Other IM + Surg Flashcards
Why do OCP’s (birth control) cause HTN?
Due to estrogen effects
(Exact mechanism is unclear, but know that estrogen is a pro-clotting, blood pressure raising hormone. Progesterone is a smooth muscle relaxant (to keep baby in) and therefore relaxes smooth muscle in vessels-> vasodilation-> lowered BP. Although progesterone may be in OCPs, estrogen is the main ingredient-> o’ all high BP.)
What is SIRS criteria? Diagnosis of sepsis vs. severe sepsis vs. septic shock vs. multi-organ dysfunction syndrome?
SIRS (systemic inflammatory response syndrome) criteria:
- Temp >38C or <36C
- WBC >12 or <4
- HR >90 (tachycardic)
- RR >20 (tachypenic)
- need 2/4 to be SIRS positive (means infection should be on your ddx)
Sepsis= SIRS positive + there’s a source
Severe sepsis= organ dysfunction (>1 organ), responsive to fluids
Septic shock= organ dysfunction (>1 organ), NOT responsive to fluids (give pressors)
Multi-organ dysfunction syndrome if >2 organs are shot—> death
If a patient has hypocalcemia, what do you first have to do to make sure the patient truly has hypocalcemia?
Correct the calcium with the albumin
Note that 99% of calcium in the body is bound to albumin (only 1% is free calcium)- so albumin influences calcium levels. Albumin plays the biggest role in hypocalcemia, so make sure to MD Calc it and check if corrected calcium level is still in the hypocalcemic range
*for every change of albumin by 1, calcium changes by 0.8
Dialysis indications (AEIOU)?
Acidosis (refractory to bicarb)
Electrolytes (hyperkalemia refractory to insulin/ beta blockers/ lasix- meds that normally drive K+ into cells)
Intoxication (aminoglycosides, polyethylene glycol, other nephrotoxic agents)
Overload
Uremia
*uremia presents as nausea/ vomiting, bleeding (disrupts platelet function, mental status changes, pericarditis)
Some IV meds that cover MRSA?
Vancomycin, Daptomycin, Telavancin
Some oral drugs that cover MRSA?
Doxycycline, Bactrim (TMP-SMX), Ceftaroline (5th gen cephalosporin), Linezolid
What is Light’s criteria?
Criteria for determining if fluid in a pleural effusion is transudative or exudative
- Transudative= protein only (due to high hydrostatic pressure like in HF or low oncotic pressure like in nephrotic syndrome or cirrhosis)
- Exudative= “extra shit in it” (like in pneumonia or malignancy where inflammation causes vasculature to become more leaky-> LDH, WBC’s, etc.)
P:S (protein: serum) ratios:
- LDH >0.6 (and 2/3rds the upper limit of normal)
- Protein >0.5
**Dirty USMLE: “PS (P:S), In sex (0.6) you want the D (LDH), up to 5 (0.5) you hope your P (protein)”
If either criteria are true, you got exudative! (Extra shit in it)
What should you always check before starting a patient on Ondansetron (Zofran)?
Their EKG!
If it’s abnormal, then the side effect of QT prolongation-> Torsades is more likely and that will likely kill your patient!
What number must the hemoglobin be under to warrant a blood transfusion?
Hb < 7
CAD with symptoms is another indication for a blood transfusion
Your patient has A-fib. What 6 things should you order/ find out?
- EKG
- Echo (check for mitral stenosis)
- Troponins
- Drug screen (check for amphetamines)
- Get an alcohol hx
- TSH (hyperthyroid can cause a-fib!)
Your patient has A-fib. What do you need to get their HR under for them to be appropriately rate controlled?
<110 bpm
Rate control usually > rhythm control and you need this rate to be <110 (based on studies)
If you cardiovert a patient (for example, to get them out of new-onset A-fib), how do you do it? (There are 2 answers)
- Shock their heart back into normal rhythm
OR
- Rhythm control with pharm using Amiodarone (type III anti-arrhythmic)
Which carbapenem does NOT cover pseudomonas?
Ertapenem
What is MRCP?
Magnetic resonance cholangiopancreatography (MRCP)
Basically an MRI of the bile ducts and pancreatic ducts (can also show the pancreas, gallbladder, and liver)
Why might a patient in septic shock have an anion gap metabolic acidosis?
From lactate
Systemic inflammation-> widespread vasodilation-> drop in BP-> inadequate perfusion to organs-> since there’s low oxygen to organs, aerobic cellular respiration gets switched to anaerobic respiration and releases lactic acid as a byproduct (we use elevated lactate in the blood as a measure of organ failure)
What is a CTA?
CT angiogram
They time when they inject the contrast and take a picture of the vessels then so you can see the blood flow
What is the CHADS-VASC score? HAS-BLED?
These are MD Calc tools to tell you if you should start your a-fib patient on anticoagulation to prevent stroke
CHADS-VASC—> tells you the patient’s risk for having stroke if you don’t anticoagulate
HAS-BLED—> tells you the patient’s risk for bleeding if you do anticoagulate
*weigh the benefits/ risks and decide what to do from there
Treatment for autoimmune hepatitis?
Corticosteroids (Prednisone + Azithroprine)
**check the TPMT enzyme prior to giving Azithroprine…this is an enzyme that breaks the drug down. If the enzyme is low, the drug will hang out in the blood longer and will increase bone marrow suppression risk.
How can you use T3 and T4 levels to figure out if a hyperthyroid patient is likely to have subactue thyroiditis (viral etiology)?
T3/T4 ratio >20 suggests viral etiology (subacute/ DeQuarvains thyroiditis) vs. Graves
- when you’re sick, your T3 (active) levels are higher
- viral would also have a hx of viral illness and textbook definition is painful. Graves would have a positive TSI antibody
What happens to cardiac output as HR increases by a lot?
It decreases
Increased HR (tachy)-> less time for the heart to fill-> decreased CO
If a-fib is NEW <48 hrs or patient is unstable (vitals are concerning- regardless of how long a-fib has been present) how do you treat?
Cardiovert (shock or give Amiodarone to correct the rhythm and attempt to get the person completely out of a-fib)
*note that the patient may come in and you diagnose a-fib for the first time ever, but if you aren’t certain when their symptoms started (not sure if onset was <48 hrs ago), do not cardiovert! This is dangerous bc if a-fib has been going on quite a while, clots may have formed in the LA appendage due to the arrhythmia and if you mess with the heart’s rhythm, you could cause that clot to be thrown-> stroke.
*so then what do you do?
Anticoagulate them for 3 weeks (make sure there are no clots)-> THEN cardiovert
OR do a TTE (transesophageal echo- invasive but takes a great pic of the LA to ensure no clots)-> THEN you can cardiovert same day
You just diagnosed a patient with a-fib, but they’ve had symptoms >48 hrs. How are you going to treat it?
Anticoagulate them for 3 weeks (make sure there are no clots that can be thrown and cause a stroke when you cardiovert)-> THEN cardiovert (with shock or Amiodarone)
OR
Do a TEE (transesophageal echo- invasive but takes a great pic of the LA to ensure no clots)-> THEN you can cardiovert same day
**Reason why you can’t jump straight to cardioversion if a-fib has been going on a while: dangerous bc clots may have formed in the LA appendage due to the arrhythmia and if you mess with the heart’s rhythm when cardioverting, you could cause that clot to be thrown-> stroke.
Some patients are chronically in a-fib (cardioversion was not indicated or did not work and they keep coming back to a-fib). How do you manage these patients?
Rate-control
-use Diltiazem, Verapamil, or a beta-blocker (Metoprolol) to keep the HR <110
Also, anticoagulate if indicated to prevent stroke! (calculate CHADS-VASC score to know their stroke risk if you don’t anticoagulate and the HAS-BLED score to know their bleeding risk if you do anticoagulate to weigh pros/ cons)
*a-fib patients are at increased risk for stroke bc the heart is beating funny-> allows clot formation, especially in the LA appendage-> these clots can be thrown and lodge into cerebral vasculature causing a stroke
Patient with angina symptoms is having chest pain. What can you give the patient for pain management?
Nitrates
*Remember, angina pain is due to narrowed coronary vessels (stenosis >70%). The heart is being starved of blood (low supply to match high demand). Nitrates cause venodilation-> dec preload (less ‘milking’ of blood to heart)-> less blood that the heart has to pump (lowers demand to meet lowered supply).