Week 3 and 4 Lectures Flashcards

1
Q

UACR cutoff

A

UACR (urine albumine:creatinine ratio) > 30 = CKD

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2
Q

Differentiate the lymphocytosis seen in chronic bronchitis vs. asthma

A

Both chronic bronchitis and asthma have airway inflammation => obstruction

Asthma- eosinophilia
Chronic bronchitis- neutrophilia

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3
Q

Criteria for multifocal atrial tachycardia

A

MAT- criteria is at least 3 morphologically different P waves w/ a HR > 100 bpm

(If HR is under 100 = wandering atrial pacemaker)

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4
Q

Hep B panel:
SAg (+)
SAb (-)
eAg (-)

What factor determines if you treat?

A

So pt has active Hep B (either acute or chronic, but probably chronic think about clinical scenario). eAg is negative so low viral load (marker of replication/activity)

Next step: measure viral load (by DNA PCR level)

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5
Q

Two categories of COPD

A

COPD usually caused by a combo of these, but can be broken down into

  1. emphysema
  2. chronic bronchitis
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6
Q

Categorization of brady arrythmias

A

Bradycardia (HR under 60) can be divided into

  1. Sinus node dysfunction
    - you’ll have sinus P waves and 1:1 P:QRS just slower
  2. AV block (all the dif types)
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7
Q

What are the final endpoints for Hep C?

A

Hep C –> cirrhosis –> a bunch of final endpoints

Hepatocellular carcinoma
Portal HTN => ascites, varices
Encephalopathy
Increased bleeding risk

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8
Q

First line tx for COPD

A

Smoking cessation

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9
Q

AVRT vs. AVNRT

(a) type of tachy
(b) focus

A

AVNRT = AV nodal reentry tachycardia
(b) focus is in the AV node

AVRT = AV reentry pathway
(b) Focus not in the AV node- is some aberrant conduction pathway btwn the atria and ventricles = WPW!!!

(a) Both are narrow complex sinus tachycardias

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10
Q

Tenofovir

A

Antiviral first line agent for Hep B

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11
Q

Drug that can help distinguish type 1 vs. type 2 second degree heart block

A

Atropine (anti-cholinergic) will improve type 1 (problem is at the AV node) , but NOT type 2 (problem is infra-nodal)

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12
Q

Describe the levels of SAg, SAb, Core Ab for Hepatitis B and what they indicate

A

Hep B lab values:

Surface antigen (SAg) shows active/current infection- either acute or chrnoic, but that you have some viral load present

then surface antibody (SAb) means your body has cleared the infection

Then there is a Window period = period where surface antigen is undetectable but surface antibody is developed yet, right after chronic infection. at this point core antibody (either IgM or IgG) is positive

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13
Q

Describe the mechanism of AVNRT

A

AVNRT = AV nodal re-entry tachycardia

Micro-reentrant circuit at the AV node + premature atrial beat (PAC)
-slow pathway repolarizes faster than the fast pathway => reentry loop

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14
Q

Who gets screened for Hep B?

A

Anyone from an endemic area

-endemic area defined as an area where there’s >2% prevalence

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15
Q

What does an ejection sound represent?

A
High frequency (harsh) sound shortly after S1- represents an abnormal opening of aortic or pulmonic valve 
-aortic stenosis
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16
Q

What does an opening snap represent?

A

Opening snap = sound of thick mitral valve (stenotic) opening

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17
Q

Consequence of Hep C- first endpoint

(a) What speeds up this process

A

in 20 years, 20% of Hep C pts will develop cirrhosis

(a) This is sped up by EtOH, HIV, and Hep B

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18
Q

2 reasons why platelets are decreased in Hep C patients

A

Low platelets b/c

  1. liver isn’t making TPO (thrombopoeitin): factor that stimulates platelet production
  2. liver fibrosis backs up into the spleen and you get splenic platelet sequestration
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19
Q

Location of the focus in AFib

(a) Tx for Afib

A

AFib focus located somewhere in the pulmonary veins => can’t easily get to the left side of the heart => harder to treat

(a) We’re getting better at burning thru the intra-atrial septum to get to the LA to ablate this out

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20
Q

2 medical tx for afib

A

Reduce complications of Afib by

  1. anti-coagulating (warfarin)
  2. rate regulation (beta blockers)
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21
Q

Describe where the following are located in the cardiac cycle

(a) Ejection sound
(b) Opening snap
(c) Pericardial knock
(d) Systolic click

A

Cardiac cycle: S1 –> S2 –> S1 etc
Overall: S1 –> ejection sound –> systolic clicks –> A2 –> P2 –> opening snap –> pericardial knock –> S3 —> S4 —> S1…repeat

(a) Ejection sound = beginning of systole, right after S1
(b) Opening snap = beginning of diastole, right after S2
(c) Pericardial knock- end of diastole, after an opening snap would be
(d) Systolic click- middle to end of systole (after ejection sound)

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22
Q

Transmission of Hepatitis

A
B
C

A

Hepatitis A: transmitted fecal-oral

B and C: transmitted thru blood/bodily fluid

  • IVDU (shared needles)
  • sex (more for C than for B)
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23
Q

QRS interval

(a) Normal duration
(b) Narrow vs. Wide

A

(a) QRS interval- normal duration is 60-100 ms (basically under 1/2 the width of a big box

(b) Narrow (normal duration) QRS = atrial
vs.
Wide (longer duration) QRS means signal is coming from the ventricles

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24
Q

Which murmur is made louder when pt leans forward

A

Aortic regurgitation- move forward to push the RVOT closer to the chest wall

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25
Q

How to categorize tachy arrhtyhmias

A

Tachycardia can be separated into narrow complex (atrial) and wide complex (ventricular)

-so get EKG and measure duration of QRS
if QRS is under 100 ms (1/2 width of a big box) = narrow = atrial
if QRS is wider than 100 ms (1/2 width of big box) = wide = ventricular

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26
Q

Clinical relevance of calculating max HR for age

A

If HR faster than 220-age, then it probably isn’t sinus

HR estimation by age estimates the max HR possible in sinus tachy

27
Q

Newly diagnosed chronic hep B

What 3 labs do you check?

A

Chronic hep B

  1. Check LFTs: track ALT, albumin
  2. DNA PCR level (viral load)
  3. eAg (envelope antigen)- this is a marker of replication/activity
    so eAg(+) basically guarantees a high viral load
    -e-antigen status helps determine who needs treatment
28
Q

When do you see Hep B surface antibody in a pt who got Hep B from vertical transmission

A

When babies get Hep B from mommy- their body’s dont clear the infection => you DONT see Hep B SAb (SAb indicates immunity)

=> chronic hepB infection = Hep B surface antigen remains high

29
Q

Name some meds used by cardiologists that can exacerbate asthma

A

NSAIDs, aspirin, ACEi, beta-blockers

30
Q

Ddx for faint/weak S1

A

Weak ventricular contraction, ex: cardiac myopathy

31
Q

What are

(a) Adenosine
(b) Amiodarone

A

(a) Adenosine = anti-arrhythmic that slows down conduction thru the AV node
=> terminates AVNRT

(b) Amiodarone = very dirty anti-arrhythmic- has properties of all 4 classes of anti-arrhythmics

32
Q

Aflutter

(a) Atrial rate
(b) Ventricular rate
(c) Focus of aberrant rhythm
(d) Tx

A

Atrial flutter

(a) Atrial rate around 300 bpm
(b) Then ventricular rate is 300/n, n being the rate at which the AV node lets beats thru
=> ventricular rate of 150 (n = 2), 100 (n = 3) etc
(c) Location of aberrant rhythm = tricuspid isthmus => very easy to get to (since r. side of heart is accessible thru peripheral veins) so
(d) Easily ablated

33
Q

How can you determine if someone immune to Hep B was exposed (and body fought it off) or they were vaccinated

A

Immune to Hep B = presence of surface antibody (SAb)

Then presence of core indicates exposure

SAb+, core + = exposed and cleared
SAb+, core - = vaccinated (aka immune w/o being exposed)

34
Q

Obese M presents w/ 20 lb weight loss and finger stick of 362

First step in management?

A

Put him on insulin (even if temporarily)! Duh you want him to lose weight but the hyperglycemia is toxic to beta-cells and you want to preserve function

35
Q

Hep B panel:
SAg (+)
SAb (-)
eAg (+)

What factor determines if you treat?

A

So pt has hepB, surface antigen (active infection) positive and surface antibody (immunity) negative

So viral load is high (indicated by eAg) => next step is ALT

If ALT elevated (aka over 60) = treat
If ALT is normal => don’t treat, even if there is a high viral load
-this is representing immune tolerance = high viral load isn’t killing of hepatocytes

36
Q

How to diagnose peritonitis

A

Tap the fluid: if the fluid has white cells > 250 (specifically high neutrophils) = diagnostic for SBP = subacute bacterial peritonitis

37
Q

Common etiology of multifocal atrial tachycardia

A

COPD

-pulm disease stretched out the heart, stretch heart is more likely to have bad stuff (ectopic pacemaker etc)

38
Q

Hep B panel:
SAg (+) SAb(-)

What do you do?

A

So this person has chronic (most likely chronic unless you’re catching them right when they got it) Hep B

-so you want to do primary prevention to prevent progression to liver cancer and/or cirrhosis

39
Q

What do you screen for in a chronic Hep B pt?

A

Chronic Hep B secondary prevention (screening)
Liver ultrasound for hepatocellular carcinoma
-can also use AFP (very nonspecific, but used)

Then these 2 can help you decide if you want to do an abdominal CT

40
Q

Differentiate chronic bronchitis and emphysema

A

Chronic bronchitis = airway disease/inflammation, not parenchymal disease

Emphysema = airways are fine, parenchyma (alveoli) are diseased- alveolar destruction

41
Q

Why is ascites dangerous?

A

B/c it’s just fluid hanging out waiting to get infected (peritonitis)

42
Q

New vs. old Hep C treatment

A

Old Hep C treatment: interferon (makes you feel awful) + ribavarin for 48 weeks (holy shit almost a year)= 40% response rate for genotype 1
-50% response rate in whites, only 20% response rate in non-whites

New Hep C tx (YAY!!!):
For genotype 1: Sotosbuvir-Ledipasvir (Harvoni): crazy expensive (like $84,000 for tx) but 95% response rate

43
Q

Key PFT feature of obstructive vs. restrictive disease

A

PFT feature

Obstructive disease: reduced FEV1/FVC

Restrictive disease: low TLC (total lung capacity)

44
Q

Ddx for Loud S1

A

Hyperdynamic state: fever, increased adrenergic tone

-mitral stenosis

45
Q

Focus of the problem in type 1 vs. type 2 second degree heart block

A

Second degree heart block (dropped QRS waves)

Type 1: problem is at the AV node

Type 2: problem is infra-nodal => a lot less stable => hence why we give these ppl pacemakers

46
Q

What is meant by the following description of a murmur

(a) Ejection
(b) Regurgitant

A

Murmur

(a) Ejection- describes blood flowing forward
ex: thru a stenotic AV valve
- crescendo decrescendo pattern is implied

(b) Regurgitant = flow from a ventricle into a lower pressure chamber

47
Q

Hep B panel:
SAg (-), SAb (-)

What do you do?

A

Testing a pt for hep B:
SAg (-) means they don’t have infection- so not acutely or chronically infected
SAb (-) means they don’t have immunity

=> they haven’t been exposed or vaccinated => we vaccinate them!!

48
Q

PIRATES mneumonic for secondary causes of AFib

A
P- pulmonary disease or PE
I- ischemia
R- rheumatic or valvular heart disease
A- anemia 
T- hyperthryoidism 
E- EtOH or other toxins (cocaine)
S- sepsis or other infection
49
Q

High clinical suspicion of asthma w/ normal PFTs, is bronchodilator response test indicated?

A

Yes bronchodilator response indicated b/c normal range for PFTs is so wide: 80-120% => what is normal may be low for that pt

50
Q

FEV1/FVC in asthma

A

Reduces FEV1/FVC ratio (under 70%)

-indicating restrictive disease

51
Q

First step when someone presents w/ tachy or bradycardia

A

Are they hemodynamically stable?

If not- cardiovert or defibrillate- aka start chest compressions asap dude

52
Q

How many Americans have

(a) HIV
(b) Hep C

A

(a) 1 million Americans have HIV

(b) 3-4 million Americans have Hep C

53
Q

Does S1 or S2 have higher frequency?

A

S2 has higher frequency- hence why emphasis is on the Dub of ‘lub-dub’

54
Q

What is DLCO for pulmonary fxn?

(a) How does it help you classify COPD?

A

DLCO = diffusion capacity of carbon monoxide- tells you how the alveolar diffusion surface is functioning

(a) Low DLCO is associated w/ emphysema (parenchymal disease), not chronic bronchitis (airway inflammation)

55
Q

ALT vs. AST clinical significance

A

Not a hard and fast rule, but basically:

ALT indicates liver inflammation/infection
while
AST elevation indicates EtOH

56
Q

Most common genotype of hep C in the US

(a) Hep C endpoint for treatment

A

Hep C: genotypes 1,2,3
-genotype 1 is the most common in the US (70%)

(a) Sustained virologic response = end point for treatment
- 3 mo after treatment, is viral load still undetectable?

57
Q

What is clinically important to tell pathology from S1 vs. S2

A

S1- the intensity is important

S2- the splitting pattern (and how it varies w/ inspiration) is important

58
Q

Describe how emphysema can progress to cause obstructive disease

A

Emphysema = lung parenchyma/ alveolar destruction, generally not an airway disease

-but increased compliance can decrease the tethered openings of the airways => obstruction

59
Q

Chances of getting chronic infection from

A
B
C

A

Chance of chronic infection

A: no chronic infection, only acute

B: very dependent on what age you get it, earlier in life you get it = higher chance of progressing to chronic infection
-so basically if you get it from vertical transmission or a kid you’ll progress, but if you get exposed as adult your body will clear it

C: high rate of progression no matter if adult or child, like 80-90% of ppl exposed will progress to chronic

60
Q

Asthma pt not well ideally controlled on low dose inhaled steroid, what is the next step?

A

Add LABA/steroid combination before increasing steroid dose

61
Q

Name a med used in COPD that isn’t commonly used in asthmatics

A

LAMA = long acting muscarinic antagonist- used in COPD and not asthma

62
Q

Varying intensity of S1 in a pt w/

(a) Regular rhythm
(b) Irregular rhythm

A

Varying intensity of S1 in pt w/

a) Regular rhythm = AV dissociation (3rd degree AV block
(b) Irregular rhythm = Nondiagnostic, but most commonly AFib

63
Q

What is your endpoint goal for Hep B treatment?

A

You’re not gonna get a cure (you wont get positive surface antibody), but 40% will transform from eAg (+) –> eAg (-)

64
Q

2 tx that improve survival in COPD pts

A

Only 2 treatments that improve survival in COPD pts- smoking cessation and O2 therapy (in those who it is indicated)