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CR&R > CR&R Final > Flashcards

CR&R Final Flashcards

1
Q

What is shown here in this photo? What may it increase the risk of?

A

Ventricular fibrosis (likely secondary to MI, dead tissue -> replaced with fibrotic tissue)

It can increase the risk of systemic thromboembolism (dead tissue doesn’t contract, leading to blood pooling)

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2
Q

What additional anatomic abnormality is found in 5% of patients with a bicuspid aortic valve?

A

Coarctation of the aorta

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3
Q

How can aortic stenosis and a bicuspid aortic valve be differentiated?

A
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4
Q

How can rheumatic fever and rheumatic heart disease be differentiated?

A
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5
Q

What are these three histological features from left to right? What disease are they associated with?

A
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6
Q

What acronym is used to describe the symptoms of infective endocarditis?

A
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7
Q

What are major differences between valve damage in RHD vs IE?

A

RHD- mostly along closure line, no chordae tindinae involvement

IE- More clumped, can destroy, vegetate CT

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8
Q

What type of cardiomyopathy can be precipitated by ethanol?

A

Dilated cardiomyopathy

*Anthracyclines (doxorubicin) are another common cause of DCM

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9
Q

Identify the diferent CM and their features using this chart:

A

Good job!

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10
Q

What is cystic medial degeneration? What 3 CT disorders is it seen in? What additional two pathologies? What is the main cause of myxoid degeneration?

A
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11
Q

Where are arterial plexiform lesions seen?

A

Pulmonary hypertension

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12
Q

What finding is characteristic of the exudative phase of ARDS?

A

Alveolar hyaline membranes

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13
Q

Which respiratory tract structure is most affected by emphysema due to smoking?

A

Respiratory bronchiole (centriacinar pattern affects respiratory bronchiole more than alveolar duct, which would be more affected in panacinar pattern from a1anti-trypsen deficiency)

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14
Q

What are major differences between centriacinar and panacinar emphysema?

A
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15
Q

What are the two notable subtypes of NSIP pattern?

A

Cellular (left)
Fibrotic (right)

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16
Q

What characteristic of end stage lung disease is seen here?

A

Honeycomb lung

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17
Q

Which arrow represents subepithelial space? Which represents subendothelial space (for deposits)?

A

Blue- Subendothelial
Purple- Subepithelial

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18
Q

What patient population would be at highest risk for a BK polyomavirus infection?

A

A kidney transplant patient (immunocompromised)

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19
Q

Which of these pictures of acute pyelonephritis? Which is chronic?

A

Chronic pyelonephritis (left)- Not as many WBC casts, mostly lymphocytes in interstitium

Acute pyelonephritis (right)- Neutrophils in the tubular lumen (contributing to WBC casts)

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20
Q

What type of pyelonephritis is visible here?

A

Chronic pyelonephritis

*Note prominant scarring

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21
Q

What type of renal artery stenosis is seen here?

A

Fibromuscular dysplasia

*Most commonly seen in young to middle-aged women

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22
Q

What is the most common disease cause of full house immunofluorescence?

A

Systemic lupus erthematosus

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23
Q

What tumor is characteristic of a triphasic appearance? What are the three layers? What do abnormally large, hyperchromatic cells (right) indicate about that particular Wilm’s tumor?

A

Wilm’s tumor (epithelium, blastema, stroma)

Anaplasia: Most common in P53 mutations. resistance to chemotherapy

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24
Q

Irregular spikes on silver stain are most indicative of what pathology?

A

Membranous glomerulonephropathy

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25
Q

How does the gross presentation help to differentiate between oncocytoma and chromophobe carcinoma?

A

The classic brown color of the renal tissue

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26
Q

Glycosuria can be associated with what two conditions?

A

Diabetes mellitus
Fanconi syndrome

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27
Q

What effect will NE have on HR, BP, and SVR?

A

BP and SVR: Increased
HR: Decreased due to reflex bradycardia

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28
Q

Will the urine Na+ be high or low in SIADH?

A

Normal Na+ in urine (just ADH secreted abnormally, not aldosterone)

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29
Q

What syndrome can directly result from a bad PE?

A

ARDS

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30
Q

A systolic murmur with a blurred S2, which is reduced by handgrip is indicative of what valvular disease?

A

Aortic stenosis

31
Q

Why does a handgrip/valsalva maneuver decrease the murmur in aortic stenosis?

A

The increased SVR translates to a higher afterload, with the ventricles unable to eject their normal amount of blood, which reduces the flow over the stenotic valve

32
Q

A late systolic ejection murmur usually has what etiology?

A

Mitral valve prolapse (Barlow’s syndrome)

*A notable feature of Marfan’s syndrome

33
Q

What can help to increase the intensity of a late systolic ejection murmur such as that due to mitral valve prolapse?

A

Squatting, which increases preload and LV volume in order to better exaggerate the murmur

34
Q

Using Left ventriular pressure versus atrial pressure, when does tension near its maximum?

A

As LV pressure > atrial pressure

35
Q

What are the four types of shock?

A

Hypovolemic
Cardiogenic
Distributive
Obstructive

36
Q

What are the expected changes in RAP, SVR, and CO in hypovolemic shock?

A

Increased: SVR
Decreased: RAP, CO

37
Q

How is hypovolemic shock treated?

A

Restore normal volume status (i.e. isotonic IV fluids, blood products etc)

38
Q

What is the expected change in PCWP, SVR, and CO in cardiogenic shock?

A

Increased: PCWP, SVR
Decreased: CO

39
Q

What is the treatment for cardiogenic shock?

A

1) Improve contracility with inotropes (dobutamine)
2) Diuresis
3) PCI for acute MI, or mechanical circulatory support in HF

40
Q

What are the expected changes in RAP, SVR, and SvO2 in distributive shock?

A

Increased: SvO2
Decreases: RAP, SVR

41
Q

What is distributive shock?

A

Hemodynamic derangement of inability to maintain vascular tone (low arteriolar/venous tone/low DBP)

42
Q

What are the three classic types of distributive shock?

A

1) Septic shock
2) Anaphylactic shock
3) Neurogenic shock

43
Q

What are the three treatments for septic shock?

A

1) Antimicobials to target infection ASAP
2) Increase preload with Iv fluids (i.e. LR)
3) Increased MAP with vasopressors (NE is first line)

44
Q

How can anaphylaxis lead to shock?

A

IgE binds to mast cells/basophils leading to massive histamine release -> dilation of arterioles and veins, tachycardia, hypotension etc

45
Q

How is anaphylactic shock treated?

A
46
Q

What is neurogenic shock? How is it diagnosed? How is it treated?

A
47
Q

What are the expected changes in RAP, SVR, and CO in obstructive shock?

A

Increased: RAP, SVR
Decreased: CO

48
Q

What are three possible causes of obstructive shock?

A
49
Q

What are the appropriate treatments for the three possible causes of obstructive shock?

A
50
Q

Why does hyperkalemia lead to the changes on MAP seen in A (black is normal, green is hyperkalemia)?

A

Hyperkalemia increases the resting MP from around -85 to less negative (maybe -60) and thus repolarization is achieved more quickly

51
Q

What pathways (G protein and second messenger) are used by alpha 1 and 2 as well as beta 1 and 2 receptors?

A
52
Q

What are the four classic features of tetrology of fallot?

A
53
Q

What are the different criteria used to diagnose RHD from IE?

A

RHD: Jones criteria
IE: Duke criteria

54
Q

What is the acronym used to remember the symptoms associated with IE?

A
55
Q

Which type of cardiomyopathy is more associated with an S3 heart sound? Which is associated with an S4?

A

DCM: An S3 can often be auscultated

HCM: An S4 can often be auscultated

56
Q

What is one common manuever to treat SVT and one common pharmacologic intervention?

A

Carotid massage

Adenosine

57
Q

What are the four stages of heart failure? What are criteria for each stage?

A
58
Q

What are the four classes of HF according to the NYHA?

A
59
Q

What are two characteristic features on atrial fibrillation on EKG?

A

1) No visible P waves
2) Irregularly irregular rythym

60
Q

What type of medication can cause the change in ventriclar myocyte action potentials as seen here? Give one example. What result is seen on EKG?

A
61
Q

What type of medication can cause the change in SA nodal cell action potentials as seen here? Give one example. What result is seen on EKG?

A
62
Q

What type of medication can cause the change in SA nodal cell action potentials as seen here? Give one example. What result is seen on EKG?

A
63
Q

What type of medication can cause the change in ventriclar myocyte action potentials as seen here? Give one example. What result is seen on EKG?

A
64
Q

How can diuretics lead to contraction alkalosis? What effect does alkalemia have on potassium-hydrogen ion exchange?

A
65
Q

What type of medium-vessel vasculitis is most likely given this presentation? What lab findings would be significant? What disease is it associated with? What is the most likely complication?

A

1) Polyarteritis Nodosa
2) Elevated ESR, possibly creatinine and BP as well
3) Hepatitis B
4) Pseudoaneurysm

66
Q

What heart disease is characterized by an anterior displacement of outflow tract portion of the IV septum?

A

Tetrology of Fallot

67
Q

What are the 5 T’s of Cyanotic CHD?

A
68
Q

What is the medication of choice in ToF patients to decrease their R to L shunt?

A

Phenylephrine

69
Q

What is a TET spell? Treatment involves increasing or decreasing SVR? What about PVR? What are four treatments?

A
70
Q

What mutations cause Down syndrome, Turner syndrome, and DiGeorge syndrome? What heart defects are common in each of these?

A
71
Q

What is Eisenmenger syndrome? What type of shunt is involved? What resulting acute complication can result?

A
72
Q

Using the table, recall the formulas for:
EER
CER
RR
RRR
RRI
ARR
ARI
NNT
NNH

A
73
Q

What pathology is indicated by the EM image shown?

A
74
Q
A

CR&R (8 decks)

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