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AAW - CRAAB 1 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Name a painfull lesions seen on the extremities related to an infectious heart disease, then name that disease

A

Oslers nodes, a type III hypersensitivity, seen in infectious endocarditis

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2
Q

The major and minor duke criteria. And what disease are they for?

A

Major:

  1. Multiple positive blood cultures
  2. Evidence of endocardial involvement (mitral or av regurg)

Minor:

  1. Predisposition (heart valve, iv drug use)
  2. Fever above 38c
  3. Vascular phenomenon (arterial emboli, janeway lesions, however you word it basically peripheral petechiae)
  4. Immunologic phenomenon (oslers nodes, roth spots, rheumatoid factor)
  5. Single blood culture
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3
Q

In what group and how hemolytic is strep pyo

A

Group a beta hemolytic

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4
Q

Most common cause of myocarditis

A

Coxsackie B

Adenovirus

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5
Q

White spots on the retina. What are they called and what disease do you see them in?

A

Roth spots, seen in endocarditis

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6
Q

2 most common alpha hemolytic strep species

A

Strep pneumo and viridians

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7
Q

What holds the cardiac cells together, and also allows action potentials to pass through them? What is the name of the protein that forms these structures?

A

Gap junctions, connexin

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8
Q

What structure between myocytes ensures the mechanical transfer of energy between them?

A

Fascia adherens and macula adherens

Aka desmosomes

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9
Q

Desribe how the pns slows the heart rate

A

Vagus nerve releases ach on the SA node, which:

  • Increases the permeability of the resting membrane to K, allowing the cell to hyperpolarize
  • decreases the current of the funny channels, so they depolarize more slowely
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10
Q

what do you call a compression of the heart caused by fluid in the pericardium

A

cardiac tamponade

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11
Q

The arterial branch that supplies the SA node comes off of which coronary artery

A

Right Coronary artery in 60 percent of people

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12
Q

coronary occlusion is most common in this artery

A

left anterior descending (aka anterior interventricular branch)

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13
Q

What does coronary arterial dominance refer to?

what are the ratios?

A

which artery gives rise to the posterior interventricular artery

70 % right coronary artery
10% left coronary artery (widow maker)
20% co-dominant

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14
Q

where is the great cardiac vain on the heart

A

curves around the left from the sinus and goes with the LAD artery

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15
Q

what is the name of the small outcropped pouch in the left atrium and what muscles are there?

A

Left auricle, pectinate muscles

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16
Q

circumflex artery comes off what

A

left coronary

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17
Q

path of sympathetic nerves that act on the heart

and what they release

A

preganglionic fibers from upper 4 or 5 thoracic spinal segments

synapse in cervical and upper thoracic sympathetic ganglia of sympathetic truck

terminate in SA node and AV node to increase contraction of heart and dilation of coronary arteries.

release NE

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18
Q

Path of the parasympathetic nerves from the CNS to the heart and what they release

A

preganglionic from the vagus

pass through cardiac plexus without synapsing

synapse onto postganglionic neurons in microganglia in the walls of the atria\

release Ach

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19
Q

Three waves of the right atrium on a pressure vs time graph

A

A wave: atrial contraction

C wave: bulging of tricuspid valve into right atrium die to ventricular contraction

V wave: right atrium and central veins re-filling behind closed tricuspid valve

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20
Q

describe the mechanism of S2 splitting

A

When you breath in, you create a drop in pressure in the thoracic cavity. This vaccuum sucks blood from the vena cavas (more so that the pulminary veins) and causes increased preload in the right ventricle, which as a result, closes later than the aortic (this vacuum also causes blood to stay in the lung longer, so there is less filling of the left ventricle)

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21
Q

Does increased preload increase the end diastolic volume?

A

yes.

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22
Q

two ways to measure the Mean Arterial Pressure

A

DP + 1/3 PP (pulse pressure)

or

2/3 DP + 1/3 SP

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23
Q

equation for ejection fraction

A

stroke volume / peak volume

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24
Q

Effect of NE on the heart

there are 5 main ones

A

Increases HR by activating funny channel currents (positive chronotropic effect)

Increases rate of action potential conduction, particularly in AV node by altering conductivity of gap junctions (positive dromotropic effect)

increases the amount that the muscle fibers can contract by activating Ca current and increasing Ca release from the SR (positive inotropic effect)

increase in the rate of cardiac relaxation by increasing Ca reuptake by the SR (positive lusitropic effect)

Decrease in cardiac action potential duration, which promotes realy relaxation via early activation of delayed K current (positive lusitropic effect)

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25
Q

what is the law that says that cardiac output increaces with preload volume?

A

starlings law

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26
Q

when do you need surgery for an aortic dissection and when can you tx it medically

A

arch - surgery

descending - medically treatable

27
Q

Mech of ceftriaxone

A

Binds to DD- transpeptidase (penicilin binding protein), preventing peptidoglycan synthesis

28
Q

Mech of Vancomycin

A

H-bonds with the D-ala-D-alanine modiety on the NAM/NAG peptide, so penicillin binding protein can’t bind it.

29
Q

Mech of penecillin G

A

beta lactamase ring in penicilin binds to the DD-transpeptidase (AKA penicillin binding protein) inhibiting cross-linking and remodeling of peptidoglycan

30
Q

Mech of TPA

A

converts plasminogen into plasmin, which breaks up clots

31
Q

equation to calculate cardiac output aka the fick principle

A

substance consumed = (what goes in (arterial) - what goes out (venous)) * flow

Xtc = (Xa-Xv) * Q

solved for flow rate

Q = Xtc/(Xa-Xv)

32
Q

What is the cardiac index

A

Cardiac output/Body surface area

33
Q

What is the mean electrical axis on an EKG and how do you figure it out (two ways)

A

it is the direction of the dipole that is strongest during the peak of contraction, or the R phase. It is normally between -30 and 90 degrees

2ways:
look at the largest peak and its corrosponding angle on the axial reference system

or the equiphasic approach: find the lead with the most equiphasic QRS complex and determine which lead lies 90 degrees away from it. (and look up that lead’s angle)

34
Q

starlings law

A

as preaload increases, so does stroke volume

35
Q

in a heart muscle pace maker cell contraction, which calcium channels are responsible for the initiation event, and which are responsible for “phase 0” or the action potential

A

transient calcium channels open first at ~30mV, and then the long lasting ones open and cause a full depolarization.

36
Q

How does the AV node slow transmission of the action potential signal?

A

it has fewer gap junctions than the SA node and the atrial myocardium

37
Q

Why is calcium necessary for muscular contraction?

A

It binds troponin, making tropomyosin leave the actin, allowing myosin to bind to actin

38
Q

Laplace law

A

its easier for the heart to contract when it is not fully expanded because there is less tension when it is not fully expanded

Tension = Pressure x Radius

39
Q

Increasing HR by activating funny channel currents would be what type of effect?

A

(positive chronotropic effect)

40
Q

Increasing the rate of action potential conduction, particularly in AV node by altering conductivity of gap junctions would be what type of effect?

A

(positive dromotropic effect)

41
Q

increasing the amount that the muscle fibers can contract by activating Ca current and increasing Ca release from the SR would be what type of effect?

A

(positive inotropic effect)

42
Q

increase in the rate of cardiac relaxation by increasing Ca reuptake by the SR

A

(positive lusitropic effect)

43
Q

Decrease in cardiac action potential duration, which promotes relaxation via early activation of delayed K current

A

(positive lusitropic effect)

44
Q

for pericarditis, what are main causitive organisms

A

coxsackie a or b, echo virus

45
Q

narrow QRS complexes signifies that the abnormility is coming from where in the heart?

A

Atria.

happens in supraventricular tachycardia

46
Q

What kind of murmur do you hear with mitral stenosis? Where is there increased pressure?

A

Diastolic. Flow moves from the atrium to the ventricle during diastole.

increased pressure in the atrium and also in the pulmonary capillaries. usually there is no significant pressure difference between the mitral valve during diastole, but here there is.

47
Q

characteristic clinical signs of aortic insufficiency?

A

low diastolic pressure, large pusle pressure, diastolic murmur

48
Q

Characteristic clinical signs of mitral insufficiency?

A

systolic murmur, may have pulmonary effects like shortness of breath

49
Q

name for nonpainful small hemmorrhagic lesions on palms and soles. commonly seen in what heart condition

A

janeway lesions. acute infectious edocarditis

50
Q

in cardiovascular disease: important virulence factors of Strep Viridans

A

Surface adhesion proteins FimA, GspB

Dextran production / glycocalyx formation

The attachment proteins are widely known as “microbial surface components recognizing adhesive matrix molecules” or MSCRAMMS

51
Q

in cardiovascular disease: important virulence factors of Strep Pneumo

A

Capsule

The attachment proteins are widely known as “microbial surface components recognizing adhesive matrix molecules” or MSCRAMMS

52
Q

in cardiovascular disease: important virulence factors of strep pyo

A

Capsule, M protein

meromyosin in heart valves in the target of anti-M protein self antibodies.

The attachment proteins are widely known as “microbial surface components recognizing adhesive matrix molecules” or MSCRAMMS

53
Q

in cardiovascular disease: important virulence factors of neisseria meningitidis

A

Capsule

54
Q

in cardiovascular disease: important virulence factors of enterococcus species

A

Biofilm formation

55
Q

in cardiovascular disease: important virulence factors of Staph Aureus

A 
capsule
biofilm
elastin, collagen, fibronectin (FnbpA) binding proteins
coagulase
leukocidin

The attachment proteins are widely known as “microbial surface components recognizing adhesive matrix molecules” or MSCRAMMS

56
Q

in cardiovascular disease: important virulence factors of staph epidermidis

A

SD-repeat containing protein-G (SdrG)

Biofilm

57
Q

in cardiovascular disease: important virulence factors of Coxsackie A and B, Adenoviruses

A

coxsackie-adenovirus cellular receptor (CAR) binding proteins that bind directly to heart tissue

58
Q

in cardiovascular disease: important virulence factors of Rickettsia rickettsia

A

OmpA and OmpB

type 4 secretion system (T4SS) used to trick cells into engulfing it.

59
Q

Splanchnic component of the lateral plate mesoderm forms what

A

the visceral layer of the serous membranes covering the lungs, heart, and abdominal organs.

60
Q

what does th epericadioperitoneal canal become?

A

the pleural cavity

61
Q

A Failure of lateral folding of an embryo can cause these defects

A

ectopia cordis with cleft sternum. Heart is outside the thoracic cavity

Congenital umbilical hernia - defect in muscle and connective tissue of anterior abdominal wall. intestines and greater omentum protrude.

Extrophy of the bladder

hemipenis and hemiscrotum

62
Q

During development, which separates the pericadial region from the developing pleural cavity?

What big nerve and vein does it contain?

What part of the pericardium does it form?

A

Pleuropericardial membrane.

Caval vein and phrenic nerve

Gives rise to the fibrous pericardium

63
Q

Congenital diaphragmatic hernia is caused by what. Which side is more common

A

failure of the pleuroperitoneal membranes to fuse with other diaphragmatic components

left side more common because it closes more slowely around the lumbocostal triangle.

64
Q

Where are the myoblasts that make up the transverse septum derived from?

A

cervical myotomes 3,4,5

this is why you get referred pain to the shoulder if your transverse septum is all fucked up.

AAW - CRAAB 1 (8 decks)

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