Internal Med 1

Question 1

What are the potential causes of anterior mediastinal masses

Answer 1

Thymus, Teratoma, Thyroid, Terrible lymphoma

Question 2

Describe the scale in time of EKG (how many seconds is one little box and one big box)

Answer 2

• 1 big box = 0.2 seconds = 5 small boxes

* 1 little box = 0.04 seconds

Question 3

How can you quickly calculate heart rate on EKG

Answer 3

• (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,

Question 4

Definition of normal sinus rhythm

Answer 4

♣ 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

Question 5

Describe how you determine normal axis on EKG

Answer 5

♣ 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

Question 6

When should you look at lead II in determining axis

Answer 6

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

Question 7

What is a normal PR interval

Answer 7

<5 small boxes (200 ms)

Question 8

What is a normal QRS interval

Answer 8

<3 small boxes (120 ms)

Question 9

What is a normal QT interval

Answer 9

less than ½ RR interval

Question 10

What does it mean to have a negative P wave in lead II

Answer 10

Ectopic atrial focus

Negative P wave in lead two which means the atria is depolarizing in the wrong direction, away from lead 2

Question 11

Define 1st degree AV block

Answer 11

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)

Question 12

Define how 2nd degree AV block is different from 1st degree

Answer 12

PR interval is slow AND there are some completely blocked atrial impulses

Question 13

Describe tx of 1st degree AV block

Answer 13

None - it is totally asymptomatic

Question 14

Describe 2nd degree AV block Mobitz Type I (Wenckebach)

Answer 14

♣ Progressive lengthening of PR interval until a beat is “dropped”

Question 15

Tx of Wenckebach

Answer 15

None - is benign

Question 16

Describe 2nd degree AV block Mobitz Type II

Answer 16

♣ “Dropped” beats without a warning

• Not preceded by change in length of PR interval

Question 17

Tx of Mobitz type II

Answer 17

♣ May progress to third degree block

♣ Treated with pacemaker

Question 18

Describe 3rd degree heart block

Answer 18

• Atria and ventricles beat independently of each other
• No correlation between P waves and QRS complex
• Atrial rate > ventricular rate

Question 19

Rank the rate of different pacemakers

Answer 19

♣ SA > AV > bundle of His/Purkinje/ventricles

Question 20

Describe what a junctional rhythm is

Answer 20

• 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

Question 21

How do you differentiate between junctional esape and ventricular escape

Answer 21

Junctional = slow rate; normal QRS; NO P wave

Ventricular = slow rate; widened QRS; still has P wave

Question 22

What are the stimulators of Renin release

Answer 22

♣ Beta-adrenergic stimulation
♣ Low Na+ in the DCT
♣ Low pressure in the afferent arteriole

Question 23

What is the function of renin

Answer 23

Renin (activated by juxtaglomerular cells) catalyzes conversion of angiotensinogen to angiotensin –> in lungs and kidney ACE converts angiotensin I to angiotensin II

Question 24

Actions of angiotensin II

Answer 24

♣ (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

Question 25

Where does ANP come from and what is its function?

Answer 25

• 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

Question 26

Where does BNP come from and what is its function

Answer 26

• 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

Question 27

Describe MOA of Digoxin

Answer 27

♣ 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

Question 28

What are the drugs that improve mortality in CHF

Answer 28

* ACE inhibitors * ARBs * Aldosterone antagonists * Certain B-blockers * Nitrates and hydralazine

Question 29

What are the drugs used solely for symptomatic relief in CHF

Answer 29

* Diuretics * Digoxin * Vasodilators

Question 30

What are the systolic murmurs

Answer 30

- Aortic/pulmonic stenosis | - Mitral/tricuspid regurg

Question 31

What are the diastolic murmurs

Answer 31

- Mitral/tricuspid stenosis | - Aortic/pulmonic regurg

Question 32

Describe presentation of aortic regurg

Answer 32

o High-pitched “blowing” early diastolic descrescendo murmur | o Wide pulse pressure with head bobbing – bounding pulses

Question 33

Causes of aortic regurg

Answer 33

♣ Aortic root dilation (e.g. syphilis or Marfan) ♣ Bicuspid aortic valve (but usually causes aortic stenosis) ♣ Endocarditis ♣ Rheumatic fever

Question 34

Describe presentation of mitral stenosis

Answer 34

o Delayed rumbling mid-to-late diastolic murmur | o Follows opening snap (after S2)

Question 35

Describe presentation of aortic stenosis

Answer 35

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

Question 36

Causes of aortic stenosis

Answer 36

♣ Bicuspid aortic valve in younger patients, senile (degenerative) calcification in older patients, chronic rheumatic valve disease, unicuspid aortic valve, syphilis

Question 37

Describe presentation of mitral regurg

Answer 37

``` o Pansystolic (holosystolic), high-pitched “blowing” murmur o Best heard at the apex, often radiates to the L axilla ```

Question 38

Causes of mitral regurg

Answer 38

• Rheumatic heart disease, endocarditis, ischemic heart disease, LV dilation, mitral valve prolapse

Question 39

Describe presentation of mitral prolapse

Answer 39

o Late systolic crescendo murmur, usually preceded by mid-systolic click (due to sudden tensing of chordae tendinae) o Best heard over apex

Question 40

Describe VSD murmur

Answer 40

o Holosystolic, harsh-sounding murmur | o Loudest at tricuspid area

Question 41

Causes of elevated lactic acid

Answer 41

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

Question 42

Causes of pancreatitis

Answer 42

I GET SMASHED: o Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypertriglyceridemia/Hypercalcemia, ERCP, Drugs (e.g. Sulfa, NRTIs, protease inhibitors)

Question 43

Components of stroke workup

Answer 43

Per chief resident: - CTA - MRA - Echo with bubble - Lipids - HbA1C - Lactic acid (really high = seizure) - PT/OT eval

Question 44

Components of chest pain workup

Answer 44

Per chief resident: - Troponin Q6H - EKG Q6H - ASA + Statin - Nitro for active CP

Question 45

What do you expect to see in normal EKG T-waves

Answer 45

Positive in V2-V6 and I, II, II, aVF

Question 46

What do inverted T waves mean

Answer 46

Ischemia

Question 47

What do Q-waves indicate?

Answer 47

Sign of old ischemia As ST elevations are resolving, Q waves begin to develop

Question 48

Tx of hyperkalemia

Answer 48

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)

Question 49

Go to empiric abx for inpatient tx of community acquired pneumonia

Answer 49

♣ Beta-lactam (e.g. Ceftriaxone) + macrolide (IV) ♣ Fluoroquinolone (IV) – respiratory fluoroquinolones = Levofloxacin, Moxifloxacin