PACES Flashcards
What are the indications for a VATS
Vats is a video assisted thoracoscopic surgery and is used primarily for pulmonary, mediastinal, and pleural pathology.
Indications include biopsy, wedge reseciton, lobectomy, bullectomy, pneumonectomy as well as treatment for recurrent pneumothorax like pleuradehesis and recurrent effusions
VATS vs Thoracotomy
VATS has a typical 3 pronged scar - but can be 2 or 1.
Thoracotomy is usually lateral and transverse scar across the anterior/posterior chest wall.
Benefits of VATS =
Quicker recovery, less pain, shorter hospital stay, quicker return to chemo, older people may qualify vs thoracotomy.
Thoracotomy may be surgically necessary and VATS has a higher pneumothorax rate post operatively vs Thoracotomy. (5% vs 1%).
Respiratory Causes of Clubbing
Lung cancer (all except small cell)
Chronic suppurative lung disease (cystic fibrosis, bronchiectasis, lung abscess, empyema)
Pulmonary fibrosis
Classify Lung Cancer
Lung Cancer can be generally grouped into small cell or non small cell lung cancer.
Non small cell is much more common and has 3 histological groups.
- Squamous Cell (Most common) Associated with smoking. Decent prognosis. Central Tumour (PTH secretion- high Ca)
- Adenocarcinoma (20%, Non smokers, Asbestos) is a peripheral tumour
- Large Cell (Central and Bad Prognosis)
Then Small cell lung Ca has the worst prognosis:
- Small cell lung cancer (30%) has a poor prognosis due to the stage of disease at presentation being advanced. (SIADH and Cushings)
Biological vs Mechanical Heart Valves
Heart Valve Replacement is still an important therapy despite the decline in rheumatic heart valve disease. Most commonly replaced valves are the aortic and mitral and the options are broadly biological (bovine or porcine) and Mechanical.
The benefits of biological valves is that the patient won’t require life long anticoagulation. However, these are more prone to mechanical damage over time and so have a much reduced life span of 10-15 years.
Mechanical valves are much more durable but require life long anticoagulation.
(Bileflet valves most common and Ball and Cage rarely used due to need for higher INR and more clot formation).
What is a paraparesis?
Paraparesis is bilateral weakness in the lower limbs
Paraparesis suggests at least a meylopathy (spinal cord issue) of the thoracic level. However, if you’ve only done the legs, you’d need to do the arms to ascertain if this was cervical myelopathy. You would be able to then find a level and also have normal cranial nerves.
What would you expect to find in cervical meylopathy?
Cervical meylopathy is disease of the spinal cord at the level of the cervical spine. My examination findings would reflect this with likely upper motor neurone signs througout the arms and legs - notably, spasticity, hyperreflexia, motor loss +/- sensory loss.
I would be expecting to be able to find a sensory level.
What are the differentials for a meylopathy?
Compressive:
Disk Herniation, tumours - intra or extra medullary - primary or secondary. and spinal stenosis
Autoimmune: MS, Lupus and sarcoidosis
Infectious: HIV / Varicella
Nutritional: Vitamin B12 / Copper
Hereditary: Genetic causes of spastic paraperesis
What is paraplegia
Total loss of movement in the legs
Tetraparesis
Loss of motor and likely sensory in all 4 limbs - pointing to a cervical spine lesion
brown sequard syndrome findings and definition
Loss of motor on the same side of the lesion
Loss of vibration and fine touch on the same side of the lesion
Loss of temperature and pain on the contralateral side of the lesion
i know that the majority of fibres decussate in the medula - like in normal stroke. So I know that the lesion will be ipsilateral in spinal cord disease.
What is bss? It is hemisection of the cause causing a partial myelopathy with ipsilateral motor and fine touch loss and contra lateral pain and temperature loss
Peripheral stigmata of chronic liver disease?
Jaundice
Asterixis (Liver flap)
Palmar Erythema
Clubbing
Jupitons Contracture
Echymosis
Signs of decompensation
Encephalopathy
Jaundice
Ascites
Coagulopathy
Differentials of Chronic Liver Disease
Most common cause of liver disease is alcoholic liver disease.
Next I would like to think about Infective causes like Hepatitis B, and C and also consider sending an HIV test. Tattoos and risk taking behvaiour like IVDU may be relevant risk factors for this
The Next cause to consider is MASH metabolic associated steotohepatitis (Formally Non Alocholic). I’d be looking to take the BMI, look for other risk factors like evidence of hypercholesteromaemia, blood pressure and blood sugars.
Following this I’d be thinking about immune causes. These would notably be autoimmune hepatitis, primary biliary colangitis and primary sclerosis cholangitis which is associated especially with IBD.
Following on from this, I would think about Iron and copper storage disorders including Haemochromatosis and Wilsons and I’d also want to conisder Alpha 1 antitrypsin deficiency if there was evidence of Emphysema.
Malignancy would also be important to consider. This could be primary or secondary.
I’d also consider various drugs - notably amiodarone if cardiovascular patient and also methotrexate
Investigations of chronic liver disease
FBC - look at anaemia / acute hb drop and also platelets - increased sequestration in portal hypertension.
Next would be Renal function.
Notably I would want to check if the patient is heading to renal failure. Are they dehydrated. Is there evidence of hyponatraemia due to the RAAS activation and is there a high urea (we’d expect low in CLD) which would therefore perhaps be suggestive of a GI bleed.
Following this I would look at the LFTs
Notably, is the bilirubin raised
Is the hepatic enzymes raised and what kind of picture is it - cholestatic suggesting a biliary cause or hepatic. I could also look at the AST: ALT ratio at this point.
Then I’d want to check the synthetic funciton of the liver. Notably looking at the ablumin and the clotting screen for the patient.
Following this my investigaitons would be more focused on cause. For this I’d want to send things like Auto antibody screens, immunoglobulins, amylase or lipase, iron studies including tranferrin saturations and ferritin. Copper and caerulosplasmin as well as viral hepatitis screens. Tumour markers may also be appropriate and I’d send the majority of these tests off in a NILS - non invasive liver screen.
Following this, we can consider imaging. The primary test I’d go with is an US due to the low radiation and good views we can achieve of the liver. Notably, we’d be able to assess for hepatosplenomegaly and the presence of ascites. Following this, we could also try to view the gall bladder.
Other radiology to consider would be a fibroscan in the context of cirrhosis as a differential as well as CT if our initial radiology didn’t find anything.
At this point in the patients work up I’d expect the gastroenterology team to be involved and we’d consult them with regards to further investigations, notably a biopsy and if this was appropriate. Dependent on the aeitiology and presence of complicaitons of Chronic liver disease, there may be a scope for endoscopic investigations like OGD, MRCP as well as colonoscopy.
Causes of a sensory peripheral neuropathy?
Metabolic causes
Commonest is diabetes
Hypothyroidism
Vitamin deficiencies. B12, B6 and B1
Toxic Causes
In this I could put alcohol at the top of my list. Then i’d think about chemotherapy agents including platinum based drugs and vincristine. Other drugs like antibiotics (Ethanbutol, antivirals)
Nitrous oxide would be an increasingly common cause from illicit drug use.
Other causes i’d think of would be immune mediated causes, in systemic disease like GPA or rheumatoid arthritis.
Or Neurological diseases like CIDP and Gillan bare.
Infection like HIV
Sensory Neuropathy Acronym
DAM IT BICH
DIABETES
Drugs/Toxins:
Heavy Metals, Vincristine, Nitrofurantoin
Alcohol
Metabolic
Diabetes, hypothyroidism, uraemia
Infection/post infection: HIV/Lymes/GBS (usually predominantly motor)
Tumor: Paraneoplastic like Lung or Myeloma / MGUS (Think of grandad)
B - B1, B6, B12
Idiopathic
Connective tissue diseases and vasculitis
Hereditary Causes
Purely motor peripheral neuropathy
GBS
Diabetes
Hereditary motor and sensory neuropathy
Rare causes like acute intermittent porphyria, lead poisoning and diptheria
Deformity and condition?
Rheumatoid arthritis
Boutonniere Deformity
Deformity and condition?
Rheumatoid Arthritis
swan neck deformity
Deformity and condition?
Heberden node of Osteoarthritis
Heberden is distal IP
Boucharrds is proximal
Deformity and condition?
Boucharrds node is proximal
Probably some heberden nodes distally here too of OA.
Mitral Regurgitation signs other than murmur
Signs of severity?
REMEMBER - MITRAL VALVE IS IN THE LA - AF, LV dilatation / failure.
Murmur
Pan systolic Murmur Apex/ going to the axilla. louder on Exhaled.
Other signs:
AF
Displaced Apex Beat
Signs of severity
Displaced Apex Beat
LV Failure
Wide Split S2
Left venticular dilatation indicated by a displaced apex beat
signs of left ventricular failure
Wide split S2 - this is because Aortic (A2) is premature due to half the blood going into the LA through regurgitant valve
Signs of Aortic stenosis other than murmur
Signs of severe Aortic Stenosis
Aortic Stenosis is a ejection systolic murmur heard loudest in the aortic region which radiates to the carotids
Signs other than the murmur are
Slow rising pulse
Narrow pulse pressure
Heave (undisplaced) due to hypertrophy of the left ventricle
Signs of Severity include
timing of the ejection systolic murmur is more delayed in increasing severity
soft s2
Narrow or reverse split S2 - A2 is increasingly delayed
Apex beat Displaced due to dilatation of the ventricle
Gallavardin phenomenon
radiation to apex of AS to mimic MR
Differentials of an ejection systolic murmur
Aortic Stenois
Pulmonary Stenosis
Aortic sclerosis - calvified valve without restricition on function - no radiation to carotids and normal pulse pressure.
Subvalular (HOCM with LV outflow tract obstruction)
Supravalvular like Williams syndrome lesions
Flow Murmur.
Causes of Aortic Stenosis
Most common is Degenerative disease
Other acquired causes include calcification accelerated by CKD or Severe Pagets.
Rheumatic Fever - normally mitral involvement
Infective endocarditis
Congential casues: Valvular - bicsupid aortic valve.
Fixed Split S2
Think ASD - there is communication between R and L side of the heart allowing for pressures to normalise on inspiration and expiration
What is reverse splitting of S2
S2 if split should increase with inspiration
This is because Aortic valve shuts before Pulmonary. Then as you inspire, the R sided volume increases and so P takes longer to shut. This increases the splitting.
However, reverse splitting is where the S2 splitting increases on expiration.
This would mean that the Aortic Valve is delaying to the point where it is shutting last. This is seen with LV outlet obstruction like Aortic Stenosis or LBBB.
Causes of Hepatomegaly
CCF
TR
Malignancy
Lymphoma
Malaria / Leishmaniasis and hepatitis
Scoring system for acute alcoholic hepatitis
Maddrey’s discriminant function test. PT and Bilirubin. if > 32 for Steroids as high mortality rate.
Treatment of Alcoholic hepatitis = supportive. Nutrition, BO, fluids, infection treatment, abstinence from alcohol and steroids if Maddrey’s > 32
AScites in the absence of stimata of Chronic liver disease?
Think Malignancy. Palpate for the spleen and for lymphadenopathy - cervical / axillary and offer others…
Causes of splenomegaly:
Malaria (Chronic)
Schistosomiasis
Kala-azar (Leishmaniasis)
Lymphoproliferative disease: normally lymphadenopathy and hepatomegaly.
CML, Meylofibrosis - massive.
Lymphoma, CLL and cirhosis with portal hypertension
EBV
CMV
Felty’s syndrome
Felty’s syndrome?
Prescence of 3 conditions
RA
Splenomegaly
NEutropenia
It effects < 1 % of people with RA.
Unkonwn aitiology but puts people of increased lung and skin infections.
Hyperpigmentation, anaemia, thrombocyptenia (splenomegaly)
S
Why low platelets in alcoholic liver disease
thromobcytopenia may be present secondary to increased sequestration of platelets in the spleen. This is due to increased portal hypertenion from cirrhosis.
There is also a direct toxic afect of alcohol on production and folate deficiency can also contribue.
May increase after 5 days off the booze.
< 50 + bleeding = transfuse
Causes of hepatosplenomegaly
Infective:
1. Malaria (Chronic)
2. Visceral Leishmaniasis - Kala-azar - severe protozoan infection spread by sandflies
3. Schistosmiasis (Bilharzia) low mortality and high morbidity.
Myeloproliferative and lymphoproliferative disesase
Cirrhosis with portal hypertension
Uncommon is storage
Wilsons disease
Haemochromatosis
Glycogen storage disorders
Kayser fleisher rings?
Wilsons
What is sarcoidosis
Inflammatory multisystem condition characterised by the formation of granumlomas
Common in black females 20-40
Pulmonary manifestations of sarcoidosis
Hilar or Mediastinal lymphadenopathy
Pulmonary Nodules
Pulmonary Fibrosis
Diagnosis of Sarcoidosis?
Blood tests
Serum ACE
CRP
Calcium
CXR
Lymphadenopathy
HR CT Chest
MRI Brain
PEt Scan
HISTOLOGY IS GOLD STANDARD - BRONCHOSCOPY / Skin Biopsy
Histological findings of sarcoidosis?
Non Caseating granuloma of epithelioid cells
Lofgrens syndrome?
Triad of
Joint pain and Skin rash (Erythema Nodosum)
On CXR
Hilar Lymphadenopathy
THIS IS SARCOID
Treatment of Sarcoid?
None - trial to see if self limiting 60% resolves in 6 months
Prednisolone Long term - need bisophosphonate replacement, as well as gastro protection
Then Methotrexate or Azothiparine
Lung Transplant
Why do you die of sarcoid?
Heart involvement - Fatal Arrythmia
Or CNS involvement
Causese of Liver Transplant
Cirrhosis, HCC, Acute Liver Failure
Side Effects /Complications of Liver Transplant immunosuppression
Ciclosporin - Gum Hypertrophy
Tacrolimus Tox - Tremor
Steroids - cushingoid
Skin malignancy / pre malignant changes - check for scars in sun exposed areas
Causes of Cirrhosis
Alcoholic Liver Disease
Non Alcoholic Fatty Liver Disease
Chronic Viral Hepatitis
Autoimmune Chronic Liver Disease
Wilsons, Haemochromatosis
Alpha 1 antitrypsin Deficiency
Contraindications to Liver Transplant
IVDU, ongoing alcohol excess,
Significant Med/Psych co morbidities
Prior Malignancy
Elective Liver Transplant vs Super Urgent
Elective: CLD / Failure with Score of 49 or more
HCC: No spread and set criteria
Super Urgent transplant example criteria?
pH 7.25 or INR > 6.5 24hrs post paracetamol
Survival Post Liver Transplant
90% 1 year, 75% 5 years
Complications post transplant
Episodes of Rejection
Immunosuppression:
Infections - viral bacterial or fungal
Increased risk of malignancy
- Skin
- Post Transplant lymphoproliferative disorder
Metabolic Syndrome - HTN, Insulin Resistance, Obesity
Avoid Live Vaccines
CKD / Chronic Liver Disease
Recurrence of certain native disease
CLD / Ascites Blood tests?
FBC
Anaemia / Infection - think SBP
Renal
Urea - usually low ? High ? Bleed
LFTs
Hepatic / Biliary disease
Albumin and Clotting
- Synthetic function
Paracetamol Level
Non invasive Liver Screen
- Ferritin and iron studies
- Copper and Caeruplasmin
- Hepatitis Screen (Viral Serology)
- Auto antibodies
- AFP - ? HCC
US - portal vein patency
Echogenicity of the liver
CXR - ? CCF
Ascitic Tap Testing
SAAG
Subract the ascitic albumin from the serum albumin taken on the same day
Prescence of 1.1 g / L Gradient = portal hypterension
Causes of a high SAAG
Cirrhosis, Budchiari CCF, Meigs, Nephrotic Syndrome
Causes of a low SAAG
Peritoneal Carcinoma, TB, Pancreatitis
Ascitic fluid assessment for infection
Rapid cell count if Neutrophils > 250 think SBP
Gram stain, ZN Stain, culture and lipase.
Haemochromatosis inheritance
HFE gene on chromosome 6
Autosomal Recessive fashion
Presentation of Haemochromatosis
- Asymptomatic either on screening of family first degree relatives or through routine blood tests with abnormally high ferritin
- Symptomatically: Multi system condition with fatigue, joint pain or swelling, skin changes.
Later complicaitons may be diabetes / cardiomyopathy
Screening of haemochromatosis
Ferritin 200 (F), Ferritin 300 (M)
Transferrin sat > 40% in F , 50% M
Variable penetrance of HFE defective gene
Monitoring of Haemochromatosis
Complications of the disease screening
HbA1c every 6 months
Liver US every 6 months looking for cirrhosis
Regular AFP - HCC
ECHO - cardiomyopathy
Liver Biopsy not required for diagnosis but may indicate severity of disease
Haemochromatosis treatment
Blood letting or venesection
Guideded by Transferrin sats - once normal can stop weekly and go to less frequent - perhaps monthly but this can be guided further by blood tests - ferritin and transferrin saturations
Other tx includes mangement of complications - Cardiomyopathy and diabetes and cirrhosis
LV dysfunction and Cirrohsis with treatment is to a degree reversible
Alcohol abstinence is important to council if there is cirrhosis
Joint pain may be treated with analgesia / inflammation
Joint swelling in haemochromatosis
Classically causes squaring of the joints
Also on X ray will have significant costrocalcinosis vs osteoarthritis
Splenectomy
L UQ
Heredetary spherocytosis
Anaemia, jaundice and splenomegaly
Autosomal dominant inheritance with 5 genes that code for proteins on the RBCs being defective.
Presentation
Neonatal Jaundice
Faitigue and anaemia in older adults
Gall stones
screening of first degree relatvies
Complications of heredetary spherocytosis
Aplastic Crisis - haemolytic - increased spelnic activity in infection or Aplastic infection (Pavovirus)
Anaemia - blood transfusions
Gall stones - cholecystectomy
Diagnosis Heredetary Spreocytosis
FBC - reticularcyte count
MCH
Blood smere - spherocytes
LDH
Haptoglobin
split bilirubin
Coombes test to rule out an immune mediated haemolysis
Heredetary Spherocytosis
EMA binding test
Osmotic fragility test
Treatment of Heredetary Spherocytosis
Folic Acid
Treatment of Anaemia - looking at replacement with blood transfusions
If severe, consideration with regards to splenectomy would be considered.
We’d want to make sure the patient had had their vaccines for encapsulated organisms such as pneumococcal before splenectomy. Following this, the patient would also require antibiotic prophylaxis normally with Pen V and ongoing vaccines.
Isolated Splenomegaly Differentials?
CML
Myelofibrosis
Malaria
EMA Binding
Heredetary Spherocytosis
This is basically a die that binds to the proteins and the mean flurescence is lower in spherocytes when looked at under eletropheresis
Osmotic Fragility
Erythrocyte resistence to haemolysis whilst being exposed to varying NaCl Solutions.
caeliac disease
Gluten intollerence
Bloods
Anaemia / mal absorption
If thinking about caeliac and ruled out kindey or liver abnormality, then go onto look at anti TTG or Anti Tissue Transgluctaminase antibodies. These may be positive if on a gluten diet but if already abstaining may be low or borderline. If Caeliac still working diagnosis, R/o with a OGD and D2 biopsy looking for villous atrophy
Pancreatic and Kidney Transplant
For type 1 but increasingly type 2 diabetics. The idea is to treat the underlying cause of the Kidney End Stage Renal Disease as well as rididng the patient of insulin therapy and allowing the graft to benefit from lack of microvascular complications of diabetes.
There is contention as to whether the pancreatic transplant improves diabetic retinopathy in these patients.
The pancreas transplant was previously plummed into the bladder for drainage but there were complications of reflux pancreatitis and frequent UTIs.
Following this, the patients now have transplanted pancreas’s drain into the small bowel.
Child Pugh Score ?
Cirrhosis
Psuedoasthetosis
Writhing movements on eyes closed
- Sensory Ataxia
differential for chorea
Sydenhams chorea is a post infection chorea that is seen in Rheumatic fever. If in conjunction with MR can consider Sydenham’s chorea
Other differentials would include huntingtons disesase
CAG repeat error on Chromosome 4
It is inherited with anticipation aka earlier onset.
Typical onset is 30-50
Neuropsychiatric and dementia symptoms as well
Other differentials :
ON blood tests rule out
Polycythemia
Thyrotoxicosis
Pregnancy
Then think drugs
OCP
Levodopa (PArksinsons over treatment)
Antipsychotics
Fibrosis Dx
CHARTS upper
Rasco Lower
CHARTS
Coal/ Silicosis
Hystocytosis
Aspergillos
Radiation
TB
Sarcoidosis
RASCO
Rheumatoid Arthritis
Asbestosis
Scleroderma
Cryptogenic fibrosisng alveolitis
Other:Drugs
Bleomycin, amiodarone, methrotrexate, Nitrofurantoin, gold
Bronchiecatsis causes
Congenital or aquired
Congenital= CF
Primary Ciliary Dyskinesia
Hypogammaglobulinaemia
Aquired
Post infection (including measles and whooping cough)
Post obstruction / local foreign body like TB or tumor
Allergic bronchopulmonary aspergillosis
Explain DLCO / TLCO
Diffusion Capacity or transfer capacity of Carbon Monoxide.
is a functional test of the lungs diffusion with surrogate CO.
Highlights pathology with 2 variables
Decreased perfusion to the lung
Decreased SA alveolar / increased diffusion distance.
Low TLCO:
Low Perfusion causes:
CCF, PE, Pulmonary Hypertension, Pulmonary Artery Damage (SLE/ SSc), Anaemia
Low Diffusion Causes:
Intrinsic Restrictive lung disease
COPD - Emphysema
Normal TLCO:
Normal Individuals
Extrinsic restrictive lung disease (Kyphoscoliosis or NM disease)
Bronchitis
Asthma
High TLCO:
You can only increase perfusion - not increase alveolar diffusion… so think increased perfusion
Athletes - literally the point of fitness
Left to Right Cardiac Shunt
CHF (Diastolic Dysfunction)
Alveolar Haemorrhage
Erythrocytosis
Blood Transfusion
treatment of idiopathic pulmonary fibrosis
pirfenidone
