im Flashcards
emergent tx for hyperkalemia
hyperkalemia is treated emergently when ECG changes (peaked t waves, widened QRS, bradycardia, disappearance of p waves, sinus node dysfunction and av node block) or when K+ is really high (like >6.5) or rises really fast. Calcium is used to stabilize cardiac membrane. Since it’s faster to shift K+ intracellular than get it out of the body, insulin is given. Glucose is also given to prevent hypoglycemia.
acute epididymitis usually due to bladder obstruction and the organism ______ in men >35 and due to ________ in men <35
men >35: e coli men < 35 N gonorrhea, Chlamydia
dermatomyositis antibodies
anti RNP, anti JO 1, anti Mi2 bonus: highly elevated creatinine kinase
in patients wither dermatomyositis, you need to screen for…
internal malignancy! they are at much higher risk for cancer also interstitial lung disease, myocarditis, dysphagia
seen with heliotrope rash, proximal muscle weakness, rash on shoulders
dermatomyositis
anti RNP, anti Jo 1, anti Mi2
give high dose glucocorticoid steroid plus glucocorticoid steroid sparing agent and screen for malignancy
how do you tell the difference between IgA nephropathy and acute post infectious glomerulonephritis?
both are nephritic syndrome (blood in urine, htn). Ig A nephropathy will affect Adults (20s-30s usually men) while postinfectious GN usually affects kids ages 6-10. IgA nephropathy shows up 5ish days after an infection while postinfectious GN takes weeks after an infection and it’s usally strep throat or impetigo so check their antistretolysin O titers. Also in IgA nephropathy complement levels are normal while in postinfectious GN complement levels are low. both tend to have benign course but IgA nephropathy can cause rapidly progressive glomerulonephritis and postinfectious GN can possibly lead to CKD in adulthood
triad of paroxysmal nocturnal hemoglobinuria
- hemolytic anemia
- pancytopenia
- thrombosis (especially in weird places like in abdomen, hepatic, cerebral)
usually in middle age b/c acquired mutation, lack CD55, CD 59 on RBCs, tx: prednisone and eculizumab
describe cardinal symptoms of ACA, MCA, posterior, opthalmic, lacunar stroke syndromes
high fever, severe polyartheritis, lymphopenia & thrombopenia, macular rash 3-7 days after travel to tropical/subtropical regions of central/south america, asia, africa
chikungunya fever
transmitted by mosquito (Aedes)
supportive care
often causes chronic arthritis, may have to give methotrexate
opening snap with mid diastolic rumble heard best at the apex
mitral stenosis,
most commonly due to rheumatic fever (usually in immigrants)
-can cause right sided, heart failure, dyspnea, left atrium dilation –> bronchus elevation and afib
Think of new onset afib with RVR as a different disease than chronic afib. What do you do for someone with new onset afib with RVR?
- Are the symptomatic? Presumably yes or you wouldnt get called
- Are they unstable? Like will they die in seconds? If yes, you shock – synchronous cardioconversion. They will need anticoag for a month afterwards
- Much more likely scenario: symptomatic and stable: You need to RATE CONTROL. Goal: below 110. Here’s the all important question: are they in heart failure exacerbation or not?
Acute decomp HF: Give Digoxin or Amiodirone
No HF: CCB like diltiazam or beta blocker like metopropolol
Think of new onset afib with RVR as a different disease than chronic afib. What do you do for someone with chronic afib
per AFFIRM trial, you can either do rate or rhythm control. Really the only time you’ll do rhythm control is for somebody who has “no good reason”to be in afib and won’t hop right back into if you convert them out and you’ll for sure anticoag those peeps.
For rate control: diltiazem or metroprolol.
Anticoag? CHA2DS2VAS score >2
for score of 1, maybe, maybe aspirin, maybe nothing
Anticoag:
Warfarin: No bridge needed for afib. Reversible. Inconvenient. Have to worry about diet. INR 2-3.
NOACs: Dabigatran, Apixiban, Rivaroxaban: easier, no reversal, insurance?
most common site of ectopic electrical foci causing afib
pulmonary veins
most common anatomic origin of atrial flutter
tricuspid annulus
status of pt with + Anti-HepB surface antibody and +Anti HepB core antibody and -HebBeAg
AntiHepB core antibody is present in acute or chronic infection but NOT after immunization; Anti-HepB surface antibody is present after immunization or succesfully clearing an infection so this person succesfully cleared an infection.
HepB e Ag indicates active infection and viral replication, infectivity
You have a patient with atypical community acquired pneumonia, GI symptoms and confusion – what tests would be really helpful besides the usual labs?
likely Legionnaire’s disease, especially if history of travel
Sputum culture Gram stain: lots of neutrophils, no organisms
Urinary legionella antigen
also low Na+ on BMP
acute symmetric arthritis in a school teacher/day care worker, maybe fever, fatigue, diarrhea
Parvovirus B19
describe areas of referred abdominal pain
test for suspected urolithiasis
abdominal US or noncontrast spiral CT
why is colonoscopy usually not performed in pts with acute abdominal pain
risk of perforation
what are 3 most common causes of esophogitis in patients with HIV?
- Herpes simplex virus
- candida
- CMV
How do you tell the difference? In Candida albicans, they will usually have oral thrush as well so that one is easy. For VIRAL esophogitis, the primary complaint is PAIN with swallowing but they can still swallow.
HSV: usually ulcers around mouth, round volcano-like ulcers in esophagus
CMV: linear ulcerations in esophagus
symptoms of hemorrhagic stroke in cerebellum
ipsilateral ataxia
nystagmus
occiputal headache, maybe neck stiffness
NO hemiparesis
facial weakness
symptoms of hemorrhagic stroke in Thalamus
contralateral hemiparesis and hemisensory loss
eyes deviate Toward hemiparesis
upgaze palsy
nonreactive miotic pupils
Pons coma symptoms
deep coma, total paralysis happens in minutes, pinpoint reactive pupils
symptoms of occipital lobe stroke
contralateral homonymous hemianopsia
euthyroid sick syndrome
happens in acutely ill patients, problems converting T4–> T3 in periphery
usually normal TSH and T4 but low T3 but everything can be low in extreme cases
pulmonary capillary wedge pressure is a measure of
left ventricle end diastolic pressure
elevated in left ventricle dysfunction
Name 3 complications of cirrhosis with portal hypertension
ascites
spontaneous bacterial peritonitis
variceal bleeding
cor pulmonale = impaired right heart function due to chronic lung disease
Name cor pulmonale signs and diagnostic tests
Elevated JVP
hepatomegaly, pulsatile liver
tricuspid regurgitation
right ventricular 3rd heart sound
edema in lower limbs
ascites
pleural effusions
Increased right heart pressures on ECHO, raised pulmonary artery systolic pressure on heart catheterization
back pain that gets better with sitting/walking uphill and worse with standing/walking downhill
spinal stenosis (better with flexion and worse with extenion)
MRI
asymmetric arthritis (even with warm swollen joints with leukocytes ), mouth ulcers, urethritis, conjunctivitis, low back pain
reactive arthritis
treat with NSAIDS
name 6 complications of ulcerative colitis
- spondyloartheritis
- colorectal cancer
- toxic megacolon
- erythema nodosum, pyoderma gangranosum
- uveitis
- primary sclerosing cholangitis
which type of IBD has skip lesions
chrons disease
age of presentation of ibd
bimodal
15-40 and 50-80
pt with large mediastinal mass
eosinophila
chest pain when drinking EtOH
elevated lactate dehydrogenase
Hodgkin lymphoma
elevated LDH associated with high tumor burden
remember to look for Reed Sternberg cells
what can happen when someone with myasthenia gravis has an infection?
myasthenic crisis
infection, surgery, preg/childbirth, tapering immunosuppressive drugs, certain meds lik beta blockers or aminoglycosides leads to extra muscle weakness. Watch out, they might be in serious respiratory distress but you don’t notice because they arent strong enough to struggle for air. Features might include dysphagia and choking sensation because they can’t clear secretions. Respiratory acidosis. They might be on death’s door before you realize it. Intubate. Plasmapharesis or IVIG. Corticosteroids.
transplanted kidney with recent increase in creatinine, proteinuria. On biopsy, lymphocyte infiltration of the intima, inflammatory tubular disruption, intimal arteritis. Transplant less than 6 months ago and pt is asymptomatic. What is it and what do you do?
Acute transplant rejection (predominantly T cell mediated)
mostly reversible
give high dose glucocorticoids and increase immunosuppressive doses
pt with kidney transplant. Pt is asymptomatic but has recent increase in creatinine. Biopsy shows intranuclear inclusions and mixed neutrophils and lymphocyte infiltration
BK virus reactivation due to immunosuppression
severe headache that came on within a few minutes with photophobia and vomiting and neck stiffness. Noncontrast CT is negative.
Get lumbar puncture to rule out subarachnoid hemorrhage.
Signs of SAH on LP: high opening pressure, xanthochromia (yellow-pink color), lots of RBCs
CT is sensitive for bleeds but might not pick up smaller or older bleed
rash
fever
AKI
eosinophilouria + WBC casts
interstitial nephritis
usually due to drugs
According to AHA, who gets a statin? (name 4)
If you are 40-75 and have diabetes
pts with known ascvd, stroke/tia, pad, other coronary revascularization procedure…
LDL >190
40-75 with ascvd 10 year risk >7.5%
symptoms/signs of the most common side effect of statins
myopathy
elevated CK
tender muscles
(you can also get elevated liver enzymes!)
which antilipid drug is best at raising HDL
niacin
remember can cause flushing and tachycardia so best to take aspirin first
fenofibrate and gemfibrozil are fibric acid derivatives used to lower triglycerides. What are their side effects?
gallstones! raised LFTs! and other gi effects
acute coronary syndrome pathophysiology
usually in situ thombosis at the site of ruptured athrosclerotic plaque
can also be due to thromboembolism causing occlusion, vasospasm, vasculitis, aortic root or coronary artery dissection, or cocaine use (cause both vasospasm and thrombobosis)
unstable angina happens when the thrombosis doesnt cause complete occlusion or there is spontaneous lysis; in chronic stable angina there is usually stenosis from an athrosclerotic plaque that’s only a problem when demand is increased due to exercise
in setting of MI, S4 suggests….
S3 suggests….
*persistent* ST elevation suggests….
S4 suggests noncompliance of the ventricles due to ischemia
s3 gallop is severe systolic dysfunction
*persistent* ST elevation is left ventricular aneurysm
what’s the difference in pathophysiology of STEMI vs NSTEMI
in STEMI we’re talking transmural ischemia whereas in NSTEMI it’s usually subendocardium
ST elevation in leads II, III, aVF suggests a problem where….
inferior surface of heart
supplied by right coronary artery
ST elevation in V2 V3 and V4 suggests a problem where?
anterior aspect of heart supplied by left anterior descending artery
ST elevation in I, aVL, V5, V6 suggests a problem where?
lateral aspect
supplied by lateral circumflex coronary artery
physical exam findings of aortic dissection
unequal pulses and BPs in each arm
widened mediastinum
murmur of aortic insufficiency
pericarditis ECG finding
diffuse ST elevation (not by vascular distribution like we see in MI)
MI Tx
- anticoagulation: aspirin, heparin
- beta blockers to lower demand
- nitrates to increase coronary blood flow
all of the above reduce mortality
patients may also be given morphine for the pain and tachycardia as well as oxygen
If pt with acute STEMI presents within 2-3 hours of symptom onset and receive ___ ideally within 90 minutes, then ____is the recommended reprofusion therapy
PCI, percutaneous reprofusion intervention
also appropriate if contraindication for thrombolytics, hypotensive or in cardiogenic shock
what are two most common causes of death in setting of an MI
ventricular arrythmia
cardiogenic shock (pump failure)
unilateral headache, ipsilateral Horner syndrome (ptosis and constricted pupil)
carotid dissection
headache, lethargy, photophobia, vomiting, CN palsy
subarachnoid hemorrhage
saccular aneurysms can compress CNs, for example compression of CNIII can cause one pupil to be dilated (think rupture of posterior communicating artery), compression of CNII can cause vision loss (internal carotid or anterior communicating artery), or compression of CN IV (trochuler) by superior cerebellar artery
or CNVI abducens by inferior cerebellar artery
blowing highpitched holosystolic murmur heard at apex plus S3
severe mitral regurgitation
Due to backflow of blood from LV to LA during systole (because mitral valve is jacked), the total amount of blood entering LV during systole each time goes way up. To compensate, the LV undergoes eccentric hypertrophy. The apical impulse will probably be displace to the left on palpation. The S3 happens when all that increased volume rushes into the dilated floppy LV and slams against the wall during systole. S3 is highly suggestive of severe mitral regurg and its absence helps rule out severe mitral regurg. Pts with bad mitral regurge will start to develop dyspnea because the floppy dilated LV has decreased output. They will also get pulmonary hypertension eventually.
wide fixed splitting of S2 occurs with…
atrial septal defect
what type of hypersensitivity reaction is this and what causes it?
this is erythema multiforme and it is type IV hypersensitivity (delayed Tcell mediated)
Herpes simplex virus, Mycoplasma pneumonia
medications like Phenytoin, beta lactams (e.g penicillins), sulfonamides
a lot of people with cirrhosis wind up with esophogeal varices and 1/3 of ppl with esophogeal varices wind up with hemorrhage. So most ppl with cirrhosis should get diagnostic upper endoscopy to look for varieces. If nonbleeding varices are found, what is 1st line prophylaxis to prevent progression?
beta blockers
eg propranolol, nadolol
(endoscopic variceal ligation is alternative if beta blockers contra indicated)
patient with few symptoms over months to years, palpable spleen, huge leukocytosis and low leukocyte alkaline phosphatase
low leukocyte alkaline phosphatase should make you think CML, chronic myeloid leukemia. Low leukocyte alkaline phosphatase distinguishes CML from leukomoid rxn and all other leukemia!
most commonly caused by t(9;22) translocation (Philadelphia) –> BCR-ABL fusion protein that is constitutively active protein kinase
if you suspect lymphoma what do you always do?
cut it out! excisional biopsy is a must
older patient with increased hematocrit, leukocyte count, and platelet count. +pruritis, dizziness, headaches, blurred vision.
what’s going on? what are potential complications? how do you treat?
Polycythemia vera caused by JAK2 mutation
complications: usually goes on for a long time without problem and then you get hypercoagulable –> thrombosis–> stroke
Treatment: repeated phlebotomy until you get hematocrit below 45% + aspirin
if you think your patient has CML, what should you do next?
get cytogenetic studies so you can see if they have t(9;22) BCR-ABL which has targeted therapy
imatinib
dasatinib
nilotinib
imatinib
targeted against BCR ABL in CML
dasatinib
targeted against BCR ABL in CML
nilotinib
targeted against BCR ABL in CML
Leukomoid reaction
what causes it?
lab findings?
Leukomoid reaction: extreme leukocytosis with increase in all of the cell lines and increase in leukocyte alkaline phophatase (LAP) score. (Decreased in CML)
Often secondary to solid tumor like lung or kidney, infections, drugs like steroids
older patient with lymphocytosis
smudge cells on smear
B cells with CD19, CD20, CD23 on flow cytometry
CLL, chronic lymphocytic leukemia
usually just watch!! patients are usually asymptomatic when diagnosed and chemo is just for symptoms not for increased survival. very slow moving malignancy
if you do tx: fludarabine, cyclophosphamide, rituximab
A_L is most common leukemia of childhood
A_L is most common acute leukemia of adulthood
ALL kids
AML adults
Auer rods
acute myeloid leukemia (myeloperoxidase positive)
t(15;17) common
pathophysiology of myasthenia gravis
autoantibodies against acetylcholine receptors at neuromuscular junction
treatment is cholineasterase inhibitor: pyridostigmine
2nd line: glucocorticoids
ptosis improved with ice pack over eyes bc it slows down breakdown of acetylcholine
first line tx for myasthenia gravis
pyridostigmine (cholinesterase inhibitor)
2nd line is glucocorticoid
IVIG/plasmapharesis in crisis
thymectomy in some cases
Name symptoms and treatment of hypercalcemia
Bones, abdominal groans, moans, neuropsychiatric overtones: Bone pain, GI distress, weakness, confusion, lethargy, stupor
For severe, **symptomatic** hypercalcemia: IV Saline hydration!!! you want to dilute that calcium. also CALCITONIN (tone down the calcium). (only if they are crazy volume overloaded will you give furosemide)
Long term: Bisphosphonates.
symtpoms of CO poisoning
lab signs
treatment
confusion, wheezes, dyspnea, nausea, headache
seizure, coma, cherry red lips
anion gap metabolic acidosis
**pulse oximeter usually normal bc can’t distinguish oxyhemoglobin from carboxyhemoglobin
can cause irreversible hypoxic brain damage
100% oxygen through nonrebreather face mask, hyperbaric O2 in extreme cases
How can you prevent renal calcium stones?
low sodium diet
pesticide (organophosphate) poisoning mechanism, symptoms, antidote
cholinergic stimulation (both muscarinic and nicotinic)
SLUDGE: Salivation (also secretion in lungs), Lacrimation, Urination, Diaphoresis/Diarrhea, GI distress/Gasping for air, Emesis
Atropine followed by Pralidoxime
what should you suspect if someone has blood on urine dipstick but no RBCs on urine microscopy
and elevated [K+] and [PO4]?
rhabdomyolysis
think crush injury, intense mm activity including seizures, drug toxicity including statins
lysed mm fibers release potassium and phosphorous
causes AKI, tubular necrosis
increased AST>ALT
dx made by hugely elevated CK
stroke that causes pure sensory loss and then weeks later may cause allodynia => severe burning pain at light touch to contralateral limbs
thalamus
symptoms of lateral medulla stroke
Wallenberg syndrome
temperature regulation probs
horner syndrome (ptosis, miosis, anhidrosis)
*crossed sensory deficit (ipsilateral face, contralateral body)
ataxia
criteria for starting long term O2 for ppl with COPD
-sat 88% on room air at rest
or
-sat 89% at rest with cor pulmonale or hematocrit >55%
(remember secondary polycythemia can result from chronic hypoxemia)
Name 2 tests to make MS diagnosis
T2 MRI - look for lesions disseminated in time and space
IgG oligoclonal bands on CSF analysis
describe 4 common types of MS symptoms/lesions
- “optic neuritis” mononuclear vision loss, afferent pupillary defect
- transverse myelitis – loss of function below of certain spinal level. first flacid paralysis (spinal shock) followed by spastic paralysis c hyperreflexia. often incontinence
- internuclear opthalmoplegia - demylelination of medial longitudinal fasiculus; the eye on the same side as the lesion cant adduct towards the nose and the eye on the contralateral side abducts with nystagmus
- cerebellar dysfunction: ataxia, intention tremor, nystagmus
what do you give elderly patients with dementia for delierium in the hospital?
low dose haldol
can also do quetiapine, risperadone
what to do for esophagitis symptoms in a pt with HIV and oral thrush?
empiric treatment for Candida esophagitis: oral fluconazole. If it doesn’t get better you can do endoscopy, culture/cytology and look for viral etiology. Remember that linear ulcers point to CMV and volcano like ulcers point to HSV. Treat CMV with ganciclovir and HSV with acyclovir
healthy kid with very low platelet count
isolated thrombocytopenia, usually due to autoimmune thrombocytopenia
a diagnosis of exclusion
usually healthy kids 2-5 or teens. Everything is normal but platelet count.
what is considered a narrow QRS (in ms)? what is considered a wide QRS?
narrow qrs is <.12 ms (three little boxes)
wide qrs is greater than 0.12 ms (three little boxes)
what rhythm is this? what do you do for it?
sinus bradycardia
if unstable, pace
if stable and symptomatic, adenosine
what is length of normal PR interval on ECG?
0.12-0.2 ms (3 to 5 little boxes)
what rhythm is this? what do you do for it?
1st AV block – the PR interval is prolonged and no beats are dropped. if the patient is unstable, you pace them (unstable signs: LOC, AMS, hypoperfusion, shock, pulmonary edema)
if stable, you can use adenosine
what rhythm is this? what do you do about it?
This is 2nd degree AV block type 1 (Mobitz 1)
the PR interval gets longer and longer until a beat is dropped.
If unstable, pace; otherwise give adenosine or atropine (anticholinergic)
what are causes of AV block?
Ischemia! STEMIs, acute coronary syndromes
infectious diseases: Chagas, Lyme, endocarditis, acute rheumatic fever, diphteria, toxoplasmosis
inflammatory/infiltrative diseases: myocarditis, sarcoidosis, rhemautic diseases like SLE, sclerosis, rheumatic artheritis, reactive artheritis,
cardiac procedures
congential
metabolic/endocrine probs like thyroid
certain drugs like beta blockers, digoxin, calcium channel blockers…
and more!
what rhythm is this? what do you do?
This is AV block type II (Mobitz II)
Prolonged PR with random dropped beats
tx: try to identify and remove underlying cause, e.g. a medication
for acute management: usually atropine and pacing
what rhythm is this? what do you do?
This is 3rd degree AV block; there is no AV conduction
definitely permenant pacing
medical therapies include atropine, beta adrenergic agonists like dopamine, dobutamine, isoproterenol, epinephrine ; also IV aminophylline
what rhythm is this? what do you do?
idioventricular rhythm – ventricles running the show but it’s not vtach. So notice slow rate but complete absence of p waves
i think the answer is pacing? same meds as other serious av blocks?
what rhythm is this? what do you do?
supraventricular tachycardia
notice fast rhythm, ABSENCE OF P WAVES, narrow QRS
Pathophys: usually some reentry pathway around AV + exacerbating factor
If unstable: SHOCK -synchronized cardioversion
If stable: try Vagal maneuver, IV adenosine
diltiazem, verapamil, propranolol, metropolol
After defibrillation, an ecg of sinus rhythm shows prolonged QT interval (this tidbit important!)
what rhythm is this? what do you do?
torsades de pointes
Note that this polymorphic vtach is not proven torsades if you don’t know there is underlying QT prolongation
I gave away treatment: If unstable: shock. If “stable” – give IV magnesium but stay close and be ready to shock.
what is considered prolonged QT?
>450-470 ms
Name antidepressants that can prolong qt
citalopram, escitalopram, TCAs
what rhythm is this? what do you do?
ventricular tachycardia
causes: structural heart probs including old infarct scars; congenital stuff like congenital long QT or hypertrophic cardiomyopathy; reversible causes like electrolyte imbalance, drugs, acute ischemia, hypoxia
Unstable: SHOCK
Stable: IV procainamid, IV amiodarone, or IV sotalol to try to stop Vtach
urgent catheter ablation
MI patient with cold extremities, elevated JVP, crackles, hypotension (systolic <80), high left and right filling pressures (measured indirectly with pulmonary capillary wedge pressure >18mmHg)
Cardiogenic shock
oxygen, vasopressors like dobutamine and dopamine, might also need reduce afterload through intra aortic balloon counterpulsation and iv nitroglyverin or nitroprusside
might have to do urgent revascularzation with PCI
MI patient with markedly elevated JVP, hypotension, but clear lungs
right ventricular infarction, tends to be a complication of inferior STEMIs
The first step to spotting RV infarction is to suspect it… in all patients with inferior STEMI!
In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:
ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle.
ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.
RV infarct is very preload sensitive DO NOT GIVE NITRATES
Name 3 MI complications that would cause systolic murmurs
- papillary muscle dysfunction –> mitral regurg
- papillary muscle rupture–> flail mitral leaflit and acute mitral regurg–> cardiogenic shock and heart failure
- new holosystolic murmur due to ventricular septal rupture
these usually happen in the first week
what should you suspect if ECG still shows ST elevation several weeks after an MI?
ventricular anuerysm
Dressler syndrome is a complication of MI that occurs several weeks later. What are symptoms?
Pleuritis
Pericarditis
Fever
(immune mediated)
tx with nsaids, sometimes prednisone
drugs for someone having a heart attack
MONA BASH C
Morphine
O2
Nitrates (unless you think its RV)
Asprin
Beta blocker
ACE-i
Statin
Heparin
Clopidegrel
underlined = they should def go home on; they might also go home on nitrates if chest pain; they will go home on clopidagrel for 1 year if they have drug eluding stent and for 1 month if they have bare metal stent
ST elevation in leads II, III, and aVF suggest an infarct in which region of the heart
inferior (right coronary artery)
you’ll often see bradycardia
which biomarker should you use to look for a re-infarct of myocardium
CK-MB
(remember that troponin stays elevated for 7–10 days so it probably wont be helpful info that troponin is elevated…from previous infarct)
a 60 smoker patient has squeezing chest for 30minutes and EMTs give him oxygen and nitroglycerin. BP is 110/70, pulse =90, and ECG is normal. What’s the next step.
Give aspirin.
remember that initial ecg and biomarkers can be normal in MI
what ecg leads show the lateral aspect of the heart
V5, V6, AVL, I
in heart failure, the renin-angiotensin-aldosterone axis and sympathetic system are activated. These help initially but in the long run make for more cardiac decompensation and remodeling. Heart failure can look like forward failure or backward failure. Describe these.
Forward failure: heart isn’t pumping enough blood out so pt has fatigue and lethargy, perhaps even hypotension
Backward failure: increased filling pressures or diastolic dysfunction. Blood backs up–> dyspnea, elevated JVP, perpheral edema, ascites and hepatic congestion
New York Heart Association functional classification of heart failure:
I: no limitation of ordinary physical activity
II: slight limitation of physical activity; develops fatigue or dyspnea c moderate exertion
III: marked limitation, even light activity produces symptoms
IV:__________________
NYHA classification IV: symptoms at rest, any activity causes worsening
name major causes of heart failure
what drugs have been shown to decrease mortality in HFrEF?
ACE-inhibitors*
beta blockers (carvedilol, metropolol, bisoprolol)
*In black pt, use HYDRALAZINE + NITRATES
spironolactone (aldosterone antagonist) can also be used for NYHA class III, IV.
digoxin can be used for symptoms but doesnt affect mortality
why is digoxin used to help relieve symptoms of heart failure
digoxin increases heart contractility somewhat
(does not improve survival - for symptomatic relief)
how do nitrates and nitrites help CHF symptoms (note that these aren’t as commonly used although hydralazine + nitrates confere improved survival in black pts)
Nitrates reduce preload and clear pulmonary congestion
(remember that’s why we don’t use nitrates for RV infarcts bc the RV is really dependent on preload)
Pts with HFrEF and advanced symptoms may have widened QRS (>120ms), indicating dyssynchronous ventricular contraction. Placement of biventricular pacemaker called………………………………..to stimulate both ventricles simultaneously can reduce symtpoms and imrpvoe mortality
Cardiac resynchronization therapy (CRT)
Pts with higher class HFrEF are at increased risk of ventricular arrhythmia and sudden cardiac death. What therapy can be considered?
implantable cardiac defibrillator (ICD)
In acute decompensated heart failure, you would treat elevated LV filling pressures with_____________.
You would treat decreased cardiac output with______________ and hypotension with ________________.
In acute decompensated heart failure, you would treat elevated LV filling pressures with IV nitroglycerin to decrease preload.
You would treat decreased cardiac output with ionotropes like dobutamine and hypotension with vasoconstrictors like dopamine.
Aortic stenosis is most common symptomatic valvular abnormality in adults. If younger than 30, think congenital bicuspid valve. Pt 30-70, think congenital stenosis or acquired rheumatic heart disease. Older than 70 think calcification. What is the classic *progression* of symptoms of aortic stenosis
angina –> syncope –> heart failure
“harsh” systolic murmur
name the three layers of the aortic vessle wall. What predisposes somebody to aortic dissection?
intima, media, adventitia. In dissection, there is hematoma in the media that propogates distally. Hypertension is biggest factor in propogation of the hematoma.
cystic degeneration of the media in connective tissue diseases like Marfans and Ehlers-Danlos
hypertension
valve dysfunction like stenois, congenital bicuspid valve
aortic coarctation
pregnancy
athrosclerosis
What do you do for someone with aortic dissection
- intravenous vasodilator like sodium nitroprusside and introvenous beta blocker like metroprolol or esmolol. Or IV labetalol does both function. Hypertension, shearing forces are what will propogate the dissection so this is most important thing to do.
- Noninvasive imaging: TTE (transesophogeal echo), CT or MRI depending on availability. You need to class the AA as Type A (involving ascending aorta) or Type B (not involving ascending aorta)
- Type A dissection requires urgent surgery. Type B only requires surgery for complications
Operative repair is indicated for abdominal aortic aneurysms > _____ cm
5.5cm or those expanding >0.5cm per year
for smaller aortic aneurysms, serial noninvasive imaging like ultrasound is indicated
A pt presents with severe chest pain radiating to his back, unequal brachial BPs and pulse strengths, and a widened mediastinum on CXR. What do you do next?
Get CT. Symptoms consistent with acute aortic dissection.
What defines first degree AV block?
prolonged PR interval - longer than 200ms (1 large box)
There is conduction delay in AV node. prognosis is good, usually dont need pacing
CCauses of secondary HTN
CHAPSS
Cushings
Hyperthyroidism, hyperaldosteronism
Aorta coarctation
Pheochromocytoma, Polycystic kidney disease
Sleep apnea
Stenosis of renal arteries
what are the initial labs you get for HTN?
UA - look for hematuria
urine albumin/creatine spot –check for proteinuria
BMP with calcium and creatinine to check kidney/GFR
Fasting glucose - diabetes
Lipid panel -cvd risk
*base line ECG*
+/- TSH, T4, ECHO, evaluation for 2* causes
Stage II hypertension (what is cut offs) need what kind of pharma therapy
Stage II >160/100
Usually need to go ahead and be on 2+ drugs
What antihypertensive drug do you use in pt with diabetic nephropathy or CKD + proteinuria?
ACE-i or Arb
SPRINT trial showed that pts 50+ with one or more cardiovascular risk factors had a 30% CVD event risk reduction if BP target was:
120 systolic
what are the two common causes of renal artery stenosis?
- Athrosclerosis
- Fibromuscular dysplasia
bilat flank masses and pain
HTN
hematuria
ask about family hx! These are symtpoms of polycystic kidney disease
carcinoid syndrome is caused by overproduction of….
serotonin , carcinoid tumors arise in GI tract and lungs
in hypertensive emergency/urgency, don’t lower BP too much…probably 160/100 range.
What are definitions of hypertensive emergency vs hypertensive urgency?
Hypternsive urgency: >180/110
Hypertensive emergency: acute elevation in BP with end organ damage
(encephalopathy, MI, aortic dissection, declining renal function, stroke, pulmonary edema from acute LV failure)
tx for hypertensive emergency vs hypertensive urgency
Hypertensive emergency: immediate lowering of BP with IV sodium nitroprusside. Lower to 25%/ or 160/110 ish.
*using nitroprusside for multiple days –> cyanide toxicity. May need to use nitroglycerin plus loop diuretics which both reduce preload,
If pt presents with cerebral infarct, don’t lower BP unless systolic >220
Hypertensive emergency: lower BP over few days with oral meds, outpt setting
Pheochromocytomas are usually in medulla of adrenal gland. Test with 24 hr urine VMA, metanephrine, catecholamine. Surgical resection AFTER alpha blockade with phenoxybenzamine.
What are symptoms of pheochromocytoma?
what medication must be given before surgical resection of pheochromocytoma?
phenoxybenzamine (alpha blocker)
beta blockers may also be given but beta blocker alone will make HTN much worse because alpha adrenergic activity will be unopposed
generally beta blockers are avoided when pt is volume overloaded bc beta blockers reduce cardiac contractility
generally beta blockers are avoided when pt is volume overloaded bc beta blockers reduce cardiac contractility
what are two most common causes of afib
htn
coronary atherosclerosis
most cases of mitral _____ are due to rheumatic fever worldwide
rheumatic fever –> mitral stenosis
opening snap after S2 followed by low pitched diastolic rumble heard best at the apex
Wolf Parkinson White (look at delta wave caused by ventricles excited by accessory pathway); pr interval is short, qrs is wide.
Most WPW pts are assymptomatic. Some will get tachy, usually SVT or afib. Afib with WPW looks like ventricular tachy bc of the wide QRS but the irregular irregular rhythm should clue you into afib
for unstable WPW with afib, direct cardioversion
for stable WPW with afib – rate will be really fast bc accessory pathway circumvents sinus pause; beta blockers or CCBs will paradoxically increase rate. Give amiodarone or procainamide
what do you give a WPW pt with afib to control rate?
amiodarone or afib
(the usual afib rate control agents, bblockers, CCBs paradoxically increase rate bc of that wiley accessory pathway)
holosystolic murmur heard at apex, radiating into axilla
mitral regurgitation
syncope is basically never from TIA bc syncope requires global hypoperfusion and TIA = regional ischemia . What are the only neurological syndromes that *commonly* cause syncope?
problems with autonomic nervous system –>orthostatic hypotension–> syncope
- Diabetes
- Parkinsons
- Idiopathic dysautonomia
also sometimes syncope can trigger seizures
differential for syncope
vasovagal - think about situational eg mictruition
cardiogenic (rhythm v structural)
orthostatic hypotension (20mmHg drop) - usually from meds
carotid sinus hypersensitivity
factitious
Sick sinus syndrome
sinus bradycardia or arrest/long pause alternates with supraventricular tachycardia, usually afib.
Second degree av block (Wenckebach) (Mobitz I)
progressive lengthening of PR interval until beat is dropped – there’s a p wave with no corresponding qrs.
due to abnormal av conduction, may be inferior MI
no need to pace unless symptomatic
Describe Mobitz II (2nd degree av block)
a dropped beat without prolongation of PR interval
usually a conduction problem in the bundle of His
usually need pacing bc Mobitz II may progress to complete heart block
describe third degree AV block
SA and AV node are completely doing their own things
atrial rhythm is faster than escape ventricular rhythm
treatment for symptomatic or severe bradycardia
atropine
differential for causes of pericarditis
infection: bacterial or viral, TB, parasite
Vasculitis: autoimmune, postradiation
Hypersenstivity/immunologic rxn: eg Dressler
Metabolic: uremia, Gaucher
underlying heart prob eg MI
Trauma
Idiopathic
Neoplasms
ECG findings of pericarditis
*diffuse* ST elevation
PR depression
(compare to regional ST elevation of MI)
How do you tell the difference between acute pericarditis and MI?
It’s really important to get it right bc thrombolytics are right for MI but can lead pericardial hemorrhage and tamponade in pericarditis
MI: crescendo pattern of pain, heaviness, squeezing; pain is not worse with respiration!; relief with nitrates. Regional ST elevation with reciprocal ST depression.
pericarditis: sharp pain worse with inspiration, leaning forward helps, nitrates don’t help. Diffuse ST elevation and PR depression
LUPUS CRITERIA
- Malar Rash
- Discoid Rash
- Photosensitivity
______________
- Arthritis
- Serositis (pleuritis, pericarditis)
- Renal prob
- Neuro prob
________________
+ANA
anti dsDNA, anti Smith, antiphospholipid
oral, vaginal ulcers
hematologic probs like leukopenia, hemolytic anemia, thrombocytopenia
It’s the renal problems that tend to be most dangerous, most likely to kill a lupus patient
Pt with JVD, distant heart sounds, pulsus paradoxus (BP drops on inspiration), dyspnea, chest pain, hypotension
pericardial effusion causing cardiac tamponade
ddx: restrictive cardiomyopathy, constrictive pericarditis
Beck’s triad
most common causes of constrictive pericarditis
TB
radiation
cardiac surgery
virus
uremia
malignancy
*constrictive pericarditis takes chronic course* Often looks like right sided heart failure (LE edema, hepatomegaly, ascites, Kussmaul sign) + pericardial knock (high pitched early diastolic sound right after S2 (closing of aortic valve)
might need biopsy to differentiate from restrictive cardiomyopathy
signs of right sided heart failure
Lower limb edema
hepatomegaly
ascites
dyspnea
JVD
Kussmaul sign
what is the most common cause of restrictive cardiomyopathy?
amyloidosis (an infiltrative disease of the elderly)
(endomyocardial fibrosis w/ eosinophilia is common in developing countries)
Of restrictive cardiomyopathy, cardiac tamponade, and constrictive pericarditis, which one(s) show pulsus paradoxus
only cardiac tamponade shows pulsus paradoxus out of these
pulsus paradoxus may also be seen in obstructive lung disease
drop in systolic BP with inspiration; if severe, peripheral pulse will disappear during inspiration
tx for cardiac tamponade: pericardiocentesis. While waiting, give IV fluids! Fluid expansion raises preload which they need to keep up cardiac output
tx for constrictive pericarditis: pericardium resection
__________________ are the most important step in diagnosis of infective endocarditis
serial blood cultures
acutely ill patients should have 3 cx drawn over 2-3 hrs before starting abx
in subacute cases, drawing 3 cx over 24 hours before starting abx is ideal
if pts are critically ill or hemodynamically ill, never wait to start abx. Start empiric treatment and draw blood cx at same time.
what bacteria cause infective endocarditis associate with UTI or genitourinary tract instrumentation?
enterococci
which bacterium in infective endocarditis should prompt a colonoscopy?
Streptococcus bovis
2 most common organisms that cause infective endocarditis
strep viridans (think dental procedures, native valves)
staph aureus (think IV drug users, tricuspid valve endocarditis)
coagulase negative staph –> prosthetic valves
Duke Criteria
Major: 1. Isolation of typical organism (strep veridans, s. aureus, HACEK, enterococcus, strep bovis) from 2 blood cx or persistently positive blood cx
- Evidence of endocardial involvement (echo, new valve regurg)
Minor: Fever, Immunologic (roth spots, glomerulonephritis, osler nodes, +RF), Predisposing valve situation or IV drug use, +blood cx not meeting major criteria , vascular phenomena (arterial or septic emboli, mycotic aneurysm, Janeway lesions)
How many do you have to meet?
2 major
1 major + 3 minor
or 5 minor
Duke Criteria
(must meet 2 major, 1 major + 3 minor, or 5 minor)
Major: 1. Isolation of typical organism (strep veridans, s. aureus, HACEK, enterococcus, strep bovis) from 2 blood cx or persistently positive blood cx
- Evidence of endocardial involvement (echo, new valve regurg)
Minor:
Fever,
Immunologic (roth spots, glomerulonephritis, osler nodes, +RF),
Predisposing valve situation or IV drug use,
+blood cx not meeting major criteria ,
vascular phenomena (arterial or septic emboli, mycotic aneurysm, Janeway lesions)
Pt with these lesions, fever and new onset valvular regurgitation
most likely infective endocarditis
These are janeway lesions = painless, thought to be caused by septic emboli, occur on palms and soles. A minor criteria (vascular involvement) of Duke criteria.
Get serial blood cultures!!
TEE (transesophageal echo) is imagining of choice
what should you always suspect in patient with fever and stroke syndrome?
infective endocarditis
Patient with fever, new onset murmur, and painful palpable erythematous lesions on pulp of fingers and toes
work up for infective endocarditis (serial blood cx and TEE). Osler nodes = immune complex deposition. Roth spots, glomerulonephritis also caused by immune complex deposition in infective endocarditis. Pts might even be +RF!
Patient with fever and new onset murmur
Work up for infective endocarditis.
These are roth spots, caused by immune complex mediated vasculitis
Treatment of Streptococcal endocarditis
4-6 weeks penincillin G
if susceptible
Treatment of staph endocarditis
4-6 weeks of nafcillin, often add gentimycin
if susceptible
(Vancomycin used for MRSA)
Treatment for HACEK endocarditis
ceftriaxone
when is infective endocarditis treated surgically?
*usually for infected prosthetic valves
otherwise, CHF that can’t be fixed and is caused by valve failure (a major complication of infective endocarditis), uncontrolled infection, huge vegetation, throwing lotta emboli, no abx treatment, abscesses, etc
A pt had prosthetic heart valve within last 6 months and needs dental procedure but is allergic to amoxicillin. What prophylaxis should she get?
clindamycin, ampicillin, or cephalosporin will work
Peripheral arterial disease workup & management
Ankle brachial index (uses doppler us) -normal is slightly above 1, PAD <0.90; Can also do exercise testing
symptomatic pad –>50% 10 year mortality rate! Stop smoking and cut MI risk in half!
supervised graded exercise
tx htn, hyperlipidemia, diabetes, etc.
aspirin, cilostazol
critical limb ischemia, pain at rest, nonhealing ulcers: maybe surgical revascularization
ddx: Takayasu (usually arms, younger women), fibromuscular dysplasia (women), Buerger disease (thromboangiitis obliterans)(smokers)
6 P’s of critical limb ischemia: Pain, Pallor, Parasthesia, Pulselessness, Poikilothermia, and (eventually) Paralysis
What is management?
In pt with known PAD, think thrombus or embolus (esp if recent procedure, a fib, etc). Give heparin to stop thrombus from propagating. Put limb below horizontal plane with no pressure. Artiography to identify occlusion and then surgical intervention.
virchow’s triad
Name 2 most common inherited hypercoagulobility problems
Factor V Leiden
Prothrombin mutation
The usual cause of death from pulmonary embolism is…
progressive right heart failure from pulomonary HTN
acute onset of hypoxemia in pt with normal CXR should be interpreted as _____ until proven otherwise
PE
wells criteria
PE unlikely? d dimer to rule out
PE likely? get chest ct with contrast
Management of PE
- Pts with severe problems, rt heart failure, hypotension, get rid of the current clot: surgical removal of clot or tPA if systolic bp<90 mmHg.
- Pts who are stable: goal becomes prevent future clots.
Start with Unfractionated Heparin, Low Molecular Weight Heparin or Fondaparinux. LMWH and fondaparinux have rapid onset, predicatble does response and don’t require constant lab monitoring like unfractionated heparin.
Bridge to Warfarin: Use LMWH or fondaparinux for at least 5 days while overlapping warfarin with at least 2 consecutive days at therapeutic INR ~2.5
or IVC filter
how many posterior ribs on inspiratory cxr?
8-10 posterior ribs (the horizontal ones)
2 drug classes of bronchodilator
anticholinergic
beta agonist
tachypnea = ___ breaths per min
>40
treatment for COPD exacerbations
bronchodilators (beta agonists, anticholinergics)
oxygen
glucocorticoids
abx if infection suspected
5 h’s of asystole and PEA
Hypovolemia
H+, acidosis
Hypoxemia
Hyperkalemia
Hypothermia
5 t’s of PEA, asystole
Trauma
Tamponade
Tension pneumothorax
Toxins
Thrombosis (heart–> MI, or PE)
painless thyroiditis
brief hyperthyroid state but low radio iodine uptake
+TPO antibody
painless, small goiter
spontaneous recovery
tx for CO poisoning
100% O2 non rebreather mask
hepatic transaminase levels in alcoholic hepatitis
elevated AST, ALT but rarely >500
AST:ALT 2:1
Name 3 symptoms of chronic pancreatitis
malabsorption (steatorhea, weight loss)
chronic epigastric pain with intermittent pain free periods (radiates to back, not improved with antacids, maybe helped by sitting up and leaning forward)
diabetes mellitus
Get CT look for calcifications
treatment for chronic pancreatitis
alcohol and smoking cessation
pain control
small frequent meals
enzyme replacement
differential for syncope
cardiogenic: LV outflow obstruction, conduction problem, Vtachy
vasovagal: prodrome?
autonomic dysfunction
hypovolemia
carotid hypersensitivity
How does acetaminophen affect warfarin?
tylenol potentiates warfarin
remember that vit K is antidote but takes 12-24hrs so give prothrombin complex concentrate (if available) or fresh frozen plasma if not for faster clotting
diagnostic tests for heart failure
BNP (right atrial stretch)
ECHO
left heart cath -tells you if ischemic or not
(you’ll prob do ecg which doesnt diagnose hf but might give clues about etiology)
HF treatment
everyone gets ACEi/Arb, and beta blocker, H2O and Na restriction. If ischemic: statin + asparin
if symptomatic: furosemide
if class III: isosorbidedinitrate hydralazine/spironolactone
if EF<35% and NOT class iv (no symptoms at rest) then they get defibrillator
class IV: inotropes, will die in a year;
Approach to HF exacerbation
Get CXR, ECG, troponin, BNP
if STEMI –> Mona bash and cath
if just CHF: LMNOP
lasix, morphine, nitrates, oxygen, position
symptoms of salicylate overdose
tinnitus, tachypnea, fever, GI probs, nausea
*mixed acid base disturbance (respiratory alkalosis + metabolic acidosis = near normal pH)
-Salicylate OD is indication for hemodialysis
describe acid/base disturbance of salicylate overdose
First aspirin overdose causes respiratory alkalosis by causing tachypnea –> blow off CO2 (acid) low pCO2
Then aspirin uncouples oxidative phosphorylation, leading to accumulation of acids like lactic acid and pyruvic acid –> anion gap acidosis which sucks up all the bicarb low bicarb
Indications for hemodialysis
AEIOU
Acidosis (<7.1)
Electrolytes (refractory hyperkalemia)
Intoxications
Overload refractory to diuresis
Uremia
metformin can cause …… deficiency
B12
gait problems , + babinski , parasthesias, neuropsychiatric changes.
metabolic acidosis
___ bicarb
low pH, low bicarb
Check anion gap
cosyntropin test is for….
primary adrenal insufficiency
tx for vasospastic angina
calcium channel blocker
tx for female pattern hair loss
topical minoxidil
causes of hyperandrogenism in women
PCOS
neoplasm (esp if rapid change)
hyperprolactinemia
Cushing
nonclassic congenital adrenal hyperplasia
acromegaly
These hands in setting of chronic hep C
porphyria cutanea tarda
also seen in hemochromotosis, alcohol, estrogen use
primary sclerosing cholangitis
pathophys?
association with what disease?
chronic inflammation of intra and extra hepatic ducts
ulcerative cholitis
increase in conjugated bilirubin, pANCA
chest pain + segmental ischemic changes on ECG in post menopausal woman –> cath shows no occlusion. What’s going on?
Ask about recent stressors. Could be broken heart syndrome. segmental ischemic changes . probably due to catecholamine surge. tx is supportive usually self resolves
Antibiotics for MRSA
Sulfamethoxazole/trimethoprim
Doxycycline
Clindamycin
Linezolid
Vancomycin
Daptomycin
antibiotics contraindicated in pregnancy
MCAT
metronidazole
chloramphenicol
aminoglycoside (streptomycin, gentomycin, tobramycin)
tetracycline
name 4 antibiotics with pseudomonas activity
ciprofloxacin
Zosyn (piperacillin, tazobactim)
cefepime
levofloxacin
azetreonam
VRE antibiotics
linezolid
tedizolid
daptomycin
tigecycline
and more
immunosuppressant drug that might cause hyperkalemia, gout attacks, tremor, htn
tacrolimus
what kind of drug is azathioprine?
immunosuppressant. stops purine synthesis–> leukocyte production
bone marrow suppression : (
hepatoxicity : (
lupus nephritis is caused by deposition of…
anti double stand DNA–> complement mediated damage
lupus nephritis kinda mixed pic of nephritic/nephrotic –
normal arterial pH and paCO2 in context of increased work of breathing indicates what…
that the pt is wearing out and can’t maintain adequate ventilation (either muscle fatigue or air trapping) and points to impending respiratory collapse
for example: pt with acute asthma attack is expected to have respiratory alkalosis with low PaCO2 due to hyperventilation. Normal or elevated PaCO2 during acute asthma attack is bad bad!
bactrim side effects
pancytopenia
nausea/vomiting
rash
hyperkalemia
interacts with warfarin
lower extremity weakness, pain swelling after drinking binge
acute alcohol myopathy
watch out for rhabdo
cocaine can also cause rhabdo
what drugs can cause rhabdomyelosis
-things that will make you pass out so much you dont move: benzos, etoh, opioids
statins
cocaine, alcohol, meth
colchinine
tx for rhabdo
IVF
(watch out for compartment syndrome)
how do you treat mycobacterium avium complex
MAC happens in aids pts with t cell count below 50
tx with macrolide +ethambutal
symptoms are diarrhea, fever, abdominal pain, hepatosplenomegaly , high alkphos
name 3 macrolids
azithromycin
clarithromycin
erythromycin
difference between secretory and osmotic diarrhea
osmotic diarrhea is because of nonabsorbed, osmotically active solute. High stool osmotic gap (290-2(Na +K)). Occurs after ingestion.
Secretory diarrhea can happen without eating. The gut secretes electrolytes and the osmotic gap is low.
-toxins, absorption issues, hormones (VIPomas). post surgery, CF, Vibreo cholerae
sepsis is common cause of mixed respiratory acidosis and metabolic acidosis
sepsis –> metabolic acidosis, requires compensatory respiratory alkalosis but muscles fatigue and you cant blow off CO2 as you approach respiratory failure leading to respiratory acidosis . look for really low pH
SIRS criteria
Temp: below 96.8 or above 100.4
HR: >90bpm
Tachypnea: >20 RR
WBCs: <4000, >12000, or bandemia
what are major signs/symptoms of sepsis
think about it by organ system
brain– AMS
kidney – BUN:Cr
cardiovas - hypotension
liver – LFTs
lung – CXR (maybe ARDS)
what’s difference between sepsis, severe sepsis, and septic shock
all SIRS 2/4 positive
severe sepsis: >= 1 organ system dysfunction; responsive to fluids
septic shock: >= 1 organ system dysfuntion, NOT responsive to fluids, will need vasopressors
BUN: creatinine ratio in ATN
10-15
pt with neck stiffness, a cranial nerve palsy, weeks of headache and malaise. CSF shows low glucose, moderately increased protein, and lymphocytosis
tuburcular meningitis
febrile neutropenia
a medical emergency
need anti-pseudomonal coverage; antipseudomonal beta lactam (cefepim, meropenem, piperacillin-tazobactam) will cover gram pos and gram neg
vancomycin has no ______ activity
gram negative
vancomycin used known MRSA, cather related infection, soft tissue, skin, pneumonia, hemodynamic instability
mild fever, pulmonary symptoms,
blastomycosis
midwest USA
can become disseminated even in immunocompetent
itraconazole or amphotericin B if really severe
cerebellar degeneration is associated with what common medical problem
alcohol use disorder
heavy alcohol use can cause cerebellar neurotoxicity – wide based gait, postural instability; cognition generally intact
triad of Wernicke encephalopathy
ocular motor dysfunction (horizontal nystagmus)
**confusion (differentiates it from alcohol neurotoxicity in cerebellum(
ataxia
risk of giving oxygen during COPD exacerbation
hypercapnia—> acidosis and vasodilation–>confusion, lethargy, seizures
Giving the oxygen will help the hypoxemia but it won’t help and may even worsen CO2 trapping in advanced COPD.
O2 may exacerbate CO2 trapping by reducing respiratory drive, loss of compensatory vasoconstriction in regions of lung where there is ineffective gas exchange; more oxyhemoglobin decreases CO2 uptake from the tissues by Haldane effect
Goal is to get to sat in low 90s
antimitochondrial antibody is associated wth
primary biliary cholangitis
cholestasis with intrahepatic autoimmune bile duct destruction
think middle aged women
ursodeoxycholic acid
many pts wind up needing liver transplant
elevated alkphos
what baseline test should pt getting traztuzamab for HER2+ breast cancer get?
baseline ECHO
traztuzamab is cardiotoxic
anastrozole and letrozole used for postmenopausal estrogen receptor + breast cancer.
What side effect should you be most worried about with anastrozole and letrozole (aromatast inhibitor)
decreased bone density
HIV predisposes pts to malignancy because T cells arent as able to target mutated cells for apoptosis and latent oncogenic viruses reactivate.
Name 3 virus-malignancy combos seen in HIV/AIDS
Epstein Barr Virus –> diffuse large B cell lymphoma, CNS lymphoma (non hodgkin lymphoma). Diffuse lymphadenopathy + B symptoms
HHSV 8 –> Kaposi sarcoma
HPV–> invasive cervical carcinoma
tick born illnesses
Rocky mountain spotted fever - rash on palms, soles;
Erlichiosis - leukopenia, thrombocytopenia
babeiosis - northeast, hemolytic anemia , thrombocytopenia, esp in older/immunocomp/asplenic ppl
heart failure in an alcoholic
alcoholic cardiomyopathy
dilated cardiomyopathy; LV function returns with abstinance
Jarish herxheimer reaction
from sudden lysis of spirochetes (syphilis, lyme)
myalgias, fever, chills
self limited
treatment for arsenic poisoning
dimercaprol
chronic arsenic poisoning symptoms
hyper/hypo pigmentation, hyperkeratosis, stocking glove neuropathy
encephalopathy + ataxia + eye dysfunction
wernicke’s encephalopathy, give thiamine
This in HIV patient without eye pain
CMV retinitis. Note the fluffiness.
liraglutide
GLP-1 agonist
weightloss
decreased CVD mortality
Old man with ESRD, back pain, normal calcium, high phosphate, high alkphos
1 what would you think it is if Xray shows mixed osteoblastic/osteolytic lesions in spine?
2 what would you think if his Xray shows widespread osteopenia and subperiosteal bone resorption in spine
3 what would you think it is if his xray shows irregular area of bone sclerosis in spine?
- normal calcium, high alkphos (not high phosphate) with mixed osteoblastic/osteolytic lesions –> Paget’s disease of the bone. Usually asymptomatic
- Phosphate will be high in ESRD. people with kidney failure get hyperparathyroidism bc of low calcium/high phosphate –> bone resorption called renal osteodystrophy
- Irregular bone sclerosis (osteoBLASTIC) and progressive back pain should make you think mets, probably prostate mets
Formula to correct calcium for albumin
=Ca +0.8 (4-albumin)
citrate in massive blood transfusions binds to…. causing low serum levels
massive blood transfusions –> hypocalcemia bc citrate binds to Ca2+
2 main factors in calcium regulation
parathyroid hormone (adjust calcium minute to minute)
and vitamin D (adjusts calcium over long term)
Hepatorenal syndrome
a complication of liver failure, often set off by peritonitis, excessive diuresis, GI bleed, other major insult
as cirrhosis progresses, the splenchnic artery dilates and there is less vascular resistance. This activates RAAS –> renal vasoconstriction and therefore decreased perfusion and GFR. acute tubular necrosis or other AKI should be on your differential but HRS patients won’t get better with fluids and they will have bland U/A.
treatment = liver transplant
Lights criteria
pleural fluid protein/serum protein >0.5
pleural fluid LDH/serum LDH >0.6
pleural fluid LDH > 2/3 upper limit of normal LDH
most common causes of bloody plural effusion
trauma
malignancy
PE
Horner syndrome
Ptosis
Miosis
Anhidrosis
associated with apical lung cancer (Pancoast tumor)
hemoptysis with blood streaked purulent sputum
Think bronchitis
chronically coughing up copious sputum
bronchiectasis
hemoptysis with acute onset of pleuritic chest pain and dyspnea
pulmonary embolism
paraneoplastic syndromes associated with small cell lung cancer
SIADH
cushings (ACTH)
CMV in immunocompromised person causes what symptoms
pneumonitis
gastroenteritis
hepatitis
vitamen D deficiency –>low calcium –> parathyroid hormone released and bone resorbed. Maybe bone pain, osteomalacia. If kidneys work, phosphate will be low and calcium will return to normal or slightly low
whats the mechanism of warfarin skin necrosis
warfarin lowers protein C first before the results of its inhibition of production of II, VII, IX, X –> transient hypercoagulable state –> VTE or skin necrosis especially in people who have hereditary protein C deficiency
TX: stop warfarin, give protein C concentrate
main 2 lung infections for immunocompromised pts
CMV (diarrhea too)
P. jirovecii
Prophylaxis: TMP-SMX, ganciclovir
severely elevated triglyceride levels (>1000) can cause…
pancreatitis!
give fibrates, fish oil, no alcohol
brown sequard syndrome
TTP is the story of ADAM and the FAT (RN)
ADAMTS-13
Fever
Anemia (hemolytic)
Thrombocytopenia
+/-Renal failure
+/- Neuro sx
platlets low + schistocytes on smear but PT/PTT, fibrinogen and D-dimer normal
Lab findings in DIC
low platelets
schistocytes on smear
high PT PTT
high D dimer
low fibrinogen
Heparin Induced Thrombocytopenia
7-14 days after heparin product started; antibodies to platelet
tx: stop heparin, start argatroban and bridge to warfarin
immune thrombocyopenia
antibodies to plt in women with autoimmune disorder
tx with steroids, IVIG
if that doesn’t work: splenectomy
if that doesnt work: rituximab
what marker is elevated in polymyositis (not antibody)? what’s treatment?
creatinine kinase is elevated in polymyositis and NOT in polymyalgia rheumatica
+ANA, +anti-Jo
furosomide cause hypo______ and hypo______
hypokalemia
hypomagnesium
what arrythmia does digitalis cause
atrial tachycardia with av block
giardia treatment
metronidazole
methotrexate side effect
impaired DNA synthesis–> seen in most rapidly dividing cells like oral mucosa (stomatitis, oral ulcers) and bone marrow (MACROCYTIC anemia
methotrexate also causes hepatotoxicity
all this can be avoided by giving folic acid along with methotrexate
Hep C with palpable purpura
cryoglobinemia
if severe: plasma xchange; steroids, cyclophosphamide
palpable purpura plus GI symptoms
henloch scholein purpura
biopsy
steroids
Pt with hemoptysis and hematuria—> what 2 weird disease should be in differential
Goodpasture and Wegners (granulomatous polyangiits)
Wegners has weird nose stuff, C-ANCA
granulomatous polyangiitis
antibody?
tx?
hemoptysis, hematuria, nose stuff
cANCA
steroid, cyclophosphamide
pt with Hep B + gut, renal and skin problems, maybe weird nerve stuff
polyarteritis nodosa!
get angiogram
steroids, cyclophosphamide
What test do you do for Wilsons?
1st: Slit Lamp
cerruplasm
urinary copper
gold: biopsy
tx: penacillamine, transplant
Wilson’s disease treatment
penacillamine, transplant
(Kaiser-Fleicher rings in eyes, cirrhosis, chorea from copper in basal ganglia)
hemochromatosis symptoms
Bronze diabetes
cirrhosis
diastolic CHF
test: ferritin >1000 or transfarrin saturation >50% or biopsy or gene mutation
blood letting
undo the iron from me: deferoxamine
primary symptoms of alpha one tripsan deficiency
test
COPD + cirrhosis in young person
biopsy and look for PAS + macrophage
dry cough, African american, hilar lymphadenopathy, hypercalcemia
sarcoidosis
also arthralgias, eye stuff, tender nodules –> granulomatous
PBC labs show increased alk phos, increased conjugated bilirubin.
What disease often co occurs with Primary biliary cholangitis?
osteoporosis
most common malignancy in people with asbestosis
bronchogenic carcinoma
what lung cancer can cause cavitary lesions?
squamous cell
hypercoagulobility + diarrhea
pancreatic cancer
signs of beta blocker overdose
cardiogenic shock
also stop endogenous catecholamines from stimulating glycogen breakdown –> hypoglycemia
give IVF, atropine, glucagon
methotrexate adverse side effects
hepatoxicity
cytopenias (give folate)
methotrexate is dmard for RA
hydroxychloroquine adverse effects
retinopathy
hydroxycholorquine is a TNF and IL-1 suppresor
chondrocalcinosis on xray of a joint associated with pseudogout. What are 3 conditions that increase chance of pseudogout
hyperparathyroidism
hypothyroidism
hemochromotosis
tolterodine
anticholinergic for urge incontinence and overactive bladder
hypercalcemia, renal dysfunction, anemia, back pain, infections
think multiple myeloma
hypercalcemia + anemia from bone marrow infiltration. hypercalcemia can cause constiption, depression, fractures
malignancy of plasma cells
tests for multiple myeloma
serum/urine protein electrophoresis (look for M spike) (have to do urine to look for light chains)
blood smear (rouleux)
bone marrow biopsy
how to calculate number needed to treat
NNT = 1/ (control rate of disease - treatment rate of disease)
for example, if 75% of control group have the event but 60% of treatment group have the event then
NNT = 1/(.75-.6)
= 7
hemi neglect is caused by stroke where…
contralateral PARIETAL lobe
euvolemic hyponatremia associated with…
SIADH
think small cell lung cancer, pituitary prob
-water restriction, maybe a salt tablet
giving isotonic fluid like NS or LR may make the problem worse bc patient will retain more water…further dilution of the sodium they have…worse hyponatremia which can lead to confusion, seizures, coma
cirrhotics have lower temperatures so temp doesnt have to be as high, just >100, to suspect spontaneous bacterial peritonitis if they have ascites
abdominal pain
+ upper limb neuropathy
+ positive urine urobilinogen
acute intermittent porphyria
port wine colored urine
it’s an autosomal dominant problem in heme synthesis. the built up precursors are neurotoxic so all the symptoms are from neuro probs but you get abdominal pain that is from neuropathy. +/- neuropsychiatric manifestations +/- autonomic dysfunction. You can also get SIADH –> hyponatremia.
Tx: glucose + hemin (heme analogue)
side effects of isoniazid
neuropathy from pyridoxine deficiency (B6). isoniazid causes B6 excretion and most people don’t have a problem bc they have a big B6 store. But pts with diabetes, malnutrition, pregnancy may not have enough B6 –> peripheral neuropathy esp vibratory sense loss.
also isoniazid causes hepatotoxicity
huntington disease causes loss of what kind of neuron?
GABA-ergic
caudate nucleus and putamen atrophy
abdominal pain and bloody diarrhea after eating undercooked meat
cambylobacter or EHEC
bloody diarrhea, often with bacteremia, associated with contaminated water or food, especially from travel outside US
Shigella
*can cause HUS (hemolysis, renal failure)
vomiting, diarrhea, abdominal pain after undercooked shellfish
Vibreo fulnificus
**really a problem for immunocompromised. immunocompromised should not eat raw oysters
colon ca chemo
FOLFOX/FOLOFIRI
plus vegf-inhibitor bavacizumab
freckled mouth…look for what cancer?
small bowel with endoscopy
peutz jager
Lynch syndrome cancers
Colorectal
Endometrial
Ovarian
(Merrill lynch was a ceo)
aka hereditary nonpolyposis colorectal cancer
defect in DNA mismatch repair
3-2-1 rule: 3 cancers, 2 generations, 1 younger than should have been
APC gene mutation causes…
familial adenomatous polyposis
1000s of polyps by teens
must do prophylactic colectomy
Turcas
think turban…brain cancer plus what other cancer?
colorectal
Gardners
jaw cancer and colorectal ca
progression of pertusis
stepwise
weeks 1-2 mild cough + rhinitis
weeks 2-6 the badness
convalescence weeks to months, gradual improvement
tx with macrolides
*lymphocyte predominant leukocytosis
signs of hyperparathyroidism
kidney stones (calcium); high blood and urine calcium
what neoplasm is mysthenia gravis associated with
thymoma
neoplasm associated with H. pylori
MALT lymphoma
metoclopromide is a ________antagonist and can cause ___________ symptoms
metoclopromide is a dopamine antagonist and can cause extrapyramidal symptoms
like acute dystonia (think neck probs), parkinsonism, akathisia
when treating for Clostridum septicum bacterima, what underlying condition should you rule out?
colon cancer
the tumors make C. speticum happy enough to create spores plus the tumor disrupts the gut/blood barrier so those spores can get into the blood
nephrotic syndrome can cause accelerated _________ and a _________________ state
nephrotic syndrome can cause accelerated athrosclerosis and a hypercoagulability state
which part of spinal cord is hurt when there is motor weakness, loss of pain and temperature but preservation of position and vibration
anterior spinal cord, usually from an injury to anterior spinal artery
UTI or pylo + alkaline urine should raise suspicion for which organisms
Proteus mirabilis (more common)
Klebsiella pneumonia
alkaline urine can cause struvite stones (magnesium ammonium phosphate)
name some causes of stephen johnson syndrome/toxic epidermal necrosis
mycoplasma pneumonia
TMP-SMX, other abx
anticonvulsants (phenytoin, lamotrigine, carbamezapine)
NSAIDs
allopurinol
sulfasalazine
vaccination
graft-vs-host
SJS <10% of body, TEN > 30%
treatment for rosacea
topical metronidazole
treatment for cholangitis
cipro + metronidazole
treatment for pyelo in someone nontoxic
cipro
tx for pyelo in someone really sick
ceftriaxone
tx for CAP
azithromycin and ceftriaxone
tx for diverticulitis
Cipro (G-) + metronidazole (anaerobes)
tx for hospital acquired pneumonia
vanc + pip/tazo
uncomplicated UTI tx
TMP-SMX
nitrofurantoin
if you find medullary thyroid cancer in a patient (elevated calcitonin), what test should you get next?
plasma fractionated metanephrine
to check for pheochromocytoma
as part of MEN2A
tests for cushings
low dose dexomethasone suppression
salivary cortisol
MEN type 1
primary hyperparathyroidism (increased calcium)
pituitary tumors
pancreatic tumors (esp gastrinomas)
antibody in granulomatosis with polyangitiis
c-ANCA
huntington’s affects what part of brain
caudate nucleus and putamen
polyarteritis nodosa
asymmetric polyneuropathy
livedo reticularis
kidney problems
ischemia and perforation in Gut
ANCA NEGATIVE
constitutional symptoms, high inflammatory markers
due to transmural inflammation of medium arteries
** Associated with Hepatitis B/C **
which TB drug causes hepatoxicity
isoniazid
don’t ever give ACEi to ….pts
cirrhosis
(RAAS important for counteracting splanchnic dilation and preventing hypotension)
low levels of what hormone can lead to SIADH?
cortisol
what kind of diarrhea happens at night
secratory
(VIPoma (in pancreas with flushing), gastrinoma, chronic infection, microscopic colitis, bile salt diarrhea
erlichiosis
no rash, fever myalgia confusion
low platelets low leukocytes
empiric doxy
what lung cancer causes cavitary lesions
squamous cell (most common among smokes)
squamous cell can cause PTHrp too
enterotoxin made in intestine …>1 day to onset….which bugs?
C diff
ETEC
Vibrio cholerae
s bovis is now known as
s gallolyticas
colon cancer!
3 major thangs of milk alkali syndrome
acute kidney injury
hypercalcemia
metabolic alkalosis
SAAG
serum albumin - ascites albumin
>1.1 cirrhosis, cardiac ascites, budd chiari
<1.1 TB, pancreatic cause, nephrotic syndrome, peritoneal carcinomatosis
consensus trial showed acei can reduce moratality for HF but ARNIs better apparently . Acei better than arb
