Transcript 10.Savige. - University of Melbourne

Some common problems in
General Medicine
Prof Judy Savige
The University of Melbourne, Northern Health
General comments
• Medicine is changing rapidly so do not
believe everything you read in books!
• Your teachers tend to have firm opinions
and do not always agree – so listen,
question and decide for yourselves
• Develop screening examinations for
diabetes and CNS
Your approach to the patient
• Always treat your patients with respect
• They are sick and worried
• Watch how they walk into the room or wake up,
and how they answer your questions
• Close the curtains, introduce yourself, and
address the patient appropriately
• Examine the patient thoroughly and not with
their clothes on!
Ward rounds each day
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Ask the patient how they are
Ask about their illness and progress
Examine for signs of recovery
Check medications
Check test results and see what they tell
you about the patient
• Don’t just ignore an abnormal test
White nails
• Only in female
medical students
• Never in a patient!
Beau’s lines
• Fingernails grow 1
mm a week
• Severe illness
interrupted nail
growth 8 weeks ago
CNS screening examination
Complete neurological examination
• when there is a history of neurological disease
• when neurological disease is suspected
• when you find an abnormality on screening
examination
Neurological assessment
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How patient walks into the room, posture
Speech
How they answer questions
History itself
Neruological signs patients are unaware of
• Memory loss
• Small, unequal pupils (glaucoma treatment, cataract
removal)
• Nystagmus
• Visual field loss, neglect
• Bell’s palsy
• Previous stroke – posture, weakness, brisk reflexes
• Parkinson’s disease – cogwheeling in upper limb
• Cerebellar disease - nystagmus, past-pointing, heeltoe gait
• Cervical spondylosis – brisk reflexes in limbs
• Peripheral neuropathy – absent ankle jerks and
vibration sense
• Absent ankle jerks – old age
CNS examination
• Higher cortical function – history taking
• Cranial nerves
– Quality of talking
– Facial asymmetry, ptosis,
– Visual fields and neglect
– Horizontal nystagmus and double vision
– Raising eyebrows, smiling
– Uvula midline, tongue pointing midline
Lower limbs
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Heel-toe walking
Stand on toes, squat
Romberg’s test
Ankle reflexes
Vibration sense at ankles
Sensory examination may be hard to
interpret
Upper limbs
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‘Play the piano’
Parietal drift, neglect
Tone including ‘unrolling the fingers’
Biceps reflex
Finger-nose test to a fixed point- looking
for past-pointing and intention tremor
Diabetes
Remember:
Diabetes is a vascular disease
Diabetes assessment
• 30% of all medical inpatients
• 90% all diabetics have type 2 disease and
sometimes have complications at
presentation
Screening questions for diabetics
• Who looks after you?
– GP, endocrinologist, diabetes nurse educator,
dietician, coordinated clinic, ophthalmologist,
podiatrist
• Do you smoke?
Check list for diabetics
• Type I or 2, LADA, duration and
treatment
• Who is responsible for your care? What
is control like? Blood sugar record,
hypo- and hyperglycemia, HbA1C
• What has BP control been like? Lipids?
• Any complications?
Complications of diabetes
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Hypertension – 70%
Dyslipidemia – 70%
Macrovascular disease – IHD, PVD, CVD
Microvascular
– Nephropathy – 20%
– Retinopathy – 33%
– Peripheral neuropathy –50%
Macrovascular disease
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Af, BP lying and standing
S1 and S2, bruits, JVP
Carotid bruits, old stroke
Renal , iliac, and femoral bruits
Dorsalis pedis, posterior tibial pulses
Diabetic foot
• Joint deformities, bunions, callus, ulcers,
hairlessness, muscle wasting, tinea, nails
• Capillary return, peripheral pulses 9both
together)
• Peripheral neuropathy – ankle jerk and VS
• Shoes
Diabetic eyes
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Cataracts – polar and cortical
Glaucoma
Macular degeneration
Diabetic retinopathy
– Background (haemorrahge and exudates)
– Proliferative (new vessel formation)
retinopathy
– Laser burns
Macular degeneration
• Commonest
irreversible cause of
blindness in the world
• Risk factors are age,
smoking,
hypertension
Result of treatment for diabetes
• Laser burns
• Treatment protects
the macula and
central vision
Check list for diabetics during admission
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FBE, U and E, LFT
HbA1c (aim for HbA1c < 7)
Cholesterol/triglycerides
Urinary albumin:creatinine
Advice to smokers
• Don’t ignore it
• You can tell them
– Most powerful addiction known
– Most patients stop by going ‘cold turkey’
– Most do not succeed the first time
– Even reducing the number of cigarettes
reduces lung damage
– Champix, nicotine patches and smoking
cessation clinics
Hypertension
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Obesity, alcohol, stress
Diabetes
Renal artery stenosis – renal doppler
Chronic renal disease – renal ultrasound, cr
Glomerulonephritis – urinary RBC, cr
Conn syndrome – aldo renin ratio – on
prazosin and amlodipine
• Phaeo – 24 hour – NOR, AD, DOP
Hypertension assessment
• 24 hour BP monitoring
• ECG
• Cardiac echo – for LVH and diastolic
dysfunction
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HbA1C
Cholesterol and triglycerides
Urine alb:cr
U and E
Treatment of hypertension
• Weight loss
• Exercise
• More vegetables, less alcohol, less salt
and less fast food
• Walk the dog, get a dog!
• Meditation, yoga, prayer
Treatment of hypertension
• ACE inhibitor
• Ca channel blocker
• Prazosin – very effective but BD
• Aldomet – should not be used long term
• Avoid thiazides
Treating pain
• Non-pharmacological methods first – heat, rest
and acupuncture
• Panadol – 2 when pain is max then try one every
2 hours to max of 4 g a day
• Add in a NSAID – and watch closely, eg Nurofen
• Only then consider codeine-based medications
– oxycontin and oxynorm
• Codeine – based meds have too many sid
effects and are becoming our commonest drug
of addiction
• Avoid tramadol in the elderly
GORD
• Non-pharmacological measures
– Avoid foods that precipitate pain - spicy, acidic (tomatoes, OJ),
fatty
– Reduce weight
– Reduce alcohol
– Stop smoking
– Avoid large and late meals
– Raise head of bed on blocks
• PPI for 8 weeks at dose that reduces symptoms
• Try stopping PPI after that if a good response. Recommence
treatment if symptoms recur within 3 months. Recurrences after 3
months can be treated with further short courses. Or use for
symptoms only
• Endoscopy only for continuous treatment to exclude Barrett’s
oesophagus or atypical features
Urinary tract infections
• Cystitis versus pyelonephritis
• Males with pyelonephritis may have a
prostatic nidus
• Most antibiotics do not enter the prostate –
need to use ciprofloxacin or norfloxacin
Heart failure
Patient with CCF
• What is the underlying cause?
• Why has this patient presented now?
• If you don’t know the answers to these
questions, you can’t treat the patient
appropriately
What else do you want to know?
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Recent chest pain
Sinus rhythm, or bradycardia, Af or tachycardia
Anaemic
Septic
JVP, crepitations, peripheral or sacral oedema
BP- lying and standing
Weight now and previously when euvolemic
What is the underlying cardiac
abnormality?
• Ischemic heart disease – in many
• Hypertension – in many too
• Other types of cardiomyopathy – eg
inherited, viral, drugs, alcohol, amyloid,
haemochromatosis, thyrotoxicosis
• Valvular disease – rheumatic, aortic
stenosis
How do you know it’s IHD?
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History of angina, infarct, stents or CAGs
ECG changes
Echo – segmental dysfunction
Troponin elevation
What are precipitants of CCF?
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Not taking tablets
Progressive disease
Further ischemia or infarct
AF, bradycardia or other arrhythmia
Fever
Thyrotoxicosis
Fluid, salt overload
Anaemia
Pulmonary embolism
Drugs – b blockers, NSAIDs
What treatment?
• Not taking tablets
• Side effects of tablets
• Further ischemia or
infarct
• Progressive disease
• Supervise, explain, box
• Stop these
• Treat ischemia, angioplasty,
increase antianginal meds
• Optimise meds
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AF
Fever
Thyrotoxicosis
Fluid, salt overload
Anaemia
PE
Control rate or revert
Treat infection
Make euthyroid
Diurese, fluid restrict
Transfuse
Anticoagulate
Treatment for CCF
• Increasing diuretics is not always best
treatment
• Work out patient’s base weight – from
asking them or from chart
• Patients often respond to pulses of
diuretics – aim for previous well weight,
ankle oedema means 3 – 5 Kg in XS,
sacral oedema is > 5 kg
Treatment for CCF
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Fluid and salt restrict – but hard for patients
Diuretics, K supplements
ACE inhibitors, ARB
b-blockers – sotalol, bisoprolol
Spironolactone
Treatment for severe fluid overload
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Fluid restriction to 1.5 or 1 L a day
Extra pulses of lasix
Lasix, chlotride, amiloride/aldactone
Strict bed rest
Stockings
Try to maintain blood pressure - risk of acute
renal failure from reduced intravascular volume
Combination of heart failure and
renal failure (end-stage CCF)
• Aim is to have patient free of symptoms
• Not SOB, not uremic (sleepy or confused) and
not dizzy when they stand up (postural
hypotension)
• Don’t worry too much about the serum creatinine
(symptoms correlate better with urea level)
• Takes days to sort out compartments
• Best done at home by GP if at all possible
• Generally poor outcome
How do you tell the difference
between heart failure and pneumonia?
• Clinical signs may be identical
• Pneumonia
– Look toxic
– Yellow-green sputum
– Fever at any time since presentation
– High CRP
– CXR – localised alveolar opacity, no
upperlobe diversion
• CCF and pneumonia commonly coexist
Pneumonia that does not
improve
How do you know a patient is improving
• Ask them
• Improvement usually starts within 12 hours of
starting antibiotics
• Less sputum
• Fever starts to subside
• Crepitations start to clear
• Arterial saturations improve, less need for O2
• Lack of progression
• CRP falls quickly
• Finally radiological abnormalities clear
When pneumonia does not improve
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Wrong antibiotic eg atypical pneumonia
Pneumonia too extensive – often in middle-aged men
Wrong disease eg acute cholecystitis
CCF present too
Continued aspiration
Poor sputum drainage – helped by physiotherapy
Elderly, frail, comorbidities impairing immune status
Pleural effusion, abscess, empyema
Bronchiectasis
TB
Cancer
Bronchiolitis-obliterans organising pneumonia (COP)
Acute renal failure
• Once renal function is abnormal, it will
continue to deteriorate (‘hyperfiltration
hypothesis’)
• Must try to get renal function back to base
line to prevent deterioration to chronic
renal failure
• Rapidly progressive glomerulonephritis – a
medical emergency – glomerular
haematuria and RBC casts
Acute or chronic renal failure?
• Ask the patient about renal function, refer
to old records
• Small kidneys in CRF on ultrasound
• Hb, Cr and Urea and Ca/P are not always
helpful, PTH takes too long
• Often acute-on-chronic renal failure - work
out baseline renal function and hope to
recover to this
Tests in RPGN
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ANCA
antiGBM antibodies
ANA and antidsDNA antibodies
ASOT and antiDNase B
Hepatitis B and C serology
Cryoglobulins
antiPLAR2 antibodies
IgA
C3 and C4
Renal biopsy
Treatment of ARF
• Treat underlying cause – hypotension,
sepsis, obstruction
• Stop or monitor all renally-excreted drugs
• Low protein, low K diet
• Treat fluid overload - fluid restriction
• Treat hyperkalemia, acidosis
• Dialysis – fluid overload, K, acidosis, uremia
Diagnostic tests
• You should use tests to confirm your clinical suspicions
• Do not ignore an abnormal test but think it means
• Always have a reason for requesting a test – there is no
need to repeat FBE and U/E more than twice weekly in
stable hospital inpatients
• CRP is a very useful test – indicates inflammation is
present and the amount of inflammation
• All medical admissions warrant FBE, U/E, LFT, Ca, P,
RBS/HbA1C and usually CRP. Vit D is often worthwhile.
We have no good test for malnutrition.
Iron deficiency
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Lethargic
Anaemic, peptic ulcer disease, aspirin use
Have a high index of suspicion
Hb and MCV may be normal
Iron deficiency
• Aspirin – even low dose for cardiac
disease
• Dieting
• Menstruation, pregnancy, breast feeding
• Renal failure
• Coeliac disease
• Gastrointestinal tract ulceration, GORD
• Ca bowel
Examination
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Conjunctival pallor – Hb < 100
Koilonychia, brittle nails
Hair loss, stomatitis, dull skin
BP lying and standing
Abdominal examination, epigastric
tenderness
• PR examination
Treatment
• Ferrogradument/VitC – one a day for at
least 4 months
• Blood transfusion
• Iron infusion
• Proton pump inhibitor
• Lower dose aspirin or clopidigrel
• Check ferritin level 3 months after end of
treatment
Rapid fall in haemoglobin
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Wrong blood sample
Haemodilution
Blood loss
Anaemia of chronic disease/active
inflammation
• Laboratory variation
Microcytic anaemia
• Iron deficiency
• Anaemia of chronic disease
• Thalassemia – MCV – constant thru’ life
Anaemia of chronic disease
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Lowish haemoglobin
Normal or low MCV
Unable to use iron, high ferritin
High CRP
Together with iron deficiency – low-N
ferritin, may respond to iron infusion
Macrocytosis
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Liver disease
Alcohol
Hypoxemia
B12/folate deficiency
Medications eg azathioprine
Myelodysplasia
Reticulocytosis, hypothyroidism, cold
agglutinins
B12 deficiency
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20% due to pernicious anaemia
B12 malabsorption
Gastrectomy
Vegans
Terminal ileal disease
Pregnancy, OC
Myeloma, elderly
Pernicious anaemia
• Blood film – larger RBC, hypersegmented
neurotrphils, cytopenias
• Intrinsic factor antibodies,
• High serum gastrin
• Schilling’s test – rarely performed now
• Holotranscobalamin II
Haemolysis
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Uncommon
Fall in haemoglobin
Increase in unconjugated bilirubin
Increased reticulocytes
Increased LDH
Low haptoglobins
Specific tests for cause
Haemolysis
• Blood film is really helpful
– Hereditary spherocytosis – spherocytes
– AIHA – spherocytes
– G6PD deficiency – bite and blister cells
– TTP – fragmented RBC
– Sickle cells
– Cold AIHA – agglutinated cells
Neutropenia
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Medications
Sepsis
Infections
Marrow infiltration
Neutrophilia
• Stress/steroids
• Infections
• PRV
Thrombocytopenia
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Severe sepsis
Medications – cytotoxics, alcohol, heparin
ITP
Aplastic marrow
Hypersplenism
Marrow infiltration
Thrombocytosis
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Inflammation
Iron deficiency
Acute blood loss
Essential thrombocystosis/PRV
C reactive protein
• Monocytes, macrophages release cytokines that
cause liver to produce CRP
• CRP binds foreign pathogens and damaged cells,
activates complement and is chemotactic for
monocytes
• Marker of inflammation
• Highest in bacterial infections (>100 mg/L)
• Increased in rheumatoid arthritis, inflammatory
bowel disease, malignancy, after surgery, gout
• Not affected by anaemia, CCF, polycythemia
(unlike ESR)
• Earlier rise, falls more quickly than ESR