Conditions Flashcards

1
Q

Anaemia

Clinical features of Fe Def vs. Haemolytic anaemia + general anaemia features

A

Fe Def

  • Koilonchyia (spoon shaped nails)
  • Glossitis
  • Angular chelitis
  • Hx of bleeding - menstrual, PR
  • Hx of low Fe diet

Haemolytic

  • Jaundice
  • Splenomegaly
  • Hx of recent medications - penicillins
  • Hx of infection - EBV, mycoplasma, malaria
  • Hx of lymphoma
  • Hx of rheumatoid conditions (RA, SLE)
  • Hx of cardiac issues (i.e. mechanical heart valve)
  • Dark urine
  • Itch/excoriation marks
  • Hx of travel

General anaemia

  • Pallor of palmer creases, conjuctivae
  • SOB
  • Palpitations
  • Systolic flow murmur
  • Dizziness (postural hypotension)
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2
Q

Anaemia

Ix for haemolytic anaemia

A
Normocytic anaemia (may be macrocytic if very high reticulocyte count)
Increased LDH (RBC enzyme)
Increased bilirubin
Decreased haptoglobin 
Blood films - spherocytes, bite cells (G6PD deficiency), fragments, polychromasia, malaria 
Reticulocytosis 
Direct coombes test - autoimmune cause 
Serology - EBV, mycoplasma
Urinary urobilinogen
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3
Q

Anaemia

Causes of haemolytic anaemia

A
Autoimmune
Drug induced (penicilin)
Infection - malaria, EBV, mycoplasma 
G6PD deficiency 
Cardiac i.e. mechanical valve 
HUS - shigella toxin 
DIC
Sepsis
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4
Q

Falls & #NOF

How can diabetes contribute to falls risk?

A
  • Visual impairment (diabetic retinopathy, hyperglycaemia, increased risk of glaucoma + cataract)
  • Hypoglycemia from medication
  • Peripheral neuropathy - decreased proprioception
  • Autonomic neuropathy - orthostatic hypotension
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5
Q

Falls & #NOF

Intra-capsular vs. Extra-capsular hip fracture, management and potential specific complication

A

Intra-capsular is subcapital fracture (through neck of femur). Risk of AVN as blood supply to head of femur (femoral circumflex artery) is distal to proximal, thus a fracture will disrupt it
Managed with open reduction + internal fixation or arthroplasty
More common in elderly, particularly elderly

Extra-capsular = subtrochanteric (below the trochanter) and intertrochanteric (fracture through the line of the trochanters)
May be stabilised with an internal dynamic hip screw

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6
Q

Complications of fractures

A
AVN - scaphoid, navicular, NOF
Malunion, non-union, delayed union 
Osteomyelitis 
DVT/PE - particularly orthopedic 
Osteoarthritis 
Nerve damage
Compartment syndrome
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7
Q

DKA

Clinical features

A
Kussmaul breathing (deep, laboured), tachypnoea 
Tachycardia 
Postural hypotension
Decreased JVP, increased capillary refill time, dry mucus membranes, decreased tissue turgur 
Acetone breath (sweat, fruity)
Generalised abdo pain 
Confusion, decreased GCS
Nausea + vomiting 
Polyuria, polydipsia
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8
Q

DKA

Precipitating factors

A
Infection
Infarction - MI, CVA
Trauma
Surgery 
Lack of insulin - compliance, inadequate dosage
Drugs - steroids, thiazide diuretics 
Pancreatitis 
Alcohol
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9
Q

DKA

Pathophysiology of DKA

A

Lack of insulin - glucose can’t enter cells - relative starvation state

  • Lipolysis - fatty acids - acetyl-CoA - ketones
  • Proteolysis - ketogenic amino acids - ketones
  • Hyperglycaemic osmotic effect - polyuria - dehydration - polydipsia

Ketones are acidic - decreased blood pH (metabolic acidosis)

  • Respiratory compensation - hyperventilation, kussmaul breathing
  • Act on CTZ - nausea + vomiting
  • Tachycardia
  • Abdominal pain
  • Exhaled - sweet, fruity (acetone) breath
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10
Q

DKA

Investigations for DKA

A

Serum/urine ketones - normally not present/low levels
BGLs - will be extremely high
ABG - Metabolic acidosis with respiratory +/- renal compensation (depending on time frame)
U&Es - normal or hyperkalaemia (body stores actually replete, shift in the compartment), bicarb low due to compensation, urea may be high from dehydration

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11
Q

IBD

Features on colonoscopy (UC vs. CD)

A

UC

  • Continuous lesions
  • Ulceration
  • Oedema
  • Affects rectum predominatly but may ascend, but never involves small bowel

CD

  • Patchy distribution of lesions (skip leisons)
  • Cobblestone appearance
  • Affects any part of bowel but spares rectum
  • Strictures may be present
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12
Q

IBD

Histological features (UC vs CD)

A

UC

  • Partial thickness of bowel wall (mucosa only)
  • Crypt abscess
  • Goblet cell depletion

CD

  • Transmural involvement
  • Non-caseating granulomatous inflammation
  • Dense lymphocyte infiltration and aggregates
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13
Q

IBD

Clinical features

A

Constitutional symptoms - fever, wt loss, anorexia
Abdominal pain (generalised)
Diarrhoea
Arthropathy

More CD
Dermatological (erythema nodosum, pyoderma gangrenosum)
Perianal disease (fissure, skin tags)
Mouth ulcers
Association with sacralilitis, AK, arthritis

More UC
Bloody diarrhoea
Tenesmus (incomplete emptying)
Urgency 
Associated with primary sclerosing cholangitis
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14
Q

IBD

Complications (CD vs UC)

A

UC

  • Toxic megacolon - risk of perforation
  • Increased risk of CRC
  • Primary sclerosing cholangitis
  • Fe-deficiency anaemia
  • VTE

CD

  • Toxic megacolin
  • Stricture - SBO
  • Fistula
  • Abscess
  • Malnutrition, osetomalacia
  • renal stones
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15
Q

IBD

Management of UC

A

Inducing remission

  • 5-ASA (rectal more effective than oral)
  • 2nd line = corticosteroids
  • If severe may require admission with supportive care
  • DVT prophylaxis

Maintenance

  • Oral 5-ASA
  • Surgery - can be cured with protocolectomy + ileostomy
  • Surgery indicated if medical treatment fails or complications
  • Infliximab in refractory disease
  • Regular gastro review, colonoscopies and LFTs for surveillence of disease activity, complications, drug side effects

5-ASA S/E - headache, rash, megaloblastic anaemia, oligospermia

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16
Q

IBD

Management of CD

A

Inducing remission

  • Oral corticosteroids
  • May use adjunct immunosuppresion (azothioprine, methotrexate)
  • 5-ASA less role but may be 2nd line to steroids
  • Metronidazole may be helpful if isolated perianal disease
  • Enteral feeding may be used initially or in addition
  • DVT prophylaxis

Maintaining

  • Immunosuppresion (azathioprine)
  • Smoking cessation
  • Methotrexate 2nd line
  • Infliximab in refractory disease
  • Regular gastro review, colonoscopies and LFTs for surveillence of disease activity, complications, drug side effects
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17
Q

Rheum

Which cervical joints most commonly affected in RA?
When should this be considered in particular?

A

C1/C2

Anaesthetic assessment consideration - may affect ability intubate due to decreased neck mobility

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18
Q

MSK

Typical management for a humeral fracture?
What is the most common injured structure?

A

80% are non-displaced # therefore can have conservative management (collar and cuff sling, pain management and early mobilisation)

Radial nerve

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19
Q

MSK

Clinical features of meniscal tears

A

Twisting movements resulting in immediate pain, instability, difficulty weight bearing
Clicking, locking of joint
Effusion may occur 24-48 hours later

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20
Q

MSK

Specific complication of a Colle’s fracture (non-displaced distal radius fracture)

A

Carpal tunnel syndrome

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21
Q

MSK

What is a positive Trendelenburg sign and what does it indicate?

A

Stand on one hip, if the pelvis drops down on the opposite side of the stance leg it is positive

The pathology is on the side of the stance leg

Weak hip abductors (gluteus medius and minimus)

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22
Q

Rheum

Poor prognostic features and increased disease activity in RA

A

High RF titre
Elevated ESR
Young age of onset

Anaemia of chronic disease
Increased platelets
Increased CRP
Erosions on xray

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23
Q

Rheum

What is the most common form of SLE renal disease?

A

Diffuse, proliferative glomerular nephritis (Class IV)

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24
Q

Derm

Risk factors for SCC of skin?

A

Topical arsenic preparations
Smoking
Sun exposure - significant burns
Immunosuppresion i.e. post-transplant

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25
MSK Management of open fracture
Remove foreign material Wash out with saline Cover with sterile dressing with antiseptic IV antibiotics Tetanus prophylaxis Reduce and immobilise Prepare for surgery - orthopaedic emergency - needs wash out
26
Rheum Diagnosis + Ix of RA
Diagnosis based on points system (>6 points for diagnosis) Criteria involves: - Pattern of joint involvement (small joints more diagnostic) - Serology - RF and/or Anti-citrullinated protein (ACPA) +ve - ESR and/or CRP +ve - Duration > 6 weeks Other Ix - FBE - anaemia of chronic disease (disease activity) - XRAY - Loss of joint space (uniform), bony erosions, soft tissue swelling, juxta-articular osteopenia RF +ve in 70%, not specific, high titre prognostic and associated with higher disease activity ACPA specific for RA
27
Neuro Features of a common fibular (peroneal) nerve leison
Foot drop (high stepping gait) Lateral leg sensory loss Inability to dorsiflex or evert the foot Bumper-bar accident, compression from plaster cast
28
Rheum Clinical features of Gout
Red, hot, swollen joint Very painful Can be associated with fever Clinically impossible to distinguish from septic arthritis Usually first MTP joint (podagra), ankle or midfoot affected Often occurs in middle of the night, sudden onset (cool temp, lower pH) Long term may be associated with deposits of crystals in soft tissue (tophi) and renal issues (stones, interstitial nephritis) Can be triggered by allopurinol, diuretics (thiazide), infection, trauma, surgery
29
Rheum Investigation features of Gout
XRAY - juxta-articular punched out erosive leisons Acute attack usually normal or low uric acid (need to remeasure after) Negatively bifringent crystals on arthrocentesis Can be associated with leukocytosis and increased ESR
30
Rheum What can be associated with gout?
CVD Renal disease HTN DM
31
Rheum Treatment of ACUTE gout
NSAIDs - good for multiple joints Colchicine Intra-articular steroids - good if one joint affected Oral steroids - if older and NSAIDs less suitable
32
Rheum Longterm management of gout
Low dose colchicine - biliary and renal excretion so caution, also risk of leukopenia and pancytopenia Individualised approach to urate lowering therapy (allopurinol) - more used in younger patients with recurrent attacks, erosive changes, long term complications or recurrent attacks Start at least 2 weeks after attack Must provide concurrent colchocine and NSAIDs for first 6months to prevent precipitation of gout Need to be consistent/compliant to avoid attacks Avoid if on azithioprine Risk factor reduction - beer, high purine foods and management of CVD risk factors and diabetes
33
Haem What is the most common type of leukaemia?
CLL
34
Haem Epidemiology and diagnosis of CLL
``` Older males (median 65 yrs) Most common leukaemia ``` Usually asymptomatic and found incidentally on routine FBE Shows marked leukocytosis with predominant lymphocytes Blood film will show small, mature lymphocytes & SMEAR cells DON'T need bone marrow biopsy to confirm
35
Haem Natural Hx and prognosis of CLL
Indolent course that is non-curable 1/3 never progress, 1/3 slowly progress, 1/3 actively progress Median survival ~8-9 years Most die from infection or transformation to lymphoma (Richter's syndrome)
36
Haem Clinical features and complications of CLL
Usually asymptomatic and found incidentally Later symptoms can include LAD, splenomegaly, bone marrow infiltration (anaemia, bleeding/bruising, infection), constitutional symptoms ``` Transformation to high-grade diffuse B cell lymphoma (Richter's syndrome) Recurrent infection (Hypogammaglobulinaemia - IgG) - usually encapsulated bacteria or fungal infection Warm autoimmune haemolytic anaemia ```
37
Haem Management principles of CLL
Non-curable Observation while symptomatic and stable If become symptomatic can provide gentle symptomatic treatment - Intermittent chemotherapy and immunotherapy (monoclonal antibodies) - Steroids (haemolytic anaemia) - Supportive - IV Immunoglobulin, blood transfusions
38
Gastro How is HCV predominantly transmitted & its risk factors
Blood-borne | IVDU, transfusion, tattoo, needle-stick injury
39
Gastro Diagnosis of HCV
Anti-HCV HCV-RNA (on PCR) Elevated ALT/AST
40
Gastro What factors influence the response to treatment of HCV?
Viral genotype (doesn't influence prognosis) - genotype 1 decreased response to treatment Co-infection with HIV Cirrhosis High HCV-RNA
41
Gastro What is the management of HCV?
``` Pegylated INF-alpha + Ribavirin (nucleoside inhibitor) 50-80% success rate Significant side effects - depression, fatigue - haemolysis - bone marrow suppression - precipitates autoimmune disorders ```
42
Gastro What percentage become chronically infected with HCV vs HBV?
HCV - 70% progress to chronic infection and chronic hepatitis HBV - 90% progress to chronic infection if infected at birth and will have asymptomatic acute disease If infected as adult much lower risk of chronic infection but more likely to have severe acute hepatitis with transmission
43
Gastro Why is there no vaccination for HCV?
Virus is difficult to culture Many strains with high international diversity and limited cross protection High mutation rate Poorly immunogenic
44
Gastro What serology will be seen with HBV in: - Vaccination - Acute infection - Acute infection that has resolved - Chronic infection
Vaccination - Anti-HBs positive only Acute infection - HBsAg, HBeAg positive, Anti-HBe (depending on timing, takes a bit to develop), Anti-HBc (especially IgM) Acute infection that has resolved - Anti-HBs, Anti-HBc, Anti-HBe (sustained for years) and HBcAg negative Chronic infection - HBeAg, Anti-HBe, HBsAg, Anti-HBc positive Anti-HBs negative Anti-HBs determines immunity - whether from vaccination or clearance of prior infection Does not develop in chronic infection and will be negative in acute infection
45
Oncology What are some differences b/w SCC and adenocarcinoma lung cancer?
SCC - Central location - Associated with smoking - Associated with clubbing, HOPA, hypercalcaemia Adenocarcinoma - Peripheral location - Not associated with smoking - Young, female asian - EGFR mutation
46
Oncology What are features of small cell lung cancer?
Less common than non-small cell lung cancer Highly associated with neuroendocrine, neurological syndromes and paraneoplastic syndromes (Lambert-Eaton, SIADH, Cushings, peripheral neuropathy, cerebellar ``` Always disseminated at presentation Poor prognosis (3-6 months or 1-2 years) ``` Centrally located Neuroendocrine 'oat cells' (small, tightly packed, darkly staining ovoid cells)
47
Oncology What are the general principles of lung cancer treatment?
Small cell carcinoma - Not resectable as disseminated at presentation (if very early disease may consider but uncommon) - Highly responsive to chemo and RTx but it is not curative - Often relapse Non-small cell - ~25% are resectable at presentation - Excision performed if lung reserve adequate, early disease with no distant spread - If early disease but poor lung reserve RTx can be curative - If advanced disease chemo or RTx, but generally poor response to chemo - Cetuximab if EGFR positive in adenocarcinoma
48
Oncology What are the complications of local invasion and mets in lung cancer?
Local invasion - Haemoptysis - Hoarseness - Dysphagia - Pericarditis - SVC obstruction syndrome Bone mets - Lytic leisons - bone pain, pathological fracture - Hypercalcaemia (SCC) - Anaemia Neurological - Confusion - Fits Liver - Abnormal LFTs, low albumin, prolonged INR
49
Haem What clinical and Ix features are suspicious for myeloma?
1. Rouleux (red cell aggregates), unexplained anaemia and high ESR 2. High ALP (normal other LFTs) - bone turnover 3. Back pain + renal impairment 4. Back pain > 50 yo 5. High total protein in setting of normal or low albumin 6. Unexplained hypercalcaemia
50
Haem Epidemiology of CML
Occurs at any age but median age is 65 years
51
Haem What is the natural hx of CML?
Slow and indolent course, often identified incidentally (30%) 3 phases of the disease 1. Chronic phase - asymptomatic 2. Accelerated phase - splenomegaly, some B symptoms 3. Blast transformation - significant B symptoms, features of acute anaemia (pancytopenia, infiltration of other organs) and may result in death Usually occurs 2-3 years after
52
Haem What features are present on blood film and bone marrow sample in CML?
Hypercellularity on BM | Myeloid leukocytosis of cells of varying stages of maturity
53
Haem What feature on blood tests is seen in both CML and AML?
Increased urate levels | Treat both with allopurinol for prevention of gout
54
Haem What are the cytogenetic features of CML?
> 80% have the philodelphia chromosome (BCR-Abl amplification) Also occurs in 20-30% ALL patients (more commonly in the adult patients than children)
55
Haem What is the management of CML?
Allopurinol - symptomatic In chronic phase 1. Tyrosine kinase inhibitor (Imatimab/gleevac) - resistance eventually occurs. Now 2nd and 3rd generations available 2. Interferon alpha Blast phase 1. Stem cell transplant may be curative if patient eligible but most are not
56
Haem What are the general features of acute leukaemias?
Occur rapidly over weeks to months They are rapidly fatal but generally curable More likely to occur in younger patients - ALL mainly occurs in childhood - AML 10-20% are children Symptomatic early
57
Haem Clinical features of acute leukaemia
B symptoms - Drenching night sweats - Fever > 38 - Wt loss > 10% over 6 mths Pancytopenia - Overcrowding of bone marrow - Anaemia - SOB, palpitations, dizziness, fatigue, pallor - Thrombocytopenia - petechiae/small bruises, bleeding Infiltration of other organs - LAD - Hepatosplenomegaly - Testes (ALL) - Mediastinum, skin (AML)
58
Haem Definition of acute leukaemia
Confirmation of diagnosis with BM aspirate | Will demonstrate > 20% blast cells (normally
59
Haem Complications of acute leukaemia. Which type are they more common in?
Leukostasis (due to significant increased WCC) - More common in AML - Increased viscosity, decreased blood flow and increased thrombus risk - SOB, blurry vision, stroke, confusion - Requires plasma exchange and urgent chemotherapy to rapidly reduce cell count DIC (due to depletion of coagulation factors) - Significant bleeding risk which can be fatal quickly - More common in AML and APML - Reverse with FFP (INR), cryoprecipitate (fibrinogen) and platelet transfusion
60
Haem Ix to differentiate between acute and chronic and sub-types of leukaemia
Blood count and blood film - AML - large blast cells with cytoplasmic granules + auer rods - ALL - small blast cells with no cytoplasmic granules or auer rods - CLL - small mature lymphocytes + smear cells - CML - increased number of myeloid cells of varying maturity Bone marrow sample - Confirms diagnosis of acute (>20% blast cells) - Not required for confirmation of diagnosis in chronic (can be diagnosed from blood film + count) Immunophenotyping - Differentiates between myeloid and lymphoid Cytogenetics - Identify different molecular changes associated with each which affects prognosis and management - Phillodelphia chromosome (BCR-Abl amplification) present in 20-30% ALL patients (mainly adults) and > 80% CML patients
61
Haem Management of acute leukaemia
1. Induction chemotherapy - Chemotherapy to rapidly reduce cell count and aims to induce remission 2. Reversal of DIC - FFP, cryoprecipitate, platelets 3. Consolidation therapy - Aims to prevent reoccurence - May increase dose of chemo drugs or use other drugs - May use stem cell transplant for consolidation in young/fit patients 4. Maintenance therapy - ALL only - Has a higher relapse rate than AML so requires ongoing treatment - Chemotherapy for 2-3 years after consolidation (intermittent & low dose) - May have stem cell transplant at any time, particuarly if poor prognosis
62
Haem What is the management of APML?
Retinoic acid Arsenic Reverse DIC
63
Haem Complications of treatment of haem malignancies?
Tumour lysis syndrome - Massive breakdown of cells leads to increases in urate, K+ and renal failure - Risk if higher if there is increased LDH, urate, creatinine and significant increased WCC and bulky disease (lymphoma), rapidly dividing cancer - To prevent treat with allopurinol and ensure adequate fluids prior to treatment
64
Haem Prognosis in acute leukaemia
ALL has a higher relapse rate than AML (requires maintenance therapy) ALL is curable in 70-90% childhood cases but much lower cure/survival rate in adults Poor prognosis in ALL is associated with being male, adult, B cell type and philodelphia chromosome AML has a lower relapse rate but is associated with high mortality (i.e. DIC) Prognosis is better with younger age and is related to cytogenetics (certain mutations have better or worse prognosis)
65
Haem Spectrum of multiple myeloma
1. MGUS - Precursor to myeloma but only 1-2% annual risk of progression - Common, particularly in the elderly - Usually incidental finding - Characterised by presence of M protein ( 30 g or > 10% plasma cells - No end-organ damage or symptoms 3. Myeloma - Symptomatic with end-organ damage
66
Haem Definition of multiple myeloma
Transition from MGUS to MM with acquisition of mutations leading to karotype instability Proliferation of malignant plasma cells Normally 10% significant Presence of M protein (polyclonal Ig) in serum and urine (Urine it is Bence jones protien - light chain only) > 30 g Symptomatic with signs of end-organ damage
67
Haem What are the clinical features of multiple myeloma?
CRAB are main clinical features - Hypercalcaemia - bones, stones, groans and moans - Renal impairment - Anaemia - BM infiltration from plasma cells - Lytic bone leisons (bone pain, compression fractures, cord compression) - BM infiltration leads to cytokine release that increase osteoclast activity leading to hypercalcaemia and leisons Others include: - Amyloidosis and hyperviscosity from significant amount of M protein 1. Amyloidosis = cardiac, gastro and neurological 2. Hyperviscosity = stroke, AMI/angina, headache - Infections due to decreased normal Ig
68
Haem Investigtions for diagnosis and assessment of multiple myeloma
Diagnosis 1. Protein Electropheresis - serum and urine M protein 2. BM biopsy - malignant plasma cell proliferation - FBE - anaemia - Blood film - rouleaux (aggregates of RBCs) - U&Es - renal impairment - Ca2+ - increased - LDH - increased is prognostic - ESR - increased - Total protein + albumin - Bone marrow - quantify plasma cells, immunophenotyping, cytogenetics (prognostic influence) - XRAY - multiple lytic lesions - MRI - if suspect spinal cord compression
69
Haem Management of multiple myeloma
Not curable but management - aim to increase QOL and decrease progression 1. Stem cell transplant if
70
Haem When to suspect multiple myeloma?
1. > 50 yo with new onset back pain, especially if unexplained renal impairment also 2. Unexplained anaemia + rouleaux + high ESR 3. Unexplained hypercalcaemia 4. High total body protein in setting of normal or low albumin
71
Haem Definition and epidemiology of Hodgkin's lymphoma
Classical or other subtypes Malignant proliferation of lymphoid cells with Reed-Sternberg cells (large pale cells) Begins at a single LN and spreads in contiguity with the lymphatics system Peaks at 20 years and again >50 years Associated with EBV
72
Haem Clinical features of Hodgkin's lymphoma
70% asymptomatic LAD - Most commonly cervical, but also axiliary and inguinal - Non-tender, rubbery - Alcohol induced tenderness 50% splenomegaly May have compressive LAD symptoms i.e. sore throat, abdominal swelling Rarely present with mediastinal mass but can cause cough, SOB, SVC syndrome (swelling of face, collaterals on chest wall, pemperton's) and pleural effusion 20% present with B symptoms Extra-nodal invovlement - may have pancytopenia (If BM infiltration but this is less common than in NHL) or hepatomegaly
73
Haem Diagnostic and other investigations in Hodgkin's lymphoma
Diagnostic 1. Excisional biopsy of LN - need architecture FBE and blood film - pancytopenia has worse prognosis LDH - increased, disease monitoring ESR - increased - prognostic LFTs - liver infiltration
74
Haem Staging of Lymphoma
Ann Arbour staging Need a CXR, CT/PET thorax, abdo, pelvis +/- bone marrow biopsy if B symptoms and Stage 3/4 Stage 1 - single node involvement Stage 2 - more than one LN involvement on same side of diaphragm Stage 3 - LN involvement on both sides of diaphragm Stage 4 - spread beyond LNs
75
Haem Prognostic factors in Hodgkin's lymphoma
``` Low albumin Low Hb Male High ESR Older age Bulky disease - mediastinal involvement Stage 3/4 disease ```
76
Haem Principles of treatment of Hodgkin's lymphoma
1. Early disease Short course of chemo (ABVD) + RTx 2. Late disease Longer course of chemo +/- RTx if bulky disease ABVD cures 80%
77
Haem Complications of lymphoma treatment
Chemotherapy - cardiac, respiratory issues (i.e. interstitial pneumonitis) - Infertility - tumour lysis syndrome - increased K+ and urate (treat with fluids + allopurinol prior to ChemoRx), can cause arhythmias and renal impairment RTx - increased risk of cancer (breast, lung) - CAD - Hypothyroidism
78
Haem Classification of NHL
1. Low grade - follicular, mantel 2. High grade - Diffuse B/T cell, most commonly B cell 3. Very high grade - Burkwitt's Malignant proliferation of lymphoid cells (mature or progenitor cells) with NO Reed-Sternburg cells Low grade is a slow progression with symptoms at end-stage, with limited curability Higher grades have more rapid progression with earlier B symptoms and are more curable
79
Haem Epidemiology of NHL
Small risk with family hx | Associated with H.pylori infection, HIV, immunosuppression, EBV (Burkwitt's)
80
Haem Clinical features of NHL
Usually widespread disease at presentation Asymptomatic LAD usually > 1 LN region involved and may have compressive symptoms B symptoms less common than in HL. If higher grade will occur earlier and more severely than in lower grades Extra-nodal involvement - GIT (i.e. MALT), testes, bones, kidney, CNS
81
Haem Principles of treatment of NHL
Low grade - Chemo not effective as slowly progressing - Only treat if symptomatic with compressive symptoms or B symptoms or Stage 1 as it may be curable with RTx High grade (diffuse) - Sensitive to chemo, curable - Treat regardless of symptoms - Use multi-agent chemo + rituximab (B cell) Very high grade (burkwitt's) - Very curable, need urgent chemo High grades need to give prophylaxis for tumour lysis syndrome 1. Adequate hydration 2. Allopurinol 3. Monitor electrolytes
82
Gastro What is the clinical picture of achalasia?
Functional oesophageal disorder Results in progressive dysphagia Initially to liquids then progresses to solids Associated weight loss
83
Gastro What is the Ix and Rx of achalasia?
Barium swallow - 'bird's beak' Oesophageal manometry - diagnostic Laporoscopic cardiamyotomy - division of lower oesophageal sphincter Oesophageal dilation
84
Gastro Compare features of inguinal vs. femoral hernia
Inguinal - Most common type (75%) - Significantly more common in males - Rarely strangulate - Above inguinal ligament and medial to pubic tubercle Femoral - More common in woman - Always repaired as high risk of strangulation and obstruction - Below inguinal ligament and lateral to pubic tubercle
85
Endo What are the management recommendations for diabetic medications pre-operatively?
Withhold OHA 12 hours prior to surgery and recommence when normal diet Never withhold basal insulin doses (can stop or modify bolus doses on day of surgery) and provide with IV dextrose Monitor BGLs and provide rapid acting insulin as necessary according to insulin correction scale Preferably diabetics should be operated on in the morning
86
Gastro What are the general trends on LFTs in hepatocellular injury, cholestatic, alcoholic hepatitis, NASH?
Hepatocellular - Marked elevation of ALT, elevation of AST Cholestatic - marked elevation of ALP and elevation of GGT Alcoholic hepatitis - moderate elevation of AST and ALT, AST > ALT NASH - ALT > AST
87
Gastro What levels and abdominal structures do the 3 anterior abdominal aorta branches supply?
Coeliac trunk - T12 - Abdominal oesophagus to the major duodinal papilla, including spleen, gallbladder, pancreas and liver SMA - L1 - Major duodenal papilla to just short of the splenic flexure (transverse-descending colon junction) IMA - L3 - Just before splenic flexure of transverse colon to the anus
88
Management for stable angina?
Sublingual GTN for acute attacks1st line = atenolol or calcium channel blocker Atenolol if have HF. Don't combine verapamil + atenolol = complete heart block (ok with long-acting dihydropyridine i.e. nifidipine)AspirinStatin
89
AmiodaroneMechanism of action?
Prolongs the refractory period in all cardiac tissuesAlso exhibits some Na, K, Ca channel blockade + mild anti-sympathetic action
90
AmiodaroneUses and indications
Most effective anti-arhythmic Atrial fibrillation - in recurrent AF - slows heart rate + acute reversion (not used in permanent AF)Ventricular tachycardia
91
What angina drug can tolerance be developed to?
Non-modified released GTN i.e. isosorbide mononitrate
92
Gastro What are features on imaging in bowel obstruction?
Erect AXR - Air fluid levels - Dilated bowel loops proximal to obstruction (> 3cm SB, >6cm LB, >9cm caecum) - Valvulae conniventes visible (SBO) - Collapsed distal colon - Signmoid volvulus - coffee bean sign - Caecal volvulus - kidney bean sign
93
Gastro What are clinical features suggesting a strangulated bowel obstruction?
Increasing pain, may be out of proportion to examination, sharper and more constant and more localised Peritonism +/- fever and increased WCC Features of mesenteric ischaemia
94
AnticoagulationHow often should INR be tested when commencing warfarin?
Every 1-2 days in first week to determine the correct individual dose.Once established monthly testing is adequate
95
AnticoagulationWhat patients require 'bridging' anticoagulation pre-operatively?What do you use for bridging?
High clotting risk patients- Recent DVT- Recent stroke- Mechanical valve- CHADsVASc score > or equal to 6Usually clexane unless mechanical valve which needs IV heparin due to extreme risk of clot
96
AnticoagulationWhat other anti-coagulation factors should be considered when STARTING warfarin?
Initially it has a pro-thrombotic effect due to decreased Protein C production It has a long half-life so its effect takes some days to be established Consider loading dose or bridging with S/C clexane or heparin if in hospital
97
Cardio Clinical features of VT
Very fast, regular heart beat Instant onset Often experience palpitations prior to severe dizziness or syncope Pre-existing HF or IHD
98
AnticoagulationFactors which DECREASE effect of warfarin
Green leafy vegetables (vit K) - don't have to reduce, need a stable consumption Chronic alcoholism Vit K supplementsBarbituates
99
Cardio Management of VT
1. DC Convert if unstable 2. O2, IV access, bloods, ECG 3. IV amiodarone 4. Consider implantable DC if EF
100
GastroWhat is the most common site for diverticular disease?
Sigmoid colon (left side)
101
GastroHow can diverticular disease and diverticulitis be diagnosed?
Diverticulae usually found incidentally on colonoscopy Barium enema can clarify if symptomatic (abdominal pain, altered bowel habit)CT gold standard for confirmation of acute diverticulitis - can identify extent of disease + complicationsAbdo XRAY can identify obstruction, free air or fistulae
102
Gastro In the acute setting of diverticulitis what Ix should be avoided?
Barium enema and colonoscopy risk perforation
103
Cardio Management of thoracic dissection
ABCD Type A - Surgery - resection of tear, graft - Aortic valve repair - Permissive hypotension - beta-blockers Type B - Medically managed if no malperfusion syndrome
104
Management for stable angina?
Sublingual GTN for acute attacks1st line = atenolol or calcium channel blocker Atenolol if have HF. Don't combine verapamil + atenolol = complete heart block (ok with long-acting dihydropyridine i.e. nifidipine)AspirinStatin
105
AmiodaroneMechanism of action?
Prolongs the refractory period in all cardiac tissuesAlso exhibits some Na, K, Ca channel blockade + mild anti-sympathetic action
106
AmiodaroneUses and indications
Most effective anti-arhythmic Atrial fibrillation - in recurrent AF - slows heart rate + acute reversion (not used in permanent AF)Ventricular tachycardia
107
What angina drug can tolerance be developed to?
Non-modified released GTN i.e. isosorbide mononitrate
108
What common drugs can cause long QT syndrome?
AmiodaroneSoltalolClass 1a antiarrythmics Erythromycin TCA (citalopram)
109
AnticoagulationWhat is the normal INR and target (therapeutic) INR range?
Normal
110
Cardio Management of ruptured AAA
ABCD Cross match and transfusion No imaging - straight to laparotomy to confirm diagnosis and control bleeding + repair (Diagnosis with CT abdo)
111
AnticoagulationWhat patients require 'bridging' anticoagulation pre-operatively?What do you use for bridging?
High clotting risk patients- Recent DVT- Recent stroke- Mechanical valve- CHADsVASc score > or equal to 6Usually clexane unless mechanical valve which needs IV heparin due to extreme risk of clot
112
AnticoagulationWhat other anti-coagulation factors should be considered when STARTING warfarin?
Initially it has a pro-thrombotic effect due to decreased Protein C production It has a long half-life so its effect takes some days to be established Consider loading dose or bridging with S/C clexane or heparin if in hospital
113
AnticoagulationFactors which INCREASE effect of warfarin?
Liver disease - decreased clotting factors NSAIDs - anti platelet effect, displace warfarin from plasma albuminAmiodarone, ciprofloxacin - interfers with its metabolism (P450 enzyme inhibitiors) Cranberry juiceAlcohol (acute consumption)Corticosteroids Macrolides
114
AnticoagulationFactors which DECREASE effect of warfarin
Green leafy vegetables (vit K) - don't have to reduce, need a stable consumption Chronic alcoholism Vit K supplementsBarbituates
115
Side effects of amiodarone
TALESThyroid - hyper or hypoArrhythmia - prolonged QT interval Liver dysfunction Eyes - corneal deposits Skin - grey discolouration
116
Cardio Investigations in Endocarditis
Blood cultures - need 3 sets separated by time and site Bloods - FBE (anaemia, leukocytosis), U&E (renal impairment), CRP, ESR Urinalysis - GN, haematuria ECG ECHO
117
GastroHow can diverticular disease and diverticulitis be diagnosed?
Diverticulae usually found incidentally on colonoscopy Barium enema can clarify if symptomatic (abdominal pain, altered bowel habit)CT gold standard for confirmation of acute diverticulitis - can identify extent of disease + complicationsAbdo XRAY can identify obstruction, free air or fistulae
118
Cardio Management of endocarditis
1. Empiric antibiotics - Benzylpenicillin, flucloxacillin and gentamycin - Vancomycin + gentamycin if suspect MRSA, prosthetic valve, nosocomially acquired, penicillin hypersensitivity 2. Tailor antibitoics once culture + sensitivity known, continue treatment for 4-6 weeks 3. Monitor for complications Surgery indicated if complications, refractory CHF, failure with medical treatment
119
Gastro What features on CT in acute diverticulitis?
Focal fat stranding adjacent to the diverticulae May see extra-luminal fluid and gas loculesBowel wall thickening May see complications - fistulae, perforation, abscess
120
Management for stable angina?
Sublingual GTN for acute attacks1st line = atenolol or calcium channel blocker Atenolol if have HF. Don't combine verapamil + atenolol = complete heart block (ok with long-acting dihydropyridine i.e. nifidipine)AspirinStatin
121
AmiodaroneMechanism of action?
Prolongs the refractory period in all cardiac tissuesAlso exhibits some Na, K, Ca channel blockade + mild anti-sympathetic action
122
Resp Features on examination consistent with PE
May have a 'clear' chest in setting of severe SOB Pleural rub Pleural effusion - stony dullness, decreased chest expansion, decreased breath sounds Cyanosis Decreased O2 sats Tachycardia, tachypnoea Fever Signs of DVT - swollen, tender calf Signs of pulmonary hypertension (often with massive PE) - TR (pansystolic murmur), elevated JVP with V waves, pulsatile liver, RV heave, Loud/palpable P2
123
Resp Diagnostic and other Ix in PE
CTPA - gold standard for acute PE, good negative predictive value, less useful for small distal PE V/Q scan - choice for chronic PE, normal scan virtually rules it out D-dimer - good sensitivity but low specificity - if positive likely PE but negative does not rule it out. Only perform if have a low index of suspicion for PE ECQ - not specific for PE but may be abnormal in 70% S1Q3T3 (Deep s in lead 1, Q wave and T inversion in lead 3) RV strain pattern - T wave inversion in V1-V4 +/- inferior leads (II, III, aVF) RBBB - M in V1/2 and or W in V5/V6 Right axis deviation ABG - not diagnostic but classically resp alkalosis due to hyperventilation ECHO - may show RV dysfunction in setting of pulmonary hypertension
124
What common drugs can cause long QT syndrome?
AmiodaroneSoltalolClass 1a antiarrythmics Erythromycin TCA (citalopram)
125
Resp What are the principles of the Well's score for clinical assessment of PE risk?
Well's score indicates clinical probability of a PE > 6 = high probability and if > 4 PE is likely 1. Clinical signs of DVT (3) 2. Other DDx less likely (3) 3. Haemoptysis 4. Hx of immobilisation, surgery in past 4 weeks 5. Malignancy 6. Previous DVT/PE
126
Anticoagulation How often should INR be tested when commencing warfarin?
Every 1-2 days in first week to determine the correct individual dose. Once established monthly testing is adequate
127
Anticoagulation What patients require 'bridging' anticoagulation pre-operatively?What do you use for bridging?
``` High clotting risk patients - Recent DVT - Recent stroke - Mechanical valve - CHADsVASc score > or equal to 6 Usually clexane unless mechanical valve which needs IV heparin due to extreme risk of clot ```
128
AnticoagulationWhat other anti-coagulation factors should be considered when STARTING warfarin?
Initially it has a pro-thrombotic effect due to decreased Protein C production It has a long half-life so its effect takes some days to be established Consider loading dose or bridging with S/C clexane or heparin if in hospital
129
Anticoagulation Factors which INCREASE effect of warfarin?
Liver disease - decreased clotting factors NSAIDs - anti platelet effect, displace warfarin from plasma albumin Amiodarone, ciprofloxacin - interfers with its metabolism (P450 enzyme inhibitiors) Cranberry juice Alcohol (acute consumption) Corticosteroids Macrolides
130
Anticoagulation Factors which DECREASE effect of warfarin
Green leafy vegetables (vit K) - don't have to reduce, need a stable consumption Chronic alcoholism Vit K supplements Barbituates
131
Side effects of amiodarone
``` TALES Thyroid - hyper or hypo Arrhythmia - prolonged QT interval Liver dysfunction Eyes - corneal deposits Skin - grey discolouration ```
132
GastroWhat is the most common site for diverticular disease?
Sigmoid colon (left side)
133
Cardio Describe features of neuropathic ulcers
- Punched out, moist ulcers - Often infected - Typically on weight bearing areas - Surrounded by thickened, calloused skin - Sensory disturbance, decreased proprioception, vibration - Hx of DM - Monofilament predicts risk
134
Cardio Clinical features of pericarditis
Sharp retro-sternal chest pain that is relieved leaning forward and worse with inspiration May have pericardial rub Fever Signs of tamponade - muffled heart sounds, increased JVP, Kussmaul's sign, pulsus paradoxis, tachycardia, hypotension Signs of pericardial effusion - SOB, raised JVP, bronchial breathing
135
Gastro What features on CT in acute diverticulitis?
Focal fat stranding adjacent to the diverticulae May see extra-luminal fluid and gas loculesBowel wall thickening May see complications - fistulae, perforation, abscess
136
Gastro What are the clinical features of diverticulosis?
Altered bowel habit Left sided colic pain, often relieved with defecation Nausea Flatulance
137
Gastro What are the complications of diverticulosis?
Diverticulitis - inflammation of the pouch - Left sided colic, fever, increased WCC/ESR/CRP, localised or generalised peritonitis - In immunocompromised patients may have few symptoms and present late Perforation - Ileus, peritonitis +/- shock - mortality 40% Abscess Haemorrphage - Sudden, painless onset - Common cause of rectal bleeding Fistuale LBO
138
Cardio Treatment of pericarditis
NSAIDs | Treat cause
139
Gastro Principles of management of bowel obstruction
Depends on site, cause and if there is strangulation Strangulated and large bowel obstructions require surgery Incomplete SBO can be managed conservatively Immediate - NBM, IV fluids and nasogastric tube on free drainage, analgesia, bloods (lipase, FBC, U&E), catheterise to monitor fluids, CT to confirm location and cause if AXR inconclusive Surgery - urgent for strangulation and laparoscopy for caecal volvulus, peritonitis, diverticulitis (no colonoscopy due to risk of perf), sigmoidoscopy for sigmoid volvulus and resection for CRC SBO due to adhesions are managed conservatively
140
Gastro What are features on imaging in bowel obstruction?
Erect AXR - Air fluid levels - Dilated bowel loops proximal to obstruction (> 3cm SB, >6cm LB, >9cm caecum) - Valvulae conniventes visible (SBO) - Collapsed distal colon - Signmoid volvulus - coffee bean sign - Caecal volvulus - kidney bean sign
141
Gastro Describe features of a Variocoele
Abnormal enlargement of testicular veins Separate to the testes Solid Left-side more commonly affected May be associated with dull ache Subfertility - surgery doesn't seem to improve much
142
Pharm What antibiotics can cause cholestasis?
Amoxicillin Co-amoxiclav TCAs OCP Clopidogrel
143
Cardio Clinical features and ECG features of SVT
``` Very fast, regular palpitations Come on suddenly and go away suddenly Shorter duration May feel fluttering May be precipitated by caffeine Vagal maneouvres improve - deep breathing, holding breath ``` Narrow complex tachycardia (QRS complex
144
Cardio Clinical features of AF
Irregular, racing heart beat May have associated SOB, chest pain, faintness and fatigue May be brought on by thyrotoxicosis (associated features of this), alcohol, caffeine, infection, exercise Hx of HTN, mitral valve disease, IHD, heart failure
145
Cardio Clinical features of VT
Very fast, regular heart beat Instant onset Often experience palpitations prior to severe dizziness or syncope Pre-existing HF or IHD
146
Cardio Management of SVT
1. Vagal manoeuvres i.e. hold breath, breath out into empty syringe, carotid massage 2. IV adenosine if fails - warn patient about side-effects 3. IV verapamil if fails 4. DC conversion if fails
147
Cardio Management of VT
1. DC Convert if unstable 2. O2, IV access, bloods, ECG 3. IV amiodarone 4. Consider implantable DC if EF
148
Cardio What causes a thoracic dissection and what are the types?
Blood splits the media of the aorta and runs in the intimal layer, forming a false lumen Type A involves the ascending aorta and Type B doesn't Most commonly caused by HTN, but less commonly by CTD (marfan's, Elhors-Danlos), trauma, congenital abnormalities (coarctation of the aorta), atherosclerosis
149
Cardio Clinical features of thoracic dissection
``` Sudden onset of tearing chest pain that radiates to the back Difference in BP/pulse between arms Symptoms depending on which branches it extends into - Carotids - stroke - coronary - MI - Anterior spinal - paraplegia - Renal - anuria - AKI - Mesenteric ischaemia - Limb ischaemia ``` May rupture into the pleural cavity, pericardium and peritonium - haemothorax, tamponade New diastolic murmur - unseating of aortic valve cusps Symptoms of shock Syncope
150
Cardio Ix of thoracic dissection
CXR - widened mediastinum, pleural effusion CT - gold standard Aortography ECG, ECHO, cardiac enzymes, lactate
151
Cardio Management of thoracic dissection
ABCD Type A - Surgery - resection of tear, graft - Aortic valve repair - Permissive hypotension - beta-blockers Type B - Medically managed if no malperfusion syndrome
152
Cardio What are some epidemiological features of AAA?
``` Normal aorta is 2-3cm, 3cm is considered an aneurysm Most occur infrarenally Increased risk with - increasing age - males > females (5:1) - Hx of CVD, PVD - family hx ```
153
Cardio Causes of AAA
``` Most commonly degenerative Also associated with - infection - atherosclerosis - CTDs (Marfans, ehler's-Danlos) ```
154
Cardio Clinical features of AAA and how they are detected
Usually asymptomatic and found incidentally or on screening (screen if have popliteal aneurysm) May have epigastric abdominal pain that radiates to the back, iliac fossa or groin Sudden death from sudden rupture Symptoms of rupture or bleeding Acute limb ischaemia due to embolus from aneurysm Uncommonly haematemesis due to aorto-duodenal fistulae
155
Cardio Clinical features of a ruptured AAA
Sudden onset epigastric pain radiating to back (or iliac fossa or groin) Signs of shock - hypotension, tachycardia, tachypnoea, cool, mottled peripheries - Ischaemic bowel, ischaemic limbs (will be bilateral) Pulsatile abdominal mass
156
Cardio Management of AAA
If 5-5.5cm then it is at high risk of rupture - surgical repair Open or endovascular - Open close aneurysm sac around graft, invasive - Endovascular insert stent, less invasive, can have endoleak occur (Type II most common - branch vessels fill sac)
157
Cardio Indications for surgery of AAA
``` > 5-5.5cm Increase in size >0.5cm in one year Symptomatic Rupture or leak If it is saccular - normally fusiform (both sides due to degeneration) ```
158
Cardio Management of ruptured AAA
ABCD Cross match and transfusion No imaging - straight to laparotomy to confirm diagnosis and control bleeding + repair
159
Cardio What pathogens cause endocarditis?
``` Most commonly S. Viridans (normal flora of skin) S. aureus (acute, virulent) S. epidermidis (subacute) Enterococcus S. Bovis - associated with bowel cancer HACEK group - fastidious organisms Fungus Coxiella (Q fever) - associated with livestock, farming ```
160
Cardio Risk factors for developing endocarditis
IVDU Immunocompromise - HIV, DM, immunosuppresive medications (chemo, steroids) Prosthetic valve Abnormal valve (more subacute compared to normal valve which is more acute) or cardiac abnormality (i.e. PDA, VSD) Previous endocarditis
161
Cardio Clinical signs of endocarditis
Peripheral stigmata - Vascular - janeway lesions (painless, non-blanching red lesions on palms and soles), splinter haemorrphage, petechiae - Immune complex - Roth spots (retinal haemorrphage, pale centre), Osler nodes (painful, raised leisons on digits) New regurgitant murmur (AR - early diastolic, MR - pansystolic) - more concerning as destruction of the vale Fever - most frequent symptom - Chills, rigors, night sweats, weight loss, anorexia Complications - HF, embolic events, glomerular nephritis & arthritis
162
Cardio Complications associated with endocarditis
Congestive heart failure secondary to MR or AR Embolic events - Right side - pulmonary infarct/abscess - Left side - renal or splenic infarct/abscess, stroke, mycotic aneurysm Immune complex - Glomerularnephritis - Arthritis
163
Cardio Diagnosis of endocarditis
Duke Criteria 1. 2 major 2. 1 major + 3 minor 3. 5 minor Major - ECHO features (osscilating intracardial mass - vegetation, abscess, dehisence of prosthetic valve) - Persistently positive blood cultures with typical organism Minor - Pre-disposing heart condition or IVDU - Fever >38 - One of vascular or immunological phenomenon
164
Cardio Investigations in Endocarditis
d
165
Cardio Which type of ECHO is performed in endocarditis - why/when?
Initially TTE usually first, particularly if IVDU TTE low sensitivity - can't exclude IE from it due to poor image quality, good for right sided valves and aorta as front of heart TOE to confirm after TTE or first if pt very unwell, prosthetic valve or suspected complications Prosthetic valves can't be seen as well on TTE
166
Cardio Management of endocarditis
1. Empiric antibiotics - Benzylpenicillin, flucloxacillin and gentamycin - Vancomycin + gentamycin if suspect MRSA, prosthetic valve, nosocomially acquired, penicillin hypersensitivity 2. Tailor antibitoics once culture + sensitivity known, continue treatment for 4-6 weeks 3. Monitor for complications Surgery indicated if complications, refractory CHF, failure with medical treatment
167
What is Virchow's triad?
3 aspects which contribute to the formation of thrombus 1. Stasis - immobilisation, surgery, inpatient 2. Endothelial damage - trauma, atherosclerosis 3. Hypercoaguable state - thrombophilia, dehydration, malignancy, pregnancy, medications
168
Resp Risk factors for development of PE
``` Prolonged immobilisation, inpatient Surgery Active malignancy - particularly pancreatic Air travel Pregnancy PHx or family Hx of DVT/PE Thrombophilia disorder Increasing age Weaker - COPD, smoking, OCP, obesity ```
169
Resp Features on hx consistent with PE
``` Sudden onset SOB Sub-sternal pain or pleuritic chest pain (if infarction) Syncope (if massive PE) Haemoptysis (if infarction) Hx of risk factors Cough Progressive SOBOE - recurrent small emboli Calf pain or swelling ```
170
Resp Features on examination consistent with PE
May have a 'clear' chest in setting of severe SOB Pleural rub Pleural effusion - stony dullness, decreased chest expansion, decreased breath sounds Cyanosis Decreased O2 sats Tachycardia, tachypnoea Fever Signs of pulmonary hypertension (often with massive PE) - TR (pansystolic murmur), elevated JVP with V waves, pulsatile liver, RV heave, Loud/palpable P2
171
Resp Diagnostic and other Ix in PE
CTPA - gold standard for acute PE, good negative predictive value, less useful for small distal PE V/Q scan - choice for chronic PE, normal scan virtually rules it out D-dimer - good sensitivity but low specificity - if positive likely PE but negative does not rule it out. Only perform if have a low index of suspicion for PE ECQ - not specific for PE but may be abnormal in 70% S1Q3T3 (Deep s in lead 1, Q wave and T inversion in lead 3) RV strain pattern - T wave inversion in V1-V4 +/- inferior leads (II, III, aVF) RBBB - M in V1/2 and or W in V5/V6 Right axis deviation ABG - not diagnostic but classically resp alkalosis due to hyperventilation ECHO - may show RV dysfunction in setting of pulmonary hypertension
172
Resp Management of acute PE
Anti-coagulation ASAP - LMWH (enoxaparin) + warfarin - overlap with LMWH until reach stable, therapeutic INR of 2.5 (+ warfarin initially has some pro-thrombotic properties) - Continue warfarin after for 3-6 months if corrected, provoked PE or 6+ months if unprovoked
173
Resp What are the principles of the Well's score for clinical assessment of PE risk?
Well's score indicates clinical probability of a PE > 6 = high probability and if > 4 PE is likely 1. Clinical signs of DVT (3) 2. Other DDx less likely (3) 3. Haemoptysis 4. Hx of immobilisation, surgery in past 4 weeks 5. Malignancy 6. Previous DVT/PE
174
Cardio What is intermittent claudication a result of? Describe the nature of this pain
Atherosclerosis resulting in chronic occlusion of peripheral arteries, as opposed to acute occlusion which results in acute limb ischaemia Intermittent claudication is pain distal to the site of occlusion - Aorto-iliac - buttocks + hip pain - Femoral-popliteal - calf Pain with walking that is improved with rest Worse going up hills/stairs
175
Cardio What are clinical features of PVD?
Intermittent claudication - leg pain with exertion, relieved with rest Hx of CVD, stroke, DM, HTN, smoking, hypercholesterolaemia, family hx, impotence Reduced or absent pulses Bruits Increased capilliary return Positive Buerger's test - rapid pallor with elevation of leg, cyanosis when legs hung off side of bed ABI
176
Cardio What are signs of critical chronic limb ischaemia vs acute limb ischaemia
Critical chronic limb ischemia - Night pain, rest pain - Ulcers, gangrene Acute limb ischaemia - 6 Ps - Pain - Paraesthesia - Pulseless - Polar (cold) - Paralysis - bad sign, impending gangrene - Pallor (mottled) - ABI
177
Cardio Investigations of PVD
ABI - compares brachial and pedal systolic BP, PVD = 0.5 - 0.9, critical ischaemia
178
Cardio Management of PVD
Risk factor and lifestyle management - aspirin - statins - BP control - weight loss, diet, exercise - Anti-inflammatories - stabilise plaque - Adequate DM control - Smoking cessation - very important If limb is not critically threatened, claudication is significant, not smoking and minimal co-morbidities then reperfusion surgery - Angioplasty +/- stenting - proximal, short segments - Bypass graft surgery - long segments, issues with wound healing, graft thrombus and cardiac issues If limb is critically threatened, smoker or significant co-morbidities then reperfusion surgery C/I - Palliation, amputation
179
Cardio Describe features of arterial ulcers
- Severe pain - Commonly located on distal part of toes, foot/ankle and pressure areas - Punched out lesion with regular smooth margins - Dry, no bleeding with debridement - Pale base - Cool, pale surrounding skin - Absent pulses - Signs of PVD - lack of hair, shiny skin, muscle atrophy, cool, pale feet, increased capillary refill time, nail changes, Buerger's test positive
180
Cardio Describe features of venous ulcers & general management
- Usually painless or mild pain - Gaiter area, particularly medial malleolus - Wet with granulation tissue at base - Irregular edges - surrounding tissue warm and oedematous - Hx of varicose veins, DVT - Other features of venous insufficiency - haemosiderin deposits/pigmentation, lipodermatosclerosis, pain with standing that can be relieved with walking, oedema, itchy skin Compression and elevation Sclerotherapy and surgery considered for varicose veins
181
Cardio Describe features of neuropathic ulcers
- Punched out, moist ulcers - Often infected - Typically on weight bearing areas - Surrounded by thickened, calloused skin - Sensory disturbance, decreased proprioception, vibration - Hx of DM - Monofilament predicts risk
182
Cardio ECG features of pericarditis and pericardial effusion
Pericarditis - Widespread saddle-shaped ST elevation Effusion - low voltage QRS complexes, electrical alternans - alternating morphologies of QRS complexes
183
Cardio Causes of pericarditis
Viral - coxsackie, flu, EBV, HIV, varicella Bacterial - pneumonia, TB, Staph or Strep Fungi Dressler's syndrome - post-MI Drugs - penicillin Rheumatoid - RA, SLE Malignancy
184
Cardio Investigations of pericarditis
ECG - saddle shaped ST elevation ECHO - if suspect effusion FBE, ESR, U&Es, cardiac enzymes, viral serology, blood cultures CXR - cardiomegaly may indicate effusion
185
Cardio Treatment of pericarditis
NSAIDs | Treat cause
186
Gastro Describe features of epididymal cysts
Separate from testes Posterior or superior to the testes May be associated with PCKD Confirm diagnosis on U/S and remove if symptomatic, otherwise supportive management
187
Gastro Describe features of a scrotal hydrocoele
Accumulation of fluid in tunica vaginalis (anterior to testes) Separate from testes Soft and non-tender Can get above it Transilluminates Can develop with testicular tumour, epidiymo-orchitis, testicular torsion
188
Gastro Describe features of a Variocoele
Abnormal enlargement of testicular veins Separate to the testes Solid Left-side more commonly affected May be associated with dull ache Subfertility - surgery doesn't seem to improve much
189
Pharm What antibiotics can cause cholestasis?
Amoxicillin Co-amoxiclav TCAs OCP Clopidogrel
190
Gastro What is Courvoisier's law?
A palpable gallbladder is not due to gallstones
191
Gastro Clinical features of carcinoma of head of pancreas
``` Painless jaundice Palpable gallbladder (Courvoisier's law) Portal hypertension - Hepatosplenomegaly (uncommon) LAD Ascites Pale stools, dark urine Acute pancreatitis Weight loss, anorexia Diabetes ```
192
Gastro What are the prefered imaging modalities in diagnosis of surgical jaundice presentations?
1st = U/S of liver and biliary tree - dilation of CBD, stones, pancreatic masses Pancreatic neoplasm - CT Liver or cholangiocarcinoma - MRI/MRCP PET scan for staging
193
Resp Outline the main pathophysiology of COPD
Exposure to pollutants/smoke results in: - neutrophilic inflammation resulting in increased protease production - destruction of alveolar walls and septa - Destruction of cilia - loss of muco-ciliary escalator - mucus plugging - airway narrowing - Goblet cell hyperplasia - increased mucus production - Chronic inflammation - airway narrowing and remodelling Narrowing of airways results in increased airway resistance - SOB Loss of tissue increases lung compliance - decreases elastic recoil - gas trapping (less air expelled in expiration) - Decreased FEV1 and hyperinflation
194
Resp What are the clinical features of COPD? What are clinical features of severe COPD?
``` SOB, reduced exercise tolerance Cough - often productive Wheeze (usually expiratory) Prolonged expiratory phase Nicotine stains Reduced breath sounds Decreased chest expansion Hyperinflation - barrel chest, hyper-resonance, ptosis of liver ``` Severe signs Pursed lip breathing Accessory muscle use Signs of pul HTN - TR (pansystolic murmur), loud/palpable P2, raised JVP with prominent V waves, pulsatile liver Signs of cor pulmonale - RV heave, raised JVP, hepatomegaly, peripheral oedema, if severe signs of portal hypertension (ascites, splenomegaly) Cyanosis Metabolic flap
195
Resp Diagnosis and other Ix in COPD
``` Diagnosis from spirometry FEV1/FVC 7 or 11 anterior/lateral ribs present Bullae Narrow heart shadow Prominant hilar vasculature if Pul HTN ``` ABG - May be chronically hypercapnic - may progress to type 2 resp failure (acidosis, hypercapnia, hypoxia) - May be in chronic type 1 resp failure (hypoxia, normal CO2)
196
Resp How can COPD be staged?
Spirometry + Gold's classification Spirometry - must have FEV1/FVC
197
Resp What are the requirements for home O2 in COPD and its benefit?
PaO2
198
Resp What is the general management of stable COPD?
Optimisation - Smoking cessation - Pulmonary rehab - Medications - SABA/SAMA, LABA/LAMA, ICS - Home O2 Prevention of exacerbations - Yearly flu vax, pneumococcal vax - Adequate nutrition and physiotherapy - Regular monitoring/follow up Develop an action plan - Home supply of antibiotics and oral steroids if signs of infection and exacerbation - Education on signs and symptoms and when to present for treatment
199
Resp What are the features of an acute COPD exacerbation and its general management?
Exacerbation is increased SOB, decreased exercise tolerance or increased RR, which may be associated with increased cough, increased sputum production and change in colour/consistency of sputum 1. Nebulised SA-bronchodilators 2. Careful O2 - maintain O2 Sats 88-92% so not to reduce resp drive 3. Oral corticosteroids - reduce the duration of exacerbation 4. Antibiotics may be beneficial if infective exacerbation (change in sputum, radiological signs) - Doxy + amoxycillin 5. Non-invasive ventilation (BiPaP) if pH 2.5 - 3.5 or invasive ventilation if indicated (Type 2 resp failure)
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Resp What are the general principles of drug management of COPD?
1. SABA or SAMA - SABA preferred due to better side effect profile - Can be used in combination If symptoms not controlled add: 2. LABA or LAMA - Response is individual, therefore choice depends on patients response If symptoms not controlled: 3. Add 2nd long-acting agent OR ICS if on LABA If still not controlled and/or FEV1
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Resp Discuss uses/features of SABA in COPD
Salbutamol, terbutaline Short-acting beta-adrenoreceptor agonists - activate B-AR to induce bronchodilation No effect on disease modification or survival, only symptomatic control S/E - tremor, palpitations, headache, very high doses - hypokalaemia Preferred to SAMAs due to risk profile
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Resp Discuss uses/features of SAMA in COPD
Ipratropium Short-acting muscarinic antagonist - reduce parasympathetic nerve activation by acetylcholine S/E - increased risk of CVD (why SABA preferred), anti-SLUD (dry mouth, dry eyes, urinary retention, constipation)
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Resp Discuss uses/features of LABA in COPD
Salmeterol, eformeterol Long acting agonist of the B-AR Improve QOL, relieve symptoms and reduce frequency and severity of exacerbations Same side effects as SABA
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Resp Discuss uses/features of LAMA in COPD
Tiotropium Long-acting muscarinic antagonist Same benefits at LABA - improve QOL, relieve symptoms, reduce frequency and severity of exacerbations Individual response to LABA and LAMA so choice depends on patient - can be used in combination
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Resp Discuss uses/features of inhaled corticosteroids in COPD
Fluticasone, budesonide Reduce the frequency of exacerbations and reduce rate of decline but no clear indication if beneficial effect on mortality Effect on reducing exacerbations enhanced when used with a LABA Indicated when FEV1 2 exacerbations S/E - dysphonia, oral thrush, long-term effects of steroids, increased risk of pneumonia (especially with fluticasone)
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Resp Compare the clinical features of typical vs. atypical pneumonia
Typical - Acute, severe - SOB, productive cough, pleuritic chest pain - Fever, rigors - Signs of consolidation - decreased chest expansion, increased fremitus, bronchial breathing, dullness to percusion - Decreased O2 sat Atypical - Gradual, insidious onset and duration - Minimal chest signs - Non-productive cough, may have some SOB - Non-resp features predominant - myalgia, arthralgia, headache, malaise - May have fever
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Resp What organisms cause typical vs. atypical pnenumonia and community vs. hospital acquired?
Typical 1. S. pneumoniae (both community + hospital) 2. HIB - less common with vaccination 3. Gram negative rods (hospital) - Klebsiella, pseudomonas 4. S. aureus Others - Morexella (elderly), anaerobes + MRSA (hospital) Atypical 1. Chlaymdia 2. Mycoplasma 3. Legionella Viral - flu, RSV, adenovirus etc Coxiella (Q fever) - farmers, vets, abattoir workers TB
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Resp What are typical patterns on CXR in typical vs. atypical pneumonia?
Typical - Lobar or patchy consolidation (bronchopnuemonia) Atypical - Reticular or recticulonodular opacities, typically in the peri-hilar region
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Resp Ix for pneumonia
Sputum sample - culture + PCR Urine - Legionella antigen U&Es, FBE Blood cultures - 10-15% of S.pneumoniae infections will be positive Serology - mycoplasma + chlamydia ABGs - if severe, may be approaching resp failure CXR ECG, cardiac enzymes if pleuritic chest pain to exclude ACS
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Resp How can the severity of pneumonia be determined?
CURB-65 Confusion Elevated Urea RR > 30 BP 65 Mild = 1, moderate - 2, severe >2
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Resp What are the empirical antibiotics for CAP?
Mild - amoxycilin (S. pneumonia, HIB) + doxycyclin (atypical cover) Moderate - Same unless require admission then replace amoxycillin with IV benzylpenicillin Severe - 3rd generation cephalosporin (Strep, Gram -ve) + azithromycin (atypical, gram +ve) +/- vancomycin (if MRSA suspected)
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Resp What is the empirical treatment for HAP?
Mild - Amoxycillin + doxycyclin Moderate/Severe - Ceftriaxone +/- metronidazole (anaerobes) +/- vancomycin (MRSA) +/- piperacillin/tazobactem (pseudomonas) MRSA and pseudomonas more likely if hospital stay > 5 days or high risk unit (ICU)
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Cardio What are the types of HF?
Chronic - HF-REF (systolic dysfunction - dilation of ventricle) - HF-PEF (diastolic dysfunction - hypertrophy of ventricle) Acute/decompensated - acute pulmonary oedema
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Cardio What are the main causes of HF and the general type of HF they cause?
IHD - 70% of cause of heart failure, mainly systolic dysfunction (dilation of ventricle) Cardiomyopathy (dilated) - also causes systolic dysfunction - dilation means decreased ability to contract efficiently to produce adequate SV Hypertension - mainly diastolic dysfunction (LV hypertrophy) Valvular disease - systolic or diastolic dysfunction, may cause left or right sided failure depending on valve and may also affect atria
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Cardio How does IHD cause HF?
- Myocardial injury leads to decreased ventricular due to loss of myocardial cells/scar tissue - Decreased SV and CO leads to activation of RAAS which causes fluid retention - increases preload - increased EDV - Frank-Starling mechanism (more volume = more stretch = more contraction) - increased SV and remodelling of LV (dilation)
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Cardio How does hypertension cause HF?
- HTN = increased afterload to LV - Increased LV EDP to eject same SV - Thickening of LV wall to dissipate increased pressure - Thickening makes it stiff - more difficult to fill
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Cardio How does valvular disease cause HF?
- Regurgitant disease - increased ventricular ESV to chamber behind valve - fluid overload - dilation to accommodate - systolic dysfunction - Stenotic disease - increased afterload to chamber behind valve - increased EDP - thickening to dissipate pressure - diastolic dysfunction
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Cardio What is the neurohormonal response to compensate HF?
- Decreased CO with HF leads to decreased BP - Decreased perfusion to kidneys - activation of RAAS - Renin - conversion angiotensinogen to Ang I - ACE converts Ang I to Ang II - Ang II acts on adrenal cortex - increase aldosterone - Aldosterone increases Na+ and H2O retention in distal tubules - Increased circulating fluid volume - increased venous return and BP - Decreased BP also increases baroreceptor firing - Increased SAN firing and decreased conduction time to ventricles - increased HR - Increased activation of sympathetic NS - increased HR, increased contractility and further activation of RAAS
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Cardio What are the clinical features of HF?
Left sided - Exertional SOB - PND - Fatigue - Orthopnoea - Tachycardia, tachypnoea - Displaced apex beat - S3 (gallop) - early sign of LV dilation (filling sound in diastole against a more compliant ventricle) - S4 - atrial kick occurring in diastolic dysfunction due to decreased compliance of ventricle - Pulsus alternans - Murmur - underlying valvular disease Right sided - SOB related to pulmonary oedema (can also occur in decompensated left sided heart failure) - Coarse bi-basal crackles - Raised JVP - Orthopnoea - Peripheral oedema - Hepatomegaly - Ascites, splenomegaly if severe (due to portal hypertension) - Signs of Pulmonary hypertension - TR (pansystolic murmur, raised JVP with prominant V waves, pulsatile liver), palpable/loud P2
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Cardio What is the NYHA classification of HF?
Describes the severity of HF based on symptoms and functional limitation 4 classes Class 1 - no symptoms or functional limitations Class 2 - mild limitation, symptoms with normal physical activity Class 3 - marked limitation, symptoms with gentle physical activity Class 4 - significant limitation, symptoms at rest and with any activity
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Cardio What investigations can be performed in HF?
ECHO - Determine if systolic or diastolic dysfunction and whether EF is preserved or reduced - Assess chamber dimensions - Assess underlying causes - valvular, cardiomyopathy, regional wall abnormalities (CAD) ECG - Supportive as may indicate LV hypertrophy (>7 large squares of combined QRS amplitude in V1+V6 or V2+V5) - Identify ischaemia/infarction, arrhythmia as cause or precipitant CXR - Supportive signs - ABCDE - alveolar congestion, kerley B lines, cardiomegaly, upper lobe divergence, pleural effusions ``` Natriuretic proteins (i.e. BNP) - Normally 400 suggestive of APO and poorer prognosis, ```
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Cardio How is HF diagnosed?
Clinical diagnosis + ECHO findings of altered chamber dimension and EF Framingham criteria European society of cardiology guidelines Diagnosis based on major and minor clinical features
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Cardio What is the pharmacological management of chronic HF?
No specific management for HF-PEF - mainly treatment of underlying cause (i.e. hypertension) and symptomatic fluid control HF-REF - BLADES - Beta-blocker - improves mortality (decreased risk of sudden death from arrhythmia) - Lasix (fruesemide) - no effect on mortality - ACEI - improves mortality, symptoms, increases EF and decreases progression - Digoxin - if have AF - Spironolactone - aim to give early as has benefit on improved mortality, but can't give if renal failure due to hyperkalaemia
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Cardio What is the management of acute HF/APO?
LMNOP - Lasix (Fruesemide) - Morphine - Nitrates - O2 if sats
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Cardio What is the non-pharmacological management of HF?
Exercise | Diet
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Cardio What ECG leads refer to which aspects of the heart and vascular territories?
Anterior - V1-V4 - LAD Inferior - Leads II, III avF - Right coronary Lateral - Lead I, aVL, V5-V6 - circumflex
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Cardio What is the definition of a STEMI vs. NSTEMI?
MI - Symptoms of ischaemia - chest pain - ECG changes - Imaging evidence of thrombus or myocardial loss STEMI - New LBBB - ST elevation > 2mm in >1 contigious chest leads or > 1mm in >1 contigious limb leads - Pathologic Q wavs - also sign of old infarction NSTEMI - ST depression - T wave flattening or inversion - may also be sign of old infarct
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Cardio What is the acute management of a STEMI?
MONASH-R Morphine - pain + reduced RR (anti-anoxylytic) O2 - only if Sats
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Cardio When do you chose PCI vs. thrombolysis in STEMI management
PCI more effective than thrombolysis Ideally PCI within 4 hours of pain onset If > 90 minutes before PCI can be achieved thrombolise first then PCI as soon as can If pain onset 12 hours CAN'T do thrombolysis (will be ineffective due to clot organisation) - Still anti-coagulate, dual anti-platelet and CT coronary angiogram (as clot retrival or stenting may still be beneficial) - After 24hrs less likely PCI will be effective Thrombolysis is absolutely C/I if CVA in last 3-6 months, any intra-cranial haemorrphage or bleeding disorder
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Cardio What types of stents can be used in PCI of ACS?
Bare-metal stent (BMS) or drug-elluting stent (DES) Stent thrombosis is higher in BMS, but requires shorter duration of dual anti-platelet therapy so consider bleeding risk Use dual antiplatelet (aspirin + ticagrelor) for at least 12 months - In BMS can reduce to just aspirin after 6 weeks and in DES after 6 months Ticagrelor reduces risk of stent thrombosis more than clopidogrel
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Cardio What is post-STEMI management?
Pharmacological (SAAB) - Continue high dose statin - ACEI - decreases remodelling, HTN, good if diabetic which commonly are, decreased risk of recurrent MI or stroke - Aspirin (+/- ticagrelor if stented) - continue for 12 months to reduce risk of reoccurrence - Beta-blocker - commence 1-2 days after, when more stable. Reduces mortality (from sudden arrhythmias), decreases remodelling and HTN. Don't use in inferior STEMI if heart block Non-pharmacological - Smoking cessation - Weight loss, diet, exercise - Cardiac rehabilitation - Education and counselling on what has happened, new medications (importance of compliance, strategies for compliance), chest pain action plan - Pharmacy involvement - information sheets, webster pack, education on side-effects - Follow-up with GP (inform them of what has happened and management) and cardiac clinic
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Cardio What is the management for NSTEMI?
Need to risk stratify High risk (i.e. ongoing pain, ECG and troponin changes, hx of infarct and CVD) - Consider for early CT coronary angiogram +/- PCI or CABGs - Dual anti-platelet - Anti-coagulation - Beta-blocker - Morphine Moderate risk (prolonged chest pain but no changes on ECG or troponins, diabetes) - Aspirin - Beta-blocker - Morphine - Monitoring and further investigation - reclassify if changes ``` Low risk (more unstable angina symptoms, normal ECG and troponin) - Discharge and manage as outpatient within 2 weeks ```
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Cardio When to do PCI or CABGs in NSTEMI?
High risk NSTEMI patient should have early CT coronary angiogram to see if PCI or CABG will be beneficial PCI - if shorter segment CABG - do better if diabetic and if longer or multiple segments If high risk features and think they may need CABG do not load up on clopidogrel/ticagrelor as need to be 5 days off it before CABG - if unsure only give aspirin until have angiogram
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Endo What is the pharmacological management of T2DM?
Lifestyle modifications first 1. Metformin (2nd line sulphonylurea) 2. Add sulphonylurea (2nd line DDP-4 inhibitor or GLP-1 agonist) 3. Triple OHA therapy or addition of basal insulin - If add basal insulin can stop other OHA except for metformin
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Endo Describe the features of metformin
Metformin = biguanoside 1st line management of T2DM Decreases hepatic gluconeogensis Not associated with wt gain or hypoglycaemia Need to renally adjust dosage and it is C/I in severe renal failure Accept a small rise in Cr (
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Endo Describe the features of Sulphonylureas
``` Medications with prefix 'Gli-' 2nd line treatment of T2DM to metformin Stimulates B-cells to increase insulin Associated with hypoglycaemia and wt gain Rapid onset C/I in severe hepatic disease ```
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Endo Describe the features of DDP-4 inhibitors
'Gliptin' medications Reduce metabolism/prolongs effect of GLP-1 - increased pancreatic glucose sensing, increased insulin secretion and decreased glucagon secretion No risk of hypoglycaemia or wt gain Reasonable efficicacy S/E - Nausea, hypersenstivitiy
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Endo Describe the features of GLP-1 agonist
Exanatide, liraglutide Increases pancreatic glucose sensing and increases insulin secretion Requires injection but good efficacy S/E - N+V C/I in those with Hx of pancreatitis or severe GI disease
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Renal What are the main principles of management in CKD?
1. Identify and treat underlying cause of disease 2. Prevent progression - management of proteinuria (ACEI), BP control, glycaemic control 3. Reduce risk of CVD - as above, plus lifestyle management (smoking, alcohol, diet, weight loss, exercise) 4. Early investigation and management of complications - Anaemia - monitor, supplement, EPO if required - Bone disease - Phosphate binders (calcium supplement), activated Vit D - Oedema - Na restriction, diuretics, fluid restriction - Acidosis - sodium bicarbonate to maintain serum levels > 20mmol/L 5. Medication adjustment/avoidance of renally excreted and nephrotoxic drugs
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Neuro What are the general clinical features of a MCA territory stroke?
Trunk of MCA - Upper and lower limb motor deficit - Global aphasia Lentinulostriate branches - Lacunar infarct (small, subcortical strokes in internal capsule, basal ganglia) - Upper and lower limb motor deficit - Language spared and sensory usually spared Superior division - Broca's area - expressive dysphasia - Upper limb motor +/-sensory - usually occur on the dominant side Inferior division - Wernicke's area - receptive dysphasia - Upper limb motor - Upper and lower limb sensory - contralateral superior quadratanopia
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Neuro What are the general clinical features of a ACA territory stroke?
Lower limb motor +/- sensory deficit | May have motivation/initiation symptoms as supplying frontal lobe (medial division of pre-frontal cortex)
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Neuro What is the acute management of stroke?
1. Admission to a stroke unit is better for outcome 2. Urgent CT to exclude haemorrphage - unlikely to see ischaemic changes early on, diagnosis made clinically 3. Other investigations - BGLs, U&Es (to exclude causes of focal neurological symptoms and C/I to thrombolysis), cardiac enzymes + ECG to exclude AMI which can be associated with concomitant stroke 4. If symptom onset
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Neuro What are the C/I to tPA in stroke?
Factors associated with increased risk of bleeding - hypertension, dementia, head injury, prolonged INR or heparin within last 48 hours Other factors - Seizure at time of onset (severe stroke), unsure of time of onset, hypoglycaemia, recent AMI (risk of ventricular rupture)
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Neuro What is the secondary management/prevention of stroke?
1. Carotid endarterectomy - If stroke or TIA and there is carotid stenosis then it should be performed within 2 weeks - If carotid stenosis also >70% it is indicated 2. Single anti-platelet therapy - 1st line Aspirin (or dipyridamole) - 2nd line Clopidogrel - modest increased effect at reducing stroke than aspirin but more expensive so less routinely used 3. Reduction of risk factors - Lifestyle - diet, weight, exercise, smoking cessation - BP control - Cholesterol - Ensure adequate diabetic control
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Urology How does prostate cancer present? What examination findings could you expect?
- Asymptomatic - incidental finding on PSA, DRE - Bone pain - sclerotic boney mets in advanced disease - Urinary retention - due to obstruction - Obstructive urinary symptoms - hesitancy, weak stream, terminal dribling - DRE - hard, irregular nodule - posterior zone most commonly affected - Bony tenderness on palpation
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Urology Ix in prostate cancer
TRUS biopsy - samples used to determine gleeson score PSA - increased (70% of increased scores not due to cancer) XRAY and bone scan - bony mets MRI for staging LFTs - spread to liver CXR - spread to lungs
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Urology How is prostate cancer managed?
Depends on age, grade and stage of cancer and if other comorbidities If local disease: 1. Watchful waiting - if older with shorter life expectancy (
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Urology What are the side effects of hormonal Prostate Ca treatment and radical prostectomy?
Prostectomy - impotence, incontinence Hormonal - impotence/decreased libido, mood swings, gynacomastia, bone loss, decreased facial hair
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Urology What are the management options for BPH?
TURP - scrape off some of prostate to reduce obstruction Alpha-antagonists - decrease smooth muscle tone in prostate & bladder to reduce obstruction 5-alpha reductase inhibitors - decrease conversion of testosterone to dihydrotestosterone
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HIV What Ix to diagnose HIV? What other Ix should you consider also?
Ab/Ag serology screening tests using an ELIZA method Diagnosis confirmed with Western blot - Abs present to at least 2 HIV protein bands Consider co-infection with other STIs and chronic infection - TB - Interferon-gamma release assay, mantaux test, CXR - Hep C & B serology - Chlamydia and gonorrhoea - urine & (increase risk of transmission)
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HIV What key messages should be conveyed at time of diagnosis?
It is HIV, not AIDS - HIV is treatable with only moderate increased risk in complications Will require regular medical checks but otherwise won't greatly interfere with future plans Use condoms
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HIV Why is mortality increased in HIV?
Chronic inflammation and immune dysfunction Drug toxicity - less of an issue now Lifestyle and risk factors often associated with HIV - smoking, alcohol, IVDU Associated with more co-moribities - DM, osteoporosis, CVD, HTN, CKD, CLD
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HIV What are important questions to ask at time of diagnosis?
- Who they have for support - Can you contact previous sexual contacts and are you willing to? - Have you donated blood or semen in last year? - Symptoms of seroconversion - as may remember and this gives a time frame for infection
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HIV What are the symptoms of HIV sero-conversion?
Very non-specific, often confused with glandular fever or the flu - Headaches, myalgia, arthralgia, sore throat, LAD, rash, weight loss
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HIV When should you consider HIV?
Opportunisitic infections - PJP, candida, CMV retinitis, toxoplasma Severe/resistant skin conditions Other chronic infections - TB, viral hep Conditions associated with it - lymphoma, karposi sarcoma Unexplained weight loss with risk factors High-risk group
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HIV What should be considered and Ix at time of diagnosis?
- Work, accomodation, relationships - Mood and lifestyle issues (alcohol, smoking, drugs) - STI risks and checks - Co-infection with TB, viral hep - Examination for associated conditions (skin, cancers) - Record and monitor wt, CD4 cel count, viral load - Department of health notification
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HIV What CD4 count are patients susceptible to opportunistic infections?
CD4
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HIV What are the general principles of treatment and considerations?
- Anti-retro viral treatment prevents replication thus reducing viral load, allows reconstitution of the immune system and stops generation of resistant strains - 3 tablets per day - 2 x nucleoside reverse transcriptase inhibitors and a protease or integrase inhibitor - Patient must know of benefits and risks of treatment and must be willing to be fully compliant - More likely to get reconstitution of immune system if started when CD4 > 200 - Monitor for complications - Monitor viral load - rising means compliance issue, resistance or both - Immune reconsitution disease can occur (opportunistic infection), particuarly if CD4 count low when commencing
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Gastro How is coeliac disease investigated?
Antibodies - anti-gliadin, anti-tG (transglutaminase), anti-endomysial Gastroscopy with small bowel biopsy FBE - anaemia Iron studies, B12
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Neuro Causes of seizures
``` Trauma Electrolyte disturbance (hypocalcaemia, hyper- or hyponatraemia) Infection - meningitis, encephalitis Hypo- or hyperglycaemia Stroke Haemorrphage Pseudoseizure Psychogenic Hippocampal sclerosis, temporal sclerosis Drug/alcohol withdrawral Drugs i.e. TCAs Space-occupying lesion Raised ICP Hypoxia ```
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Neuro What are some precipitants of seizure?
``` Flashing lights Reading/righting Tiredness Emotional - stress Fever Alcohol ```
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Neuro Clinical features that distinguish between seizure and syncope
Before 1. Seizure - moan or cry, sudden onset, may be associated with aura (strange feeling in gut, jamais vu/deja vu), presence of trigger (flashing lights, tiredness, stress, fever, alcohol) 2. Syncope - only when standing (unless seated if cardiac cause), prodrome (N+V, sweeting, light-headed, change with vision and hearing), often warning it is going to happen, hypoglycaemia, dehydrated, fear/anxiety/stress, hx of valvular or heart disease During 1. Seizure - tonic clonic movements, cyanosis, frothing, tongue biting, incontinence, automatisms (i.e. picking at clothes, smacking lips) 2. Syncope - pale, may have a few very brief convulsions, usually no loss of continence (but rarely can) After 1. Seizure - injury (sore tongue, back shoulder - posterior dislocation), post-ictal confusion, fatigue, drowsiness, aphasia, temporary muscle weakness (Todd's palsy), amnesia 2. Syncope - Not confused or tired, on examination may find postural hypotension, bradycardia, ejection systolic murmur (AS), irregularly irregular pulse
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Neuro Investigations of a seizure
EEG or video telemetry (continuous EEG with recording) - Diagnosis of epilepsy syndrome, not a seizure - May have abnormal inter-ictal epileptiform patterns - During a seizure there will be abnormal discharges - VEEG is useful to classify seizure and distinguish from pseudoseizure MRI - may show epileptogenic leisons CTB - rule in or out specific causes of seizure i.e. space-occupying lesion, haemorrphage Genetic epilepsy syndromes confirmed with recurrent seizures with no clinical or radiological evidence of brain damage, Epileptiform discharges > 3 hertz and response to therapy usually good
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Neuro Principles of management of seizure/epilepsy
Do not treat first seizure - unless abnormal EEG/imaging, known underlying neurological condition, use of a motor vehical or dangerous activities for occupation/lifestyle Always attempt monotherapy and introduce drug slowly, change if not effective Education on drugs to ensure compliance Don't acutely treat a seizure unless it is prolonged (status epilepticus) - benzodiazepine Drug choice depends on type of seizure - Generalised seizures (absence or tonic clonic) 1. Valproate 2. Lamatrigine (T-C) or ethosuxamide (absence) - Partial seizures 1. Carbamezipine 2. Lamatrigine 3. Valproate
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Neuro What safety issues need to be considered in epilepsy?
``` Occupation - dangerous if seizure? Safety around heights and water Driving restrictions Education about avoiding triggers of seizures Pregnancy and medications ```
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Derm Non-surgical treatment options for skin cancers
Topical imiquimod or fluorouracil Cryotherapy Phototherapy RTx - usually adjunct to surgical excision of SCC if it its high risk Pre-malignant lesions such as Bowen's disease and solar (actinic) keratoses
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Urology Imaging of renal stones
Initial - KUB Xray - 80% stones will be visible CT (non-contrast) abdo - superior to IV pyelogram, can exclude other causes of acute abdomen IV pyelogram (contrast + Xray) - need a plain film as control for interpretation KUB US
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Urology Non-imaging Ix of renal stones
FBE (infection) U&E (obstructive nephropathy) Ca2+, phosphate, urate - causes of stones Urine MC&;S, urinalysis - haemturia and infection
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Urology What are common sites for renal stones to obstruct?
Pelvicureteric junction Ureters at point of pelvic brim Vesicoureteric junction
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Urology What is the management of renal stones?
Analgesia & supportive If 5mm - alpha-blockers (tamulosin) or calcium channel blockers (nefidipine) to help expel (reduces smooth muscle tone) - Can consider shockwave lithotripsy to break stone up and surgical removal of stone (rare)
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Rheum Interpretation of DEXA bone scan
T score compares patient's bones to that of healthy 30 year olds T score >/ -1 = normal T score - 1 to -2.4 = osteopenia T score -2.5 = osteoporosis
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Rheum What is osteoporosis & what are risk factors?
Loss of bone mass (loss of cells and matrix) - Late menarch, early menopause - Low BMI/malnutrition - Malabsorptive disorders - Sedentary/immobile - Failure to reach peak bone mass - Other disease - RA, malignancy with bone mets - Increasing age - Cushing's/steroids - Hyperparathyroid - Smoking and alcohol - Decreased calcium
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Rheum What is osteomalacia and what are the causes?
Loss of bone mineralisation (as opposed to bone mass) - Inadequate Vitamin D - malabsorption, diet, lack of sun - Renal osteodystrophy - decreased activation of vitamin D - Liver disease - decreased vitamin D activation
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Renal How does CKD result in bone disease?
- Decreased activation of Vitamin D by the kidneys reduces absorption of calcium in the gut - Increased phosphate due to inadequate clearance by kidneys - Excess phosphate binds to calcium causing further loss via excretion in gut - Low calcium levels and high phosphate levels leads to increased PTH secretion (2o hyperparathyroidism) which results in bone resorption to correct low calcium levels - Due to constant inadequate activation of Vit D and increased phosphate levels, PTH are constantly high which means bone is constantly demineralised - Eventually to keep up with continued PTH secretion the parathyroid glands undergo hyperplasia (3o hyperparathryoid) Provide activated Vitamin D supplement and Phosphate binders with meals
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Rheum Compare Ix and results between osteoporosis and osteomalacia
Osteoporosis - ALP, calcium and phosphate normal - DEXA T score - 2.5 = osteoporosis Osteomalacia - Vit D decreased - Decreased calcium and phosphate - Increased ALP and phosphate
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Rheum Treatment of osteoporosis
Lifestyle - decrease smoking & alcohol - increase exercise + weight bearing - Increase diet intake of Ca + Vit D Drugs - Bisphosphonates (aldrenoate) - weekly dose, directly toxic to osteoclasts which uncover them when they are resorbing bone, S/E of osteonecrosis of jaw, atypical fractures and oesophagitis - RANKL inhibitor (denosumab) - monoclonal Ab that binds to RANKL. RANKL on Oc interacts with RANK on Ob causing it to become activated - Selective oestrogen receptor modulators (raloxifen) - increases oestrogen effect on bone (increases OPG which binds to RANKL) and decreases RANKL, therefore reducing activation of Oc + prolongs survival of Ob
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Gastro What are features of acute cholecystitis on U/S?
Thickened gallbladder wall Peri-cholecystic fluid Gallstones in gallbladder - small, round, hyperechoic masses with posterior acoustic shadowing
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What are the ultrasound features of a cyst?
Round, regular anechoic mass which is wider than it is taller (not invading other planes) Posterior acoustic enhancement
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Oncology What are radiologic features of breast malignancy?
U/S - Hypoechoic, ill-defined mass - Taller than is wide - Hyperechoic, thick halo surrounding - Posterior acoustic shadowing - Calcifications Mammogram - Ill-defined hyperdense mass - Spiculate margins - Microcalcifications
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Oncology What are the principles of breast cancer management?
Surgery 1. Lumpectomy with WLE + RTx 2. Mastectomy - if very large tumour vs. breast size, C/I to RTx Endocrine - If ER/PR positive - Tamoxifen (oestrogen receptor antagonist) - pre or post-menopausal woman, increased risk of uterine cancer + VTE but still beneficial, 5-10 year course - Aromatase inhibitor (inhibits enzyme converting androgens to oestrogen) - post-menopausal woman only, requires adjunct bisphosphonates (increased risk of osteoporosis), 5 year course Chemo - Taxanes and/or anthacyclins - Used when there is high risk of reoccurence or advanced disease - 3-6 month course - Risk of reoccurence predicted by - younger or post-menopausal woman (more aggressive cancers), nodal status, receptor status (HER2 more aggressive), size and grade Targeted - Transtuzumab (herceptin) if HER2 receptor amplification (tyrosine kinase activity) - HER2 amplification occurs ~20% early cancers - More aggressive cancer with higher risk of reoccurrence