Internal Med 1 Flashcards
What are the potential causes of anterior mediastinal masses
Thymus, Teratoma, Thyroid, Terrible lymphoma
Describe the scale in time of EKG (how many seconds is one little box and one big box)
- 1 big box = 0.2 seconds = 5 small boxes
* 1 little box = 0.04 seconds
How can you quickly calculate heart rate on EKG
• (1) Count the number of QRS complexes on the full strip and multiply by 6
• (2) Count how many dark lines the QRS complexes are apart
o If two adjacent QRS complexes are one big line apart, the HR is 300
o If two adjacent QRS complexes are 2 big lines apart, the HR is 150
o . . . 300, 150, 100, 75, 60, 50,
Definition of normal sinus rhythm
♣ All of the following MUST be true:
• P wave must preceded every QRS
• QRS must come after every P
• P wave must be upright in lead II
Describe how you determine normal axis on EKG
♣ Normal axis is between -30 and 90 degrees
• Basically everything between lead I and aVF (even though this is technically only 0 to 90)
• In a normal ECG, you would see a positive deflection of QRS in leads I and aVF
When should you look at lead II in determining axis
o The only time you need to look at lead II is if you are positive in lead I and negative in lead aVF
o Usually this means this is L axis deviation UNLESS it falls between -30 and 0
o So you need to check lead II
♣ If lead II is positive, then it is normal (between -30 and 0)
♣ If lead II is negative, then it is real L axis deviation
What is a normal PR interval
<5 small boxes (200 ms)
What is a normal QRS interval
<3 small boxes (120 ms)
What is a normal QT interval
less than ½ RR interval
What does it mean to have a negative P wave in lead II
Ectopic atrial focus
Negative P wave in lead two which means the atria is depolarizing in the wrong direction, away from lead 2
Define 1st degree AV block
Prolonged PR interval (>200 ms)
And PR interval is consistent (not irregular)
And every P still has a QRS following it (never any dropped beats)
Define how 2nd degree AV block is different from 1st degree
PR interval is slow AND there are some completely blocked atrial impulses
Describe tx of 1st degree AV block
None - it is totally asymptomatic
Describe 2nd degree AV block Mobitz Type I (Wenckebach)
♣ Progressive lengthening of PR interval until a beat is “dropped”
Tx of Wenckebach
None - is benign
Describe 2nd degree AV block Mobitz Type II
♣ “Dropped” beats without a warning
• Not preceded by change in length of PR interval
Tx of Mobitz type II
♣ May progress to third degree block
♣ Treated with pacemaker
Describe 3rd degree heart block
- Atria and ventricles beat independently of each other
- No correlation between P waves and QRS complex
- Atrial rate > ventricular rate
Rank the rate of different pacemakers
♣ SA > AV > bundle of His/Purkinje/ventricles
Describe what a junctional rhythm is
• When there is a heart block, then one of the slower automatic pacemakers will take over for the faster SA node
• Usually have slower rates (40-60 bpm)
• Will NOT have a P wave
o Basically looks like sinus brady, will be regular rate with normal narrow QRS
o No P waves are the only reason you can distinguish from other things
How do you differentiate between junctional esape and ventricular escape
Junctional = slow rate; normal QRS; NO P wave
Ventricular = slow rate; widened QRS; still has P wave
What are the stimulators of Renin release
♣ Beta-adrenergic stimulation
♣ Low Na+ in the DCT
♣ Low pressure in the afferent arteriole
What is the function of renin
Renin (activated by juxtaglomerular cells) catalyzes conversion of angiotensinogen to angiotensin –> in lungs and kidney ACE converts angiotensin I to angiotensin II
Actions of angiotensin II
♣ (1) Acts on the zona glomerulosa cells of the adrenal cortex to stimulate synthesis of aldosterone
• Aldosterone acts on principal cells of renal distal tubule and collecting duct to increase Na+ reabsorption and increase K+ and H+ excretion
♣ (2) Stimulates Na+/H+ exchange in the renal proximal tubule
• Leading to increased reabsorption of Na+ and HCO3-
♣ (3) Acts on the hypothalamus
• Increases thirst and water intake
• Increases release of ADH
♣ (4) Acts directly on arterioles to cause vasoconstriction
• Leads to an increase in TPR increased BP
♣ (5) Constricts efferent arteriole of the glomerulus
• Increases filtration fraction to preserve renal function (GFR) in low volume states
Where does ANP come from and what is its function?
• Released from atrial myocytes in response to increased blood volume
• Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule
o Dilates afferent arteriole and constricts efferent arterial, promoting diuresis
Where does BNP come from and what is its function
• Released from ventricular myocytes in response to ventricular stretch
• Similar action to ANP, with longer half-life
o Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule
o Dilates afferent arteriole and constricts efferent arterial, promoting diuresis
• BNP blood test used to diagnose heart failure
Describe MOA of Digoxin
♣ Inhibits Na+/K+ ATPase at the cell membrane (usually responsible for pumping K+ into the myocyte)
♣ Inhibition of this pump prevents K+ from being pumped into the cell and Na+ from being pumped out
• Increase in intracellular sodium concentration
♣ Increase in intracellular sodium promotes activation of Na+/Ca2+ exchanger
• This promotes calcium influx
♣ Increased cytoplasmic Ca2+ will lead to a rise in sarcoplasmic reticulum Ca2+ stores, resulting in improved myocyte contractility and LV function
What are the drugs that improve mortality in CHF
- ACE inhibitors
- ARBs
- Aldosterone antagonists
- Certain B-blockers
- Nitrates and hydralazine
What are the drugs used solely for symptomatic relief in CHF
- Diuretics
- Digoxin
- Vasodilators
What are the systolic murmurs
- Aortic/pulmonic stenosis
- Mitral/tricuspid regurg
What are the diastolic murmurs
- Mitral/tricuspid stenosis
- Aortic/pulmonic regurg
Describe presentation of aortic regurg
o High-pitched “blowing” early diastolic descrescendo murmur
o Wide pulse pressure with head bobbing – bounding pulses
Causes of aortic regurg
♣ Aortic root dilation (e.g. syphilis or Marfan)
♣ Bicuspid aortic valve (but usually causes aortic stenosis)
♣ Endocarditis
♣ Rheumatic fever
Describe presentation of mitral stenosis
o Delayed rumbling mid-to-late diastolic murmur
o Follows opening snap (after S2)
Describe presentation of aortic stenosis
o Crescendo/decrescendo systolic ejection murmur
o Ejection click may be present
o Murmur may radiate to carotids (turbulent blood pushed out of aorta may still be turbulent when it reaches the carotids)
o Associated with weak pulses
o Can lead to: SAD
♣ Syncope, angina, dyspnea
Causes of aortic stenosis
♣ Bicuspid aortic valve in younger patients, senile (degenerative) calcification in older patients, chronic rheumatic valve disease, unicuspid aortic valve, syphilis
Describe presentation of mitral regurg
o Pansystolic (holosystolic), high-pitched “blowing” murmur o Best heard at the apex, often radiates to the L axilla
Causes of mitral regurg
• Rheumatic heart disease, endocarditis, ischemic heart disease, LV dilation, mitral valve prolapse
Describe presentation of mitral prolapse
o Late systolic crescendo murmur, usually preceded by mid-systolic click (due to sudden tensing of chordae tendinae)
o Best heard over apex
Describe VSD murmur
o Holosystolic, harsh-sounding murmur
o Loudest at tricuspid area
Causes of elevated lactic acid
Lactic acid levels get higher when strenuous exercise or other conditions-such as heart failure, a severe infection (sepsis), or shock-lower the flow of blood and oxygen throughout the body. Lactic acid levels can also get higher when the liver is severely damaged or diseased, because the liver normally breaks down lactic acid
Causes of pancreatitis
I GET SMASHED:
o Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypertriglyceridemia/Hypercalcemia, ERCP, Drugs (e.g. Sulfa, NRTIs, protease inhibitors)
Components of stroke workup
Per chief resident:
- CTA
- MRA
- Echo with bubble
- Lipids
- HbA1C
- Lactic acid (really high = seizure)
- PT/OT eval
Components of chest pain workup
Per chief resident:
- Troponin Q6H
- EKG Q6H
- ASA + Statin
- Nitro for active CP
What do you expect to see in normal EKG T-waves
Positive in V2-V6 and I, II, II, aVF
What do inverted T waves mean
Ischemia
What do Q-waves indicate?
Sign of old ischemia
As ST elevations are resolving, Q waves begin to develop
Tx of hyperkalemia
Shift :: Insulin + glucose; beta-2 agonists (Albuterol)
Poop :: Kayexalate; Lactulose
Spin :: Hemodialysis
THINK :: C BIG K DROP (Calcium, beta agonists, insulin, glucose, kayexalate, dialysis, repeat labs, observation, poop)
Go to empiric abx for inpatient tx of community acquired pneumonia
♣ Beta-lactam (e.g. Ceftriaxone) + macrolide (IV)
♣ Fluoroquinolone (IV) – respiratory fluoroquinolones = Levofloxacin, Moxifloxacin
