  • Bone protection

Pharmalogical:

  • NSAIDs
  • Sulfasalazine
  • Biologicals: infliximab
  • Methotrexate:
    • Discourage alcohol
    • Monitoring 4-8 weeks
    • Folic acid supplements
  • Atherosclerosis risk factor modification
  • Vaccinations
119
Q

What is carpal tunnel syndrome? and how is it managed?

A

There is compression of the median nerve at the wrist by teh flexor retinaculum. There is noctural tingling and pain in the hand )and/or forearm) followed by weakness of thenar muscles. Wasting of abductor pollicis brevis develops, with sensory loss in the palm and radial 31/2 finger. Confirm with nerve conduction studies.

Treatment:

  • A wrist splint at night
  • Steroid injection
  • Surgical decompression
120
Q

What are the extra-articular manifestations of RA?

A
  • Eye: episcleritis, scleritis, perforation, sicca symptoms
  • Heart: valvular disease, conduction abnormalities, pericardial effusions
  • Lung: effusions, nodules, basal fibrosis
  • Splenomegaly (Felty’s syndrome)
  • Peripheral neuropathy, sensorimotor, motor, mononeuritis, multiplex
121
Q

What is the difference between RA and SLE?

A

RA causes erosive, non suppurative, type of destruction synovitis, whereas SLE causes non erosive synovitis with little deformity

122
Q

A patient presents with, exertional dyspnoea, noctural cough. PMHx MI, stenting, HTN and hypercholesterolaemia. Current medications are Ca2+ blocker, statin, aspirin. He has a 40 pack year smoking Hx.

Given this clinical picture what organ systems are involved and what are the DDx that should be considered?

A

Cardiovascular:

  • CHF
  • Ischaemic cardiomyopathy
  • Alcoholic cardiomyopathy
  • Arrythmia
  • Hypertensive cardiomyopathy
  • Valvular

Respiratory:

  • COPD
  • Asthma/allergy
  • Occupational diseases
  • Respiratory infection - ?Flu
  • Thrombo-embolism
  • Obstructive sleep apnoea
  • Lung cancer

Haematological: Anaemia

Endocrine:

  • Thyrotoxicosis
  • Hypothyroidism
123
Q

A patient presents with, exertional dyspnoea, noctural cough. PMHx MI, stenting, HTN and hypercholesterolaemia. Current medications are Ca2+ blocker, statin, aspirin. He has a 40 pack year smoking Hx.

What further questions would you like to ask?

A
  • Define symptoms more accurately: SOCRATES, especially time line
    • Cardiovascular:
      • Exercise tolerance
      • Orthopnoea
      • Paraxysmal nocturnal dyspnoea
      • Chest pain/palpitations/oedema
    • Resp:
      • Cough/sputum/haemoptysis
      • Pleuritic pain
      • Wheeze
      • Sleep pattern
    • Haem:
      • Digestive symptoms
      • GI bleed
      • Hx of PU
    • Endocrine:
      • Heat/cold intolerance
      • Sweaty
      • Anxiety
      • Diarrhoea
    • Associated features:
      • Fever
      • Joint/skin symptoms ?autoimmune
      • Recent illness/conact illness
  • PMHx:
    • Weight/DM/diet
    • Recent surgery/trauma
  • POSHx:
    • Smoking/drinking
    • Medications
    • Travel
    • Allergies
  • FHx
124
Q

Describe the cause of a gallop rhythm, and how it is produced?

A

S3 early diastole, and S4 late diastole, are thought to be ventricular filling sounds, and are herd during the rapid filling (passive) and atrial filling phases of the ventricle respectively. S3 can be physiological (e.g. in fit young men), but S4 is pathological. With a tachycardia they can combine to become a “summation gallap”

(Ken tuc-ky or Ten-ne see)

125
Q

A patient presents with, exertional dyspnoea, noctural cough. PMHx MI, stenting, HTN and hypercholesterolaemia. Current medications are Ca2+ blocker, statin, aspirin. He has a 40 pack year smoking Hx.

What test would you order and why?

What would you expect in the results? for this patient.

What tests can the GP do in his office that may assist his diagnosis?

A
  • FBC: Normal
  • UEC: normal or slight raised urea and creatinine
  • Lipids: probably mild to moderately raised
  • HDL: normal or low
  • LFT: probably raised transaminases - ?fatty liver, ?alcohol induced.
  • Blood glucose: Normal or borderline
  • TFT (TSH only): NOrmal
  • Urine dipstick (office): normal or borderline
  • ECG (office): signs of ischaemia and old infarct
  • CXR: enlargement of heart with pulmonary venous congestion, ?pleural effusion.
  • Echo: Reduced ejectionfraction, maybe mitral or tricuspid murmure
  • Coronary angiogram: May be done later to define ventriuclar function.
126
Q

What is the New York classification of heart failure?

A
  • Class I: No limitations
    • Ordinary physical activity does not cause fatigue, dyspnoea or palpitaitons (asymptomatic LV dysfunction.
  • Class II: Slight limitation of physical activity.
    • Ordinary physical activity results in fatigue, palpitations, dyspnoea or angina pectoris (mild CHF)
  • Class III: Marked limitation of physical activity
    • Less than ordinary physical activity leads to symptoms (moderate CHF).
  • Class IV: Unable to carry on any physical activity without discomfort.
    • Symptoms of CHF present at rest (severe CHF)

Normal EF is >55%, <40% significant

Class II-III ~35%

Class IV EF ~15%

127
Q

What is hte management plan for a patient with mild CHF?

A

First line agents:

  • Diuretics
  • Beta blockers
  • ACE-inhibitor
  • Aldosterone anatgonist

Second line:

  • Digoxin: for tachycardia

Management:

  • Stop Ca blocker - negatively inotropic
  • Start diuretic first - there must be no excess water on board before the beta blocker
  • Start beta blocker - once dried out
  • Start ACE inhibitor - with beta blocker long term ventriuclar remodelling
  • Maintain statin and aspirin due to MI risk and stent
  • If remains fluid overloaded consider aldactone but watch Na+
  • If remains HTN >160/100, consider AIIR
128
Q

What non-pharmacological recommendations can you make to manage CHF?

A
  • Smoking cessation and avoidance of passive smoking
  • Reduce or eliminate alcohol consumptions
  • Modify diet: Dietician
  • Regular physical activity
  • Weight reduction
  • Reduce salt intake
  • Fluid management
  • Vaccination: influenza and pneumococcal
129
Q

How is obstructive sleep apnoea relevant to heart failure?

A

OSA can aggravate HF, particularly in the obese patient, contributing to reduction in left ventricular eject fraction. CPAP has been shown to improve left ventricular function

130
Q

How do you treat AF?

A
  • Commence anticoagulation: heparin initally
  • If hypotensive and unwell straight to electrical cardiovaersion
  • If stable consider pharmacological cardioversion first:
    • Amiodarone/Sotalol/Digoxin (many revert spoonatneously in 24 hours)
  • Discourage cardioversion if certain AF present for less than 48 hours
  • If doubt about time AF present then anti-coagulate with warfarin, and perform an elective cardioversion in 4-6 weeks.
131
Q

What are the risk factors for cardiac failure?

A

Modifiable:

  • Low physical activity
  • Smoking
  • Alcohol abuse
  • Obesity
  • HTN
  • Diabetes
  • Valvular heart disease
  • Coronary artery disease
  • LV hypertrophy
  • AF

Non-modifiable:

  • Advanced age >60
  • Low SES
  • FHx of cardiomyopathy
132
Q

What is the difference between systolic heart failure and disatolic heart failure? Are they managed differently?

A

SHF has a low ejection fraction, often a dilated ventricle with remodeling. In SHF need to:

  • Correct systemic factors
  • Lifestyle modifications
  • Review drugs
  • Pharmacotherapy
  • Implantanle devices.

DHF has a normal or near normal EF, and has abnormal filling and filling pressure. The failure is thought to relate to ventriuclar wall abnormalities. IN DHF need to:

  • Control systolic and diastolic HTN
  • Control the ventricular rate
  • Contorl pulmonary congestion with diuretics
  • Coronary re-vascularisation in those in whom ischaemia is though to have an adverse effct on diastolic function.
133
Q

A patient presents with change in vision in one eye. Feels like “looking through a frosted glass shower door”, red and green are less vibrant when monocularly viewed. Occasional bright white steaks of light on moving eye.

What are your DDx?

A
  • Ophthalmic:
    • Posterior vitreius detachment
    • Retinal tear/hole
    • Retinal detachment
    • Optic neuritis - photopsia on eye movenemt, retrobulbar pain.
    • Cataract
    • Posterior uveitis
    • Diabetic retinopathy
    • Papilloedma
    • Vitreous haemorrhage
    • Retinal venous occlusion
    • Retinal arterial occlusion
  • Non-ophthalmic:
    • Migraine
    • Postural hypotension
    • Occipital tumours
    • TIA
    • Stroke
134
Q

A patient presents with change in vision in one eye. Feels like “looking through a frosted glass shower door”, red and green are less vibrant when monocularly viewed. Occasional bright white steaks of light on moving eye.

What further information would you seek from the Hx?

A
  • Further assessment of eye issues: SOCRATES
    • Associated features:
      • Is the eyelid affected? (ptosis)
      • Pain on eye movement?
      • Is the eye dry or gritty
      • Photophobia? (glaucoma, migraine)
      • Is there a glare in sunlight or difficulty driving at night due to the glare from headlights (cataracts)
      • Is vision impaired (glaucoma, cataract, uveitis)
      • Are there any floaters/flashes/haloes (rentinal disease)
      • Headache?
      • Systemic features: fever, malaise, vomiting, arthralgia, rashes, facial pain?
  • PMHx:
    • HTN - associated with vascular eye disease, central retinal vein occlusion
    • Diabetes: retinopathy
    • Sarcoidosis: uveitis
    • Ank spon: uveitis
    • Medications - some drugs have ocular side effects
  • FHx: HTN, diabetes, glaucoma, MS
  • POSHx:
    • Smoking/alcohol
    • Sexual hisotry - Reiters syndrome
135
Q

What are the side effects of steroid use?

Use a mnemonic

A

CUSHINGOID:

  • Cataracts
  • Ulcers
  • Skin: striae, hirsutism, bruising
  • Hypertension/ Hirsutism/ Hyperglycaemia
  • Infections
  • Necrosis: avascular necrosis of the femoral head
  • Glycosuria
  • Osteoporosis, obesity
  • Immunosuppresion
  • Diabetes
136
Q

What do Staph aureus look like on gram stain?

A

Clusters of gram +ve cocci.

137
Q

What does Strept pneumonia look like on gram stain?

A

Gram +ve diplococci

138
Q

What does Neisseria meningitidis gram stain as?

A

Graim -ve diplococci

139
Q

What does pseudomonas aeruginosa stain as on grain stain?

A

Gram -ve rod

140
Q

What are the DDx for pain on eye movement, loss of central vision and colour vision?

A
  • Optic neuritits:
    • MS, sinusitis, syphillis, collagen vascular disorders
  • Trauma/ head injury
  • Myopia and colour blindness
  • Infectious: neuritis
  • Ocular myopathy
  • Globe issues:
    • Uritis
    • rental trauma
  • Migraine
141
Q

What physical exams would you perform on a patient with ? optic neuritis?

A
  • General observations
  • Vital signs
  • Cranial nerve exam: II, III, IV, VI, VIII
  • Lower and upper neuro exam
  • Cardio: carotids
  • Respiratory
142
Q

Define optic neuritis.

A

A demyelination inflammation of the optic erve that often occurs in association with MS or neuromyelitis optica.

Gradual recovery of visual acuity with time is characterisitic of optic neuritis.

50% of MS have optic neuritis in lifetime, only 20% of optic neuritis will develop MS.

143
Q

What investigations would you order in a patient with optic neuritis? What results would you expect?

A
  • CRP/ESR: Assess inflammation
  • Serum IgA/G.M, oligoclonal bands: compare with CSF
  • CSF for oligoclonal bands: MS
  • MRI brain: disseminated lesions → MS, exclude cord compression.
  • FBC: increase WBC with infection
  • ACE: sarcoid
  • ANA/dsDNA/ENA: autoimmune screen
144
Q
A

Year 3 (11 decks)

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