VENI VIDI VICI Flashcards
Diagnostic criteria- Lewy Dementia
Central: Progressive decline in cognition - dementia + >= 2 of the following: Core: 1. Fluctuation in cognition 2. Visual hallucinations 3. Spontaneous parkinsonism features 4. rREM sleep behavior disorder (Dream enactment). THYE HAYVE ANIPSYCHOTIC HYPERSENSITIVITY
Most common causes of Dementia
1st is AD, 2nd Lewy Body ( survival time after diagnosis is 8 years)
Tto for lewy dementia
Donepezil (Cognition), Carbidopa-levodopa (Parkinsonism), Melatonin(rEM disorder), Antispychotic( Hallucinations- BUT MAY WORSEN CONFUSION, PARKINSONISM AND AUTONOMIC DYSFUNCTION
Patient with Lew Dementia treated with Donepezil, Carbidopa-Levodopa, and Risperidone, that comes with worsening confusion
They have antipsychotic hypersensitivity- may worsen the confusion, parkinsonism, orthostatic changes. IF ANTIPSYCHOTIC NEEDED TRY QUETIAPINE (risk is lower). In addition to worsening confusion, antipsychotics are associated with increased mortality in patients with dementia
Brain death algorithm
say it
why can brain death pts have some movements
because these originate for peripheral nerveso spinal cords
Transverse myelitis
Progressive lower extremity weakness, urinary retention, loss of sensation in the setting of URI
RF for Tunnel Syndrome
Obesity, Pregnancy, DM, Hypothyroidism, RA
Dx Carpal Tunnel Syndrome
Nerve conduction studies
Tto Carpal Tunnel syndrome
wrist splint, glucocorticoid injection,
the striatal dopamine transporter scan
imaging that can be considered when Parkinson disease diagnosis in unequivocal
TTO Parkinson
If < 60 and mild Pramipexole or Bromocriptine. For odler levodopa carbidopa.
Traumatic LP
Often has > 6000 RBCs. iT may also elevate WBCs usually 1 per 750-1000. If WBC/RBC< 0.01 is less likely that is meningitis
SAH vs traumatic LP
Xantochromia is seen with SAH
Amaurosis fugax
Is a marker of carotid artery atherosclerosis - Carotid bruit indicates obstruction
Triad of SAH
Sudden onset headache, nausea, nuchal rigidity- often due to aneurysm rupture ( can be posterior cerebral artery causing compressinon of third nerve -diplopia- can also have anisocoria, proptosis)
Brainstem glioma
Has more brainstem involvement , multiple CN involvement , ataxia, motor and sensory involvement
Patient with DVT that 2 days after develops hemiparesis and Facial paralysis
Paradoxical embolism- Transesophageal echocardiogram
Meningovascular syphilis
low grade infection in the subarachnoid space can affect intracranial vessels and cause stroke
Stroke in young- Cardiac causes
Patent foramen ovale, congenital heart disease, arrhythmia
Stroke in young Heme causes
HIT, Sickle cell anemia, inherited hypercoagulable disorders
Stroke in young- Infectious causes
Meningovascular syphilis, Endocarditis, TB meninigits, Bacterial meninigits, vzv
Stroke in young- other causes
Cocaine, amphetamines, nflammatory arteritis, cerebral artery dissection
TTO of meningovascular syphilis (stroke)
Penicillin
Red flags for headaches: SNOOP
Systemic signs(fever) or illnesses(Cancer), Neurologic signs/symptoms, Onset is new, Other associated conditions ( head trauma), Previous headaches with changes in frequency, quality.
NSAIDs induced headache
Patients who take analgesics (eg, acetaminophen) for headaches >10 days/month for >3 months can develop a secondary headache disorder due to medication overuse.
Prophylaxis Cluster
The first-line therapy for cluster headaches that typically last >2 months is verapamil. This medication is usually initiated at 240 mg and titrated up as needed.
Trigeminal Neuralgia tto
Carbamazepine
Ages of febrile seizure
6 months to 5 years
Prognosis of febrile seizure
Risk of epilepsy is 1-2%, if complex increases to 5-10%. In addition, abortive antiepileptic drugs do not alter the outcome of a child who has had a febrile seizure, even with an abnormal EEG.
Spina bifida complications
Neurogenic bladder/bowel, hydrocephalus, scoliosis, motor or sensory dysfunction.
Vertebrobasilar insufficiency
Eldery who presents with dizziness, unable to speak, nauseated, sensation of tingling in face, body, lasting 8-10 minutes. Common in patients with hypertension, DM, hypercholesterolemia. vertigo, dizziness, dysarthria, diplopia, and numbness.
Patient with NPH by clinic and then imaging, next step?
LP ALWAYS FIRST- TO CONFIRM THAT THIS IS NORMAL PRESSURE. MILLER FISCHER TAP- looks if patient improves after removal of 30-50 cc of CSF. THE TREATMENT IS THEN VP SHUNT
MS and pregnancy
lower MS activity during pregnancy, but at delivery higher likelihood of cesarea or instrumented delivery. If exacerbation during pregnancy– short term steroids.- After delivery there is high MS activity.
Major risk factor for stroke
HTN! , THEN SMOKING, THEN DM. Maintain < 150/90 in > 60 years old
Subtypes of syncope
Cardiovascular: .1Arrhythmia 2. Aortic stenosis. NonCardiovascular: vasovagal, carotid sinus hypersensitivity, orthostasis, seizure TIA
Opoiod withdrawal medications and when to use one over the other
Opioid agonists ( Methadone and buprenorphine): require supervision program - so patient needs to be adherent. Clonidine and adjunctive medis( antidiarrheal, antiemetics)
Prior to giving aspirin in stroke what should you consider?
Swallowing study! Some patients may have dysphagia. quick swallowing screening evaluation (eg, water swallow test, Toronto Bedside Swallowing Screening Test)
Management of Hypertension in patients with stroke
In pastients who do not receive the tPA <220/120 is allowed to assure good perfusion to brain . In patients who receive tPA 180/105.
How do you monitor the respiratory function in Guillain Barre
vital capacity and negative inspiratory force. NOT THE PEAK EXPIRATORY PHASE
In whom do you give IVIG or plasmapheresis in Guillain Barre
Non ambulatory and within 4 weeks of onset. If ambulatory and doing well generally do not require treatment.
Botulism characteristics
symmetric descending paralysis, does not have sensory compromise.
Guillain Barre Progression
2 weeks of progressing weakness and can arrive to full paralysis , 2-4 weeks of full plateau, slow recovery over months
Diagnostic criteria for Narcolepsy
Recurrent lapses into sleep and multiple naps in the day, at least 3 times a week for 3 months. aT LEAST 1: Cataplexya, low hyporexin, REM< 15 min
MOA modafinil
Direct, non direct dopamine receptor agonist
tto of cataplexy
SSRIs
MOA methylphenidate
inhibits the reuptake of dopamine and norepinephrine, increased dopaminergic and noradrenergic activity in the prefrontal cortex may explain its efficacy in ADHD.
Childhood absence prognosis
CAE often spontaneously remits by early puberty with no major long-term sequelae. When the patient has been seizure-free for 2 years, the antiepileptic medications frequently can be tapered.
Neurofibromatosis I and II
Type I: Tumor suppression gene chromosome 17, neurofibromin. Cafe au lait, neuromas, lisch nodules, can have optic gliomas. Type II: Merlin, chrom 22, bilateral acoustic neuroma and cataracts.
Nerve injuries during endarterectomy
hypoglossal nerve ( ipsilateral deviation of tongue when is protruded), recurrent laryngeal nerve (unilateral vocal cord paralysis- is distal to lesion) facial nerve( damage the mandibular brnch innervates orbicularis oris muscle- asymmetric smile),vagus nerve, ansus hypoglossal nerve innervates neckm can be sacrificed.
Parinaud Syndrome
pineal gland. 4 things: vertical gaze paralysis, loss of pupillary reaction, loss of optokinetic nystagmus , ataxia
Cremasteric reflex - level, and causes
Diabetic neuropathy, L1, L2
gET UP AND gO TEST
To assess postural stability
Valproate SE
Dose-related Thrombocytopenia , hepatotoxicity,pancreatitis, teratogen
Psychogenic coma
normal reaction to caloric stimulation : transient, conjugate, slow deviation of gaze to the side of the stimulus (brainstem-mediated), followed by saccadic correction to the midline (cortical correction).
unilateral facial nerve palsy, hepatomegaly, and lymphadenopathy
Extrapulmonary manisfestations of sarcoidosis
Extrapulmonary manifestations of sarcoidosis
Skin: erythema nodosum,
If you suspect sarcoidosis, next step in management?
Chest X ray
Confirm diagnosis of sarcoidosis
Excicional lymph node biopsy - Biopsy reveals noncaseating granulomas
Contraindications tpa
Presence of active internal bleeding
Bleeding diathesis (eg, platelets <100,000/µL)
Hypodensity in >33% of an arterial territory on CT scan
Presence of intracranial hemorrhage on CT scan
Intracranial surgery in the last 3 months
Blood pressure >185/110 mm Hg
Alzheimer
Donepezil, rivastigmine, galantamine
Wernicke’s Korsakoff triad
Encephalopathy, ophtalmoplegia, Gait ataxia
Wernicke’s Korsakoff tTO
IV thyamine- Intravenous thiamine usually improves ocular abnormalities within hours, but confusion and gait ataxia may persist for days or weeks; many patients never fully recover. - DO NOT GIVE GLUCOSE PRIOR TO THIAMINE! WORSENS IT
Initial workup of Tuberous sclerosis
MRI for hamartomas, and EEG
MC cause of death in tuberous sclerosis
epilepsy, renal
ASTHMA IN BABY
maternal asthma may be associated with an increased risk of preterm birth, pre-eclampsia and caesarean delivery.
Scissors gait
spastic CP
Evaluation of CP
MRI-eg, periventricular leukomalacia, brain malformation, ischemia. MRI is superior to CT!
Gerstmann syndrome
Dominant parietal lobe: acalculia, agraphia, R/L
ataxia, weakness, and absent deep tendon reflexes after a camping trip to Washington State
tick paralysis - normal sensation
prolactinoma
bromocriptie and cabergoline- dopamine agonists
Prolactinoma presentation and definition
PRL>200. Rule out renal insuff or thyroid problems. Microadenoma (<10mm or 1 cm). Macroprolactinoma(>10mm, >1cm). If macroprolactinoma or micro but symptomatic try dopamine agonists- that decrease PRL (Bromocriptine, cabergoline). If > 3 cm surgery
Dx of Myasthenia gravis
acethylcholine receptor antibodies, if negative- muscle specific tyrosine kinase antibodies. CT chest
Myasthenia gravis
NM junction
Tto of myasthenia gravis
Pyridostigmine/neostigmine ( acethylcholinesterase inhibitor), if doesn’t work and patient < 60 thymectomy.
Triggers for myasthenia gravis
surgery, childbirth, pregnancy, surgery, infection. TTO is plasmapheresis
Definition of concussion
Transient neurological disturbance ( dizziness, amnesia, disorientation), and NO intracranial injury
Management of concussion, recs on returning to physical activity
suspend from same day play. Rest for 24 hours. If without ss start exercise ( light aerobic exercise, non contact sports, then contact sports) . For mental: decreased screen time, and school accomodations. Potentially returning to full contact sports in one week.
Unilateral headache and partial horner ( anisocoria, transient vision impairment)
Carotid artery dissection- so always do imaging
MCC of carotid dissection
Trauma, HTN, Smoking or connective tissue disease
Presentation of carotid artery dissection
unilateral head and neck pain, transient vision loss, ipsilateral horner disease ( ptosis and miosis without anhidrosis), signs of focal cerebral ischemia( focal weakness)
Dx of carotid artery dissection
CT angiography head and neck
TTO OF carotid artery dissection
Thrombolysis if < 4.5 hours ( dissection leads to thrombi formation), aspirin, anticoagulation
presentation of temporal arteritis
head ache, jaw claudication, fever, anemia, high ESR. No anisocoria.
Peripheral Facial palsy and hx of cold sores, tto
Steroids within the first 3 days of onset . Bell palsy. If there is a central facial nerve palsy it requires further imaging . Although HSV can be a cause, there is NO BENEFIT og given antiviral therapy
PECARN rule
say it
Blepharospasm presentation and treatment
type of dystonia, involuntary closeure of the eye, usually trigger by bright light, irritants ( like smoke). Older women are predisposed potentially due to dry eye. TTO: Botulin toxin
Wallenberg Syndrome, etiology
aka lateral medullary infarction - caused by intracranial vertebral artery occlusion- or PICA
Wallenberg Syndrome presentation
Vestibulocerebellar findings ( dizziness, ipsilateral limb ataxia), ipsilateral horner, contralateral loss of pain and T, Ipsilateral cerebellar ataxia, nausea, nystagmus, vertigo,
lateral pontine syndrome
anterior inferior cerebellar artery is occluded
lateral pontine syndrome
Afftect motor and sensory trigemin. Weakness of muscles of mastication, diminished jaw jerk reflex, impaired tactile sensation. In contrast dysphagia, hoarseness, and dimished gag reflex are more lateral medulla.
Patients with late life depression are more likely to develop alzheimer
true , this is in contrast with patients who develop depression at any age.
Medial Medullary Syndrome etiology
aka alternating hypoglossal hemiplegia, occlusion of vertebral or the anterior spinal artery
Medial medullary Syndrome presentation
Contralateral paralysis of the arm and leg. And tongue deviation towars the side of the injury.
Presentation of vit B12 deficiency
Dementia and subacute combined degeneration ( dorsal column: loss of vibration, impaired Romberg)( Lateral corticospinal tract: spastic paresis and hyperreflexia)
Cause for increase in indirect bilirrubin in patients with vit B12def
ineffective erythropoiesis - defective DNA and cell production– intramedullary hemolysis.
Clinical suspicion of spinal/epidural abscess, next step
MRI with gadolinium (preferred) or CT with contrast
MCC bacteria in spinal epidural absces s
S.aureus
tto od epidural abscess
CT guided aspiration and culture for antibiotic, most pts require immediate surgical decompression.and drainage
fOR DEMENTIA TEST FOR
TSH,VITB12, AND DEPRESSION
Pt with forgetfulness, responses are very slow, gait is slow and cautious,
TSH- IS ASSOCIATED WITH HYPONATRMIA AND MICROCYTOSIS
Phenytoin toxicity
Horizontal nystagmus is the first sign! Blurred vision, diplopia, ataxia, slurred speech, drowsiness and decreased mentation . Oif this happen phenytoin should be decreased and look for resolution of nystagmus.
Never do an LP prior to MRI if suspecting tumor
TRUE
ss of postconcussive syndrome and prognosis
amnesia, headache, confusion,difficulty concentrating, vertigo, hypersensitivity to stimulus, mood alteration, sleep disturbances, and anxiety. Ss often resolve with symptomatic treatment within few weeks and months but some patients may have persistent ss lasting >=6 months.
Normal glucose, protein, cell count in CSF
glucose : 40-70, protein < 40, cell count 0-5
Bacterial meningitis glucose, protein, cell count in CSF
cell count >1000, glucose < 40, protein >250
Viral meningitis glucose, protein, cell count in CSF
cell count 100-1000, glucose normal, protein <100
TB meningitis
cell count 5-1000, glucose <10, protein >250
treatment of meningitis -empiric
vancomyicin, ceftriaxone, steroids + Ampi for Listeria
glucose less than 10 IN CSF, and lymphocytosis predominance
TB, cells 5-1000, glucose <10, protein >250, elevated adenosine deaminase
meninigits + yellow white nodules in bilateral optic discs, basilar enhancement
TB tuberculosis
TB meningitis dx
serial lumbar punctures with CSF examination for acid fast bacilli
In patients with altered mental status check
TSH , CMP,Urinalysis, infection. Thyrotoxicosis or hypothyroidism can present as confusion, altered mental status
Apathetic thyrotoxicosis is often misdiagnosed with dementia
TRUE
MVP
Non ejection click due to snapping of the mitral chordae as the valve cusps extend to the left atrium during systole, followed by a systolic murmur or mitral regurgitation. WORSE with low venous return( standing valsalva) and better with handgrip or squatting that increases left ventricular size.
Ejection murmur followed by crescendo-decrescendo
Aortic or pulmonic valve stenosis
Harsh holosystolic murmur with palpable thrill
VSD
Compartment syndrome presentation
pain out of proportion, increased pain with passive stretch, paresthesia “ ants crawling”, burning pain.
Dx of compartment syndrome
Compartment pressure > 30, or DBP-Compartment pressure < 20-30.
HF with preserved EF
Diastolic HF
Most common cause of Diastolic HF
htn –> concentric hypertrophy and impaired diastolic filling.
BNP in HF and obesity
BNP IN HEART FAILURE IS VERY SENSITIVE. HOWEVER, OBESITY LOWERS THE BNP, MAKING IT UNRELIABLE IN THIS PATIENTS.
Newborn with respiratory distress and murmur, son of diabetic mother
transient hypertrophic cardiomyopathy due to increase glycogen storage in the heart, and particularly interventricular. Flow can be obstructed and patient can have congestive heart failure,
Hypoplastic left heart syndrome
seen in children of prediabetic mothers.
Most common complication of Compartment syndrome
Renal failure due to myoglobin release –rhabdomyolysis
Left foot pain likely due to arterial thrombosis + diastolic murmur
left cardiac myxoma
Hypertension,who to treat?
If >=60 with >= 150 or 90. If<60, CKD, DM >=140/90
Tto of HTN
Black: thiazides or CCB, alone or in combination . Other ethnicities: thiazides, ACEi, ARB or CCB Other ethnicities with DM or CKD: ACEi and ARB
alpha blockers are not 1st line HTN meds but can be used in BPH
yes
Classification of pulmonary hypertension
WHO Classification 1.Pulmonary arterial Hypertension 2. Due to left heart disease 3. Due to chronic lung disease ( COPD, ILD), 4. Chronic thromboembolic disease 5. other causes(sarcoidosis)
progressive dyspnea with exertion, prominent S2, Chest X ray with prominent pulmonary arteries but no infiltrate, ECG right axis deviation Dx?
Pulmonary hypertension
If clinically you suspect pulmonary HTN, next step?
Transthoracic TTE – mean arterial pressure >=25
TTO pulmonary HTN
- Endothelin antagonists ( bosentan, Ambrisentan): vasodilation, and delay progression of disease
- PD5 inhibitors (Sildenafil, tadalafil)
- Prostacyclin pathway agonists ( epoprostenol, treprostenol)
Prgnosis of postural tremor
incidence increases with age, familiar cases may present younger, no disability and normal life expectancy
Tto of essential tremor
propanolo, primidone
Trastuzumab cardiotoxicity PROGNOSIS
is a monoclonal antibody that targets HER 2 , Causes decline in LVEF. Cardiotoxicity is REVERSIBLE , is due to loss of myocardial contractility. It should be withheld by 4 weeks if EF decreases > 16% from baseline, and if symptomatic heart failure discontinue.
Anthracycline(Doxorubicin) cardiotoxicity PROGNOSIS
IRREVERSIBLE, there is myocyte destruction. Toxicity is associated with accumulative dosing
Tto of post MI perdicarditis
high dose aspirin, is preferred over NSAIDs and if refractory may consider Colchicine. NSAIDs not ideal because they interfere with myocardial healing. Steroids should be avoided as well.
Tto of idiopathic or viral pericarditis
Naproxen and colchicine
Patient with blunt thoracic trauma, mildly hypotensive, next step?
Bedside US or Focused assessment with sonography in trauma. Bedside Chest X rays ( Anteroposteroir) are performed after and are preffered over the posterior anterior and lateral that require the patient to stand up.
Causes of prolonged QT
Reemember that Sinus bradycardia can also cause it!
Pulmonary edema -exacerbation CHF
Can present with hypoxia, tachypnea, sensation of choking.
tto of acute decompensation of HF
fUROSEMIDE, OXYGEN, NITROGLYCERIN IV, MEXT STEP? ECHO
After LMNOP in acute HF exacerbation , next step?
Echo, to assess for type of HF and any valvular abnormalities that may be contributing to it . If there is signficant left ventricular dysfunction – then pt may require stress testing or coronary angiography
TIMI score
say it
Aortic dissection tto
IV B blocker, morphine, Sodium nitroprusside IV if SBP>120, emergent surgical repair.
TTO for chronic HF
NYHA classification
Tto for cocaine induced MI
BZD and nitrates. NO B BLOCKERS, CCbs if persistent chest pain , phentolamine if persistent hypertension, +/- PCI if MI
Chest pain cocaine induced and new neurologic symtpom, and negative CT head, diagnosis and next step?
acute dissection of ascending aorta– Ctangiography– that is a surgical emergency
Meds for redcuing TRG
Fibrates ( Gemfibrozil)
Niacin
Increased HDL, modest decrease of LDL
Bile acid sequestrants function
cholestyramine, colestipol, colesevelam– decrease LDL levels but no impact on cardiac outcomes.
Interaction between warfarin and amiodarone
amiodarone (for Afib) increases warfarin level, so warfarin dose should be reduced by 25-50%.
SE of amlodipine
Peripheral edema - are arteriolar vasodilators . To reduce it you can add ACEis
difficulty breathing ECG with narrow QRS complex, different P wave morphology , not able to talk
Multifocal atrial tachycardia
Multifocal atrial tachycardia
Seen in patients with pulmonary disease, but can be triggered by exacerbation of pulmonary disease, electrolyte disturbance, or cathecolamine surge(sepsis)
ECG findings multifocal atrial tachycardia
R-R interval irregular, P waves of at least 3 different morphologies atrial rate of >100
tto of multifocal atrial tachycardia
underlying disease, can be electrolyte replacement, NIPPV or O2 supplementation
short apical low pitch diastolic rumbling murmur, notched p waves, opening snap
mitral stenosis
Mitral stenosis presentation
Dyspnea, orthopnea, hemoptysis, SOB, cough at night.
Sudden cardiac death in young patients– think of 2 things
HCM, and Anormalous Aortic Origin of Coronary Artery
Types of Aortic Origin of Coronary Artery
- LAD originating from the right aortic sinus 2. RCA originating from the Left aortic sinus
Why is AAOCA dangerous
it creates a curvature that is less amenable for high flow, and in situatins of high flow like exercise when pulmonary and aortic vessels are dilated these may cause external compresion as the anomalous coronary is in the middle.
AAOCA DX
ECG resting is normal, Echo sometimes can show it, but the best is CT coronary angiography.
Medications that should be withheld prior to any surgery
ACEi/ARBs unless heart failure( they have peri and postoperative risk of hypotension), Diuretics, Metformin, Raloxifen.
Ortner syndrome
Hoarseness due to recurrent laryngeal nerve compression due to left atrial enlargement- seen in mitral stenosis
Brugada Syndrome ECG characteristics
Right bundle branch block and ST elevation on V1-V3,can cause SCD but not in exertion
Define long QT syndrome
> 450 in men, > 470 in females
Raloxifen SE
Venous thromboembolism, should be discontinued 4 weeks prior to any surgery
Treatment of Afib
say it
Algiruthm arrythmias, PE/Asystole, and Vfib/pulseless Vtach
say I t
Chronic heart failure tto
1) ACEi/ARBs + B blockers 2. Same 1 + Furosemide 3. Same as 2 + spironolactone , hydralazine+nitrate
Indications for hydralazine+nitrate in CHF
African americans and if ACEi/ARBs are not tolerated
Patient with sudden onset of SOB, diaphoresis, hypotension, hyperdynamic pre-cordium and early decrescendo holosystolic murmur
Acute mitral regurgitation - can be seen in patients with ehler Danlos, Marfan, or in patients with papillary muscle rupture in the setting of MI. THE MURMUR IS OFTEN ABSENT!!! ( due to severity, and equalizationof LA and LV pressures
Tto of acute Mitral regurgitation
Echo at beside, emergent surgical eval
What do Ehler and Marfan share in common and what is different
Common things: JPSM: Joint hypermobility, Pectus excavatum, Scoliosis, MVP. Ehler danlos: Easy bruising, velvety skin, atrophic scars, uterine prolapse, inguinal and abdominal hernias, high arched palate. Marfan: tall stature, aortic root dilation, lens and retinal detachmen, spontaneous pneumothorax.
Definition of peripartum cardiomyopathy
occurs between 36 weeks and 5 months postpartum, signs of left heart failure, and LVEF =<45
RF for peripartum cardiomyopathy
MATERNAL AGE>30, PRE-ECLAMPSIA,MULTIPLE PREGNANCIES
Prognosis of peripartum cardiomyopathy
Some may resolve spontaneously and completed. If at time of diagnosis LVEF<20 the risk of recurrence is higher. Patients need to be followed with Echo for years. If persistent or recurrent, may be adviced not to pursue another pregnancy
3 Complications of cardiac catheterization
- Hematoma: +/- mass, no bruit 2. Pseudoaneurysm: bulging, pulsatile mass, systolic bruit 3. AV fistula: continuous bruit, no mass.
Patient post catheterization, leg pain, pulsatile mass, next step
US leg
Main RF for pseudoaneurysm after catheterization
inadequate post-procedural manual compression
tto of pseudoaneurysm post catheter
Small can be treated with US guided compression or intraluminal thrombin injection, larger or rapidly expanding can rupture so surgery.
Criteria for biventricular pacing in HF
- LVEF < 35% 2. NYHA II,III,IV with ss despite tto 3. LBBB with QRS > 150. These patients also meet criteria for cardioverter defibrillator implant.
wHAT DOES Deep Q waves indicate
prior infarct
MC location of abdominal aneurysm
infrarenal > 3cm
What intervention will more likely decrease the expansion risk of aortic aneurysm
stop smoking
aortic aneurysm screening
Abdominal US, 65-75 yo who have ever smoked
Indications for aortic aneurysm repair
large > 5.5 cm, rapidly progressive > 0.5 in 6 months, AAA associated with PAD or aneurysm
Management of AAA
Smoking cessation, ASA, statin, and evaluate If candidate for surgery
Follow-up of aortic aneurysms
Medium : 4-5.4 (US every 6-12 months), Small( every 2 -3 years)
Patient with hypertensive emergency who received IV labetalol and IV nitroprusside , 2 days after presents with confusion and seizures
Cyanide toxicity
Cyanide toxicity presentation
Cherry red color first, then cyanosis, altered mental status to seizures, arrythmias, respiratory depression and then tachypnea, pulmonary edema, METABOLIC ACIDOSIS
Cyanide toxicity treatment
sodium thiosulfate
Beck’s triadforcardiac tamponade:
hypotension, muffled heart sounds, JVP
The most specific finding of cardiac tamponade indicating that emergent treatment is needed
early diastolic collapse of the right ventricle and right atrium. Other signs pulsus paradoxus . LOW VOLTAGE QRS IS NOT SPECIFIC OF CARDIAC TAMPONADE, THAT CAN BE FOUND IN OTHER CAUSES. THIS IS DIFFERENT FROM ELECTRICAL ALTERANS
Most significant predictor of cardiovascular risk ?
Diabetes Mellitus , other CHD equivalents are: CKD, and noncoronary atherosclerotic isease
Strict glycemic control improves microvascular complications but not macro
Micro include retinopathy, nephropathy, neuropathy. Macro: CHD, stroke
Criteria for Aortic valve replaement
Severe AS (JET>0.4, GRADIENT>40,) PLUS >=1: onset of symptoms, LVEF< 50%, undergoing other cardiac surgery (CABG)
men died steering wheel , motor vehicle accident. Cause of sudden death?
Aortic rupture. NOT CARDIAC CONTUSSION! IT CAN CAUSE BUT WHEN THERE IS INVOLVEMENT OF VESSELS AND CHAMBERS.
Management of statin myopathy or rhabdomyolysis
Symptomatic patients-discontinue statin. Asymptomatic patients with CK increased >10 times stop. BECAREFUL because statin can also potentiate myopathy in the setting of exercise so if pt did a marathon presents with high CK, discontinue statin, and then recheck CK, and if levels have normalized re-start statin as it was initially tolerated.
Patient developing cardiogenic sshock in the setting of inferior MI and bradyarrhythmia. Not responsive to atropine, hemodynamically stable, next step
temporary pacing, and then PCI
Patient diagnosed with bicuspid aortic valve, next step?
First degree relative screen with echocardiography. Patients are followed with echo every 1-2 years. And can require valvuloplasty.
Complications or risks of having bicuspid valve
Endocarditis, Severe aortic stenosis or regurgitation, aortic root dilation, dissection.
Treatment of Wolff Parkinson white Afib
unstable: cardioversion. Stable: procainamide or ibutilide
Meds CI in Wolff Parkinson White
Digoxin, CCBs, b blockers, verapamil, adenosine
INR target with aortic and mitral mechanic valve
Warfarin 2-3: aortic valve replacement with no risk factors(
Patients with bicuspid valve should be assessed for
thoracic aortic aneurysm, or dissection.
Afib but pulseless
Pulseless electrical activity- any type of arrythmia. Start compressions and then give Epinephrine
Syncope in patient with prior mI
think that cause can be ventricular tachyarrhythmia due to scarring tissue.
Causes of cardiogenic syncope
Aortic stenosis/HCM, Ventricular tachyarrhythmia, Sick sinus syndrome, Torsades de pointes, advanced AV blocl
Athlete asymptomatic with low heart rate, next step
reassure, and routine care
Patients with suspected marfan syndrome require an echo prior to initiation of physical activity
if there is root dilation, they are advised not to do strenous activity.
Patient with cardiogenic shock secondary to MI, presenting with sinus bradycardia and infarct on II, III, Avf, next step
Intravenous atropine. Inferior infarcts can be associated with sinus bradycardia because the the SA node is irrigated by the RCA. In RV infarcts its true that they can be preload dependent and may require IV fluids, but its not the case for patients who have cardiogenic shock, where fluids can worsen it
Perioperative stratification for cardiac risk, High risk and low risk procedures.
High risk procedures: aortic surgery , or peripheral vascular. Low risk : ABCE: Ambulatory or superficial, Breast, Cataract, Endoscopy. Low risk no further testing unless decompensated HF, or unstable angina. For high and intermediate risk based on RCRI risk, and if they are able to do brisk walking or climb 2 flight of stairs no further testing.
Lateral wall of the heart Is irrigated by
LCA
LAD irrigation
anterior interventricular groove and irrigates the anterior wall of the left ventricle
RCA irrigation
right ventricle and inferoposterior wall of left ventricle
TCA overdose
CARDIAC ARRHYTHMIA, ALTERED MENTAL STATUS, Hyperthermia, confusion, flushing, blurred vision, urinary retention, mydriasis
TCA antidote
sodium bicarbonate for stabilization of the heart. , if not resolve give Mg, or lidocaine.
Management of TCA OVERDOSE
O2,intubation as needed, IV fluids. Activated charcoal if within 2 hours of ingested( unless ileus is present) and sodium bicarbonate for WIDE QRS arrhythmias
patients with CAD that are elderly > 80 may present more often with anginal ss ( shortness of breath) rather than chest pain in CAD!!!
TRUE
Patient with MI leading to acute decompensated HF, what medication should NOT BE GIVEN
B blockers, as it may worsen pulmonary edema
Resume sex after MI
If they are asymptomatic they can resume ot. Guidelines say within 3-4 weeks after MI, and as early as 1 week.
ECG findings in constrictive pericarditis
nonspecific, Afib, low voltage QRS complex. Imaging shows calcifications
Causes of constrictive pericarditis
Idiopathic or viral, cardiac surgery or radiation, TB
T wave abnormalities in ECG may raise suspicion for CAD
always do troponin (at least 2 in 3 hours apart) and serial EKG every 30 minutes.
indications of implantable cardioverter-defibrilator in HCM
- Prior history of cardiac arrest or sustained Vtach 2. family history of SCD 3. Recurrent or exertional syncope 4. Nonsustained SVT, 5. Hypotension with exercise 6. Extreme left ventricular hypertrophy
PCI timing
ideally 90 minutes from when patient is seen by physician (independent of when the ss started) and 120 if will be transfer
Epigastric pain associated with exercise, think of CAD!
WARRANTS ECG
Management of Afib
b blocker or CCBs!and assess need for cardioversion and CHA2DS2VASc
PAD management
Aspirin + High dose statin , then supervised exercise progrma > 3 x/week for 3 months. If despite this persist cilostazole, if persists revascularization
Antiarrhythmics for Afib indication and what to use
Indications: 1. inability to maintain adequate HR control with rate drugs 2. Symptomatic despite rate control agents. For LVH AND HF: Amiodarone. Nothing: flecainamide, propafenone, CAD:Sotalol.
What has the major impact inHTN
Weight loss ( < 25%), BASH diet, and exercise.
Digoxin toxicity
nausea/emesis, anorexia, fatigue, confusion, visual disturbances, cardiac abnormalities
What drugs cannot be given with Digoxin, otherwise there is Digoxin toxicity?
VASQ–Verapamil, Amiodarone, Spironolactone, Quinidine.
Patients in TPN should be closely monitored for which electrolyte and why?
Phosphorous. It is possible that they develop silent hypophosphatemia ( in the setting of IV dextrose in TPN- Dextrose–insulin production–insulin drives serum phosphate into the cell for ATP generation– and there is hypohosphatemia. It is also seen in refeeding syndrome
Complications of refeeding syndrome
seizures, rhabdomyolysis, arrhythmias, CHF
First line tto for DVT/PE in cancer and non cancer patients
in non cancer: oral X inhibitors (Rivaroxaban) for at least 3 months. In cancer LMWH (this is non oral)
Alternative for horomone replacement therapy for hot flashes due to risk of DVT
SSRIs OR NSRIS
Risks of hormone replaceent therapy
Increase risk of breast Ca, stroke, and DVT
Down is associated wiith which conditions
Endocardial cushion defect, duodenal atresia, hirschprungs, atlanto axial instability, hypothyroidism
Patients with Down syndrome are at risk of developing
ALL, Alzheimers, autism, ADHD, depression and seizures
characteristics of AS murmur,
single S2 ( delay in aortic equalizing pulmonic), pulsus parvus et tardus ( diminished and delayed carotid pulse), soft S2 in severe, and loud S2 in mild and severe.
in vasovagal syncope prodromal symptoms may persist briefly AFTER the syncope
true.
HCM treatment
B blocker, if not work verapamil, and disopyramide. Implantable cardioverter defibrillator.
Single most important RF for CAD
DM
Is stress a RF for CAD
NO
RF fo0r CAD (8)
DM- IS THE MOST IMPORTANT. Others: HTN, smoking, Obesity, sedentarism, hyperlipidemia, PAD, family history (female < 65, men <55)
Chest pain in CAD
Dull chest pain, lasts 15-30 mint, occurs in exertion, substernal location, and radiates to the jaw or left arm.
The most common cause of pain that is not cardio related
GERD
NSTEMI tto
DNA BSG. Dual anticoagulation( Aspirin, clopidogrel), nitroglycerin, anticoagulation( heparin) , b blickers, statin
EKG changes in CAD
ST depression, elevation, and T wave inversions
Types of troponins and function
T- tropomyosin C- binds calcium to activate actin-myosin interaction, and Troponin I blocks or inhibits actin-myosin interaction.
When do CKMB levels go down and and then up
go down at day 2-3 and then elevate after if re-infarct. While troponins will remain elevated
Best initial treatment for CAD
Aspirin
Aspirin lowers mortality?
Aspirin alone reduces mortality by 25% for acute MI, reduces mortality by 50% in unstable angina.
MOA clopidrogrel, prasugrel, ticagrelor
P2Y12 antagonists- block aggregation of platelets to each other by INHIBIYING ADP-induced activation of the P2Y12 receptor.
Angioplasty and thrombolytics both lower mortality in STEMI
true , IBUT IN STABLE ANGINA it does not decrease mortality more than medical therapy
Stable angina tto
ABNS - Aspirin, B blocker, Nitrate, Statin
Timing for angioplasty and thrombolytics
angioplasty > thrombolytics. Angioplasty 90 min of arrival to ED. If not able to PCI then thrombolytics within 30 minutes of arrival to the ED, BUT CAN BE GIVEN UP TO 12 HOURS FI THERE IS ST ELEVATION >=2 leads.
ACEis lower mortality in STEMI?
ONLY IF there is LV dysfunction or systolic dysfunction
When to add prasugrel inSTEMI
If they go to Angioplasty
Mechanism of thrombolytics and why time matters
thrombolytics convert plasminogen to plasmin. Plasmin cleaves fibrin clot into D dimer. Normally, once fibrin clot is formed after a couple of hours it is stabilized by factor XIII, Once is stabilized plasmin will not cleave fibrin.
Mechanism of B blockers in STEMI
Slow heart rate– increases coronary artery perfusion, and ncreased left ventricular time increases both stroke volume and cardiac output.
Meds in ACS that lower mortality
Aspirin, thrombolytics, primary angioplasty, metoprolol, statins, clopidogrel, prasugrel ticagrelol.
Heparin lowers mortality in MI?
only if ST DEPRESSION- NSTEMI
When do you give prasugrel, clopidogrel,?
aspirin allergy, they go to PCI, or MI.
SE of ticlopidine
neutropenia
When to give CCBs in MI
intolerance to b-blockers: asthma patients, cocaine induced chest pain, or Prinzmetal angina
When do you give lidocaine or amiodarone in MI
When is Vtach or Vfib. NEVER prophylaxis.
In which patients prasugrel cannot be given
> 75years and in stroke. It increases bleeding.
When is a pacemaker needed in MI
Symptomatic bradycardia, Mobitz II, 3rd degree block, bifascicular block, New LBBB.
All complications of MI lead to hypotension
TRUE
Dx and tto of cardiogenic shock post MI
Echo, swan-Ganz catheter. ACEI, and urgent revascularization
Dx and tto of valve rupture post MI
Echo, ACE, nitroprusside, intraortic ballon bump to bridge into surgery
Dx and tto ofseptal rupture post MI
Echo, right heart will show step up in Oxygen. ACE, nitroprusside, and urgent surgery.
Dx and tto of Myocardial wall rupture inMI
Echo, pericardiocentesis, urgent cardiac repair.
Dx and tto of sinus bradycardia in MI
ekg, and give ATROPINE , followed by pacemaker if ss persist.
Dx anf tto of 3rd degree AV block
EKG showing canon a waves(high amplitude), and give atropine and pacemaker.
All patients POST-MI should go home on
Aspirin, clopidogrel( or prasugrel), b blocker, statin, ACEi.
How is NSTEMI management different from STEMI
NO thrombolytic use, We use heparin ( lMWH>unfractionated), Glycoprotein Iia/IIIb INHIBITORS(ABCIXIMAB) LOWER MORTALITY
Abciximab lowers mortality in NSTEMI
yes, particularly in those going for angioplasty
ACE and ARBs SE
both cause hyperK, but cough is only caused by ACE
In chronic CAD and pain persists despute all treatment
ranolazine- antianginaal- blocks inward sodium currents
LDL goal of statins in coronary artery disease and DM
<70
Proprotein convertase subtilisin/kexin type 9 (PCSK9). Moa and use
binds (LDL-R) on the surface of hepatocytes, leading to the degradation of the LDL-R and higher plasma LDL-cholesterol (LDL-C) levels. if patients on ACS already on statins and they cannot control severe hyperlipidemia. Injected meds that block clearance of LDL BY THE LIVER FROM THE BLOOD. NO impact on mortality.
Alirocumabandevolocumab
Proprotein convertase subtilisin/kexin type 9 (PCSK9). Inhibitors
Erectile dysfunction causes post MI
MC is anxiety, but can be due to B blockers.
mechanism of rales in CHF
increased hydrostatic pressure develops in the pulmonary capillaries from the left heart pressure overload. It transudates into alveoli. In inhalation the alveoli open with a popping sound referred as rales.
Management of Pulmonary edema as manifestation of CHF
LMNOP -I first prior to imaging!
Labs to order when patient is with pulmonary edema as complication of CHF
Chest X ray ( pulmonary vascular congestion, cephalization of flow, effusion, cardiomegaly). EKG, Oximeter, Echo
MOA dobutamine, inamrinone, milrinone
Phosphodiesterase inhibitors. Increase contractility and decrease afterload.
If after LMNO in pulmonary edema patient continues symptomatic
positive inotrope.- dobutamine 30-60 min
neVER USE DIGOXIN IN ACUTE TREATMENT OF CHF AND PULMONARY EDEMA
Digoxin can be used in chronic treatment.
Treatment of systolic dysfunction chf
ACE/ARBs, b blockers, furosemide, sspironolactone, digoxin if persistent, if still persistent jhydralazine+ nitrates, sacubitril with valsartan
Side effects of Mineralocorticoids receptor antogonists (Spironolactone, eplerenolne)
hyperK. Spironolactone can cause gynecomastia and erectile dysfunction. Eplerenone has no andorgenic. IF HYPERK and needed to decrease mortality then five Patiromer.
Spironolactone decreases mortality in SYSTOLIC CHF
TRUE
Treatment of diastolic CHF
Spironolactone, or eplerenone.
Patient with pulmonary edema that has Vtach, next step
Synchronized cardioversion , pulmonary edema is not considered hemodynamically stable.
when to do synchronized cardioversion in pulmonary edema
if Vtach, a fib, flutter or SVT- These are considered hemodynamically UNSTABLE!
Escalation in treatment of acute pulmonary edema
LMNOP –Inotropes ( Dobuitamine,iunamrinone, milrinone)–> nesitiride (SYNTHETIC FORM OF ATRIAL NATRIURETIC PEPTIDE)
What is wedge pressure
Left atrial pressure
When to order echo inpulmonary edema secondary to CHF
Once the patient has been stabilized.
In systolic CHF what to do if ACE/ARBs cannot be given
hydralazine+nitrates in addition to other meds.
Digoxin and diuretics in CHF do not reduce mortality
TRUE
what CHF med causes transient excess brightness or vision
ibravidine (Sa nodal inhibitor of funny channels that slow heart rate.
Pacemaker in CHF
LVEF <35%, and QRS >120msec
All valvular heart disease can be expected to have murmurs and rales on lung exam.
True, can also have peripheral edema, carotid pulse findings, gallop.
Tto of most of the murmurs
ACE/ARBS or diuretics.
Tto of MVP
B blocker if ss
tto of Mitral Stenosis
Furosemide and Na restriction, Balloon valvuloplasty, warfarin and rate control for Afib.
Early diastolic decresecendo best heard in the lower left sternal border
Aortic regurgitation.
Intensity of murmurs
I/VI only heard with special manuevers ( handgrip, valsalva) , II/VI AND III/VI majority, no obkective difference between these. IV/VI: palpable thrill. V/VI: can be heard with the stethoscope partially off the chest VI: stetoscope no needed to hear it.
Best initial test for Valvular lesions, and most accurate
BIT: Echo, MAT: Left heart catheterization.
Prognosis of AS
coronary disease: 3-5 year survival, syncope 2-3 year survival, CHF 1.5-2 year survival.
AS treatment
Diuretic and TRANSCATHTER valve replacement.
Management of bio vs. mechanical valve in AS
Boioprostethic valve will last 10 years but requires no anticoagulation with warfarin. Mechanical valve will last longer but requires warfarin goal INR 2-3.
Antithrombotic therapy in mechanical valve
Warfarin with INR 2-3 in Aortic valve replacement without risk factors. Warfarin 2.5-3.5 for mitral valve replacement, and for aortic valve replacement with risk factors: Afin, LV dysfunction, thromboembolism, hypercoagulable state. Always ADD ASPIRIN FOR MECHANICAL VALVES
how long mechanical valves last
10-15 years.
Causes of AR
HTN, endocarditis, rheumatic heart disease, Marfan, AS, cystic medial necrosis, Syphilis, reactive arthritis.
When do you repair Bicuspid aortic valve
> 5 cm
Complications of bicuspid aortic valve
aneurysm, and endocarditis
AR treatment
ACEi/ARBs, NIFEDIPINE.- but these are not proven to decrease velocity of disease. Surgery if LVEF < 55%
Murmur in MS
opening snap followed by diastolic rumble, loud S1, as it gets worse the opening snap moves towars S2
BIT and MAT in Mitral Stensois
Best initial therapy diuretics, MAT: ballon valvuloplasty
Pregnancy is NOT A Contraindication for Ballon valvuloplasty
TRUE
Operative criteria for AR and MR
AR: EF<55% AND LV end systolic volume > 55. MR LEVF<60% and LVESD >40
Mechanism of fixed splitting of S2 in ASD
LA/RA pressure no change in respiratrion = no change in splitting
When is percutaneous repair indicated in ASD
SHUNT RADIO EXCEEDS 1.5:1
Causes for Wide splitting of S2, delayed P2
RBBB, Pulmonic stenosis, RVH, Pulmonary HTN
Causes for PARASOXICAL splitting of S2, delayed A2
LBBB, AS, LVH, HTN
TTO of dilated cardiomyopathy
same as systolic HF- ACE/ARBs, b blockers, furosemide, spironolactone
Tto of hypertrophic cardiomyopathy
distolic HF- Spironolactone, or eplerenone.
Most accurate diagnositic test in Restrictive cardiomyopathy
endomyocardial biopsy, but usually we do first echo and EKG
Amyloid cardiomyopahty ECG and Echo findings
Low voltage ECG and spleckled pattern on echo
Treatment of Tako Tsubo Cardiomyopathy
ACEi, diuretics, b blockers.
pleuritic vs ischemic pain
pleuritic is sharp, positional. Ischemic is dull and sore.
Best initial test in pericarditis
EKG- ST elevation everywhere, and PR segment depression in lead II but this last one is always present.
Electrical alternans is seen in which condition
cardiac tamponade
earliest finding in cardiac tamponade in echo
diastolic collapse of the right atrium and right ventricle, later findings include equalization of all pressures in the heart during diastole.
tto of cardiac tamponade
pericardiocentesis, DO NOT USE DIURETICS
Best initial treatment in constrictive pericarditis
diuretic, the most effective treatment is removal of pericardium (pericardial stripping)
BIT and MAT in aortic dissection
cHEST X RAY, AND THE MAT is CT.
Aortic dissection in CSS
Give b blocker, order EKG and Chest X ray. Then order CT angiography and start nitroprusside to control BP. ICU AND SURGERY CONSUTL,
Normal ankle brachial index
> =0.9
BIT and MAT in PAD
Ankle brachial test, angiogram
Treatment in PAD
Aspirin + High dose statin , then supervised exercise progrma > 3 x/week for 3 months. If despite this persist cilostazole, if persists revascularization
CCS, Patient with Afib
Echocardiogram ,TSH,T4, CMP,
if severe bleeding occur with warfarin, next step
Prothrombin complex concentrate (II, VII,IX, X)or FPP
If bleeding occurs with Xa inhibitors
give andenaxet
if bleeding occurs with dabigatran
gice idarucizumab
Factor X inhibitos and dabigatran( inhibitoer thrombin) decrease more mortality in Afib than warfarin
TRUE
When is obligatory to use Warfarin in Afib
metallic valves or MS
Atrial flutter is managed the same as Afib
true
Treatment for multifocal atrial tachycardia
If PO2< 55 give O2 first, then diltiazem. NO B BLOCKERS
SVT tto
unstable: cardioversion. Stable: first vagal manuevers, IV adenosine, if doesn’t work b blocker, CCBs, or digoxin
Best long term tto for SVT
radiofreq catheter ablation
CCS syncope
EKG, CMP, CBC, Cardiac enzymes, oxymetry, echo if murmur if present, head CT is neuro exam focal.
What class of antihypertensive agent is best known for severe, first dose orhtostatic hypotension
terasozin ( alpha 1antagonist)
List 4 primary categories of shock
Hypovolemic, cardiogenic, distributive( septic, anaphylactic shock, neurogenic shock), and obstructive shock ( tension pneumothorax, impeding venous return)
Fluids in shock
generally 10-20 cc/kg, but in distrubutive shock be more aggressive 30cc/kg
If fluid challenge fail to raise BP in shock patient, next step
Norepinephrine is first line tto for SEPTIC AND CARDIOGENIC SHOCK. Epinephrine for anaphylactic
Types of shock and parameters CO, PCWP, SVR, SVO2
Septic: high CO, low PCWP, Low SVR, High SVO2. Hypovolemic: low CO, low PCWP, high SVR,low SVO2. Cardiogenic : low CO, high PCWP, high SVR, Low SVO2. Anaphyactic: high CO, low PCWP, SVR, and SVO2
Pulmonary embolism can cause shock
TRUE
aortic dissection can cause cardiac tamponade
true
What clues suggest Addison disease as a cause of shock
history of steroid, traima, hypotension, eosinophilia, hyperK, and hyponatremia. Treat with steroids and high volumes of fluids
Norepinephrine MOA and when to use in shock
alpha1 and beta 1 agonist effects. For hypotension to increase peripheral resistance. 1st line in septic shock and cardiogenic shock
Dobutamine MOA and when to use in shock
B agonist to increase cardiac contractility
Dopamine
at low doses: affects dopamine receptors–> vasodilation. At higher doses its beta 1 agonist effect increases contractility. At even higher doses has alpha 1 agonist effects and causes vasoconstriction. The b1 agonist activity makes it first line symtpomatic bradycardia.
Stages of hypertension
normal <120/<80. PreHTN 120-139/80-89, HTN stage 1 140/90 , stage II >=160/100
HTN tto
black: thiazides or CCB, alone or in combination . Other ethnicities: thiazides, ACEi, ARB or CCB Other ethnicities with DM or CKD: ACEi and ARB
HTN in pregnancy
Labetalol, hydralazine and alpha methyldopa are safe.
Define Hypertensive urgency
> 200/120 without ss, if ss is called emergency
What tests should be ordered in HTN
ECG, CMP, Urinalysis, CBC, Lipid panel
ST changes in leads V5 and 6 are often seen with left ventricular hypertrophy from systolic overload and are termed a “strain pattern.”
TRUE
Hyperthyroidism algorithm
say it
Hypothyroidism algorythm
say it
Thyroid nodule algorithm
say it
Types of Ca in thyroid
say it
Indications for treating in subclinical hyperthyroidism
TSH < 0.1 , or TSH 0.1- 0.5 IF >=65, hear problems, osteoporosis, and nodular disease . TTO is indicated due to the risk of developing overt hyperthyroidism
Precocious puberty algorithm
say it
Patient with acne, no testes enlargement, and advanced age. No CNS ss, cause?
Peripheral precocious puberty - CAH. There is significant acne, may exhibit hypotension, hypoNa, hyperK.
Dx of Congenital adrenal hyperplasia, classic
Elevated 17 hydroxyprogesterone on ACTH stimulation test.
Dx of glucagonoma
pancreatic alpha cell tumor. Glucagon > 500. Necrolytic erythema migrans, new diagnosis of DM, weigh loss, GI ss ( diarrhea, constipation), venous thrombosis , neuro ss(ataxia, dementia, proximal weakness)
Treatment of glucagonoma
octeotride or surgery
Treatment of hyperthyroidism
Anthythyroid drugs ( Methimazole prefered over PTU, unless is 1st trimester pregnancy), radioactive iodine, and thyroidectomy. IN ACTIVE SYMPTOMS ADD B BLOCKER
Patients candidate for Antithyroid medications
Mild hypothyroidism, older with limited life expectancy, preparation for radioactvie iodine, pregnancy
Patients candidate for radioactive iodine
Moderate to severe hyperTSH with or without ophtalmopathy, patient preference in mild hyperTSH
Patients candidate for thyroidectomy
large goiter, suspect cancer, concurrent hyperparaTSH, Pregnant who cannot tolerate antithyroid meds, severe ophtalmopathy, retrosternal goiter with obstructive ss
When do you check labs in thyroid disease once starting antithyroid meds?
4-6 weeks after initiating meds, and then every 2-3 months. TSH levels remain suppressed for a while so check with T3 and T4
iF YOU WANT TO MONITOR FOR EFFICACY OF antithyroid medications what are the labs you check
TSH levels remain suppressed for a while so check with T3 and T4
SE of anithyroid
agranulocytosis and hepatotoxicity
Patient with hypertension and hyperK, what do you think of?, next step in management
Hyperaldosteronism - plasma aldosterone to renin ratio
Causes of primary hyperaldosteronism and labs
Primary hyperaldosteronism (Conn Syndrome), bilateral adrenal hyperplasia. Low renin and high aldosterone (PAC/PR>20) – Do CT scan
Causes of secondary hyperaldosteronism and labs
High renin, high aldosterone. Renovascular HTN, Malignant HTN, Renin producing tumor, diuretic use, coartaction, cirrhosis (PAC/PR~10)
causes of decreased renin and decreased aldosterone, hypertension, and hypoK
Non aldosterone causes: CAH, Cushings, Exogenous mineralocorticoids
treatment of bilateral vs unilateral adrenal hyperplasia
unilateral may benefit from surgery, bilateral just medical therapy ( spironolactone, eplerenone)
Aldosterone escape mechanism
sodium and water retention volume expansion → secretion of atrial natriuretic peptide (ANP) and pressure natriuresis (other mechanisms may be responsible, although how these operate remains unclear)→ compensatory diuresis → “escape” from edema and formation and frank hypernatremia
Why patients with hyperaldosteronism have polyuria
hypokalemia → desensitization of renal tubules to antidiuretic hormone (ADH) → increased water excretion (polyuria) and excessive thirst (polydipsia)
The best way to assess diabetic neuropathy
tuning fork
First line treatment for diabetic neuropathy
glycemic control + First line meds: duloxetine (SNRI), pregabalin- alter neuronal transmission and decrease pain. TCA decrease pain but not alter transmision. Other meds are gabapentin, lamotrigine, or carbamazepine.
what is the advantage of using Glargine or other long acting insulin over NPH
Less risk of hypoglycemia
Short acting insulins
Analogs (Lispro, aspart, glulisine), and Regular
Peak and duration of short acting insulin
analogs (Peak 0.5-1.5, Duration 3-5hours), Regular ( Peak 2-4h, duration 5-8hrs)
Intermediate acting insulin
NPH
Peak and duration of NPH Insulin
Peak 4-12 and duration 14+
Long acting insulins
Detemir, Glargine, and Degludec
Duration of detemir, glargine, and degludec
12-24, 20-24, 42+
hypertension, hyperglycemia, osteoporosis, mood swings, and hypoK with metabolic alkalosis
Cushing syndrome
Clinical presentation of cushing
central obesity, bone fractures/osteopenia, mood swings, skin atrophy, proximal muscle weakness, glucose intolerance, skin pigmentation
Dx of cushing syndrome
24 hour urine cortisol, late evening salivary cortisol, low dose dexamethasone test
high cortisol, high/normal ACTH, next step
MRI. If >6mm –> dexamethasone suppression test and CRH suppresion test. If suppressed cortisol but elevated ACTH- cushing disease. If < 6mm or no mass: inferior petrosal venous sampling: high cushing
Dexamethasone supression test for Cushing
dexamethasone administration woul decrease cortisol levels
Presentation of pseudoparathyroidism
Seizures, muscle cramping, hyperreflexia, basal ganglia calcifications and cataracts- are sign of hypocalcemia.
Vit D deficiency related changes in Ca and pphos
Ca and phos are decreased
Scuvadiving an epistaxis
barotrauma, generally decongestants and pain control
Macrocytosis (MCV >110 fL), diarrhea and neurologic symptoms
Vit B12 def - Diarrhea from celiac sprue, bacterial overgrowth or pancreatic insufficiency can be seen with vitamin B12 deficiency because these are malabsorptive syndromes. Also pernicious anemia
folate deficiency does not cause neurologic deficits
develops faster than B12 def, but is often asymptomatic. Causes include nutritional deficiency, alcoholism, malabsorption, pregnancy, chronic hemolytic states and the administration of drugs that interfere with folate metabolism (for example, trimethoprim and methotrexate).
MCC of travelers diarrhea
E.coli
gas gangrene in a diabetic foot, pathogen?
C. perfringens
Carcinoid tumor presentation with and without metastasis
cutaneous flushing, abdominal cramps, bronchospasm and diarrhea, Gastrointestinal carcinoids that have not yet metastasized are much less likely to produce carcinoid syndrome, because the liver metabolizes and clears the portal blood of the vasoactive substances.
Carcinoid tumor cardiac complications
Right-sided endocardial fibrosis, with pulmonary stenosis and tricuspid regurgitation
Hypersensitivity types
Describe all and examples.
extrahepatic manifestations of hep B
polyarteritis nodosa, and glomerulonephritis.
Elderly, smoker, Recurrent pneumonia in same place, and imaging also shows some scarring
Bronchogenic carcinoma , in young patients and non-smokers may think of carcinoid tumor.
Indications for screening for lung cancer
55-80 years with Hx of 30 packs/year AND currently smoking or stopped within the last 15 years. Diagnosis is with CT and done yearly.
SIADH management
1st water restriction, and if still asymptomatic demeocycline
The best diagnostic test for diagnosing endobronchial obstruction
Is flexible bronchoscopy is the best first initial tool to assess persistent or nonresolving pneumonia, if they ask about the next step in management would have been CT chest.
Well’s score
3 Signs of DVT, alternate diagnosis less likely. 2.5 Previous PE, DVT, HR>100, Recent surgery or immobilization. 1 hemoptysis and cancer. > 4 PE likely
PE presentation
sudden onset pleuritic chest pain ( hurts with inspiration and movement), loud S2, friction rub, hypoxia, tachypnea and tachycardia, can have small pleural effusion ( in the setting of pulmonary infarction due to inflammation)
V/Q scan pretest results
If normal rules out PE, if abnormal ( saying low , medium probability) then it DOES NOT RULE IT, AND IF HIGHLY SUSPECTED BASED ON WELLS START ANTICOAGULATION. High probability on V/Q scan confirms PE
Test of choice for diagnosis pneumothorax in the acute setting
Bedside US ( in the ED, ICU). In non acute setting is the UPRIGHT POSTEROANTERIOR CHEST X RAY
Patients with OSA are at higher risk for residual anesthesia effect and decreased respiratory drive
True because there is decrease in pharyngeal muscle dilator tone, and they have prior propensity for obstructive apneic or hypoapneic events.
patients with respiratory failure due to residual anesthesia effect
respiratory acidosis with normal anion gap, and hypoxemia typically correct with supplementary oxygen.
Atelectasis when do they occur?
2-5 days POP, hypoxemia fails to correct with O2 and it is elevated anion gap.
cough variant asthma presentation
nonproductive cough triggered by exercise(particularly cold weather), allergens, and forced expiration. Occurs also at night and can present chest tightness. Wheezing and rhonchi are often absent
cough variant asthma tto
same as asthma, but If cough is resistant to bronchodilators or inhaled corticosteroids then leukotriene receptor agonists (montelukast) can be used
upper airway cough syndrome
sam is postnasal drip
Indications of palivizumab in bronchiolitis
Preterm birth <29 weeks, chronic lung disease of prematurity, hemodynamically significant congenital heart disease.
Complications of RSV
Apnea ( those premature, chronic lung disease and congenital heart failure are more likely to develop), and respiratory failure
Labs in pertussis
lymphocyte predominant lymphocytosis: > 20,000 with >50% lymphocytes.
Why does tachycardia in asthma exacerbation occurs, is it contraindication for albuterol?
hypoxia– activates carotid chemoreceptors that release catecholamines drom adrenal gland, not a contraindication to give albuterol.
Weight loss in COPD
Pulmonary cachexia syndrome: =<20 BMI or weight loss > 5%. Caused by: 1. Increased WOB, caloric use, energy imbalance- 2. Inflammation 3. skeletal muscle hypoxia and sometimes glucocorticosteroids.
tto of pulmonary cachexia syndrome
optimization of lung function, nutrition supplementation, and exercise.
asthma exacerbation+fever, malaise, brownish sputum, eosinophilia, patches in upper lobes
bronchopulmonary aspergillosis – do either allergy skin testing for Aspergillus or IgE.
tto of bronchopulmonary aspergillosis
MAINSTAY IS ORAL STEROIDS , and also voriconazole or itraconazole.
How to differentiate pulmonary contusion from pulmonary embolism
pulmonary contusion often occurs in the setting if blunt trauma, has SOB, chest pain, tachycardia, hypoxia BUT respiratory ss can present even 24 hours after insult, and the XRAY SHOWS IRREGULAT , LOCALIZED OPACIFICATION.
tto of pulmonary contusion
supportive- pulmonary hygiene, supplemental oxygen, pain management. Most resolve by 3-5 days.
patients with pulmonary contusion are at higher risk of pneumonia
true but prophylaxis antibiotics are not indicated
Why is the hypoxemia in COPD
low V/Q mismatch. Poor ventilation leads to hypoxic vasoconstriction.
Why do COPD patients that are hypoxic improve with supplemental oxygen
despite low V/Q mismatch, supplemental oxygen is able to reach alveoli, decrease the vasoconstriction increasing Q, and overal V/Q.
Croup presentation
Inspiratory stridor, cough, hoarseness
Croup tto
mild(no stridor at rest): humidified air +/- corticosteroids. Mod/severe (stridor at rest): corticosteroid + racemic epinephrine.
Suspects croup, next step?
TREAT! CORTICOSTEROIDS. NO NEED FOR IMAGING, DX is clinical.
STOPBANG Questionnaire for OSA
Snoring, Tiredness during day, Observed apnea or chocking/gasping, Pressure high, BMI>35, aGE>50, Neck size M>17 and women >16, Gender Male.
Elimination of bedtime alcohol and smoking are preferred strategies for isolated snoring- no OSA
TRUE
Factors increasing the malignancy of solitary nodule
Large size (>2cm), Female, advanced age, smoker(previous or active), personal or familiar hx of Ca, spiculated, upper lobe
Algorithm of solitary nodule.
say It
hypotension and hypoxemia in the absence of infiltrates, requiring intubation
massive pulmonary embolism- patients can have massive RH strain causing RBBB, dilation of the RV and tricuspid regurgitation
suspect massive PE, next step
bedside Echo, but first stabilize the patient like with intubation
postextubation stridor and hypoxemia, what is it and tto?
laryngeal edema, re-intubate if impending respiratory failure
Signs of impending respiratory failure
pH<7.35 AND PCO2>45. clinical signs of respiratory failure, , RR > 25 X 2 HRS, Hypoxemia
RF for extubation failure
weak cough, frequent suctionin, poor mental status, positive fluid balance, pneumonia as initial cause of respiratory failure, Age > 65, Comorbid conditions
Administration of multiple doses of corticosteroids prior to intubation can prevent laryngeal edema and extubation failure
TRUE
Acute respiratory failure due to OSA postop causes
hypoventilation (evidenced by bibasilar atelectasis in the chest X ray) and hypercapnic and hypoxic respiratory failure. With respiratory acidosis.
definition of acute bronchitis
persistent cough> 5 days up to 3 weeks, cough can present with purulent yellow or green discharge and this is associated with epitelial sloughing. 90% have a previous URI
Presentation of acute bronchitis
persistent cough > 5 days up to 3 weeks, can have purulent sputum, rhinchi at auscultation that clear when coughing. , wheezin, chest wall tenderness an mild dyspnea.
tto of acute bronchitis
symptomatic( NSAIDs and bronchodilators), no antibiotics! If pt has fever, suspect bacterial pneumonia or bronchitis with influenza
Spirometry in symptomatic and asymptomatic asthma
asthma overall has decreased FEV1/FVC and normal or high DLCO. In symptomatics if we give albuterol there is increase of FEV1 > 15%, and in asymptoamtic and we give metacholine there is a reduction of FEV >=20%
Elderly with confusion, hypothermia, tachypnea, hypoxia and hypotension, not responsive to fluids. Next step
Fluids + empiric antibiotics== qSOFA ( RR>22/MIN, AMS, SBP=<100)
qSOFA
( RR>22/MIN, AMS, SBP=<100) IF>=2
Inhaled bronchodilators in RSV, are they recommended?
Can be used but they do not show evidence that they reduce illness, admission rates, r length of hospital stay.
Patients with RSV are at risk of?
Apnea ( those premature, chronic lung disease and congenital heart failure are more likely to develop), and respiratory failure, AND RECURRENT WHEEZING 30%.
Low dose chest CT in lung cancer, if positive what is the probability of having cancer?
<10%, has a false positive rate of 96%.So any postiive finding may need confirmation. Screening reduces 20% mortality.
Pulmonary embolism and fever
15%, likely due to pulmonary necrosis in the setting of infarction.
risk factors for TTN
cESAREA, PREMATURE, MATERNAL DM.
Chest X ray finding in TTN
Hyperinflatio (flattened diaphgram), mild cardiomegaly, prominent vascular markings, fluid in the interlobal fissures, and pleural,.
prognopsis of TTN
usually resolve by 72 hrs and no long term complicatiosn
Management of tension pneumothorax
Needle decompression ins appropriate in the acute setting where cardiac arrest is imminent. However, needle decompression must ALWAYS be followed by chest tube placement. In patients that you identify pneumothorax but there is not yet a big compromise chest tube is the answer!
