Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MS3 > Internal Med 1 > Flashcards

Internal Med 1 Flashcards

1
Q

What are the potential causes of anterior mediastinal masses

A

Thymus, Teratoma, Thyroid, Terrible lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A
  • 1 big box = 0.2 seconds = 5 small boxes

* 1 little box = 0.04 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can you quickly calculate heart rate on EKG

A

• (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,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Definition of normal sinus rhythm

A

♣ 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe how you determine normal axis on EKG

A

♣ 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When should you look at lead II in determining axis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a normal PR interval

A

<5 small boxes (200 ms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a normal QRS interval

A

<3 small boxes (120 ms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a normal QT interval

A

less than ½ RR interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Ectopic atrial focus

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define 1st degree AV block

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe tx of 1st degree AV block

A

None - it is totally asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tx of Wenckebach

A

None - is benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe 2nd degree AV block Mobitz Type II

A

♣ “Dropped” beats without a warning

• Not preceded by change in length of PR interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Tx of Mobitz type II

A

♣ May progress to third degree block

♣ Treated with pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe 3rd degree heart block

A
  • Atria and ventricles beat independently of each other
  • No correlation between P waves and QRS complex
  • Atrial rate > ventricular rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Rank the rate of different pacemakers

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe what a junctional rhythm is

A

• 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

21
Q

How do you differentiate between junctional esape and ventricular escape

A

Junctional = slow rate; normal QRS; NO P wave

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

22
Q

What are the stimulators of Renin release

A

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

23
Q

What is the function of renin

A

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

24
Q

Actions of angiotensin II

A

♣ (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

25
Q

Where does ANP come from and what is its function?

A

• 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

26
Q

Where does BNP come from and what is its function

A

• 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

27
Q

Describe MOA of Digoxin

A

♣ 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

28
Q

What are the drugs that improve mortality in CHF

A
  • ACE inhibitors
  • ARBs
  • Aldosterone antagonists
  • Certain B-blockers
  • Nitrates and hydralazine
29
Q

What are the drugs used solely for symptomatic relief in CHF

A
  • Diuretics
  • Digoxin
  • Vasodilators
30
Q

What are the systolic murmurs

A
  • Aortic/pulmonic stenosis

- Mitral/tricuspid regurg

31
Q

What are the diastolic murmurs

A
  • Mitral/tricuspid stenosis

- Aortic/pulmonic regurg

32
Q

Describe presentation of aortic regurg

A

o High-pitched “blowing” early diastolic descrescendo murmur

o Wide pulse pressure with head bobbing – bounding pulses

33
Q

Causes of aortic regurg

A

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

34
Q

Describe presentation of mitral stenosis

A

o Delayed rumbling mid-to-late diastolic murmur

o Follows opening snap (after S2)

35
Q

Describe presentation of aortic stenosis

A

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

36
Q

Causes of aortic stenosis

A

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

37
Q

Describe presentation of mitral regurg

A 
o	Pansystolic (holosystolic), high-pitched “blowing” murmur
o	Best heard at the apex, often radiates to the L axilla
38
Q

Causes of mitral regurg

A

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

39
Q

Describe presentation of mitral prolapse

A

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

40
Q

Describe VSD murmur

A

o Holosystolic, harsh-sounding murmur

o Loudest at tricuspid area

41
Q

Causes of elevated lactic acid

A

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

42
Q

Causes of pancreatitis

A

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

43
Q

Components of stroke workup

A

Per chief resident:

  • CTA
  • MRA
  • Echo with bubble
  • Lipids
  • HbA1C
  • Lactic acid (really high = seizure)
  • PT/OT eval
44
Q

Components of chest pain workup

A

Per chief resident:

  • Troponin Q6H
  • EKG Q6H
  • ASA + Statin
  • Nitro for active CP
45
Q

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

A

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

46
Q

What do inverted T waves mean

A

Ischemia

47
Q

What do Q-waves indicate?

A

Sign of old ischemia

As ST elevations are resolving, Q waves begin to develop

48
Q

Tx of hyperkalemia

A

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)

49
Q

Go to empiric abx for inpatient tx of community acquired pneumonia

A

♣ Beta-lactam (e.g. Ceftriaxone) + macrolide (IV)

♣ Fluoroquinolone (IV) – respiratory fluoroquinolones = Levofloxacin, Moxifloxacin

MS3 (88 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions