general Flashcards
what are the important Q’s for SOB presentation?
general health fever cough sputum wheeze chest pain swollen legs Fix of cardiac or pulmonary disease risk factors for VTE (smoking, obesity, diet, etc)
list potential causes of sudden onset of breathlessness
pneumonia pulmonary embolism pericarditis costochondritis pneumothorax panic attack
what investigations are important in a pt presenting with SOB?
RR O2 sats pulse BP JVP chest legs breast exam general
what is the Well score used for?
stratifies pt’s for PE and provides an estimate pre-test probability
what investigations would you perform pc SOB and swollen leg
FBC - anaemia can cause breathlessness, though unlikely to be sudden onset. raised WCC could point toward infective cause
CRP - raised CRP could also point to an infective cause
N-terminal pro-B-type natriuretic peptide - a normal level rules out heart failure
CXR - often normal in PE but should be done to look for potential diagnosis such as pulmonary oedema, pneumonia or pneumothorax
ECG: can be abnormal in acute PE and would pick up other potential causes of acute SOB such as tachyarrhythmias
D-dimer: if Wells score if hight, a D-dimer is not indicated
what is D-dimer used for?
- essentially a rule-out test for PE
- sensitivity but low specificity
- common other diagnoses are infection, trauma and cancer. aortic dissection
- used if low well score (if high well score –> imaging)
what are the ECG changes seen in PE?
- comments ECG abnormality in acute PW is sinus tachycardia
- the S1Q3T3 pattern is uncommon but when present usually indicates high clot load
- right axis deviation, right bundle branch block, clockwise rotation of the heart and atrial dysrhythmias
- sinus rhythm
- evidence of right ventricular strain, recognised by simultaneous presence of T wave inversion in leads V1-4, III and aVF
what are the risk factors for venous thromboembolic disease?
- major general or orthopaedic surgery
- immobility
- leg trauma
- active cancer
- COCP
- pregnancy
- inherited thrombophilias
- obesity
- long plane or care journeys
an acute PE should be considered in pt’s presenting with acute SOB, are hypoxaemic and have clear lung fields on CXR. ECG may provide further clues and raised cardiac biomarker. what Ix would be beat to confirm Dx of PE?
CTPA
- clot load determines the outcome
- large = central aa. +/- peripheral aa.
- small = peripheral aa. only
why might an echocardiogram be requested in diagnosing PE?
assess RV dilation
what medication is prescribed based on findings suggesting PE?
anticoagulant e.g. dalteparin (daily SC injections)
how else could acute PE present?
- commonest = dysponea and pleuritic chest pain
- large clots loads likely to present with retrosternal chest tightness rather than pleuritic chest pain
- may also present with cough, fever, haemoptysis and syncope
- around a quarter of pt’s with PE will have clinically evident DVT (most PE result from DVT)
how do you classify PE?
massive = shock and hypotension
sub-massive = pulmonary trunk or one or both pulmonary aa. but the pt is not shocked
small = involve lobar or segmental aa. only
once you have confirmed Dx of PE, is there any other test you might want to perform?
- consider Ix to exclude cancer as an underlying cause
- CT scan of chest, abdomen and pelvis
- breast exam in women, PSA in men
what are the management options for VTE?
- thrombolysis is indicated in massive PE (defined as SBP <90mmHg or drop >/=40mmHg from baseline for a period of >15min, not otherwise explained by hypovolaemia, sepsis or a new arrhythmia
- LMWH is one Tx option. recommended over warfarin or DOACs when PE is associated with active Ca
- for most pt’s, (not associated with active Ca or massive PE) then choice lies between initial Tx with LMWH before moving onto warfarin as maintenance therapy or a DOAC as both initial and maintenance therapy
- anticoagulant Tx is recommended for 3months for first provoked PE and 6months for first unprovoked PE. decision to Tx for longer will depend on clot load, the likelihood that PE will recur and the risk of bleeding
what is the site of action of the following drugs..?
a) Apixaban
b) Dabigatran
c) Warfarin
a) Xa inhibitor in the combined pathway
b) direct thrombin inhibitor
c) vitamin K antagonist in the extrinsic pathway
do all pt’s with PE need to be treated in hospital?
the simplified PE severity index can help identify low-risk pt’s who may be eligible for outpatient Tx, but it should not replace clinical judgement
briefly discuss the metabolic changes during rest-to-exercise transitions
- O2 uptake increased rapidly, generally reaching steady state within 1-4mins
- the term oxygen deficit applies to the lag of oxygen uptake (anaerobic) at the beginning of exercise before steady state is reached (aerobic)
- the failure of O2 uptake to increase instantly suggest anaerobic pathways contribute to the overall production of ATP early in exercise
- after SS, ATP requirement is met via aerobic metabolism
what happens with oxygen levels when recovering from exercise?
- remains elevated above rest during recovery
- oxygen dept -> repayment for oxygen deficit at onset of exercise
- exercise post-exercise oxygen consumption (EPOC) -> the amount of O2 required to restore your body to its normal, resting level of metabolic function/homeostasis
EPOC/oxygen debt = the temporary oxygen shortage in the body tissues arising from exercise. there are two portions of O2 debt; rapid and slow. what happens in each?
rapid:
- resynthesis of stored Pc
- replenishing muscle and blood O2 stores
slow:
- elevated heart rate and breathing = increase energy need
- elevated body temperature = increase metabolic rate
- elevated epinephrine and norepinephrine = increase metabolic rate
- conversion of lactic acid to glucose
define the term oedema
excessive accumulation of fluid within the interstitial space, outside the vascular system
describe the physiological processes that maintain the normal distribution
Starling forces act on the capillary bed and govern the exchange of fluid between the capillary and interstitial fluid
these forces determine the direction of net water movement and the rate of movement
describe the physiological processes that maintain the normal distribution
Starling forces act on the capillary bed and govern the exchange of fluid between the capillary and interstitial fluid
these forces determine the direction of net water movement and the rate of movement
- hydrostatic pressure of the cap (Pc)
- hydrostatic pressure of the interstitium (Pi)
- oncotic pressure in the capillary (pc)
- oncotic pressure in the interstitium (pi)
(remember lymphatics)
net driving pressure = [(Pc-Pi) - (pc-pi)]
what protein is the main contributor to oncotic pressure?
albumin
(these proteins are large and can’t move freely out vasculature. therefore, stay in the plasma. the plasma will always have greater oncotic pressure than the interstitial fluid)
list causes of low albumin
- liver disease
- nephrotic syndrome
- malabsorption
- protein losing enteropathy (disease of the intestines)
describe the pathophysiological processes which lead to oedema formation
arise because of localised or generalised disruption of the starling forces (or problems with lymphatic damage)
- reduction in plasma oncotic pressure
- increase in cap wall permeability
- increase venous hydrostatic pressure
- lymphatic blockage
(oedema is not dependant on starling’s forces alone. in most cases of generalised oedema, the kidneys avidly retain salt and water)
list causes of oedema
- infection/trauma:
- damage to capillary and leakage
- localised
- e.g. cellulitis of the finger. associated swelling around the infection. - DVT/obstruction:
- increased venous hydrostatic pressure
- localised (distal to block)
- e.g. obstruction of venous return to the heart (DVT or stenosis or extrinsic compression), stop draining properly. - lymphatic obstruction:
- damage to lymph vessels (radiotherapy)
- localised
- e.d. any damage, commonly seen as a result of surgery (i.e. breast Ca axillary lymphatic system) or radiation - drugs:
- CCB (cause fall in arterial BP, venous BP stays the same. therefore, pressure difference across the cap’s increases, pushing fluid out)
- lower limb
- CCB; commonly associated with oedema (10% of pt’s that are on dihydropyridine e.g. amlodipine)
- (ACEi and ARBs normalize hydrostatic pressure by causing post-capillary dilation) - idiopathic:
- oedema in women in absence of another cause
- intermittent, premenstrual
- Dx of exclusion.
*3 causes of generalised oedema:
- congestive cardiac failure:
- increased venous hydrostatic pressure that can lead to increase in cap P
- reduction in CO that can cause reduction in cap filling -> activates RAAS system –> retention of salt and water
- raised JVP is not interstitial fluid it is intravascular; can be a feature, especially of right sided HF - cirrhosis:
- reduced oncotic pressure
- peripheral vasodilation as a result of NO generation, can lead to reduction in arterial filling and renal salt and water retention. ascites in this case
- lower limb, and ascites - nephrotic syndrome:
- primary increase in salt and water retention and decrease in plasma oncotic pressure
- can get marked lower limb and also climbing body oedema. facial oedema is a sign of nephrotic syndrome
describe the clinical assessment of a patient presenting with oedema and formulate a differential diagnosis
Hx:
- onset (sudden or more insidious)
- duration
- variability
- distribution
- rings/belts/shoes
- collateral Hx
systemic review:
- focus on symptoms of underlying potential
- HF: SOBE, orthopnoea and PND
- liver disease: malaise and anorexia
- nephrotic syndrome: frothy urine
PMHX:
- diabetes
- heart/liver/renal disease
- Ca surgery or radiation therapy
- chronic alcohol abuse
- hyper coagulable disorders/previous DVT/ immobilisation or recent surgery
DHX:
- CCB
- NSAIDs
- oestrogens (has aldosterone effect -mild sodium retention)
- thiazalidinediones (glitazones) (can cause fluid retention due to action on Na transporters)
- IV fluid (iatrogenic oedema; some have a lot of sodium load)
exam:
- generalised
- localised
- scrotal
- facial/peri-orbital
- sacral/thighs
- ankles
- hands (periphery stigmata of liver disease, palmar erythema, clubbing)
- > symmetry, temperature, tenderness, pitting
- pulse
- jvp (intravascular fluid status)
- precordium (signs of HF, additional heart sounds or murmurs)
- lungs (pleural effusion -> sign of reduced air entry or dull percussion note)
- abdomen (hepato/splenomegaly or massess or ascites)
- weight
Ix:
- urine dip - protein/blood (quantify after)
- bloods - FBC, U+Es, eGFR, LFT (albumin), D-dimer
- ECG - features of HF
- CXR
- liver USS
- duplex USS
- echo
define the term nephrotic syndrome, list causes
triad: oedema, proteinuria >3.5g/24h and hypoalbuminaemia
not a Dx. it is a syndrome
always due to glomerular disease (e.g. glomerulonephritis or systemic diseases that affect the kidney)
*causes (REMEMBER THIS):
3 primary:
1. minimal change disease (MCD) - common cause in children and young adults
2. focal segmental glomerulosclerosis (FSGS) - all age groups, recurs in transplanted kidneys
- scarring in the kidney, limited to small sections of each glomerulus
3. membranous glomerulonephritis: - older patients, can be secondary to viral infections or malignancy. specific type of glomerular nephritis that develops when inflammation of the kidney structures causes problems with the functioning of the kidney
2 systemic disease:
- diabetes - usually >10yrs, other microvascular complications
- amyloid - older pt’s
explain the complications of nephrotic syndrome
- hypercholesterolaemia:
- increase lipoprotein synthesis
- atherosclerosis - hyper coagulability:
- loss of coagulation factors (antithrombin) in the urine
- venous thromboembolism - infection:
- urinary loss of immunoglobulins causing hypogammaglobulinaemia
- infection by encapsulated organism (e.g. pneumocococcus)
list causes of transient proteinuria
- fever
- exercise
- orthostatic proteinuria
what structures comprise the kidneys filtration barrier?
- capillary endothelium
- glomerular basement membrane
- podocytes
outline how oedema is managed
treat the underlying cause:
- HF
- nephrotic syndrome caused by minimal change disease is often steroid responsive
- anti=proteinuric effect of ACE-i
treat oedema:
- diuretics (high dose)
- sodium restriction (2g/day)
prevention of complications:
- anticoagulation in nephrotic syndrome
a resp Hx may cover what symptoms?
chest pain dysponea cough sputum haemptysis wheeze systemic upset
list differential causes of SOB with an onset of…
a) minutes
b) hours to days
c) weeks to months
d) months to years
a) PE pneumothorax acute LVF acute asthma inhaled foreign body
b) pneumonia
asthma
exacerbation of copd
c) anaemia
pleural effusion
respiratory neuromuscular disorders
d) copd
pulmonary fibrosis
pulmonary TB
