AH1 Flashcards
Red flags for pneumonia
RR>30 systolic BP<90 O2 sats less than 92 acute onset of confusion Heart rate >100 Multilobar involvement of the chest
COPD-X
Confirm the diagnosis Optimise function prevent deterioration develop a plan of care manage eXacerbations
What kind of rehabilitation is MUST with COPD
pulmonary rehabilitation- patient assessment, exercise training, education, behaviour change, nutritional intervention and psychosocial support
What co-morbid condition do we need to worry about in COPD
Osteoporosis- due to the medications and lack of activty and COPD presents in the elderly patient
Beck’s triad for cardiac tamponade
JVP distension
muffled heart sound
Hypotension
Carcinoid triad syndrome
Facial flushing
Diarrhea
Right-sided heart failure
Charcot’s triad of Multiple sclerosis
Nystagmus
Intention tremor
Scanning or staccato speech
Cushing’s triad for increased ICP
Hypertension(progressively increasing systolic pressure +/- widened pulse pressure)
Bradycardia
Irregular breathing
Mackler triad for Boerhaave syndrome
Rupture of the oesophagus during forceful emesis
- vomiting
- lower chest pain
- subcutaneous emphysema
Which test for supraspinatus tendinopathy
Hawkins Kennedy test
What are the tests for a supraspinatus tear
Drop Arm test and empty can test
What is the test for dislocation or anterior shoulder instability
Apprehension and relocation test
walking on heel is done by L
L5
Walking on toes is done by
S1
Which drugs give steven-johnson syndrome
Ethosuximide, Carbamazepine and lamotrigine
All patients with suspected TIA should have stroke risk assessment, which may include the ABCD2 tool
age>60 years
BP-140/90
Clinica features- unilateral weakness(2 points), speech impairment without weakness(1 point)
Duration >60 minutes(2 points), 10-59 minutes(1 min)
Diabetes- 1 point
Which 3 organs are most likely to be damaged by emboli
Brain
Kidney
Spleen
3 complications of long-standing AF
- Acute left heart failure → pulmonary edema
- Thromboembolic events: stroke/TIA, renal infarct, splenic infarct, intestinal ischemia, acute limb ischemia
- Life-threatening ventricular tachycardia
What are 4 ECG characteristics of AF
- Irregularly irregular RR intervals
- P-waves are indiscernible
- Tachycardia
- Narrow QRS complex (< 0.12 seconds)
State some investigations for AF you would like to do and why
- Troponin levels: to rule out myocardial infarction
- D-dimer levels: if risk factors (e.g., DVT) or clinical features of pulmonary embolism are present
- Brain-natriuretic peptide (BNP): to rule out heart failure
4.CBC: to identify anemia, infection - TSH, fT4: to screen for hyperthyroidism
6Serum electrolytes (Na+, K+, Mg2+, and Ca2+): to identify electrolyte imbalances - BUN, serum creatinine: to identify chronic kidney disease
- Ethanol levels, digoxin levels and/or urine toxicology (e.g., cocaine, amphetamines)
ECHO for imaging
What are the general principles of treating AF(3)
- Correcting reversible causes and/or treatable conditions (e.g., hyperthyroidism, electrolyte imbalances)
- Controlling heart rate and/or rhythm
- Providing anticoagulation
Controlling heart rate in AF
- what to do if they are stable
- what to do if they are unstable
Unstable AF: emergent electrical cardioversion
Stable AF: rate control or rhythm control strategies to control AF and prevent long-term recurrence
What are the rate control methods for AF
Normally good for the ELDERLY patient
1st choice: beta blockers (esmolol, propanolol, metoprolol) OR nondihydropyridine calcium channel blockers (diltiazem, verapamil)
2nd choice: digoxin
3rd choice: amiodarone
If not working albative procedures
What is a prerequisite for cardioversion in a patient in AF
Anticoagulation
New-onset AF (< 48 hours) in patients with:
-Tell me what you would do for low risk
-for high-risk patient
and what’s your medication choices
Low thromboembolic risk (see CHA2DS2-VASc score below) → consider anticoagulation directly before or after cardioversion
High thromboembolic risk → start anticoagulation immediately before or after cardioversion
Anticoagulation options: IV heparin or LMWH, direct thrombin inhibitors (e.g., dabigatran), or factor Xa inhibitors (e.g., rivaroxaban, apixaban)
AF ≥ 48 hours in patients with:
-Stable vs unstable
Unstable AF (require urgent cardioversion): IV heparin or LMWH immediately before cardioversion followed by warfarin for up to 4 weeks after cardioversion
TEE to rule out atrial thrombi recommended if anticoagulation has not been administered at least 3 week prior to cardioversion
Stable AF (do not require urgent cardioversion): warfarin with bridging therapy for 3 weeks before and up to 4 weeks after cardioversion
Anticoagulation therapy should be considered in all patients who are about to undergo cardioversion.
Write down CHA2DS2-VASc score for
-Non-valvular AF- like what is the treatment, what are the indications for each of these treatments(medications)
Nonvalvular atrial fibrillation: The need for anticoagulation therapy is based on the CHA2DS2-VASc score
Score = 0: no anticoagulation
Score = 1: no anticoagulation OR treatment with oral anticoagulants
Score ≥ 2: oral anticoagulation with either warfarin or newer oral anticoagulants (dabigatran, rivaroxaban, apixaban) - NOACs are avoided in patients with renal insufficiency
If warfarin is chosen then needed to monitor INR and has to be 2-3
Valvular AF and CHA2DS2-VASc score
Valvular atrial fibrillation: anticoagulation with warfarin is required regardless of the CHA2DS2-VASc score
The risk of stroke among patients with AF and mitral stenosis is 4 times greater than the risk of stroke with non-valvular stenosis.
A higher therapeutic range for INR of 2.5–3.5 is allowed. Dabigatran is not recommended among AF patients with a mechanical heart valve.
Acute management of AF
Mx dependant on Haemodynamic stability
- Haemodynamically unstable- Emergency electrical cardioversion
- Haemodynamically stable- Consider the risk of thromboembolism before cardioverting with either a drug or a direct current (DC) shock. Mx further dependent on duration of Afib (if in doubt mx as per >48 hours.
- AFib lasting less than 48 hours –> low risk of acute thromboembolic complications–> Consider initial rate/rhythm control stratergy. If using rhythm control, ensure anticoagulation (LWMH) at the time of electrical cardioversion and continued long term depending on thromboembolic risk.
- AFib lasting longer than 48 hours–> increased risk of developing a left atrial thrombus –> do not perform acute cardioversion unless left atrial thrombus has been excluded (using TOE, start anti-coag at time of cardioversion and continue for atleast 4 weeks), or the patient has had therapeutic anticoagulation for the previous 3 weeks. If not excluded/ no prior anti-coag- use rate control method.
Can I give antiplatelet therapy to reduce the risk of AF and reduce the risk of stroke from it
Recommendation: Antiplatelet therapy is not recommended for stroke prevention in Non-VAF patients, regardless of stroke risk.
1st choice drug for focal seizures
eTG states–> Carbamazepine(carbs are bad, that why you get rid of them first)
Lamotrigine–> cause he is a LAMO, that why he can only do focal control
and it causes SJS- cause its lame :P
1st choice of drug for generalized seizures
Valproate–> cause val means honour, they can do more
1st choice of drug for typical absence seizures
Ethosuximide
What is Todd’s paralysis and when does it occur
Occurs in focal seziures/simple partial seizures
Todd’s paralysis: Postictal weakness or paralysis of the affected limb or facial muscles (for minutes or up to hours)
What is the difference between simple partial and complex seizures- focal seizures
Focal seizure with intact consciousness (simple partial seizures)
Focal seizure with impaired consciousness (complex partial seizures)
What is an aura in seizures
Can get it tonic-clonic seizures-prodromal
A class of symptoms present in ∼ 25% of patients with migraines. Characterized by paroxysmal, reversible, focal neurologic symptoms that typically precede migraine headaches and last up to one hour. Symptoms may be visual (e.g., flashing lights), motor (e.g., paresis), somatosensory (e.g., paresthesia), vestibular (e.g., dizziness), or vocal (e.g., aphasia).
What is Adam-stokes attack
A sudden loss of consciousness, usually without warning and lasting for a few seconds, due to an abnormal heart rhythm (especially complete atrioventricular block).
What is the important factoid that can differentiate seizure from syncope
Postictal disorientation is key to differentiating between seizures and syncope. Syncope may be accompanied by twitches; however, patients become completely reoriented after a few seconds!
What is the biggest complication with status epilepticus
Status epilepticus is a life‑threatening event! If not interrupted, it can lead to cerebral edema, a dangerous rise in body temperature, rhabdomyolysis, and cerebral cardiovascular failure!(death)
Traveller’s diarrhea
Enterotoxigenic Escherichia coli (ETEC)
May be exudative-inflammatory diarrhea or secretory diarrhea
Erythromycin
Erythromycin promotes emptying of the stomach, improving visibility during gastroscopy.
What are the 2 types of gastritis and what are the clinical features
-investigations
AMAG(Autoimmune destruction of the parietal cells)
Associated with major histocompatibility haplotypes HLA-B8 and HLA-DR3
Associated with other autoimmune diseases (e.g., autoimmune thyroiditis)
Autoantibodies against intrinsic factor → vitamin B12 deficiency → pernicious anemia
EMAG(Environmental metaplastic atrophic gastritis) Helicobacter pylori infection (most important risk factor of atrophic gastritis overall) Dietary factors (e.g., N-nitroso compounds , alcohol intake, high salt intake)
Clinical features
Intensity of symptoms may be inconsistent and vary widely
Hematemesis (coffee-ground appearance or bright red in color), possibly melena
Epigastric pain is possible
Nausea, vomiting
Abdominal paresthesia and dyspepsia
IDA and Vitamin b12 deficiency
Ix
Vitamin B12 levels: decreased in AMAG
Serum gastrin levels: increased in AMAG
Serology : anti-intrinsic factor and anti-parietal cell antibodies
ALARMS symptoms of dyspepsia
ALARM Symptoms [mnemonic]
Anaemia (iron deficiency) Loss of weight Anorexia Recent onset of progressive symptoms Melaena/haematemesis Swallowing difficulty
If dyspepsia and either >55yrs or ALARM Symptoms then ENDOSCOPY
What is the empirical therapy for GERD
If GERD is clinically suspected and there are no indications for endoscopy, empiric therapy – ranging from lifestyle modifications to a short trial with PPIs – should be initiated. A GERD diagnosis is assumed in patients who respond to this therapeutic regimen.
What are some side effects of PPIs
Clostridium difficile infection
pneumonia
decreased serum vitamin B12 concentration (long-term use >2 years)
chronic kidney disease
fracture (long-term use); for patients at risk of osteoporosis and taking PPIs long term (>1 year), consider daily calcium intake and vitamin D status
Vitamin B12 deficiency and neurological damage- what are they
Patients with vitamin B12 deficiency present with signs of symmetrical damage to large sensory fibres
- decreased vibration sense
- decreased proprioception
- paresthesias
- hyporeflexia
What are the 2 main functions of Vitamin b12/cobalamin
- An essential role in enzymatic reactions responsible for red blood cell (RBC) formation
- Proper myelination of the nervous system
What is the main cause of vitamin b12 deficiency and state some others causes
Pernicious anemia: most common cause of vitamin B12 deficiency
Atrophic gastritis (e.g., secondary to H. pylori infection)
Gastrectomy
↓ Reduced uptake of IF-vitamin B12 complex in terminal ileum: e.g., Crohn’s disease, celiac disease, pancreatic insufficiency, surgical resection of the ileum
Other causes
Malnutrition: e.g., chronic alcoholism, anorexia nervosa, or strict vegan diets
What is the triad of condition to look out for if you have pernicious anaemia
Associated with other autoimmune diseases (e.g., hypothyroidism, vitiligo)
What is your ddx for polyneuropathies
Diabetic polyneuropathy- affects all kinds of nerve
Vitamin B12 deficiency-only large sensory fibres
Alcoholic polyneuropathy- Does not affect the autonomic fibers
Guillain-Barré syndrome
Exposure to lead, dapsone, amiodarone, or vincristine
Uremia
Vasculitis
Out of all the polyneuropathies, why does vitamin b12 have a positive Romberg’s test
Due to subacute combined degeneration of the spinal cord. Only affects the Large sensory fibers.
Vanish DDT- Cerebellar signs in the neuro exam
vertigo ataxia- during the gait, the patient will fall onto the side of the lesion nystagmus intention tremor staccato speech hypotonia dysmetria dysdiadochokinesia titubation.
Romberg’s test is a test of
proprioception
I say(Related to liver) you say
- pANCA
- anti-smooth antibodies
- Anti-mitochondrial antibodies (AMA)
PSC
Autoimmune hepatitis
PBC(affects women and women need a lot of energy-mitochondrial to do household and they are more introverted so they are only in the intrahepatic ducts)
What is the test used to check for albuminuria/proteinuria(mean the same thing cause the main protein peed out is albumin)
-what do you need to tell the patient
urinary albumin:creatinine ratio (urine ACR).
Need first void urine
If this is not possible, your doctor can still do the test on a sample of urine collected at any time during the day (called a spot random sample).
State the kidney function stage
1 ≥90 2 60-89 3a 45-59 3b 30-44 4 15-29 5 <15 or on dialysis
State the albuminuria stages and what is the unit
Normal
(urine ACR mg/mmol)
Male: < 2.5
Female: < 3.5
Microalbuminuria
(urine ACR mg/mmol)
Male: < 2.5 -25
Female: < 3.5-35
Macroalbuminuria
(urine ACR mg/mmol)
Male: > 25
Female: > 35
24 hour urine collection – the “gold standard”
Most patients with CKD are morelikely to DIE from CVD than get kidney failure
Proteinuria is not just a disease marker,
it influences disease progression
Mnemonic for indications for dialysis: A-E-I-O-U
Acidosis Electrolyte abnormalities (hyperkalemia) Ingestion (of toxins) Overload (fluid) Uremic symptoms
Metabolic acidosis of pH < 7.1
Hyperkalemia, hypercalcemia
Toxic substances (e.g., lithium, toxic alcohols)
Refractory fluid overload
Signs of uremia, including pericarditis, encephalopathy, and asterixis on exam
Complications of Nephrotic Syndrome(5)
- Edema
- Malnutrition
- Hypercoagulability
- Hyperlipidemia
- Increased risk of infection
What is included in the haemolytic screen
Common laboratory findings, such as elevated indirect bilirubin and lactate dehydrogenase, reticulocytosis, and decreased haptoglobin levels. The Coombs test helps to distinguish autoimmune (positive Coombs test) from non-autoimmune anemias (negative Coombs test).
Increased
- absolute reticulocyte count
- LDH (elevation is more pronounced in intravascular haemolysis)
- Indirect Bilirubin (i.e. unconjugated)
- Plasma free haemoglobin (PFHb)
Decreased
5. Haptoglobin (intravascular haemolysis)
Urine
Haemoglobin
Haemosiderin (useful in the diagnosis of intravascular haemolysis)
Blood film- look at spherocytosis, G6PD deficiency
Native valve endocarditis-Triple therapy
Gentamycin IV
Benzylpenicillin IV
Fluclocaxillin IV(MSSA better)
if MRSA–> change flucloxacillin to Vancomycin IV
Prosthetic valve endocarditis-Triple therapy
Gentamycin IV
Benzylpenicillin IV
Vancomycin IV
DDX for angina-4
- Anaemia
- Aortic stenosis
- Thyrotoxicosis
- Hypertrophic cardiomyopathy
Which heart failure does not show improvement with drugs
HFpEF–> Diastolic heart failure
What are some causes of heart failure
- Coronary artery disease, myocardial infarction
- Arterial hypertension
- Valvular heart disease
- Diabetes mellitus (diabetic cardiomyopathy)
- Renal disease
- Infiltrative diseases (e.g., hemochromatosis, amyloidosis)
What are some clinical features for heart failure-5
SOB Nocturia Fatigue Tachycardia Heart sounds--> S3/S4 Pulus alternans
What are the three main causes of heart failure
Hypertension
T2DM
CAD
Chronic compensated CHF definition
clinically compensated CHF; the patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable
Acute decompensated CHF definition
Acute decompensated CHF: sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition (e.g., myocardial infarction)
Why use CXR in heart failure
Useful diagnostic tool to evaluate a patient with dyspnea and differentiate CHF from pulmonary disease
State some lifestyle modification for heart failure patients
Salt restriction (< 3 g/day)
Fluid restriction in patients with edema and/or hyponatremia
Weight loss and exercise
Cessation of smoking and alcohol consumption
Immunization: pneumococcal vaccine and seasonal influenza vaccine
Contraindicated in acute decompensated heart failure!- which drug
Beta-blockers
Digoxin is contraindicated in HF when there is
Contraindicated in severe AV block
Which three drugs are contraindicated in HF
- NSAIDs
Worsen renal perfusion
Reduce the effect of diuretics
May trigger acute cardiac decompensation - Calcium channel blockers (verapamil and diltiazem): negative inotropic effect; worsen symptoms and prognosis
- Thiazolidinediones: promote the progression of CHF (↑ fluid retention and edema) and increase the hospitalization rate
