1) blood, emerg, CV system Flashcards
Iron deficiency anaemia:
- type of anaemia seen?
- GROUPS of causes? 4 (give specific examples)
which group most common causes
insufficient iron to support Hb production -> microcytic, hypochromic anaemia
nb iron is absorbed in duodenum
1) POOR DIET
= children / infants (rarer in adults)
2) MALABSORPTION = coeliac disease - IBD (- gastric bypass) - PPIs reduce iron absorption - low Vit C reduces - H Pylori reduces
4) BLOOD LOSS (commonest)
= menorrhagia
= GI bleed (incl NSAIDs)
- colonic / gastric Ca
IRON DEFICIENCY ANAEMIA
- initial symptoms? 2
- late / chronic signs? 4
- worrying symptoms/signs? 7
= SOB on exertion (1st)
= fatigue
- Koilonychia – spoon nails w/ longitudinal ridging
- Atrophic glossitis
- Angular cheilosis – ulceration at corners of mouth
- Pale conjunctiva
WORRYING
- Acute dyspnoea
- Dizzy / Syncope
- Palpitations
- chest pain
- ↑HR
- ↓BP
- bounding pulse
IRON DEFICIENCY ANAEMIA
- bloods (1 all, 2 consider)
- other investigations to consider to investigate cause? 5
BLOODS
= FBC (↓MCH ↓MCV ↓Hb)
- Ferritin
- blood film
TO FIND CAUSE
- coeliac screen (TTG +/-endoscopy)
- urine dip (bladder Ca)
- endoscopy (GI bleed)
- urea breath test (H Pylori)
- DRE (if fresh blood / malaena)
MANAGEMENT of IRON DEFICIENCY ANAEMIA:
- lifestyle? 1
- if not too serious? 1 (incl DOSE)
- if serious? 1 (incl when to give!)
EAT IRON RICH FOODS
- dark green veg, red meat, apricots, prunes, raisins
- have w vit C / orange juice
- less cows milk for kids
FERROUS SULPHATE
- 200mg TDS PO (can get IV)
- continue for at least 3 months to replensih stores
- check FBC 2-4wks after, then 2-4m after
BLOOD TRANFUSION
= if Hb < 70 (<80 if ACS)
Side effects of ferrous sulphate? 6
- nausea
- abdo discomfort
- reflux
- diarrhoea
= constipation - black stools
(don’t worry too much about learning these exactly - just know GI)
Causes of anaemia:
- microcytic? (2c, 3r)
- normocytic? (2c, 3r)
- macrocytic? (4c, 1r)
MICRO = iron-deficiency = chronic inflammation - lead poisoning - sideroblastic - thalassaemia (high no of cells, but small)
NORMO = chronic disease (incl CKD) = acute blood loss - haemolytic - bone marrow disorders - hyposplenism
MACRO = vit B12 deficiency / pernicious = folic acid deficiency = liver disease = hypothyroidism - reticulocytosis
EARLY reactions from blood product transfusions? 6
(within 24hrs)
just list them here (inidividual flashcards for each)
- febrile reactions
- bacterial contamination
- Transfusion-associated circulatory overload (TACO)
- transfusion related acute lung injury (TRALI)
- acute haemolytic reactions
- anaphylaxis
LATE reactions from blood product transfusions? 4
(after 24hrs - norm 5-10 days post)
DESCRIBE cause of each briefly
Late Reactions (> 24hrs, usually 5-10 days post transfusion)
1) INFECTIONS (HIV, Hep B/C, prions, protozoa)
- Risk very small < 1/100,000 due to screening procedures
2) GRAFT VS HOST DISEASE
- Due to T lymphocyte reaction, Immunocompromised most @ risk
3) POST TRANSFUSION PURPURA
- Fall in platelets 5-7 d post (can be lethal)
4) IRON OVERLOAD
- repeat transfusions most at risk
Possible symptoms of all late reactions to blood transfusion? 4
management of each of the 4 types of late reaction?
- fever
- jaundice
- falling Hb
- haemoglobinuria
1) INFECTIONS (HIV, Hep B/C, prions, protozoa)
- Risk very small < 1/100,000 due to screening procedures
= treat infection if poss
2) GRAFT VS HOST DISEASE
- Due to T lymphocyte reaction, Immunocompromised most @ risk
= No effective treatment
3) POST TRANSFUSION PURPURA
- Fall in platelets 5-7 d post (can be lethal)
= Treat with IV Ig
4) IRON OVERLOAD
- repeat transfusions most at risk
= Chelation therapy for @ risk groups
FEBRILE REACTION to blood transfusion:
- who most at risk?
- symptoms? 4
- timing of symptoms?
- management? 2
(1-2% of patients)
From HLA Abs
Pts w/ multiple Hx of transfusions (eg multiparous women) most @ risk
- Fever
- chills
- pruritis
- urticaria
symptoms start 1/1.5 hrs from transfusion
- slow transfusion
- give paracetamol
Paracetamol/antihistamines pre-transfusion reduces incidence of febrile reaction
BACTERIAL CONTAMINATION during blood transfusion:
- what blood product more common with?
- symptoms? 3
- management? 4 (3 to do, 1 to give)
More common in Platelets (stored @ higher temp)
- ↑Temp
- Rigors
- hypotension
- Stop transfusion
- call haematologist
- take blood cultures
- start broad spec Abx
blood transfusion causing FLUID OVERLOAD:
- other transfusiuon-specifc name for this?
- which patients at higher risk? 2
- management? 2 (to give)
Transfusion-associated circulatory overload (TACO)
@ Risk patients incl:
- chronic anaemia
- Heart failure
- give Oxygen
- IV furosemide
(consider central line and exchange trasfusion if still need the blood products)
Give transfusion slowly w/ Diuretic for HF patients
acute haemolytic reaction during transfusion
- aka?
- what nearly always due to?
- symptoms / signs? 6
- tming of onset of symptoms?
- management? (5 to do, 1 to give)
ABO/Rh incompatibility
nearly always due to incorrect labelling (never event)
- ↑Temp
- Flushing
- Hypotension
- Agitation
- Abdo or Chest Pain
- Oozing venepuncture sites
MANAGEMENT
- stop transfusion
- check identity / name on unit
- keep IV line open
- IV FLUID RESUS
- send blood back to lab
- direct coombs test
TRALI
- what does it stand for?
- what is it?
- symptoms/signs? 4
- investigations? 3
- management? 3
TRALI (transfusion related acute lung injury)
ARDS due to anti-leucocyte Abs in plasma (is a diagnosis of exclusion)
- Dyspnoea
- cough
- ↓Sats %
- fine creps B/L
INVESTIGATIONS
- repeat ABGs
- CXR
- anti-leucocyte Abs
MANAGEMENT
- 100% oxygen
- treat as ARDS (CPAP, ventilation, circulatory support)
- removedonor from pool
ANAPHYLAXIS caused by blood transfusion:
- symptoms/signs? 5
- management? (2 to do, 4 to give - incl DOSES)
- Cyanosis
- Bronchospasm/Stridor/SOB
- Soft tissue swelling
- urticaria
- hypotension
(basically symptoms of anaphylaxis)
- stop transfusion
- secure airway / call anaesthetist
- adrenaline 0.5mg (1:1000) IM
- chlorphenamine 10mg
- hydrocortisone 200mg
- salbutamol 5mg nebs
just treat as normal anaphylaxis - but don’t forget to stop transfusion!!
Difference between TACO and TRALI
- pathology?
TACO is just pure fluid overload - similar to acute HF
TRALI is a reaction to something in donor blood which triggers infalm response in lungs
eg BNP and heart size go up in TACO (which also has good response to diuretics - but not TRALI
also see pleural effusions / fluid on lungs in TACO, but not TRALI
TRALI is effectively a diagnosis of exclusion
MACROCYTIC ANAEMIAS
- two different types?
give the 2 conditions that cause one of them and the 4 commoner + 2 rarer conditions that cause the other
MEGALOBLASTIC
- abn. Erythroblasts in bone marrow have delayed maturation of nucleus relative to cytoplasm → defective DNA synthesis
= B12 deficiency
= FOLATE deficiency
NON-MEGALOBLASTIC = liver disease (incl alcohol) = pregnancy = hypothyroidism (severe) = reticulocytosis - myelodysplasia - cytotoxic drugs (eg azathioprine)
Causes of:
- B12 deficiency? 3
- folate deficiency? 4
B12 DEFICIENCY
- coeliac disease
- addison’s
- pernicious anaemia
FOLATE DEFICIENCY
- diet
- malabsorption
- leukaemia
- hepatitis
MACROCYTIC ANAEMIA
- initial symptoms? 2
- late / chronic signs? 3
- worrying symptoms/signs? 7
= SOB on exertion (1st)
= fatigue
- Glossitis (B12/pernicious)
- Angular stomatitis (B12/pernicious)
- Pale conjunctiva
WORRYING
- Acute dyspnoea
- Dizzy / Syncope
- Palpitations
- chest pain
- ↑HR
- ↓BP
- bounding pulse
Investigations for macrocytic anaemia:
- blood for all? 3
- other bloods to find cause? 4
- other investigation if can’t find cause?
= FBC
= B12
= Folate
- blood film (B12/liver/folate)
- LFTs
- TTG (coeliac screen)
- intrinsic factor auto-antibodies (pernicious)
bone marrow biopsy (if no obvious cause, must exclude leukaemia)
Most worrying complication of B12 deficiency:
- speed of onset?
- describe the clinical signs? (incl 1st thing to notice)
SUB-ACUTE COMBINED DEGENERATION of SPINAL CORD (SCDSC)
- insidious onset
SYMMETRICAL LOSS of:
DORSAL COLUMN
-> sensory + LOWER motor neurone signs
CORTICOSPINAL TRACTS -> motor + UPPER motor neurone signs
1st thing = sense of VIBRATION + proprioception
then ATAXIA -> stiffness + weakness
(don’t worry too much about specific signs - just know is symmetrical, slow and pathology)
nb CLASSIC TRIAD
- extensor plantar (UMN)
- absent ankle jerk (LMN)
- absent knee jerk (LMN)
Management of macrocytic anaemia:
- 1st step?
- replacement of vitamins? 2 (incl drug + route + which to start first)
1) TREAT UNDERLYING CAUSE
2) REPLACE VITAMINS
- vit B12 (1st!! - to avoid risk of SCDSC)
- folic acid
B12 = IM injections
- initially alternate days for 2 weeks, then every 3 months for life!
FOLIC ACID = PO tablets OD
- can also increase dietary intake: green veg, nuts, yeast, liver
if deficient in both, replace B12 first + wait for B12 to normalise before starting folic acid
Pernicous anaemia:
- pathology (incl where B12 absorbed)
- age of onset?
- common clinical sign? (incl why)
- bloods? 2
- management? 1
autoimmune gastritis -> reduction in INTRINSIC FACTOR -> reduced B12/IF binding so that B12 cannot be absorbed in TERMINAL ILEUM
tends to be >40s
LEMON TINGE (due to pallor AND mild jaundice)
BLOODS
- parietal cell Ab
- intrinsic factor auto-Ab
B12 injections every 3 months for life (initially more frequently to get levels up)
HAEMOLYTIC ANAEMIA
- pathology + two different types?
Premature breakdown of RBCs before their natural limyfespan (120 d)
may be INTRAVSCULAR (leading to jaundice) or EXTRAVASCULAR (due to immune complex formation or RBC defect spleen)
HAEMOLYTIC ANAEMIA - GROUPS of causes:
- acquired? 2
- hereditary? 3
ACQUIRED
1) Immune-mediated
2) NON-Immune mediated
HEREDITARY
1) enzyme defects
2) membrane defects
3) haemoglobinopathies
Acquired Immune-related Haemolytic Anaemias:
- aka?
- give examples of causes (all rare but be aware)
- give basic management (if relevant)
which are coombs +ve and whive -ve
ACQUIRED (immune mediated – all Coombs +ve except*)
A) DRUG-INDUCED
- penicillin, quinine
B) AI HAEMOLYTIC ANAEMIA (AIHA)
- Warm AIHA (IgG, pts. Require steroids/ immunosuppressants – CLL/SLE)
- Cold AIHA (IgM, worse in cold, pts. Avoid – lymphoma)
C) PAROXYSMAL COLD HAEMOGLOBINURIA
- inf. w/ syphilis/viruses predisposes AI reaction to cold
D) COOMBS -VE AIHA*
- Hepatitis (AI, B/C)
- post-flu/vaccine
- drugs (piperacillin, rituximab)
(don’t worry too much about understanding this alll…)
Acquired NON-immune-related Haemolytic Anaemias:
- causes? (2 commoner, 1 v rare)
1) MALARIA
- RBC haemolysis, Haemoglobinuria → black-water fever
2) MICROANGIOPATHIC HAEMOLYTIC ANAEMIA (MAHA)
- mechanical disruption of RBCs
3) Paroxysmal nocturnal hemoglobinuria (PNH)
- rare stem-cell disorder w/ bone marrow failure + thrombophilia
Give three commonest causes of MICROANGIOPATHIC HAEMOLYTIC ANAEMIA (MAHA)
nb condition is rare though
Haemolytic uraemic syndrome (HUS)
DIC
Pre-eclampsia
HEREDITARY causes of HAEMOLYTIC anaemia:
- enzyme defects? 2
- membrane defects? 1
- haemoglobinopathies? 2
for all list:
- recessive or dominant
- epidemiology
- management (if any)
ENZYME DEFECTS
1) G6PD deficiency (most common)
- X-linked
- middle-east
- precipitated by drugs e.g. aspirin, cipro, sulphonamides, fava beans (avoid these)
2) Pyruvate kinase deficiency
- ↓ATP production limits RBC survival
- autosomal recessive
MEMBRANE DEFECTS
A) Spherocytosis
- spherical RBCs trapped in spleen → extravascular haemolysis + splenomegaly
- autosomal dominant
= mx with folate ± splenectomy
HAEMOGLOBINOPATHIES
1) Sickle cell anaemia
- african / afrocarribean
= autosomal recessive
- see paeds notes
2) thalassaemias
- Mediterranean (incl Italy, Greece + Cyprus)
- Indian subcontinent
- Middle East
- China + southeast Asia
= autosomal recessive
- see paeds notes
CLINICAL PRESENTATION of HAEMOLYTIC anaemia
- general symptoms of anaemia? 5
- symptoms / signs specific to haemolytic anaemias? 4 (say which causes may indicate)
- what FHx symptoms to ask about? 2
GENERAL
- SOB on exertion
- fatigue
- lightheaded
- palpitations
- pallor
SPECIFIC
- jaundice (all haemolytic)
- dark urine (ie haemoglobinuria -> intravascular cause)
- splenomegaly (extravascular, eg CLL, SLE, malaria)
- fever (recent travel? malaria)
FHx
- jaundice
- anaemias
^may indicate hereditary cause
COOMBS TEST
- aka?
- what is it?
- what means if positive?
- when direct + indirect used?
ANTIGLOBULIN TESTING
= immunology laboratory procedure used to detect the presence of antibodies against circulating RBCs in the body, which then induce hemolysis
So if positive then aquired immune-mediated (AIHA) cause of haemolysis
DIRECT - if suspect acquired immune-mediated haemolytic anaemia (AIHA)
INDIRECT - used in ant-natal screening
APPROACH to determine CAUSE of HAEMOLYTIC anaemia - how answer each Q?
1) if there RBC breakdown?
2) is there increased RBC production?
3) Is haemolysis mainly extra or intravascular?
4) Why is there haemolysis?
1) IS THERE ↑RBC BREAKDOWN?
- Anaemia with normal or ↑MCV
- ↑Unconjugated Bilirubin from haemolysis (pre-hepatic)
- ↑Urinary urobilinogen (no urinary conjugated bilirubin)
- ↑Serum LDH (released from red cells during turnover)
2) IS THERE ↑RBC PRODUCTION
- ↑Reticulocytes (large immature RBCs) causing a ↑MCV
3) IS HAEMOLYSIS MAINLY EXTRA OR INTRAVASCULAR?
Extravascular = Splenomegaly
Intravascular:
- Haemoglobinuria
- ↑Free plasma Hb (released from RBC)
- ↓Plasma Haptoglobin (this mops up free Hb)
- Haemosiderinaemia (excess Hb is processed by kidneys)
WHY IS THERE HAEMOLYSIS?
- history (FHx, travel, DHx)
- see causes on other flashcard
(don’t worry too. much about this flashcard… went too much in depth…)
Investigations for HAEMOLYTIC ANAEMIA
- bedside test? 1
- bloods? 6
- imaging to consider? 2 (why)
URINE - haemoglobin + urobilinogen
BLOODS
- FBC
- reticulacytes
- blood film
- coombs test
- LDH
- LFTs (bilirubin)
IMAGING TO CONSIDER
- USS Spleen
- CXR (cardio-pulm status)
Blood film findings for haemoltic anaemia: - low MCH, low MCV? - sickle cells? - schistocytes? - heinz bodies / bite cells? - spherocytes? - thick + thin blood film? list which conditions would produce this finding
↓MCH ↓MCV → Thalassaemia
Sickle cells → sickle cell anaemia
Schistocytes (haemolysis) → MAHA
Heinz bodies/Bite cells → G6PD def.
Spherocytes → Hereditory spherocytosis or AIHA
Thick + Thin blood film → Malaria
HODGKINS LYMPHOMA
- what is it?
- characteristic types of cells you see? 2
malignant proliferation of lymphocytes → accumulate in LN (lymphadenopathy) and peripheral blood/organs
REED-STERNBERG cells (large, abnormal lymphocytes that may contain more than one nucleus)
LACUNAR cells (only in some sub-types)
HODGKINS LYMPHOMA
- gender + age?
- other risk factors? 4
M > F (2:1)
YOUNG! (early 20s)
- EBV
- obesity
- SLE
- post-transplant
HODGKINS LYMPHOMA:
- Main symptom / sign (describe fully + what makes it WORSE)
- what are A symptoms?
- what are the B symptoms? 3
LYMPHADENOPATHY (75%)
- painless + non-tender
- rubbery
- superficial
- asymmetirical
- typically cervical (also axillary + inguinal)
- size increases + decreases spontaneously
- become PAINFUL WITH ALCOHOL
(if mediastinal -> SVCO, recurrent laryngeal nerve -> hoarseness)
A SYMPTOMS
- no systemic upset, except PRURITIS
B SYMPTOMS
- weight loss (>10% in 6mo)
- fever >38
- night sweats (needing to change clothes)
HODGKINS LYMPHOMA
- bloods? 3
- other investigation? (and findings)
incl prognosis of findingd
- ESR (high = poor)
- FBC (low Hb = poor)
- LDH (increased dt increased cell turnover)
Tissue biopsy via LYMPH NODE EXCISION BIOPSY (US guided needle if can’t do excision)
REED STERNBERG and LACUNAR cells
nb 4 different histological classifications (here for ref, but don’t learn!)
A) Nodular sclerosis (70%) most common – good prognosis, Lacunar cells, usually female
B) Mixed cellularity (20%) – good prog, Reed-sternberg
C) Lymphocyte predom (5%) – best prog
D) Lymphocyte deplet (rare) – worst prog
HODGKINS LYMPHOMA
- how stage?
- staging system used?
- management?
- prognosis?
Staging via CXR, CT/PET thorax/abdo/pelvis + marrow biopsy
Ann Arbor System (I-IV) – influences Mx + prog
ChemoTx (ABVD) – Adrimycin, Bleomycin, Vinblastine, Dacarbazine
(don’t learn specific chemo drugs - just know have chemo!)
the 4 Ss of hodgkins lymphoma
‘S’ervical LAD
Systemic A + B sx
Splenomegaly
Sternberg cells (reed)
HON-HODGKIN LYMPHOMAS
- definition?
- which cell line norm come from?
- mechanism of action which normally precipitates / causes? (give examples)
- age group norm affected?
all lymphomas WITHOUT Reed-Sternberg cells
typically derived from B-cell lines (diffuse large B-cell lines (DLBCL) most common)
Normally linked with an IMMUNE DEFICIENCY process (either acquired or congenital)
- chemo
- HIV (EBV transformed cells)
- H.Pylori
- Toxins
- congenital
patients tend to be OLD (although some childhood)
NON-HODGKINS LYMPHOMA - main symptom / sign? additional symptoms/signs if: - skin affected? - oropharynx affected? - gut affected? - systemic symptoms?
Superficial LYMPHADENOPATHY (75% at presentation)
Skin Lympho -> Sezary syndrome (T-cell lymphoma)
Oropharynx Lympho ->
Odynophagia, Obstructed breathing (Waldeyer’s ring lymphoma)
Different types of Gut Lympho
1) Gastric MALT – caused by H.Pylori, involves antrum, multifocal and metastasises late
Gastric Ca w/ systemic Sx like fever, sweats
∆ Important to give triple therapy early in H.Pylori
2) Non-MALT Gastric – DLBCL, high-grade, do not respond well to H.Pylori eradication
3) Small bowel – immunoproliferative (IPSID), MALT or enteropathy/coeliac a/ T-cell lymphoma
Vomiting, abdominal pain, weight loss (poor prognosis)
Systemic symptoms – fever, night sweats, weight loss are LESS COMMON than Hodgkin’s lymphoma
NON-HODGKINS LYMPHOMA: what three features / complications can occur from bone marrow involvement?
ANAEMIA
- reduced RBCs
INFECTIONS
- reduced WBCs
BLEEDING
- reduced platelets
ie PANCYTOPENIA
Investigations for non-hodgkin’s lymphoma:
- 1st line?
- how stage?
- staging systom used?
Marrow biopsy (1st line) for classification and grade
Staging via CXR, CT/PET thorax/abdo/pelvis + marrow biopsy
Ann Arbor System (I-IV) – influences Mx + prog
Two main groups of non-hodgkins lymphoma?
principles of management + prognosis for each?
LOW GRADE
- indolent, incurable, widely disseminated
- E.g. follicular lymphoma, marginal zone lymphoma, MALT etc.
HIGH GRADE
- aggressive, but curable
- Treat with R-CHOP regimen
Burkitts lymphoma:
- high or low grade?
- age affected?
- characteristic sign?
high grade non-hodgkins lymphoma
childhood
characterised by JAW lymphadenopathy
What complication of all blood cancers can lead to AKI?
which cancer especially high risk?
TUMOUR LYSIS SYNDROME -> AKI
high-grade non-hodgkins lymphoma’s at especially high risk
Blood film appearance / buzz word for high grade non-hodgkins lymphoma?
‘starry sky’ appearance on blood film
MYELOMA
- what is it?
- describe the pathology?
- describe the three organ systems it most commonly affects and the pathology behind this
plasma cell dyscrasia (PCD) due to malignant proliferation of plasma cells
i.e. neoplasm of bone marrow plasma cells (occurs during terminal differentiation of B cells to plasma cells) →
A) Diffuse bone marrow infiltration → bone destruction (↑osteoclast/ ↓osteoblast → ↑Ca2+) + marrow failure
B) Secretion of Ig or paraprotein (detectable in urine) → organ dysfunction esp. renal disease
nb Sub-classified by Ab produced – IgG (66%), IgA (33%), some IgM, IgD
SYSTEMS AFFECTS
- blood
- bone
- kidneys (+ other end organs, incl heart)
MYELOMA
- three organ systems it affects?
- symptoms / signs of each of these?
BLOOD = symptoms dt bone marrow infiltration - anaemia -> lethargy - neutropenia -> infections - thrombocytopenia -> bleeding/bruising
BONE
= due to ↑osteoclast ↓osteoblast activity
- backache (common)
- bone pan
- pathological fractures
- vertebral collapse
- HYPERCALCAEMIA (↑bone resorption) – polyuria, polydipsia, fatigue, constipation, N+V, confusion, renal stones
KIDNEYS
= due to light Ig chain deposit w/ Tamm-Horsfall protein in distal loop of Henle
- ↓urine output
- AKI
MYELOMA risk factors
- age?
- ethnicity?
Age 70 yo
afro-carribeans > Caucasian (2:1)
nb RAS + oncogene mutation are often pathological cause
MYELOMA
- findings in FBC, U+E and LFTs, ESR?
- SPECIFIC findings on blood film?
FBC – normocytic normochromic anaemia (↓Hb)
Persistently ↑ESR or PV (plasma viscosity)
U+E = ↑Urea ↑Creat ↑Ca2+ (40%)
LFTs = ALP if healing fracture
Blood film = ROULEAUX FORMATION (red cells stack on each other → ↑ESR)
MYELOMA
- specific diagnostic tests for myeloma? 3
(think buzz words!)
(excl imaging)
SERUM electrophoresis
= MONOCLONAL PROTEIN BAND (paraprotein)
URINE electrophoresis
= BENCE JONES protein
“jones = a common name and urine is a common bedside test!”
BONE MARROW BIOPSY
- find plasma cells
(think about it, don’t normally find loads of plasma cells in bone marrow, normally just a few circulating in blood)
MYELOMA:
- two main types of imaging?
findings on these (incl buzz words)
what sort of bone lesions seen?
1) SKELETAL SURVEY X-Ray: - chest - spine - skull - pelvis
find LYTIC (punched out) bone lesions
e. g.:PEPPER-POT SKULL, Vertebral collapse, Fractures, Osteoporosis
2) nuclear imaging (Tc-99m MIBI) and PET
MYELOMA:
- diagnostic criteria?
- major criteria?
- minor criteria?
Criteria requires 1 major and 1 minor
MAJOR
- Monoclonal protein bands (paraprotein) in serum or urine electrophoresis
- > 30% Plasma cells on marrow biopsy
- Plasmacytoma on marrow biopsy
MINOR
- 10-30% plasma cells on marrow biopsy
- Minor ↑Monoclonal protein in serum or urine EP
- Osteolytic bone lesions on X-ray, CT/MRI, tc99-m MIBI, PET
- Low Ab levels (not produced by cancer cells) in blood
DON’T BOTHER LEARNING THESE PRECISELY - just be vaguely aware
MANAGEMENT of MYELOMA:
- to treat the cancer? 1
- to manage bone efffects? 1 (drug class + name examples)
- to manage haem effects? 2
- to manage renal effects? 1
- to manage infections? 2
- what to monitor? 5
TREAT MYELOMA
- chemo (intensive or low intensity)
BONE
- Bisphosphonates (help ↓fractures ↓bone pain ↓Ca2+) - clondronate, zolendronate
BLOOD
- blood transfusions
- erythropoetin
RENAL
- fluid + follow AKI guidelines
INFECTIONS
- antiobiotics (as appropriate)
- regular IV Ig infusions
MONITOR
- FBC
- U+E (creatinine)
- Ca 2+
- serum electrophoresis
- urine electrophoresis
^every 2-3 months
MYELOMA
- prognosis?
- two serious complications? (not incl bone, blood + renal issues as described in other flashcards)
INCURABLE
- chronic: relapsing + remitting
- treatment aimed at controlling disease + prolonging survival
AMYLOIDOSIS
- presenta as heart failure + nephrotic syndrome
METASTATIC SPINAL CORD COMPRESSION (MSCC)
- high risk for this
what is MGUS?
Monoclonal gammopathy of undetermined significance (MGUS)
If raised monoclonal proteins (paraprotein) but don’t meet criteria for MYELOMA
DIC
- what stand for?
- describe pathological process?
Disseminated Intravascular Coagulation (DIC)
dysregulation of coagulation + fibrinolysis → widespread clotting → all coagulation factors used up → resultant massive haemorrhages
Release of tissue factor (TF) from trauma or vasc damage → exposed to circulation (not normally)→ binds to coag factors → activation of extrinsic pathway → triggers intrinsic pathway
Thrombin and plasmin activation
(don’t know in detail but be aware of general principles)
DIC
- common groups of causes? 5
- Malignancy (leukaemia)
- sepsis
- trauma
- obstetric events (HELLP, amniotic fluid emboli, pre-eclampsia)
- Anti-phospholipid syndrome
DIC
- clinical presentation?
Large Bruising
/ Bleeding – can be anywhere
> 3 unrelated sites is highly suggestive (ENT, GI, resp, venepuncture site)
Skin: Petechiae, Purpura, Acral cyanosis, Necrosis of lower limbs, local infection
Renal failure
ARDS
DIC: specific findings on:
- clotting? 2
- FBC? 1
- blood film? 1
CLOTTING
- ↑PT
- ↑APTT
bleeding time gets longer
FBC
- ↓Platelets (get used up)
(also ↓Fibrinogen)
BLOOD FILM
- broken RBCs (shistocytes)
MANAGEMENT:
- criteria for platelet trasfusion?
- other potential management? 2
(nb management aside from treating the underlying condition!)
<50 platelets → Platelet transfusion
Replace clotting factors → FFP (fresh frozen plasma)
Activated protein C (reduces mortality in sepsis/organ failure)
DDx for DIC? 2
blood findings for both of these?
Von Willebrands Disease – bleeding into mucosa → only ↑bleeding time and ↑APTT
Vitamin K def - only ↑INR and ↑APTT
(don’t bother learning these! - this flashcard is just for interest!)
THROMBOPHILIA
- what is it?
- what most commonly present with?
increased tendency to clot
unprovoked DVT or PE
(nb can also present with recurrent miscarriages)
THROMBOPHILIA:
- most common cause?
- other causes to be vaguely aware of? 4
Factor V leiden
- aka activated protein C resistance
- heterozygous (5%), homozygous (0.5%)
- prothrombin gene mutation
- protein C + S deficiencies
- anti-thrombin III deficiency
- anti-phospholipid syndrome
THROMBOPHILIA:
- investigations? 5
- management? (regardless of cause)
- FBC
- clotting
- blood film
- lupus
- assays for anti-thrombin + protein C+S
^clotting anf FBC first then talk to specialist
long-term prophylactic ANTI-COAGULATION (eg warfarin or DOAC)
THROMBOCYTOPENIA
- what is it defined as?
- what level of platelets do you give platelet transfusion?
low platelet count
< 150
transfuse platelets if < 50
THROMBOCYTOPENIA CAUSES:
- congenital? 4
- decreased production of platelets? 8
- reduced survival of platelets? 7
- platelet dysfunction? 4
CONGENITAL
- Fanconi’s
- Wiskott-Aldrich
- Bernard-Soulier
- Leukaemia
↓PRODUCTION
- EBV
- rubella
- mumps
- HIV
- aplastic anaemia
- malig
- chemo
- alcohol
↓SURVIVAL
- ITP
- SLE
- RA
- sarcoidosis
- DIC
- HUS
- HELLP
PLATELET DYSFUNC.
- vWD
- CKD
- valve disease
- myeloma
don’t bother learning all!
clinical presentation of thrombocytopenia:
- signs on skin? 4
- bleeding from orifices? 8
DERM SIGNS
- Spontaneous bruising
- Petichiae
- Purpuria
- Ecchymoses
BLEEDING FROM ORIFFICES
- Epistaxis (frequent and prolonged)
- Bleeding gums (common in vWD)
- Haemoptysis
- Haematemesis
- Haematuria
- Menorrhagia
- Haematochezia (fresh blood PR)
- Melaena
THROMBOCYTOPENIA:
- investigations to consider? 4
- two main components of management?
- FBC
- clotting
- blood smear
- bone marrow biopsy (if >60)
MANAGEMENT
- treat underlying cause
- replace platelets + monitor as necessary
PANCYTOPENIA:
- three groups of blood cells that are reduced? (+ describe how each may present)
- which blood test used as screening? 1
ANAEMIA
- dyspnoea, fatigue, weak, pale, tachy
NEUTROPENIA
- infections
THROMBOCYTOPENIA
- epistaxis, bruising, bleeding
(nb depending on the cause, may also get other symptoms but these are the symptoms of the pancytopenia itself)
FBC
- low RBC, neutrophils + platelets
PANCYTOPENIA
- infections that can cause? 3
- other causes? 5
- iatrogenic cause?
- Hep B
- EBV
- parvovirus B19
- vit B12 def
- folate def
- aplastic anaemia
- lymphoma
- myeloma
adverse drug reactions:
- trimethoprim, chloramphenicol penicillamine, carbimazole, carbamazepine, tolbuatamide
Management of pancytopenia (aside from treating underlying cause)
- options? 3
- emergency? (how define + how to manage)
- blood transfusion
- platelet transfusion
- bone marrow transplant
FEBRILE NEUTROPENIA
- fever AND neutrophils < 1
- bufalo
- broad spec abx (eg tazocin)
Von Willebrands Disease
- inheritance pattern?
- 4 most common symptoms?
- management options? 3
autosomal dominant
- most common inherited bleeding disorder
(acts as a platelet deficiency disorder)
- bruising
- menorrhagia
- epistaxis
- bleeding gums
MANAGEMENT OPTIONS
- tranexamic acid (for mild)
- desmopressin (increases levels of vWF)
- factor VIII replacement
LEUKAEMIAS:
- which cells affected?
- demographics affected?
of:
- ALL
- AML
- CLL
- CML
ALL
= lymphoblasts
- children (“L for Little people”)
- most common malignancy affecting children (peak 2-5 years)
AML
= myeloidblasts
- “M for Middle aged + Mature (elderly)”
CLL
= Lymphocytes (almost always B lymphocytes)
CML = granular cells (basophils, eosinophils, neutrophils) - elderly pts 60-70yo "M for Mature" - can progress to AML (80%) or ALL (20%) - poor prognosis
“makes sense that the acute leukaemias would be blasts as these reporoduce fast!”
Which leukaemia is almost always caused by a translocation of a chromosome?
and what is the name of this chromosome?
CML
philadelphia chromosome
“philadelphia is a Massive area of land = cMl”
ACUTE LYMPHOBLASTIC LEUKAEMIA
- describe pathology?
- finding on blood film?
- staining finding that’s specifric to ALL?
↑No of Lymphoid Blast cells push other cells out of bone marrow acutely → rapid onset of Anaemic, Neutropenic, thrombocytopenic Sx
blood film = lymphoblast cells (blast cells >20% blone marrow)
+ve TDT staining
ACUTE MYELOID LEUKAEMIA
- findings on blood film?
- staining finding that’s specifric to AML?
blood film = myeloidblasts
AUER RODS
(seen with myeloperoxide stain - don’t bother learning name)
ACUTE LEUKAEMIAS (ALL + AML)
- groups of symptoms of bone marrow failure? 3
- other systemic symptoms? 3
- other symptoms? 2
RAPID onset MARROW FAILURE:
Anaemia – dyspnoea, pallor, lethargy
Thrombocytopenia – bruising, purpura
Neutropenia – recurrent infections
SYSTEMIC SX
- weight loss
- fever
- malaise
OTHER
- splenomegaly
- bone pain
CHRONIC LEUKAEMIAS (CML + CLL) - symptoms common to both? 2 - other CLL symptoms? 3 - other CML symptom? 1
finding on blood film for CLL
BOTH
- ↓Weight
- Loss of appetite
CLL
- Bleeding
- infections
- Lymphadenopathy
CML
- splenomegaly (significant)
“think of CML as all the granulocytes, and there’s so many different types of them + the whole of philadelphia that they all have to fit in the spleen”
BONE MARROW TRANSPLANT:
- indications? 5
- what does it involve?
basically anything that causes bone marrow failure
- severe aplastic anaemia
- leukaemias
- lymphomas
- myeloma
- other conditions (eg sickle cell anaemia, thalassaemia, severe combined immunodeficiency (SCID) and Hurler syndrome)
1) matching donor
2) marvest donor cells
3) conditioning (w chemo + radio)
4) transplanting cells
cariogenic + obstructive shock:
- difference between them?
- causes of cardiogenic shock?
- causes of obstructive shock?
Cardiogenic shock is due to inadequate function of the heart
In obstructive shock, hypoperfusion due to elevated resistance (there is an obstruction to the outflow of the heart)
CARIOGENIC
- acute MI
- heart failure
- valvular dysfunction
- arrythmias
“so anything strusturally wrong with heart itself = cardiogenic”
OBSTRUCTIVE
- cardiac tamponade
- pulmonary embolism (maasive)
- tension pneumothorax
- management of cardiogenic shock? 2
- management of obstructive shock? 1
CARDIOGENIC
- inotropes
- diuresis
^plus treat underlying cause!
OBSTRUCTIVE
- relieve obstruction
(drain pericardial effusion or pneumothorax + treat PE)
- common causes of distributive shock? 3
- common causes of hypovolemic shock? 3
DISTRIBUTIVE
- septic
- anaphylactic
- neurogenic (CNS damage)
HYPOVOLEMIC
- haemorrhage
- burns
- pancreatitis
FOUR TYPES of SHOCK:
- which cold/hot peripheries?
all cold, except DISTRIBUTIVE = HOT
so cardiogenic, hypovolemic + obstructive all cold
difference between neurogenic shock + spinal shock?
Neurogenic shock describes the hemodynamic changes resulting from a sudden loss of autonomic tone due to spinal cord injury. It is commonly seen when the level of the injury is above T6.
Spinal shock, on the other hand, refers to loss of all sensation below the level of injury and is not circulatory in nature.
ALTHOUGH different conditions - can occur simulateously in same pt following a spinal cord injury or can have one without other
SPINAL SHOCK
- cause?
- symptoms/signs?
- prognosis?
caused by acute spinal cord injury
BELOW SPINAL LEVEL INJURED
- decreased reflexes
- loss of sensation
- flaccid paralysis
HOWEVER
after a few weeks you have regain in function as nerves regrow (get UMN features first, hyperreflexia, spasticity etc, but then approach normal)
prognosis depends on extent of injury and other factors
- sooner start to regain function, the better!
Salicylate poisoning:
- most common drug caused by? 1
- which pts most at risk? 2
aspirin
old people and children more affected
(nb aspirin should not be given to children <12 - except for kawasaki)
SALICYLATE POSIONING
- initial / mild symptoms? 7
- signs in severe poiosoning? 3
INITIALLY
- vomiting
- dehydration
- tinnitus
- deafness
- sweating
- vasodilation
- hyperventilation
SEVERE
- confusion
- coma
- convulsions
nb rarely can also get:
- non-cardiogenic pulm oedema
- cerebral oedema
- renal failure
SALICYLATE POISONING
- bedside investigation? 1
- bloods? 5
- effects on blood gas?
- electrolyte disturbance that can occur?
- ECG (and full obs monitoring, esp if severe)
- Blood gas (ideally ABG!)
- FBC
- U+Es
- clotting
- glucose
- salicylate levels (take 2 hrs after ingestion for symptomatic pts + 4 hrs after ingestion for asymptomatic pts)
^as takes a while for levels to peak (esp if tablets are enterically coated
Blood gas
- MIXED metabolic acidosis AND respiratory alkalosis
- ie may be unclear
may get HYPOKALAEMIA!!!
SALICYLATE POISONING
- levels of salicylate (in mg/L) which indicate mild, moderate or severe poisonings?
- when should these levels be checked?
Salicylate plasma levels:
MILD = < 300mg/L
MODERATE = 300-700mg/L
SEVERE = > 700mg/L
but should also take into account clinical signs + symptoms too
this is different to how much aspirin pt has INGESTED - if taken < 125mg/kg body weight of aspirin then harm very unlikely
SALICYLATE LEVELS
= take 2 hrs after ingestion for symptomatic pts
= take 4 hrs after ingestion for asymptomatic pts
repeat after 2 hrs if levels high or still symptomatic
^as takes a while for levels to peak (esp if tablets are enterically coated
SALICYLATE poisoning MANAGEMENT
- if present within 1 hr of ingestion?
- mild poisoning? 1
- moderate poisoning? 3
- severe posioning?
also define salicylate levels that are considered mild, mnoderat + severe
activated charcoal if < 1 hr since ingestion
MILD
= < 300mg/L
- observe for 6hrs and, if normal VBG, can go home after this
MODERATE = 300-700mg/L - replace K+, if low - sodium bicarbonate (aka urinary alkalisation) - fluids (get dehydrated)
SEVERE
= > 700mg/L
- urgent haemodialysis / haemofiltration
(+ all above)
Iron overdose
- most common cause?
- other causes?
kids mistaking iron tablets for sweets
is also present in some weed / seed preperations
iron overdose
- inital signs + symptoms? 4
- features in severe poisoning? (6 early, 6 late)
what is timescale for early and late for severe poisoning?
INITIAL
- nausea
- vomiting
- diarrhoea
- abdo pain
vomit + stools often black / grey in colour
vast majority of patients don’t have further symptoms!!
SEVERE EARLY
= from ingestion -> 6-12 hrs post (then resolve)
- haematemesis
- drowsiness
- convulsions
- coma
- metabolic acidosis
- shock
SEVERE LATE
= deterioration 24-48hr post ingestion (following resolution of early features)
- metabolic acidosis
- shock
- hypoglycaemia
- jaundice
- hepatic encephalopathy
- renal failure
(occassionally bowel infarction too)
iron overdose
- bloods? 6 (+ findings)
- imaging if unsure of dose taken? 1
- serum IRON
- FBC
- VBG
- LFT
- INR
- glucose
(may get hyperglycaemia + increased WCC)
severe poisoning -> metabolic acidosis + may cause RBCs to haemolyse
ABDO X-RAY
- iron tablets are radio-opaque so can count on x-ray
iron overdose
- what management should avoid? 1
- management? (1 general, 1 specific)
- who to refer to? (and when)
- after how long does an asymptomatic pt have to be observed before can be safely discharged?
avoid charcoal (iron doesn't bind to it) - but can use whole bowel irrigation if still see un-disolved tablets on x-ray
1) SUPPORTIVE
2) IV infusion DESFERRIOXAMINE (infuse slowly!!)
nb if severe posioning, administer desferrioxamine before checking iron levels
REFER EARLY if severe (call poisons expert +/or ICU for help)
monitor asymptomatic pts for 6 HOURS - if still no symptoms - unlikely a toxic dose has been ingested - send home with safety-netting!
iron overdose
- complications of severe overdoses?
- how long after ingestion do they occur?
2-5 weeks after overdose may get:
- gastric strictures
- pyloric obstruction
Antidotes to common things overdosed on:
- paracetamol? 1
- aspirin (salicylate)? 2
- opiates? 1
- benzos? 1
- TCA? 1
- lithium? 2
- warfarin? 1
Paracetamol = Parvalex (n-acetylcysteine)
Aspirin (salicylate) = NaHCO3/haemodialysis
Opiates = naloxone
Benzo = Flumezanil
TCA = IV sodium bicarbonate
Lithium = saline and haemodialysis
Warfarin = vitamin K
Antidotes to common things overdosed on:
- iron? 1
- Ca channel blockers? 2
- Heparin? 1
- digoxin? 1
- Beta-blockers? 1
- non-depolarising muscle relaxant? 1
Iron = desFERRioxamine (FERRous)
Ca2+ channel blockers = calcium/glucagon
Heparin = protamine
Digoxin = digibind
Beta-blocker = glucagon
non-depolorising muscle relaxant = glycopyrrolate
RESPIRATORY ARREST:
- definition?
- most common cause?
- other causes? (2 CVS, 3 systemic, 4 neuro)
nb these are causes in adults (lots more can cause in kids as airways narrower!)
when a person stops breathing (ie apnoea) - no air movement at all
normally PROGGRESSION from resp distress -> resp failure (type 1 or 2) -> resp arrest!
OTHER CAUSES
- stroke
- MI
- drowning
- suffocation
- drug overdose
- head injury
- neuromuscular paralysis
- spinar injuries
- post-op cervical laminectomy (remove disc)
RESPIRATORY ARREST
- how to prevent?
- two principles of management? 2
know SIGNS of RESPIRTATORY DISTRESS so you can recognise before someone arrests
1) URGENT AIRWAY / RESP SUUPORT
- get help
- ventilate using bag-mask until able to get definitve airway
- also suctioning if necessary
2) TREAT UNDERLYING CAUSE
nb be careful not to overventilate (go at regular pace and not too much tidal volumne (a big enough squeeze to slightly raise the chest is enough)
HYPOTHERMIA
- at what temperature is this?
CORE body temp < 35 deg C
HYPOTHERMIA
- two main groups of causes in young adults?
- causes in elderly? 9
YOUNG ADULTS
- ENVIRONEMENTAL exposure (eg hill-walking ior cold water immersion)
- immobility / incapacity from ALCOHOL and/or DRUGS
ELDERLY
more commonly occurs indoors
- unsatisfactory housing
- poverty
- immobility
- lack of cold awareness (autonomic neuropathy, dementia)
- drugs (sedatives, anti-depressants)
- alcohol
- acute confusion
- infection
- hypothyroidism
HYPOTHERMIA
- clinical features at 32-35 degs? 4
- clinical features < 32 degs? 5
- what may happen if < 28 degs? 1
32 to 35 DEGS
- apathy
- amnesia
- dysarthria
- ataxia
LESS than 32 DEGS
- consciousness drops -> coma
- respiratory depression
- BP drops
- arrythmias
- muscle rigidity
shivering is an unreliable sign!
VF may occur spontaneously <28 degs
severe hypothermia can mimic death!! - as core temp drops, cerebral + CVS function deteriorates
nb check pulse for 1 min before diagnosing cardiac arrest! - as may just have very slow arrythmia!
HYPOTHERMIA
- what used to diagnose?
- bedside test? 1
- bloods?
- imaging to consider?
(justify all of the above)
use tympanic or rectal thermometer (oesophageal more acurate but need equipment)
nb typmanic + rectal temp may lag behind core temp during rewarming
- ECG (get lots of weird stuff! - AF and bradycardias are most common)
BLOODS
- FBC
- U+Es
- toxicology (incl alcohol)
- clotting
- blood glucose (don’t trust BM)
- amylase/lipase (often raised)
- ABG
- blood cultures (if suspect infective cause)
nb hypothermia often causes problems with clotting (as enzymes stiop working and clot cascade works slower)
CONSIDER
- CXR (to look for pneumonia / aspiration)
- CT head (if head injury or stroke suspected)
also consider other x-rays (eg for fractured hip) after rewarming complete
HYPOTHERMIA MANAGEMENT
- principles for all? 4 (regardless of severity)
- what to do if patient has cardiac arrest while hypothermic? 2
see specific re-warming methods on next flashcard
- treat in warm room (>21 degs)
- remove wet clothes + dry skin
- givewarmed, humidyfied oxygen by mask
- secure IV access but don’t pump with fluids (use a bit of warmed saline if need, but don’t overload or rely on warming this way)
- correct hypoglycaemia with IV glucose
CARDIAC ARREST
- if cardiac arrest - do CPR normally but don’t use drugs until >30degs
- can defib but if 3 shocks unsuccessful, wait till >30degs before trying again
^ warming is what’s going to treat the arrest!
HYPOTHERMIA MANAGEMENT
- rewarming option if mild? 1
- rewarming options if severe? 5
see general principles of management of hypothermia on previous flashcard
IF TEMP >32 degs = AIM FOR PASSIVE REWARMING (ie just allow the body to reheat itself)
- wrap in warm blankets +/- polyethene sheets (remember to cover tops and side of head)
ACTIVE RE-WARMING
- water bath at 41 degs (don’t use if other injuries, insecure airway or arresting)
- hot air blanket (ie bear hugger - is better, bit of warming and reduces heat loss)
CORE REWARMING
- inhale heated, humidified air
- consider peritoneal lavage (with warm water)
- cardiopulmonary bypass (ie bringing blood out , warming it, then putting back in) is ghold-standard if severe / cardiac arrest
DON’T BOTHER LEARNING OFF BY HEART (general prinicples and causes are more important!)
ACUTE LEFT VENTRICULAR FAILURE:
- commonest cause? 1
- other causes/ triggers? 3
acute MI = commonest cause
- arrhythmias
- iatrogenic (eg too much fluids in frail elderly w impaired LV function)
- sepsis
ACUTE LEFT VENTRICULAR FAILURE
- most predominant symptom?
- what exacerbates this?
- other symptoms? 2
- possible symptoms/signs related to underlying cause? 3
RAPID-ONSET SHORTNESS OF BREATH
- exacerbated by lying flat (improves on sitting up)
- looking + feeling unwell (often nauseous)
- cough (frothy white/pink sputum)
nb if right ventricuklar failure too - will get raised JVP and peripheral oedema
may also be signs + symptoms of cause:
- chest pain (ACS)
- sepsis (fever)
- palpitations (arrythmias)
ACUTE LEFT VENTRICULAR FAILURE
- most common changes to obs? 3
- possible findings on auscultation? 2
- what would hypotension indicate?
- raised RR
- low Sats
- raised HR
- 3rd heart sound
- bibasal crackles
hypotension would indicate cardiogenic shock!
ACUTE LEFT VENTRICULAR FAILURE
- bedside tests? 2
- immediate imaging? 1
- imaging later? 1
- KEY bloods to consider? 2
ie would probs do U+E, FBC etc as well
- ECG
- ABG (norm type 1 resp failure)
- CXR
- transthoracic echo
- BNP
- Troponin (especially if chest pain and/or ECG ischaemic changes)
U+Es also important - esp for monitoring
ACUTE LEFT VENTRICULAR FAILURE
- four main medications used? 4 (incl acronym)
- which 2 are most important?
- what super simple thing is also done to aid breathing?
- 2nd line management options if above aren’t working? 2
OMFG
- OXYGEN (sats >95%)
- Morphine (nb used less, act as vasodilators)
- FUROSEMIDE (40-80mg IV)
- GTN spray
O2 and furosemide are key ones for you to start then talk to senior before GTN or morphine!
SIT PATIENT UP!!!
to consider if not working (should have called for help by this point):
- nitrate infusion (if sys BP >100)
- CPAP
if BP<100 then treat as cardiogenic shock and get senior help (obvs you would have already!)
ALSO:
- monitor fluid balance and daily weights etc!
What ejection fraction is considered normal?
anything above 50%
CXR findings in left ventricular failure? 5
incl way to remember
A = Alveolar oedema (bat wing shadow) B = curley B lines C = cardiomegaly (>50% on PA) D = Dilated prominenet upper lobe vessels (upper lobe Diversion) E = pleural Effusion
ALSO fluid in horizontal fissure
scary DDx for rapid-onset breathlessness? 5
- PE
- pneumothorax
- pneumonia
- aspiration
- acute LV failure
this is NOT extensive - but is just things to consider as DDx
difference between low and high output heart failure?
which is most common?
- groups of causes of low output?
- causes of high output?
LOW OUTPUT
- demand for blood flow is norm, but heart is unable to meet demand -> decrease in renal perfusion -> activation of RAAS -> salt and water retension -> expansion of interstitial fluid + blood volumes -> pulm/peripheral oedema
causes of LOW OUTPUT:
1) pump failure (HF, bradycardia, negatively inotropic drugs)
2) excessive pre-load (mitral regurg, fluid overload)
3) excessive afterload (aortic stenosis)
HIGH OUTPUT
- cardiac output may be norm or a little high but demand for blood flow is high! therefore heart is unable to meet increased demand
- often presents with RVF initially
- much rarer
causes of HIGH output:
- anaemia
- pregnancy
- hyperthyroidism
What classification is used to rate the severity of heart failure (ie on functioning)
describe the 4 levels
NYHA classification
CLASS I
- ordinary physical activity, does not cause undue fatigue, palpitations, dyspnoea and/or angina
= ie NO SYMPTOMS w PHYSICAL ACTIVITIES
CLASS II
- ordinary physical activity does cause symptoms (see above)
= ie SYMPTOMS w PHYSICAL ACTIVITES
CLASS III
- less than ordinary physical activities causes symptoms (see above)
= ie SYMPTOMS w LITTLE PHYSICAL ACTIVITY
CLASS IV
- symptoms at rest
= ie SYMPTOMS AT REST
MEDICAL MANGEMENT OF HEART FAILURE:
- preserved ejection fraction? 1
- reduced ejection fraction? (1 symptomatic, 2 help mortality, 1 2nd line to help)
PRESERVED ejection fraction
- low-med dose loop diuretic
(- if also have HTN treat this too!)
REDUCED ejection fraction
- ACE inhibitor
- beta-blocker
- loop diuretics (for symp)
- mineralocoritcoid antagonist (eg spironolactone) is 2nd line
if still not working, refer to cardiology
nb see CCC notes for other stuff on chronic heart failure!
surgical management of heart failure:
- if valve problem?
- implantable devices? 2
- other option? (norm only if youngish)
if severe aortic stenosis / mitral prolapse etc then can have valve replacement etc
- cardiac resynchronisation therapy with defibrilator (CRT-D) or with pacing (CRT-P)
heart transplant - if severe and otherwise fit
nb see CCC notes for other stuff on chronic heart failure!
SUPERFICIAL THROMBOPHLEBITIS
- what is it?
- how does it present?
- name if in breast?
nb aka superficial vein thrombosis
inflammation of superficial vein (norm great saphenous) due to a blood clot
painful hard lumps under the skin with redness of surrounding skin
mondor’s disease = in breast
nb can occur anywhere!
SUPERFICIAL THROMBOPHLEBITIS
- main risk factor? 1
- other risk factors?
- two main risk factors for concurrent infection? 2
VARICOSE VEINS
basically anythign that increases your risk of VTE!! (smoking, overwieght, immobile, COCP/HRT, pregnancy, prev VTE, cancer, thrombophilia)
risk factors: (but also specifically increase your risk of a septic thrombus (ie infection as well as inflammation)
- recent cannula
- IVDU
SUPERFICIAL THROMBOPHLEBITIS:
- main DDx/complications? 3
- red flags for these? (or how to differentiate from thrombophlebitis)
- DVT (whole leg swllen, instead of lumps)
- infected thrombophlebitis (thrombophlebitis plus pus/surrounding cellulitis/ fever/ malaise)
- cellulitis (hot and red etc and over a lrger area)
SUPERFICIAL THROMBOPHLEBITIS
- diagnosis?
- investigation if repeated or concerned? 1
- medical management? 1
- self-care advice? 3
- how to dress/what to give to wear? 1
- prognosis?
- when to consider using Abx as well? 2
- when to consider anticoagulation? 2
norm clinical diagnosis
- venous USS if concered that close to groin or behind knee (ie where superficial veins meet deep)
- simple analgesia (paracetamol, nsaids) - norm use ibuprofen gel
- warm, moist towel/flannel to area may help pain
- keep leg elevated when sitting
- continue to use leg / be mobile (to reduce risk of DVT)
- COMPRESSION STOCKING (only after ruled out arterial insufficiency w ABPI)
norm lasts 2-3 weeks (then tender lump afterwards but not constantly painful)
Abx signs of infection:
- high fever
- malaise
consider LMWH if:
- increased risk of DVT/PE
- if thrombophlebitis is behind knee or near sapheno femoral junction (ie close to deep veins)
nb For people with recurrent superficial vein thrombosis with no obvious cause or risk factor, consider investigating for a coagulation disorder and/or cancer
nb Recurrent thromboses in superficial veins at various sites are called migratory thrombophlebitis. This is a pointer for malignancy, especially carcinoma of the tail of pancreas
CANNULA-RELATED PHLEBITIS
- what score is used by nurses to assess risk/presence of this?
- include the symptoms/signs that they look for at which stage
- also when do you re-site cannula and when do you treat? (ie Abx)
Visual infusion phlebitis (VIP) score
0 = NO SIGNS OF PHLEBITIS
- IV site appears healthy
= observe
1 = POSSIBLE 1ST SIGN OF PHLEBITIS - one of: --- slight pain at IV site --- redness near IV site = observe
2 = EARLY PHLEBITIS - two of: --- pain --- erythema --- SWELLING = resite cannula
3 = MEDIUM PHLEBITIS - all of: --- pain ALONG PATH OF CANNULA --- erythema --- INDURATION (hardening of soft tissue) = resite cannula = consider treatment
4 = ADVANCED PHLEBITIS / START THROMBOPHLEBITIS - all of: --- pain along path of cannula --- erythema --- induration --- PALPABLE VENOUS CORD = resite cannula = consider treatment
5 = ADVANCED THROMBOPHLEBITIS - all of: --- pain along path of cannula --- erythema --- induration --- palpable venous cord --- PYREXIA = inititate treatment = resite cannula
only remove a cannula once a new one has been sited!!!
CANNULA-RELATED PHLEBITIS
- how to prevent? 2
- which specific drug commonly gives phlebitis? 1 (non-infective)
- put cannulas in aseptically as possible
- don’t leave cannulas in for too many days and keep checking site
- AMIODARONE can cause phlebitis/thrombophlebitis
nb phlebitis can be: - mechanical - chemical - infectious (or all 3 / a combo)
CANNULA-RELATED PHLEBITIS
- symptomatic management medication?
- other things to do to reduce pain? 2
- medication to use if signs of infection? 1
- ibuprofen gel on area
- elevate limb
- warm, wet flannel on site
antibiotics - check trust guidelines! (assuming fluclox? but unsure?)
give Abx if VIP 5 (and consider if 3 or 4)
HEART BLOCK
- two commonest causes? 2
- classes of drugs that can cause/worsen? 3
- causes of cardiomyopathy -> heart block? 2
- infections -> heart block? 2
- metabolic cause? 1
= idiopathic (nb can also be pysiologicl in athletes)
= ischaemic heart disease
= beta blockers
= calcium channel blockers
= digoxin
nb cardiac interventions, eg surgery or septal ablation can also cause
cardiomyopathy, eg dute to:
- amyloidosis
- sarcoidosis
infections, eg
- lyme disease
- bacterial endocarditis
hyperkalaemia can also cause
four different types of heart block? (list them)
what PR interval is considered 1st degree heart block? (in squares and seconds)
is pulse regular in each?
1ST DEGREE
- fixed PR interval >200ms (5 little squares)
- regular pulse
2ND DEGREE:
MOBITZ TYPE I
- aka wenkiback
- gradually prolonging PR interval until drop a beat and then back to short PR
- irregular pulse
MOBITZ TYPE II
- fixed ratio between atrial contraction and ventricular contraction (eg 2:1 or 3:1 block)
- nb there is still relationship between atrial and ventricular contraction
- regularly irregular pulse
3RD DEGREE / COMPLETE
- no relationship between atrial and ventricular contraction
- regular pulse
nb in 3rd degree: if narrow QRS then ventricular ryhthm originates close to AV node, if wide then originates more distally
HEART BLOCK:
- possible signs/symptoms? 6
- which types tend to be symptomatic?
- fatigue
- dyspnoea
- palpitaitons
- chest pain
- dizzy
- syncope
mobitz type 2 and third degree more likely to be symptomatic
Acute management of heart block:
- which ALS algorithm to follow?
- summarise the key points of this guideline
- what are the 4 adverse features? what would you do if any of these features? (incl dose)
BRADYCARDIA ALGORITHM
A-E assess
- give O2 if hypoxic
- monitor ECG + BP
- IV access
- identify + treat reversible cause
adverse features = HISS
- heart failure
- ischaemia
- shock
- syncope
if adverse features:
- atropine 500micrograms IV
also give atropine if any risk of asystole:
- recent asystole
- mobitz II block
- complete heart block
- ventricular pause >3 sec
if satisfactory response then observe
if not:
- can repeat atropine or other drugs or transcutaneous pacing
**see algorithm for full guidance
HEART BLOCK:
- which types get pacemakers?
- what drugs to consider stopping?
mobitz type 2 and 3rd degree get pacemaker
consider stopping:
- beta blockers
- calcium channel blockers
- digoxin
(but look at why on these drugs - risk vs benefits)
ECG FEATURES OF:
- bivasicular block?
- trivasicular block?
and what do each of them actually mean?
BIVASICULAR BLOCK
- right bundle branch block PLUS left anterior OR left posterior block
= ECG: RBBB + left axis deviation
TRIVASICULAR BLOCK
- right bundle branch block PLUS left anterior AND left posterior block
= ECG: RBBB + left axis deviation PLUS 1st degree beart block
SUPRAVENTRICULAR TACHYCARDIA
- technical definition?
- what actually normally referring to?
- pathophysiology?
- what look like on ECG?
supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin - eg could include AF, flutter etc
BUT normally referring to PAROXYSMAL SVT
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
- symptoms of all types? 5
paroxisms of:
- palpitations
- dizziness
- SOB
- chest pain
- syncope
nb these can self-resolve or progress to haemodynamic instability
SVT acute management in hospital
- what algorithm to use?
- what are 4 adverse features?
- what to do if any adverse features?
- what to do if no adverse features and is REGULAR and NARROW TACHY? describe 2 steps
incl drug doses
adult tachycardia algorithm
HISS
- heart failure
- ischaemia
- syncope
- shock
if adverse features:
- SYNCHRONISED DC shock (up to 3) - do bedside echo before to check for clot!
(then can give amiodarone)
if stable:
1) vagal manouveres (sinus massage and valsalva manouveres)
2) adenosine (6mg, 12mg, 12mg)
3) synchronised DC shock (if still in rhythm)
DDx for SVT? 5
- paroxysmal SVT
- wolf-parkinson white (have bundle of kent)
- AF
- atrial flutter
- ventricular tachycardia (with pulse)
SVT:
- as well as ECG, what other investigation should all pts probably have? 1
- management options if recurrent? 3
should have an ECHO
- beta blockers
- ablation
- amiodarone
Congential cause of SVT?
features on ECG? 2
management?
Wolf-parkinson white
congenital accessory pathway between atria + ventricles
resting ECG
- short PR interval
- wide QRS (dt slurred upstroke: delta wave)
patients present with episodes of SVT
refer to cardiology for electrophysiology + ablation
MITRAL REGURG
- causes? 5
- gender and age most affected? 2
- other risk factors? 5 (think about causes)
CAUSES
- POST-MI (if MI affects papillary muscles or chordae teninae)
- MITRAL VALVE PROLAPSE (norm iatrogenic and mild)
- infective endocarditis
- rheumatic fever
- congenital
RISK FACTORS
- Female sex
- Age
- Lower body mass
- Renal dysfunction
- Prior myocardial infarction
- Prior mitral stenosis or valve prolapse
- Collagen disorders (e.g. Marfan’s or Ehlers-Danlos)
MITRAL REGURG:
- describe murmur? (when and quality etc)
- at what severity do you get symptoms? what are these symptom due to (ie complications)? 3
MURMUR
- pansystolic
- ‘blowing’
- heard best at apex (5th intercostal space, mid-clav) + radiates to axilla
- S1 may be quiet dt incomplete closure of valve
- severe MR may -> widely split S2
(nb a VSD can lso give a similar murmur)
mild + moderate tend to be asymptomatica
severe get symptoms mainly due to:
- LV failure
- arrhythmias (often get AF)
- pulm hypertension
so amy present as SOB, fatigue, oedema, palpitations etc
nb can present as ACUTE PULM OEDEMA: following an acute MI, papillary muscle rupture can occur → acute mitral regurgitation (→haemodynamic compromise) Murmur may be inaudible
MITRAL REGURG:
- key investigation to get?
- what must be high on differnetial for acute mitral regurg?
- what may see on ECG?
- what may see on CXR if severe?
ECHO REALLY IMPORTANT TO ASSESS SEVERITY and if any HF!
MI: check ECG if acute mitral regurg - to rule out MI! (also do trop!)
ECG may show:
- a broad P wave, indicative of atrial enlargement
- may also have concurrent AF!
(- may also have LV hypertrophy if chronic)
Cardiomegaly may be seen on CXR
Management of mitral regurg:
- immediate medical management if acute? 2
- medical options for chronic? 3
- surgical options? 3
- indications for surgery? 2
- what do you need to do before surgery? 1
treat the acute pulm oedema:
- nitrates
- furosemide
(consider inotropes if low BP and resynchronisation if AF)
chronic MR (basically treating the heart failure): - loop diuretics - ACEi - beta blockers
surgery
- valve repair (better if poss) or valve replacement (pig or mechanical)
do surgery
- ALL acute MR need URGENTLY
- chronic MR with failure of medical management (LVEF 30-60% - lower than 30% success rate is too low!)
need a transOESOPHAGEAL echo before surgery (?? even if need urgently)
nb can also use intra-aortic balloon pump as a bridging measure
Drugs that cause QTc prolongation:
- which betablocker? 1
- which Abx? 1
- which opioid? 1
- which classes of antidepressants? 2
- which other psychoactive group of drugs? 1
- sotalol
- erythromycin
- methadone
- TCAs
- SSRIs (esp citalopram)
- antipsychotics (incl haloperidol)
MITRAL STENOSIS:
- main 4 causes? (which most common)
- what complications normally present with? 2
= RHEUMATIC FEVER
- degenrative calcification
- infective endocarditis (nb technically this mimics it - large vegetation on valve)
- congenital
- autoimmune conditions (RA, SLE)
complciations often present with:
- pulm HTN/oedema (dt backflow then -> RVH)
- AF (dt stretch of pacemaker cells as left atrium enlarges)
MITRAL STENOSIS
- peripheral sign on examination?
- murmur / sounds heard on auscultation?
- other findings on cardiac exam?
MALAR FLUSH (mauve discolouration of the cheeks due to low cardiac output and systemic vasoconstriction)
AUSCULTATION
- DIASTOLIC murmur WITH loud first heart sound (S1)
can also get:
- raised JVP
- RV heave
- laterally displaced apex beat
- signs of LV failure (although actually only left atrium that’s failing) -> RV failure signs
MITRAL STENOSIS
- diagnostic investigation? 1
- possible findings on ECG? 2
- possible findings on CXR? 2
ECHO (TTE for all, TOE if surgery plan)
ECG
- P mitrale (biphasic and/or wide P wave - also often tall) - dt left atrium hypertrophy
- AF (complication)
CXR
- get left atrium enlargement (can see double heart border)
- signs of pulm oedema (kerley B lines, fluid in fissure etc)
MITRAL STENOSIS
- medical management options? 3
- what class of drug SHOULDN’T you use?
- what prophylactic mx can you give? 1 (to who?)
- surgical options? 2 (who gets?)
MEDICAL
- diuretics for the HF
- beta blockers
- calcium channel blockers
DON’T give ACEi/ARBs as can cause dilation of peripheral blood vessels -> cardiac decompensation
can give infective endocarditis prophylaxis if hig risk, eg prosthetic valve or Hx of IE
SURGICAL OPTIONS:
1st line) percutaneous balloon commissurotomy of valve
2nd line) open commissurotomy or mechanical or bio valve replacement
indications for surgery:
- severe mitral stenosis
- symptomatic mitral stenosis
nb can only do 1st line if no calcifications on valve, no left atrial thrombus, no/mild mitral regurg
MITRAL STENOSIS:
- cardiac complications? 3
- other complcations? 2
- AF (-> thromboembolic stuff)
- pulm HTN/congestion/oedema
- congestive heart failure
if left atrium get’s really enlarged can get (rare):
- oeseophageal compression (dysphagia)
- recurrent laryngeal nerve palsy (hoarse voice)
AORTIC REGURG
- describe pathophysiology (incl what major complication can occur)
aortic root dilatation OR valvular disease → Aortic valve does not close properly (incompetent) → leakage of blood from aorta, via aortic valve, into left ventricle (regurgitation) during diastole → ↑Stroke volume in LV → ↑Systolic BP ↓Diastolic BP → ↑Pulse pressure (= systolic – diastolic) → eventually LV hypertrophy
AORTIC REGURG
- causes of acute? 3
- causes of chronic? (1 congenital, 2 infective, 3 other chronic med conditions)
ACUTE
- infective endocarditis
- aortic dissection (ascending aorta)
- chest trauma
CHRONIC
= congenital bicuspid valve (commonest in developed countries)
= rheumatic heart disease (commonest in developing)
- tertiary syphillis
- collagen diseases (marfans, ehlers danlos)
- RA/SLE
- ank spond
nb can also divide them by:
- causes dt valve disease (rheum fever, IE, RA/SLE, bicuspid valve)
- causes dt aortic root disease (dissection, ank spond, HTN, syphillis, marfans/ehlers danlos)
which valve defect causes a water hammer / collapsing pulse?
describe the pathophysiology
aortic regurg
Regurgitation of blood from the aorta into the left ventricle (LV)
→ Increased systolic blood pressure and decreased diastolic pressure
→ Widened pulse pressure → water hammer / collapsing pulse
aortic regurg presentation:
- acute? (1 main symptom, other symp)
- chronic? (1 symptom, 1 complication norm present with, 1 additional sign unique to AR)
ACUTE
- sudden, severe SOB (pulm oedema) dt sudden heart failure
- symptoms related to underlying disease (eg fever if IE, chest pain if dissection)
CHRONIC
- may be asymptomatic for years despite LV dilitation
- palpitaitons
- symptoms of left heart failure (exertional SOB, orthopnoea, fatigue)
- signs of high pulse pressure (nodding of head = de musset sign)
nb other weird signs for high pulse pressure (don’t bother learning):
Corrigan’s sign – carotid pulsation
Quincks sign – capillary pulsation in nail bed
Duroziez’s sign – groin, finger compresses femoral artery → systolic murmur 2cm proximal to stethoscope gives systolic murmur and then diastolic murmur as blood flows back
Traube’s sign- pistol shot sound over femoral arteries
Austin Flint murmur – cooing dove sound at aortic region indicates valve has collapsed and is absolutely incompetent, this indicates severe AR → valve replacement
AORTIC REGURG
- finding on auscultation?
- main other sign on cardiac exam? 1
AUSCULTATION
- early diastolic murmur (best heard L or R sternal border) (intensity of the murmur is increased by the handgrip manoeuvre)
- collapsing pulse
- wide pulse pressure (eg BP of 140/50)
nb can get other weird murmurs in later stages
AORTIC REGURG:
- main investigation?
- finding on ECG? 1
- finding on CXR? 1
echo (TTE or TOE if surgery)
ECG: LV hypertrophy
CXR: cardiomegaly +/- pulm oedema
AORTIC REGURG:
- medical mx?
- surgical mx? 2 (2 indications)
MEDICAL
- treatment for HF (ACEi, beta blockers +/- loop diuretics or spironalactone)
surgery = valve replacement (bio or mechanical)
indications for surg
- symptomatic pts w acute severe AR
- asymptomatic pts with EF <50% or really increase LV size
nb if mechanical need warfarin for life!
nb occassionally valve reconstruction is possible, but norm replace!
AORTIC STENOSIS
- commonest cause <65years? 1
- commonest cause >65 years? 1
- other rarer cause? 1
- what can mimic it? 1
is most common valvular disease (2nd is mitral regurg)
= bicuspid aortic valve (<65)
= calcifcation (>65)
- rheumatic fever (rare)
nb can be mimiced by pseudo-stenosis
- ie LVF means perssure can’t open aortic valve much (use dobutamine stress echo to tell difference)
AORTIC STENOSIS:
- typical triad of symptoms? 3 (way to remember)
- auscultation finding? 1
- what happens to BP?
- exertional SOB
- angina
- syncope (on exertion)
think SAD: syncope, angina, dyspnoea
get a loud EJECTION SYSTOLIC MURMUR (radiates to CAROTIDS)
get a narrow pulse pressure if severe (ie systolic + diastolic BP are close to each other - opposite to aortic regurg)
nb DDx is anything that causes: SOB, angina or syncope - ie BROAD!! - so always listen to heart if any of these symptoms!
AORTIC STENOSIS:
- main investigation? 1
- sign on ECG? 1
- why do a CXR?
- what other investigation do get before surgery? 1
echo (TTE for all, TOE if surgery)
ECG signs of LVH
do CXR to rule out other causes of dyspnoea!
do coronary angiography before surgery so can see how much of angina is dt aortic stenosis and hopw much due to narrowibng of coronaries!
AORTIC STENOSIS:
- if asymptomatic mild-moderate?
- if symptomatic or severe?
if asymptomatic and mild/moderate
- annual TTEs to assess porogression
if symptomatic OR severe stenosis (incl significatly low EF)
- surgical replacement of valve!
ie presence of exrtional dyspnoea, angina or syncope is an indication for surgery!
nb can also do percutaneous balloon valvuplasty in child or young person w no calcification
nb
Asymptomatic patients: Mortality rate is < 1% in a given year
Symptomatic patients: Mortality rate in the first 2 years is > 50% if left untreated
nb remember do coronary angiogram as well is having surgery!
Common BACTERIA to cause INFECTIVE ENDOCARDITIS:
- commonest overall?
- commonest in IVDU?
- commonest in prosthetic valves?
- commonest in poor dental hygiene / dental procedure?
- associated w colorectal cancer?
commonest overall (incl in prosthetic valves etc) = staph aureus
IVDU
= staph aureus (nb norm tricuspid valve that’s affected)
prosthetic valves
= staph epidermis
(nb if early <1 year diff organisms to late >1 year post-surgery)
poor dental hygiene / dental procedures
= strep viridans (eg strep mitis, strep sanguinis)
colorectal cancer
= strep bovis (esp strep strep gallolyticus)
nb can also rarely be caused by SLE or malignancy too
nb can also be pseudomonas aruginosa or HACEK organisms (haemohilus, actinobacillus, cardiobacterium, eikenella, kingella)
Risk factors for infective endocarditis:
- biggest risk? 1
- other main risk factors? 4
- what % have previously normal valves? 1 (ie not prosthetic or damaged)
biggest risk = prev episode of IE!
- rheumatic valve disease
- prosthetic valves
- congenital heart disease
- IVDU
nb also recent piercings or dental procedures or poor dental hygiene
50% have previously normal valves!!
“Don’t TRI drugs for the sake of your TRIcuspid valves”
acute vs subacute infective endocarditis
- time scale?
- normal or prosthetic/damaged valves?
- which organism more likely to be caused by?
- describe symptoms / presentation of each
nb don’t list clinical signs - this is on another flashcard
ACUTE
= hrs-days
= normal valves
= staph aureus
- fever AND CHILLS/rigors
- night sweats
- malaise / fatigue
- symptoms of acute HF (SOB, or peripheral oedema etc)
SUBACUTE
= weeks-months
= damaged/prostheritc heart valves or or other structural heart defects
= viridans streptococci
- Fever and chills (90%)
- night sweats
- General malaise, weakness
- weight loss
- Dyspnea, cough, pleuritic chest pain
- Arthralgias, myalgias
^ie flu-like symptoms
nb elderly pts may not have a fever!
Fever of unknown origin AND new murmur is IE until proven otherwise!
INFECTIVE ENDOCARDITIS
- what criteria used for diagnosis?
- what two investigations do you need to be able to use these criteria? 2
- describe the criteria (main points)
MODIFIED DUKES CRITERIA
need:
- echo (TTE 1st then TOE if see nothing)
- blood cultures (repeated)
MAJOR
- 2 or more positive blood cultures for typical organisms
- classic ECHO findings (vegetation, new valve prolapse, abscess)
MINOR
- pre-disposing condition (underlying heart or valve abnormality, IVDU)
- fever >38
- vascular abnormalities
- immunological phenomina
- one positive blood culture
PATHOLOGICAL
- bacteria present on tissue culture / histology of bit of heart valve
definite IE if:
- 2 major
- 1 major and 3 minor
- 5 minor
- 1 pathological
possible IE if:
- 1 major and 1 minor
- 3 minor
VASCULAR ABNORMALITIES:
- Septic infarctions (eg stroke)
- conjunctival or intracranial hemorrhages
- mycotic aneurysm
- Janeway lesions (painless)
- splinter haemorrhage
IMMUNOLOGICAL PHENOMINA
- Glomerulonephritis
- Osler nodes (painful)
- Roth spots (retinal haemorrhage)
- positive rheumatoid factor
nb left sided tends to present with systemic emboli signs, right sided only really get infective PEs
nb negative blood cultures don’t rule out IE - could be due to Abx being taken prior to sampling OR fastidious bacteria (eg coxiella or bartonella)
nb norm also have anaemia and raised inflamm markers and WBCs
nb wopuld also do an ECG (PR elongation may indicate a aortic root abscess)
MANAGEMENT of INFECTIVE ENDOCARDITIS:
- if unstable / septic? 6
- after taken blood cultures, who to consult?
- what medication to start?
- what determines targetted Abx choice?
- how long have Abx for?
- indications for surgery?
BUFALO if septic!
consult infectious diseases about what empirirc therapy to start
- give more Abx if prosthetic valves!
once cultures are back - give targetted Abx depending on:
- what grown
- native or prosthetic valves
(- also pen allergy)
(see amboss and passmed for which Abx)
2-6 weeks (depends on which valve affected, what grown, native or prosthetic etc)
indications for surgery:
- prosthetic valve endocarditis
- aortic root abscess (ie new heart block)
- infections resistant to Abx/antifungals
- refractory heart failure
- severe vavular incompetence
- recurrent emboli after Abx therapy
nb fluclox if native valve with staph aureus
Complications of infective endocarditis:
- local infection? sign on ECG?
- other heart complications? 2
- major non-heart complicaiton? 1
aortic root abscess (get widening PR interval - ie 1st deg heart block)
- heart failure
- ongoing valvular disease/damage
septic emboli (scariest is stroke)
can also get other ones like kidney damage etc but these are main 3 to worry about!
ANEURYSMS
- definition of an aneurysm?
- difference between true and pseudo?
- common sites? 4
an artery with a dilitation >50% of its original diameter
true = all layers pseudo = only outer layer (adventitia)
- aorta (infrarenal most common)
- iliac
- femoral
- popliteal
nb two main types:
- Fusiform aneurysms e.g. AAA
- Sac like e.g. Berry Aneurysms
ANEURYSMS
- types of complications? 4
- rupture
- thrombosis/emboli
- fistulae
- pressure on other structures
CAUSES/RISK FACTORS OF ANEURYSMS:
- infective? 2
- collagen disorders? 2
- inflamm? 1
- other? 2
- mycotic in endocarditis
- tertiary syphillis
- ehlers danlos
- marfans
- takayasu’s aortitis
- atheroma
- trauma
nb also specific RFs for AAA and berry aneurysms - covered in other flashcards
VARICOSE VEINS:
- age and gender risk?
- lifestyle risks? 2
- other main risk factors? 3
- female
- increased age
- obesity
- long periods standing/sitting (esp teachers!)
- FHx of varicose veins
- PMHx of DVT
- pregnancy
VARICOSE VEINS
- main symptoms? 4
symptoms not always present - people often just don’t like appearance of them
- pain, aching, discomfort
- swelling, heaviness
- itching
- burning sensation / parasthesia
VARICOSE VEINS
- complications? 6
- bleeding
- superficial thrombophlebitis
- DVT
- venous ulcers
- changes in skin pigmentation
- saphena varix (dilation in saphenous vein at confluence w femoral vein -> get a cough impulse and can be mistaken for an inguinal/femoral hernia!)
nb these are UNCOMMON!
management of VARICOSE VEINS:
- if bleeding? 2
- if not bleeding:
- – self-care advice? 4
- – other conservative mx option? 1
- management during pregnancy?
IF BLEEDING
- first aid to stop bleeding
- refer to vascular
IF NOT BLEEDING:
advice:
- loose weight (if applicable)
- light-moderate exercise
- avoid sitting/standing for long periods
- elevate legs where possible
compression stockings (if no arterial insufficiency - do ABPI)
in pregnancy:
- rare to treat - will get a lot better after birth! - so tend to just wait! (can have compression stockings)
VARICOSE VEINS
- when to refer to vascular surgery? 5
- what investigation will they do 1st line? 1
- management options they may do? 3
REFER IF:
- very symptomatic (pain, aching, sweling, itching)
- pigmentation / skin changes / venous eczema
- superficial thrombophlebitis
- active or healed venous leg ulcers (>2 wks to heal)
- bleeding
vascular will do an USS
surgical options (refer to vascular):
- endothermal ablation
- foam sclerotherapy
- surgery
Chronic lower limb ischaemia
- risk factors? 5 (which is biggest?)
- inital and predominant symptom?
- other signs/symptoms?
aka Peripheral vascular disease (PVD)
= SMOKING
- increased age
- high BP
- high cholesterol
- diabetes
intermittent claudication in calves (both, although one may be worse than other)
- stops after a few mins of rest
(think of as angina in legs!)
- hair loss
- brittle/slow-growing toe nails
- pale/blueish legs (also shiny)
- arterial ulcers
- numbness / weakness
- muscle wasting
- erectile dysfunction
nb can also get claudicatin in buttock or thigh as well - but calf most common
Peripheral arterial disease:
- classification used?
- describe 4 stages of this
Fontaine Classification of PAD
Stage I (20-50%) = Asymptomatic PAD
Stage II
= Pain on exertion
IIa: claudication at a walking distance > 200m
IIb: claudication walking distance < 200 m
Stage III
= Ischemic pain at rest
Stage IV
= Necrosis, ulcers or gangrene (can be dry or humid)
nb ischaemic pain at rest IMPROVES when sit/stand (ie worse when lying down)
CHRONIC LOWER LIMB ISCHAEMIA
- inital investigation for all? 1 (incl rough values)
- other possible investigations? 3
ABPI
- <0.8 indicative of disease
- 0.5-0.8 will likely have intermittent claudicaiton
- <05.5 needs urgent referral
- USS
- Digital subtraction angiography (DSA): gold standard
- CT or MRI angiography
nb Greater than 1.3 may suggest the presence of arterial calcification, such as in some people with diabetes, rheumatoid arthritis, systemic vasculitis, atherosclerotic disease, and advanced chronic renal failure. For values above 1.5, the vessels are likely to be incompressible, and the result cannot be relied on to guide clinical decisions
- if greater than 1.3 consider referring to vascular!
CHRONIC LOWER LIMB ISCHAEMIA
- main lifestyle advice? 1
- 1st line mx for intermittent claudication?
- two main options if 1st line fails? 2
- medications to manage cardiovascular risk in ALL people with PVD? 2
- other things that should be managed in all? 3
STOP SMOKING!
1st line) 3 MONTHS of supervised graded exercise (exercise to point of maximal pain)
if failure to improve after 3 months
1) refer to vascular for angioplasty or bypass surgery
2) if person doesn’t want surgery: trial NAFTIDROFURYL OXALATE (try for 3-6 months, stop if no benefit after this)
MEDS FOR ALL:
- statin (regardless of QRISK)
- aspirin (consider PPI)
manage cardiovascular risk
- loose weight / less fat in diet
- control HTN
- control diabetes
ACCELERATED HYPERTENSION:
- definition in terms of systolic and/or diastolic BP?
- drug-related causes? (1 adherence, 3 med, 4 recreation)
- medical conditions? (2 endocrine, 1 obstetric, 4 other)
an ACUTE increase in blood pressure:
- systolic ≥ 180
AND/OR
- diastolic ≥ 120
CAUSES
- non-adherence to anti-hypertensives
- TCAs
- MAO inhibitors (esp when eat tyrosine foods too)
- NSAIDs
- cocaine
- amphetamines
- ecstasy
- stimulant diet pills
- pheochromocytoma
- hyperthyroidism
- eclampsia / preeclampsia
- acute + rapidly progressing renal disorders
- collagen vascular diseases (eg SLE)
- head trauma
- spinal cord disorders
ACCELERATED HYPERTENSION:
- non-specific symptoms?
end-organ dysfunction:
- cardiac? 3
- neurologic? 2
- renal?
- opthalmic?
- other?
describe event that happens and then some symptoms to indicate this
NON-SPECIFIC
- headache
- dizziness
- epistaxis
CARDIAC
- Heart failure exacerbation / pulmonary edema (dyspnea, crackles)
- MI (chest pain, diaphoresis)
- Aortic dissection (chest pain, asymmetric pulses)
NEUROLOGIC
- Hypertensive encephalopathy (headache, vomiting, confusion, seizure, blurry vision, papilledema)
- Ischemic or hemorrhagic stroke (focal neurological deficits, altered mental status)
RENAL
- acute renal failure (U+E damage, oligouria, oedema)
OPTHALMIC
- Acute hypertensive retinopathy (blurry vision, decrease in visual acuity, retinal flame hemorrhages, papilledema)
OTHER
- microangiopathic haemolytic anaemia (fatigue, pallor)
nb may also get signs indicating a cause:
- Signs of sympathomimetic drug toxicity
- eclampsia symptoms
- other signs of phaeochromocytoma
difference between pericardial effusion and cardiac tamponade?
what is the triad of features seen in cardiac tamponade? 3 (incl name of this triad)
Pericardial effusion: an accumulation of fluid in the pericardial space between the parietal and visceral pericardium. May be acute or chronic.
Cardiac tamponade: a pathophysiological process whereby elevated intrapericardial pressure from a pericardial effusion causes compression of the heart (especially the right ventricle)
BECK TRIAD
- Hypotension
- Muffled heart sounds
- Distended neck veins (+/-raised JVP)
Other features of tamponade:
- Tachycardia, pulsus paradoxus
- Pallor, cold sweats
- Left ventricular failure
- Symptoms of right heart failure
- Obstructive shock, cardiac arrest (presenting as PEA)
nb Cardiac tamponade is not necessarily associated with a larger amount of fluid in the pericardial space; a rapid but small pericardial effusion can also lead to tamponade physiology.
PERICARDIAL EFFUSION:
- causes of a haemopericardium? 4
- causes of serous pericardial effusion? 7
BLOOD
- Cardiac wall rupture (e.g., complication of myocardial infarction)
- Aortic dissection
- Chest trauma
- Cardiac surgery (e.g., heart valve surgery, coronary bypass surgery)
SEROUS
- Idiopathic
- Acute pericarditis (especially viral, but also fungal, tuberculous or bacterial)
- Malignancy
- Uremia
- Autoimmune disorders
- hypothyroidism
- Postpericardiotomy syndrome (wks after cardiac surg)
PERICARDIAL EFFUSION:
- main two symptoms?
- other possible symptoms? 4
Initially asymptomatic in most cases
= Shortness of breath, especially when lying down (orthopnea)
= Retrosternal chest pain
Can cause compressive symptoms
- Hoarseness
- Nausea
- Dysphagia
- Hiccups (compression of phrenic nerve)
CARDIOMYOPATHIES
GENETIC
hypertrophic obstructive
- what can it cause?especially in which group?
- what see on echo? 2
- inheritance?
arrhythmogenic right ventricular dysplasia
- what happens to heart?
- inheritance?
MIXED (genetic + enviro)
dilated
- classic causes? 4
restrictive
- classic causes? 3
ACQUIRED
peripartum
- when develop?
- risk factors? 3
takotsubo
- trigger?
- what happens to the heart?
GENETIC
HYPERTROPHIC OBSTRUCTIVE
- leading cause of sudden death in young athletes (often asymptomatic)
- see asymmetric septal hypertrophy and mitral regurg (+ mitral valve thing as well) - LVH on ECG
- autosomal dominant
ARRHYTHMIC RIGHT VENTRICULAR DYSPLASIA
- R ventricular myocardium is replaced by fatty + fibrofatty tissue
- autosomal dominant
^nb both of these need implantable defib
MIXED (genetic pre-disposition + trigger)
DILATED
- alcohol
- wet beri beri (thiamine deficiency)
- coxsackie B virus
- doxorubicin (chemo drug)
RESTRICTIVE
- amyloidosis
- post-radiotherapy
- Loeffler’s endocarditis (eosinophils infiltrate heart muscle)
ACQUIRED
PERIPARTUM
- last month of preg - 5 months post-partum
- RFs: older women, greater parity, multiple gestations (twins/triplets)
TAKOTSUBO
- ‘stress’-induced cardiomyopathy - eg from grief
- transient, apical ballooning of myocardium
- treatment is supportive
nb can get other weird and wacky ones too!
RAYNAUDS
- age of onset and bilateral or not in raynauds disease compared to raynauds syndrome/phenomenon
- most common cause of secondary raynaud’s?
- other secondary causes of raynauds?
raynaud’s disease (primary)
- young women (<40)
- bilateral
raynaud’s syndrome (secondary)
- norm >40
- unilateral
- also digital ulcers + calcinosis
- also have other symptoms in keeping with the underlying disease
causes of secondary
= SYSTEMIC SCLERODERMA / CREST
- RA
- SLE
- leukaemia
- type I cryoglo9bulinaemia, cold agglutinins
- use of vibrating tools
- cervical rib
- drugs: oral contraceptive pill, ergot
nb this is a list 3 condition - don’t need to know detail
RAYNAUDS
- most common triggers? 2
- what is the order of the three colour changhes in fingers /toes?
- lifestyle advice? 2
- medication if severe? 1
- what med is contraindication in raynaud’s? 1
- cold
- emotion
1) white
2) blue
3) red
they also ache / are painful
- keep warm
- stop smoking
if severe: nifedipine (calcium channel blocker) (and other meds…)
beta blockers are contraindicated! (make it worse!)
LYMPHOEDEMA
- what condition is primary lyphoedema found in?
- causes of secondary oedema? (2 iatrogenic, 4 not iatrogenic)
primary lyphoedema
- rare
- seen in turner’s syndorme
CAUSES OF SECONDARY
- surgery (eg post mastceomy)
- radiation therapy
- tumours
- trauma
- inflammation
- infection (recurrent cellulitis, leprosy, syphillis, other weird stuff..)
LYMPHOEDEMA
- two characteristic things on exam to differentiate from venous oedema? 3
venous oedema
= pitting
- toes / finger not affected
- normally bilateral
lymphoedema
= non-pitting (although early on can be pitting)
- Swelling of toes and feet with deep flexion creases
- often unilateral dt localised disease process
nb management can be conservative (compression stockings, exercise, mx of underlying disease) or surgical options too
CAUSES OF PERIPHERAL PITTING (ie venous) OEDEMA
- why does heart failure -> oedema? (ie decribe pathology)
- what cardiac drug has a side effect of peripheral oedema?
protein deficiency causes? 4
hydrostatic causes? 4
increased capillary permeability causes? 6
1) FLUID RETENSION
= RIGHT HEART FAILURE
reduced cardiac stroke volume → impaired renal perfusion → activation of RAAS system → increased renal fluid retention → increased hydrostatic pressure in the capillaries → secretion of fluid into the interstitium (oedema formation)
= calcium channel blockers
2) PROETIN DEFICIENCY (norm albumin)
- nephrotic syndrome
- liver cirrhosis
- malnutrition
- protein-losing enteropathy (eg IBD, coeliac, infection)
3) HYDROSTATIC
= chronic venous insufficiency (commonest!)
- pregnancy
- DVT
- post-thrombotic syndrome (basically chronic venous insufficiency following a DVT)
4) INCREASED CAPILLARY PERMEABILITY
- inflammation
- infections
- toxins
- allergic reactions
- burns
- trauma
causes of peripheral oedema (pitting and non)
- acute + generalised? 3
- chronic + generalised? 4
- acute + localised? 5
- chronic + localised? 3
ACUTE + GENERALISED
- nephrotic syndrome (norm get peri-orbital too)
- acute renal failure
- acute cardiac failure
CHRONIC + GENERALISED
- chronic kidney disease
- chronic heart failure
- liver cirrhosis
- malnutrition
ACUTE + LOCALISED
- inflammation
- allergic reaction
- burns
- trauma
- thrombosis (incl DVT)
CHRONIC + LOCALISED
- lymphoedema
- chronic venous insufficiency (norm localised to legs, ie not sacram, abdo etc)
- post-thrombotic syndrome
nb can use stockings for Mx - but only if ABPI is fine!
