Acute medicine- station 5 Flashcards
What are the steps in the management of asthma?
- SABA
- Add ICS regularly
- Add LABA (only continue if benefits), consider increasing ICS to 800mcg/day
- Increase dose ICS. Consider adding leukotriene receptor antagonist or LAMA or theophylline or B2 agonist tablets
- Oral steroids
What are the criteria for life threatening and severe asthma?
Life threatening
- PEFR <33%
- Sats <92%
- PO2 <8kPa
- Normal or raised PCO2
- Silent chest
- cyanosis
- poor resp effort
- arrthmyia
- Exhaustion/altered consciousness
Severe attack
- PEFR 33-50% predicted
- RR >25
- HR >110/min
- Inability to complete sentences on 1 breath
- Pts whose PEFR >75% 1hr after initial treatment may be discharged
What are the differential diagnosis of a TIA?
Migraine Focal epilepsy Metabolic disturbance eg hyper/hypoglycaemia Transient global amnesia MS
What are the risk factors for a TIA?
Age Previous TIA and stroke HTN DM Dyslipidaemia Cardiac disease Obesity Cigarette smoking Alcohol Recreational drug use Carotid stenosis AF
What would your investigation plan be for a patient presenting with a possible TIA?
Bloods- FBC- polycythaemia/thrombocythaemia
Glucose- exclude hypo/hyperglycaemia
HBA1C
Lipid profile
ECG and 24hr ECG for AF
ECHO- assess for LV dyskinesia or other structural cause of cardioembolism
Carotid artery imaging
Duplex US
CT angiography/MR angiography
Brain imaging= MRI including diffusion weighted imaging and gradient echo imaging
What score do you use to calculate risk in TIA?
ABCD2 score
Age >60yrs= 1
BP >140/90= 1
Clinical features:
Unilateral weakness= 2
Speech impairment without weakness = 1
Duration
10-59mins =1
>60mins = 2
Diabetes = 1
Score more than or equal to 4 high risk and need specialist assessment and investigation within 24hrs
IF <4 then within 1 week (risk of stroke 1% when score=1-3)
How do you manage a TIA?
Commence aspirin and dypiradamole as dual antiplatelet
Start anticoagulation if in AF
Control BP <130/80
Cholesterol <3.5mmol/L
HBA1C <7.5%
Carotid endarterectomy shoul dbe offered within 2 weeks to those with carotid stenosis 50-99%
Lifestyle- reduce salt, sat fat, weight loss, stop smoking, reduce alcohol
What should you advise somebody that has had a TIA?
At high risk of stroke and they need to ACT FAST. Facial weakness Arm weakness Speech problems Time to call 999
What are the red flag features of headache?
New headache in patient >50yrs Develops within minutes- SAH Inability to move limb or other neurological abnormalities Mental confusion Recent trauma Woken by headache Worsens with change in posture and straining Scalp tenderness Visual loss/abnormalities Jaw claudication Neck stiffness Rash Fever Pre-exisiting HIV, cancer, risk factors thrombosis
What are your investigations for headache
FBC, U+E, ESR (GCA), CRP, clotting WCC/CRP Brain imaging LP Temporal artery biopsy
How would you treat a cluster headache and hemicrania?
Hemicrania (constant unilateral headache): indomethacin
Cluster headache: SC/nasal triptans, 100% oxygen
What are the causes of pericarditis?
Viral infection: coxsackie, EBV, influenza, Echovirus
Rheumatological: Sarcoid, scleroderma, RA, SLE, PAN, AS
Drugs: hydralazine, procainamide, isoniazid, phenytoin
Neoplastic: sarcoma, mesothelioma, mets
Bacterial: staph, haemophilis, pneumococcus
Other: chest trauma, uraemia, radiation
What investigations would you do of somebody with pericarditis?
ECG- saddle ST elevation CXR: boot shaped heart Bloods: U+E, FBC, troponins, ESR/CRP ECHO- effusion or tamponade or myocarditis Surgical: percardiocentesis
What criteria would cause you to admit a patient with pericarditis?
- Fever (>38ºC) and leukocytosis.
- Evidence suggesting cardiac tamponade.
- A large pericardial effusion (ie an echo-free space of more than 20 mm).
- Immunosuppressed state.
- Patients taking warfarin.
- Acute trauma.
- Failure to respond within seven days to non-steroidal anti-inflammatory drugs (NSAIDs).
- Elevated cardiac troponin, which suggests myopericarditis.
How would you manage pericarditis?
NSAIDs + PPI
Colchicine
What are the symptoms of hypertensive encephalopathy?
Headache Drowsy Confusion Nausea.vomiting Visual disturbance
Caused by severe small blood vessel congestion and brain swelling and reversible if BP lowered
Name some causes of hypertension
Renal: GN Chronic atrophy pyelonephritis Adult PCKD Analgesic nephropathy Renal artery stenosis
Endocrine: Conn's Cushings Phaeochromocytoma Acromegaly Thyrotoxicosis Hyperparathyroidism
What are the thresholds for treatment of blood pressure
Stage 1 hypertension >140/90 (ABPM >135/85) + one or more of the following:
• target organ damage
• established cardiovascular disease
• renal disease
• diabetes
• 10-year cardiovascular risk equivalent to 20% or greater.
If >160/100 offer to anybody
What are the steps in hypertension management?
< 55yrs = ACE-I
>55yrs or black= CCB
A+C
A+C+D (indapamide)
Consider adding spironolactone if K+ <4.5 or increasing indapamide
How would you manage somebody with an UGI bleed?
Check Hb
IVF + Hb replacement
If platelets <50 then transfuse
FFP if fibrinogen <1g or INR >1.5x normal
Beriplex if on warfarin
PPI prior to endoscopy not currently in NICE guidelines
Endoscopy within 24hrs
What investigations would you do for somebody with GI bleed?
FBC + crossmatch U+E LFTs- CLD and varices? INR and clotting Erect CXR and AXR ? perf Endoscopy
What scores are used in UGI bleeds?
Blatchford score: scores are added using the level of urea, haemoglobin, systolic blood pressure, pulse rate, presentation with melaena, presentation with syncope, hepatic disease and cardiac failure. A score of 0 is the cut-off with any patient scoring >0 being at risk of requiring an intervention.
Rockall score
- pre-endoscopy: age, shock, co-morbidity
- post-endoscopy: also uses diagnosis (Mallory Weiss tear=0, all other=1, GI malignancy=2) and evidence of active bleeding. Predicts rebleed and mortality
If >1 need to stay in
What are the causes of haematemesis?
In order of frequency Peptic ulcer 44% Oesophagitis 28% Gastritis/erosions 26% Erosive duodenitis Varices Portal hypertensive gastropathy Malignancy Mallory-Weiss tear Vascular malformation
Who can be discharged with an UGI bleed?
Urea<6.5
Hb>130 in man, >120 in women
SBP >110
Pulse <100
What questions would you ask if somebody presented with palpitations?
Onset, freq, exacerbation Chest pain SOB, leg swelling Exercise tolerance Syncope/light headed Fatigue Vascular risk factors (htn, DM, hyperlipidaemia) Endocrine: thyroid issues- hot/cold, tremor, anxiety Drug/alcohol
What investigations would you perform for somebody presenting with palpitations?
FBC- anaemia U+E, calcium, magnesium- electrolyte disturbance Glucose Lipids TFTs ECG 24hr tape ECHO
Who should be rate controlled and who should be rhythm controlled in AF?
Rate controlled in patients: >65yrs with IHD CI to anti-arrythmics/cardioversion Without cardiac failure
Rhythm control in patients:
<65yrs who are symptomatic
Presenting with lone AF (no other CV/resp disease)
With AF secondary to treated/corrected precipitant
With cardiac failure
Can consider ablation or pace and ablate
How would you rate limit in AF?
Beta blockers
Rate limiting calcium antagonists
Digoxin only if sedentary
What do you use to decide whether to anti-coagulate in AF?
CHADSVASc score
CCF= 1 HTN >140/90 = 1 Age >75 =2 Diabetes= 1 Stroke/TIA = 2 Vascular disease (MI, PVD)= 1 Age 65-74= 1 Sex= female= 1
Offer anticoagulation to anyone except score= 0 or 1 for being females
What is the HASBLED score?
Risk of bleeding with anticoagulation
Hypertension >160 Abnormal liver or renal function (1 point each) Stroke history Bleeding history or predisposition Labile INR Elderly >65yrs Drugs or alcohol (1 point each)
What are the causes of AF?
IHD Rheumatic heart disease Hypertensive heart disease Thyrotoxicosis Acute infection Electrolyte imablance Cardiomyopathy (toxic, metabolic, endocrine, collagen disease related, infiltrative, infective, genetic) Constrictive pericarditis
How do you differentiate AF from other pulse irregularities?
Irregular pulse due to controlled AF is differentiated from that of multiple extrasystoles by the long pauses which occur in groups of 2 or more, whilst with ectopic beats the compensatory pause follows a short pause because the ectopic is premature. Exercise may abolish extrasystoles but worsen irregularity of AF. AF may be difficult to distinguish from atrial flutter with a variable block, multiple atrial ectopics due to shifting pacemaker and paroxysmal atrial tachycardia with block but only in AF is the rhythm truely chaotic
What are the differential diagnoses of pyelonephritis?
Peritonitis Cholecystitis Appendicitis Renal colic PID Ectopic pregnancy Pneumonia
What factors predispose to urinary sepsis and pyelonephritis?
Mechanical: structural abnormalities of renal tract, vesicourethral reflux, renal calculi, catheter/stent, incomplete emptying
Constitutional: DM, immunocompromised, atrophic urethritis
Behavioural: change in sexual partner
Positive FH
How would you investigate somebody with possible peripheral vascular disease?
Full examination with assessment of pulses, for ulcers, hair loss, bruits over aorta/iliac/femoral/politeal, assess neuropathy
Buergers test- elevate leg and assess for peripheral pallor
Measure ABPI
Urine dip for glycosuria
FBC, U+E, glucose, HBA1C, lipid, autoantibody
ECG
arterial duplex
angiography
How would you manage somebody with PVD?
Lifestyle advice and control of vascular risk factors as for TIA
Anti-thrombotic medication (anti-platelets)
Treatment of claudication:
- supervised exercise programme
- pharmacological agents: cilostazol, pentoxifylline
- endovascular tx: stenting, angioplasty
- Bypass surgery
Treatment of critical limb ischaemia:
- parenteral prostaglandins
- thrombolysis
- endovascular tx: stenting, angioplasty
- surgery
What signs/symptoms would encourage you to involve surgeons in PVD?
6 P’s pain, paraesthesia, paralysis, pallor, pulselessness, perishingly cold
Why do patients with more severe disease often have pain at rest in bed?
In bed at night there is physiological decrease in cardiac output and a reactive dilatation of skin vessels to warmth in bed
What is phantom limb pain?
Pain appearing to come from where an amputated limb used to be. Suggested mechanisms for pain include damage to nerve endings and subsequent erroneous re-growth leading to abnormal and painful dischagre of neurons in stump and altered nervous activity within the brain as a result of loss of sensory input from the amputated limb
What are the risk factors for DVT?
Age Obesity Immobility/recent long-haul travel Previous VTE Pregnancy/puerperium OCP use Cigarette smoking Thrombophilia Recent surgery Cancer CCF
Describe the Wells score for DVT
Active cancer: 1
Paralysis, paresis or recent plaster immobilisation: 1
Bedridden for >3 days or major surgery in last 12 wks: 1
Tenderness along distribution of deep veins: 1
Entire leg swollen: 1
Calf swelling >3cm compared to other leg: 1
Pitting oedema confined to symptomatic leg: 1
Collateral superficial veins present: 1
Previous DVT: 1
Alternative diagnosis at least as likely as DVT: -2
Likely if 2 or more
Unlikely if 1 or less
Describe the Wells score for PE
Clinical signs and symptoms of DVT: 3
No alternative diagnosis more likely than PE: 3
HR >100bpm: 1.5
Immobilisation for >3 days or surgery in last 4 wks: 1.5
Previous PE/DVT: 1.5
Malignancy: 1
Haemoptysis: 1
How long do you treat a DVT for?
Proximal DVT 3 months and reassess, consider continuing if unprovoked
In cancer at least 6 months
Which patients need more careful monitoring of warfarin treatment?
Drugs: broad spectrum antibiotics
Liver disease
Hyperthyroidism
ETOH
What is the triad of nephrotic syndrome?
Proteinuria, hypoalbuminaemia and oedema (hyperlipidaemia)
What are the causes of nephrotic syndrome?
Glomerulonephritis (80%)
- minimal change
- Membranous
- focal segmental glomerulosclerosis
- mesangiocapillary
Other
- DM
- amyloidosis
- SLE
- drugs- penicillamine
- allergies
- infection
What are the complications of nephrotic syndrome?
Increased susceptibility to infection- partly due to Ig loss in urine
Thromboembolism- increased platelet abnormalities and clotting factors
Hyperlipidaemia
Hypertension
How do you manage nephrotic syndrome
Monitor U+E, BP, fluid balance and weight
restrict salt intake
Diuretic- furosemide +/- metalazone or spiro
If chronic ACE-i decrease proteinuria and slow renal deterioration
Treat hypertension with ACE-i
What are the causes of nephritic syndrome?
Post strep glomerulonephritis (diffuse proliferative)
Infective endocarditis
IgA nephropathy
Membranous GN
SLE (Diffuse proliferative is most common)
HSP
Cryoglobulinaemia
What is Goodpastures disease and how do you treat it?
Develop autoantibodies to type IV collagen essential component of renal basement membrane
Haemoptysis and macroscopic haematuria
Anti-GBM Ab in serum on ELISA
Biopsy: cresecentic
Tx: plasma exchange, steroids, cytotoxics
WHat is the classification in Granulomatosis with polyangitis?
ELK
Ears/nose/throat= almost 100%
Lungs- most patients
Kidneys 75%
Rare vasculitis
How do they test for HIV?
COmbination test of HIV antibodies and p24 antigen (fourth generation test)
Generally accepted need to be rechecked in one month if negative and suspected
Name some aids defining conditions?
Oesophageal candidiasis Candidiasis of bronchi, lung Invasive cervical cancer CMV reitine HIV encephalopathy Kaposis sarcoma Toxoplasmosis of brain Progressive multifocal leukoencephalopthy PCP TB Lymphoma- Burkitts, brain
How do you treat HIV?
Everyone starts HAART
COmbination of 3 ARTs from at leaxst 2 groups
- Nucleoside reverse transcriptase inhibitors (NRTI): Tenofovir, Lamivudine, Zidovudine
- Non-nucleoside reverse transcriptase inhibitors (NNRTI): Efavirenz
- Protease inhibitors: Indinavir, ritonovir
- Integrase inhibitors
- FUsion inhibitors
Atripla can be given once a day
Septrin prophylaxis if CD4 <200
What are your differentials of microcytic anaemia?
Iron deficiency
Anaemia of chronic disease
Thalassaemia
Sideroblastic anaemia
What are your differentials in macrocytic anaemia?
Megaloblastic (delayed nuclear maturation in relation to cytoplasm in red blood cells in bone marrow due to defective DNA synthesis)
- vitamin B12 def
- folate def
- drug induced
Non megaloblastic
- alcohol
- myelodysplastic syndromes
- liver disease
- pregnancy
- hypothyroidism
What are the causes of vitamin B12 deficiency?
Low dietary intake- vegans (B12 in meat and dairy products)
Stomach
- pernicious anaemia
- gastrectomy
- congenital def in intrinsic factor
Small bowel
- ileal disease or resection eg Crohns
- coeliac disease
- tropical sprue
- bacterial overgrowth
Abnormal utilisation
- nitrous oxide- inactivates B12
- congenital transcobalamin II def
What is pernicious anaemia?
Autoimmune condition in which there is atrophic gastritis with loss of parietal cells and hence failure of intrinsic factor production and vit B12 malabsorption
What do you need to remember to ask if a patient has a macrocytic anaemia caused by possible B12 def?
Neurological features- polyneuropathy, weakness, ataxia, subacute combined degeneration of spinal cord. Dementia and visual distubance
How do you investigate a patient with possible pernicious anaemia?
Hb
Blood film
vit B12
Anti-parietal cell Ab- sensitive but not specific
Intrinsic factor antibodies- specific but not sensitive (found in 50%)
May be necessary to do
- bone marrow biopsy
- Small bowel barium follow through
Schilling test is no longer used
If you have a megaloblastic anaemia of underdetermined cause, how do you manage this?
Always replace B12 prior to folate so you don’t aggravate the neuropathy
