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Cardiology > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

Nascent chylomicron

  • where is it formed?
  • what does it consist of?
  • how does it undergo maturation?
A
  1. Formed in the intestinal epithelium
  2. Consists of
    - TGs
    - cholesterol esters
    - phospholipids
    - Apo B48 (truncated ApoB100) -> does NOT bind to LDLr
  3. Maturation
    - released into lymph -> blood stream
    - picks up ApoE, ApoCII, and ApoCIII from HDL
    - apoCIII blocks ApoE binding site
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2
Q

How do TGs get into adipocytes and muscle cells? Describe the mech

A

Binding of ApoCII with LPL found on endothelial cells

LPL secreted by tissues in response to insulin

TGs -> broken down into 3 FAs + glycerol -> FAs taken up by tissue and glycerol taken up by liver

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3
Q

What is the fx of hepatic lipase?

A

Digestion of chylomicron remnant

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4
Q

Nascent VLDL

  • where is it made?
  • what does it consist of?
  • what happens to it?
A

Made in the liver

Consists of

  • endogenous TG + TG from chylomicron remnant
  • endogenous cholesterol + cholesterol esters
  • phospholipids
  • apoB100

Picks up ApoE, ApoCII and ApoCIII from HDL -> bind to LPL -> releases FFAs -> becomes IDL

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5
Q

What are the 2 fates of IDL particles?

A
  1. Endocytosed by liver (ApoE mediated) -> recycled to VLDL

2. Further digested by LPL -> becomes LDL -> delivers cholesterol esters to cells through endocytosis

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6
Q

HDL related enzymes/proteins

  • ABC-1
  • LCAT
  • CETP (include disadvantage)

What is a major role of HDL?

A

ABC-1 - transporting cholesterol from cell to HDL
-helps get cholesterol across plasma membrane

LCAT - Forms cholesterol ester
-activated by ApoA-I

CETP - exchanges cholesterol for TGs from
-can promote atheresclerotic disease -> cholesterol uptake by tunica intima of arteries -> oxidation

HDL -> carry cholesterol back to the liver
-SRB-1r on liver binds to HDL -> internalization -> recycling of cholesterol

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7
Q

What mediates LDL endocytosis by cells?

A

Presence of ApoB100 -> binds to LDLr

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8
Q

Describe the sxs of LPL deficiency w/ regards to

  • chylomicrons
  • LDL
  • VLDL

What other deficiency shows the same sxs

A
  • chylomicrons -> elevated
  • LDL -> low
  • VLDL -> normal

ApoCII deficiency = same sxs

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9
Q

Hepatic lipase def leads to?

A

Hypertriglyceridemia

-inc duration of LDL and HDL in circulation

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10
Q

How does the chylomicron remnant get into hepatocytes

A

ApoE -> binds to LDLr and LRP

ApoB48 -> bind to LRP

ABSORPTIVE ENDOCYTOSIS

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11
Q

If there is an excess of cholesterol, which enzyme promotes storage?

A

aCAT -> Stimulate production of reesterification to form cholesterol esters (storage form)

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12
Q

What allows LDL to fall of the LDLr in the endosome?

A

-dec in pH which is sensed by the EGF region -> dissociates the receptor from the particle

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13
Q

How can we inc HDL levels?

A
  1. exercise

2. Alcohol

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14
Q

SR-B1

  • where is it found?
  • what role does it play?
A

Found on hepatocytes

Allows for uptake of HDL-2

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15
Q

Role of scavenger receptors in atherosclerosis

A

UNREGULATED uptake of oxidized LDL by macrophages

-receptors are NOT downregulated

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16
Q

Product and substrate for HMG-CoA reductase

A

Substrate - HMG-CoA

Production - Mavalonate

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17
Q

Describe the hypothesis for muscle pain associated with statins

A

Reduction in CoQ10 (ubiquinone) due to decrease in Farnasyl PP

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18
Q

Protein prenylation requires which 2 intermediates of the cholesterol synthesis pathway

A

GPP and FPP

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19
Q

HMG-CoA reductase activity regulation

  • what increase
  • what decreases

What controls rate of synthesis?

A
  1. Insulin -> inc activity by blocking adenyl cyclase
  2. Glucagon and AMP dependent phosphorylation -> decreased activity
    - the phosphorylated form of HMG-CoA reductase in INACTIVE

Rate of synthesis -> SREBP (Sterol levels)

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20
Q

Tangier disease

  • defect
  • inheritance
  • pathognomonic signs
  • presentation
A
  • defect in ABCA1
  • autosomal recessive
  • orange tonsils

Presentation

  • inc level of immature HDL (reduced HDL)
  • inc cellular level of cholesterol esters
  • inc atherosclerosis risk
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21
Q

LCAT deficiency

  • observed effects
  • risk of atherosclerosis?
A

Observed

  • reduced HDL and LDL
  • inc phospholipids

No inc in atherosclerosis

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22
Q

Abetalipoproteinemia

  • defect
  • effects
A

Defect -> MTP
-needed for chylomicron (ApoB48) and VLDL (apoB100) synthesis

Effect

  • low chylomicron and VLDL levels
  • reduced absorption of dietary fats and fat soluble vitamins
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23
Q

Defect in LDL bind to LDLr effects

A

Defective LDLr -> familial hypercholesterolemia

  • achilles tendon xanthoma
  • corneal arcus

-increase serum cholesterol due to inc in serum LDL levels

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24
Q

Hepatic lipase deficiency effects

A

Triglyceride rich HDL and LDL

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25
Q

Dysbetalipoproteinemia

  • defect
  • effects
A

-apo E2 isoform -> doesn’t bind to LDLr properly

Effects

  • elevation of chylomicron and VLDL remnants
  • elevated blood levels of TGs and cholesterol
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26
Q

Fx of PCSK9? implications in controlling cholesterol

A

Binds to LDL + LDLr complex and PREVENTS recycling of the receptor back to the membrane

mAb against PCSK9 dramatically lowers LDL levels

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27
Q

What is the tetrad for metabolic syndrome?

A
  1. Impaired glucose regulation/insulin resistance
    - fasting glucose > 100
  2. Abdominal obesity
  3. High BP
    > 130/85
  4. Hyperlipidemia (
    - High TGs > 150
    - Low HDL < 40 in men and < 50 in women
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28
Q

BMI

  • obese
  • pre-obese
A

OBESE > 30

Pre-OBESE = 25-30

kg/m^2

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29
Q

Summarize relationship between obesity and atherosclerosis

Hint: discuss the effects on increasing BMI

A

Inc BMI -> inc TNF-alpha

Inc TNF-alpha -> inc serum FFAs

  • inc activity of HSL
  • dec activity of LPL

Inc TNF-alpha -> inc IL-6

  • dec in LPL
  • in the liver:
  • > inc TG synthesis -> inc VLDL

VLDL is atherosclerotic

Summary - obesity related hypertriglyceridemia due to:

  • inc synthesis of TG and secretion of VLDL (IL-6)
  • dec in LPL activity (TNF-alpha + IL-6)
  • inc in HSL activity (TNF-alpha)

THIS IS EFFECT IS MOSTLY DUE TO ABDOMINAL (OMENTAL) FAT -> acts more like an endocrine system

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30
Q

Summarize the relationship b/w obesity and insulin resistance (diabetes)

hint: 2 mechanisms stemming from same primary problem

A

Insulin resistance due to INCREASED serum FFAs in basal state leading HIGH levels of insulin (poorly regulated) -> downregulation of insulin receptors

  1. Dec uptake of glucose by muscle -> inc gluconeogenesis using the FFAs
    - inc levels of circulating glucose -> inc insulin secretion
    - dec uptake of insulin by the liver
  2. Inc FFA -> take up by pancreas -> buildup of acetyl-CoA -> conversion of pyruvate to OAA -> INC levels of NADPH -> inc insulin release
    - pancreas becomes insensitive to glucose
    - downregulation of insulin receptors (downstream effects)
    - exhaustion of beta cells in the pancreas
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31
Q

3 categories of afib etiology

A
  1. Conditions that stretch the atria
  2. conditions that irritate the atria
  3. metabolic abnormalities
    - thyrotoxicosis
    - Alcohol
    - Sympathomimetics, theophylline
    - hypoxia
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32
Q

In general, where do the drugs used to control ventricular rate in afib act? Give some examples

A

AV node

  • digoxin
  • diltizem
  • beta blocker
  • amiodarone
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33
Q

Drug used to cardiovert in afib

A

Ibutilide

  • given IV
  • can cause vfib
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34
Q

Features which favor return of NSR

A
  • Reversible precipitating cause
  • Short duration of atrial fibrillation
  • Limited left atrial enlargement (LA <5 cm by echo)
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35
Q

Best drug to maintain NSR in afib

A

Amiodarone

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36
Q

T/F - VF NOT associated w/ acute MI or reversible metabolic/drug cause has a high risk of recurrence

A

TRUE!!!

-30% w/ in 1 year

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37
Q

tx of choice for patients resuscitated from VT/VF?

A

Implantable cardioverter/defib

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38
Q

What’s the cutoff at which an aortic aneurysm has risk of leaking and should be txed?

A

5 cm

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39
Q

Most common site for atherosclerosis

2nd MC?

A

Lower aorta and iliac arteries

2nd - proximal coronary arteries

40
Q

Chronic cocaine use hits which arteries in the heart?

A

Intramural coronary arteries

41
Q

Hypovolemic shock due to what type of infarct

A

Subendocardial infarct

-subendocardial myocardium gets most of O2 from LV lumen -> cells high in glycogen content (huh?)

42
Q

When can a myocardial infarct be seen grossly?

Peak of neutrophilic infiltrate?

highest risk of myocardial rupture?

A

12-24 hours -> light or dark mottling

Days 1-4

Days 4-7

43
Q

Troponin

  • complex specific for myocardium
  • time to become abnormal post MI
  • time to max elevation
  • duration of elevation
A

Troponin I -> myocardium

  • time to become abnormal post MI = 4-6 hours
  • time to max elevation = 14 - 18 hours
  • duration of elevation = 7 - 14 days
44
Q

CK-MB

  • why is it used
  • time it takes to return to normal
A

Used to dx REINFARCTION

Back to normal in 48 hours

45
Q

What is the metabolic regulator involved with matching flow to myocardial oxygen demand

A

ADENOSINE

46
Q

Most common anginal equivalent? more common in males or females?

A

DYSPNEA

-anginal equivalents more common in females

47
Q

NY heart association classification of angina

A

Class I - Ordinary physical activity does not cause angina

Class II - Slight limitation of activity

Class III - Marked limitation of activity
-angina with 1-2 blocks of walking and climbing one flight of stairs

Class IV - Inability to carry on any physical activity without discomfort
-anginal symptoms may be present at rest.

48
Q

Microvascular angina

-patient population

A
  • Peri-menopausal women

* Disease of micro vessel’s inability to vasodilate -> can’t recruit coronary vascular reserve

49
Q

Most sensitive ECG finding for ischemia?

A

ST depression (horizontal)

50
Q

Exercise stress test

  • positive
  • negative
  • non-diagnostic
A
  1. . POSITIVE: ECG: Ischemic ST segment depression - ≥1mm horizontal or downsloping ST depression
  2. NEGATIVE: Patient reaches 85% maximum predicted heart rate (MPHR)* without ST depression
  3. NONDIAGNOSTIC: No ischemia but patient fails to reach 85% of their maximum predicted HR.
51
Q

Tx of chronic stable angina - most drugs designed to:
A) increase supply
B) decrease demand

A

B

52
Q

3 subtypes of acute coronary syndrome

A
  1. Unstable angina
  2. Non-STEMI (NQMI)
  3. STEMI
53
Q

Hallmarks of unstable angina

A
  • Key feature - abrupt new onset of anginal sxs or sudden change in severity of previously stable angina
    * hx is very important
    • New onset of angina = acute coronary syndrome/unstable angina until proven otherwise
      • last month or 2 onset
      • particular focus on accelerated pattern of sxs - this is a clear hallmark of unstable angina
    • High risk of coronary thrombosis if not taken care of
      • Clinical evaluation is EXTREMELY important
54
Q

Non-STEMI presents with?
But does not have?
Difference from unstable angina?

A

Non-STEMI angina WITH positive biomarkers….but WITHOUT total coronary occlusion (no ST elevation, no development of Q waves.)

“interrupted MI”

unstable angina does NOT have pos biomarkers (no necrosis)

55
Q

List 5 things than should be done for initial medical management of unstable angina/Non-STEMI

A

 Inhibit platelet aggregation (ASA)

 Prevent thrombus formation (heparin)

 Maximize supply:
– Nitrates, O2

 Minimize excessive demand
– Pain control (morphine), Beta blocker

 Stabilize plaque -> STATINS

  • 80 mg atorvastatin
  • better blood flow to ischemic beds
56
Q

Fill the blanks:

Women < 55 have (blank) prevalence of CAD but (blank) mortality compared to men

A

LOWER; HIGHER

57
Q

Door to ballon time =

A

60 min

58
Q

Higher risk of arrhythmia (VT/VF) following MI is in patients with?

A

reduced EF (<30%)

59
Q

Complete the sentence:

In civil cases, to show medical malpractice, the standard that the plaintiff has to prove is

A

Preponderance of the evidence

60
Q

What are the 4 criteria to prove medical malpractice

A
  • Breach
    • Damages/harm
    • Causation
    • Duty
61
Q

Is pneumonia an immediate life threatening cause of chest pain?

What are others?

A

NO!

  • acute coronary syndrome
  • pulmonary embolus,
  • aortic dissection,
  • tension pneumothorax,
  • pericarditis with pericardial tamponade,
  • esophageal rupture.
62
Q

Characteristics associated with increased inadvertent discharge of a patient with missed cardiac ischemia (8)

A 
Younger patient age
Atypical symptoms
Women
Nonwhite race
Physician inexperience
Lower-volume EDs
Failure to detect ischemia on initial ECG 
Failure to obtain an ECG
63
Q

Is cocaine a classic risk factor CAD?

List the rest (7)

A

NO!!!

Advanced age
Male sex
Hypertension
Diabetes mellitus
Hypercholesterolemia
Premature CAD in a first-degree relative
Cigarette smoking
64
Q

4 risk factors for CV events that can’t be controlled

A

Father/brother w/ heart disease or stroke before 55

Mother/sister w/ heart disease or stroke before 65

Being male

Early menopause

Age

65
Q

MCC of myocarditis

Describe the postinflammatory possibilites

A

VIRAL

Possibilities

  • return to normal
  • cardiac dilation -> systolic dysfx
  • can also get myocardial fibrosis
66
Q

How can influenza pneumonia cause myocarditis?

A

CYTOKINE RELEASE by macrophages in the lung

67
Q

MCC of myocarditis in infants?

A

Coxsackie virus A and B

68
Q

Which vaccine can cause hypersensitivity myocarditis?

A

Smallpox

69
Q

Most common worldwide cause of restrictive cardiomyopathy?

A

Amyloidosis

70
Q

Differentiate systolic vs diastolic HF w/ regards to EF and contractility

A

Both are normal in diastolic dysfx (compliance prob)

Both are decreased in systolic dysfx (contractility problem)

71
Q

Defective contractile protein associated w/ HCM?

A

beta-myosin heavy chain

72
Q

Most common underdxed condition that affects the heart and leads to HF is

A

systemic htn

73
Q

4 receptors that mediate myocardial hypertrophy

A

AGII, endothelin, insulin-like GF, carditropic cytokines

74
Q

matrix metalloproteinases (MMPs) are involved in which pathology?

A

myocardial remodeling

75
Q

Rheumatic fever

  • causative organism
  • pathogenesis
  • dxic features
  • which valves are hit?
A

ORGANISM
-Group A beta hemolytic streptococci

PATH

  • type II hypersensitivity
  • Abs to M protein x-react w/ self Ags

VALVES

  • mitral - almost always
  • mitral + aortic -> less common

DIAGNOSIS - JONES criteria
-elevated ASO or anti-DNase B titers

FEVERSS
Fever
Erythema marginatum
Valvular damage (vegetation and fibrosis)
ESR
Red-hot joints (migratory polyarthritis) Subcutaneous nodules
St. Vitus’ dance (Sydenham chorea)

ANOTHER MNEMONIC

  • J - joint problems
    • migratory polyarthritis
      • Wrists, knees and ankles
  • O - heart probs
    • Pancarditis
      • All 3 layers of the heart
    • THIS IS THE KEY PROB
  • N - nodules
    • Subcutaneous
  • E - erythema marginatum
    • Appears more red at margins of rash
    • Annular
  • S - sydenham’s chorea
76
Q

Histology for rheumatic fever myocarditis

A
  • Granulomatous w/ macrophages
    * Chronic inflammation
    * Giant cells w/ fibrinoid material
    • Lymphocytes
    • Called Aschoff nodules - pathognomonic for RF
      • REMEMBER THIS
      • Caterpillar nucleus cells are found here
        • Anitschkow cells - enlarged macrophages
          w/ ovoid, wave , rod like nucleus
77
Q

List 3 complications of aortic stenosis

A

LVH

CHF

Impairment of coronary outflow
-syncope w/ exertion

78
Q

Mitral valve prolapse heart sound

More common in men or women

pathology?

A
  • Midsystolic click and late systolic crescendo murmur (click-murmur)
  • > click due to sudden tensing of chordae tendineae (think of parachute opening)

Dec preload -> sound closer to S1
Inc preload -> sound closer to S2

WOMEN > MEN

Myxomatous degeneration of mitral valve

79
Q

Fill in the sentence:

Strains w/ a selective advantage in adhering to (what 3 things) produce disease w/ a lower bacterial inoculum

A

Platelets, fibronectin or fibrin

80
Q

What does the following adhere to?

S. aureus

Oral streptococci

Strep viridans

Candida albicans

A

S. aureus -> fibronectin binding properties

Oral streptococci -> dextran
-also plays role in cavity formation

Strep viridans -> fim A

Candida albicans -> adhesins

81
Q

Blood culture criteria for infectious endocarditis

A

Major blood culture criteria for IE include the following:
• Two separate blood cultures positive for organisms typically found in patients with IE (including viridans streptococci, Streptococcus bovis, Staphylococcus aureus or HACEK* group)

  • Blood cultures persistently posiOve for one of these organisms, from cultures drawn more than 12 hours apart
  • Three or more separate blood cultures drawn at least 1 hour apart

DRAW BLOOD BEFORE GIVING ANTIBIOTICS

82
Q

MC pathogen associated w?

  • native valve IE
  • IE of prosthetic valves
  • IE of IV drug users

Next most common?

A
  • native valve IE -> staph aureus and viridans streptococci
  • IE of prosthetic valves -> Staph epidermidis (coag neg)
  • IE of IV drug users -> staph aureus
  • > less commonly fungi + gm neg bacilli

Next most
Streptococci and enterococci

83
Q

Staph aureus

  • characteristics
  • pathogenesis mechs
A

Gm pos, catalase pos, coag pos

  • Microcapsule
    • prevents phagocytosis
    • adherence
  • Adhesins
    • allow for binding to host cell proteins (damaged tissue)
  • Protein A
    • Messes up the Ab by binding to Fc site
84
Q

Staph aureus

  • colonizers of?
  • primary reservoir?
  • transmission?
A
  • mucosa and skin
  • anterior nares
  • autoinoculation
85
Q

Streptococci - groups

  1. Endocarditis
  2. RF
A
  1. Endocarditis
    - Group D
    - viridans strep (no group) -> alpha hemolysis (INCOMPLETE)
  2. RF
    - Group A
    - beta hemolytic -> COMPLETE HEMOLYSIS
    - M protein = antigenic
86
Q

Enterococci

  • hemolytic?
  • grow in presence of?
  • 2 types of infections they can cause
  • pathogenesis
A
  • non hemolytic (most)
  • grow in presence of salt and bile
  • nosocomial (hospital acquired)
  • endocarditis

BIOFILM production
-resistant to many antimicrobial agents

-found in normal gut flora

87
Q

Strep viridans

  • hemolytic?
  • normal flora?
  • sensitive to which antibiotic
A

alpha hemolytic
-viridans = green

YES - normal flora

PENICILLIN

88
Q

40-60% of native valve endocarditis in community practice due to?

A

Viridans strep and strep bovis

89
Q

List 2 gm neg aerobic bacilli that cause IE

A

Pseudomonas aeruginosa

Enterobacteriaceae
-health care contact

90
Q

Definition of critical aortic stenosis

A

FIXED CO -> no inc on demand

Valve area <0.6cm^2

91
Q

Cardinal sxs of severe/critical aortic stenosis

Implications?

A
  • dyspnea
  • angina
  • syncope

High risk for sudden cardiac death

92
Q

List 3 reasons for syncope w/ critical AS

A
  • Syncope - 3 reasons
    * Extreme LVH -> inc in risk of VT/VF
    * Aortic ring abuts IV septum
   * Calcification get into upper part of IV septum -> heart block 

* Critical AS -> fixed CO
   * Exertion can’t be accommodated by an inc CO
   * Can’t meet the demand
93
Q

Most sensitive for differentiating mild/moderate from critical AS

A

Single S2
-absent aortic component of S2

tighter stenosis -> longer murmur + later peak + softer A2

94
Q

How can you differentiate HOCM from AS?

A

-HOCM
Valsalva -> dec venous return -> dec preload -> inc obstruction of LVOT outlet tract -> INCREASE in intensity of murmur

-AS
Valsalva -> DECREASED intensity of murmur

95
Q

How to conduct a systematic review

  • 5 A’s
  • PICOTT
A 
! Ask
• Define the question
• PICOTT
o Population
o Intervention
o Comparison
o Outcome
o Type of question (therapy, diagnosis, prognosis, harm) o Type of study (i.e. RCC in therapy questions)

! Acquire
• Conduct the literature search

! Appraise
• Apply your own inclusion/exclusion conclusion

! Apply
• Summary effect statement

! Assess? Assess? Anyone? No? Ok.

96
Q

Tests for heterogeneity

I^2 statistics should what percentage?

Z-score

Forest plots

A

I^2 stats
< 40%
-means that studies are low enough to compare

Z-scores
<0.05

Cardiology (6 decks)

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