Brainscape's Knowledge GenomeTM

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


See full index

USMLE step 2 cardiology > cardio 10 > Flashcards

cardio 10 Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

Which type of shock will have increased mixed venous O2 saturation?

A

Septic shock because of increased cardiac output but low tissue oxygen utilization.

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

What is Mvo2 saturation?

A

Venous blood o2 saturation measured in a pulmonary artery by catheter. or
The tension represents the oxygen remaining in the venous bloodstream after the extraction of oxygen by the tissues.

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

What are normal SVCO2 and MSVo2 values?

A

SVCo2–60-80

MSVo2–65–75

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

Svo2 and Scv02 diference?

A

Svo2–Pulmonary artery

Scvo2–Superior venacava

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

What leads to a decrease in ScvO2 and Svo2 values?

A

1) Decrease CO
2) High tissue metabolic rate
3) All other causes factors lead to decrease arterial total oxygen content..

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

What factors will lead to an increase in Svo2?

A

1) High flow state (sepsis, hyperthyroidism, severe liver disease.
2) Increase o2 delivery(high Fio2, hyperbaric 02, and hyperoxia)
3) Low tissue O2 uptake(Anesthesia, hypothermia, and neuromuscular blockade, and severe tisue inflammation)

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

Why is Scv02 < S/Mvo2?

A

The high metabolism of the brain –Low SVC o2 saturation to that of IVC(low lower body metabolism especially kidney)—Low SVCO2 to that of MVO2

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

In which type of shock have high CVP?

A

Cardiogenic

Obstructive

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

In which type of shock have low CVP?

A 
Hypovolemic
Distrubitive (all type)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In which type of shock have High PCWP?

A 
Cardiogenic
Obstructive (Onley In case of pericardial effusion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In which type of shock have Low PCWP?

A 
Hypovolemic
Obstructive(Exept in case of Pericardial temponad)
Distributive all type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In which type of shock have a High cardiac index(LVO)?

A

Distributive (Septic or anaphylactic shock)

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

In which type of shock have a Low cardiac index(LVO)?

A

Hypovolemic
Cardiogenic
Obstructive
Distributive (In case of neurogenic one)

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

In which type of shock have a Low Svo2?

A

Hypolumic
Cardiogenic
Obstractive
Distributive(Nurogenic one)?

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

In which type of shock have a High Svo2?

A

Distributive(exept nurogenic one)

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

Cause of aortic stenosis?

A

3(three)
1-senile calcific aortic stenosis(in age >70)
2-Biscupid aortic valve (the most common cause under the age of 700.
3-Rheumatic fever.

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

What are the components of CHADSVAS?

A 
CHF 
Hypertension
Age>75
Diabetes
STROKE/TIA/TE
Vascular disease(MI, PAD, or aortic plaque)
Age 65-75
Sex(female)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

all score criteria have a value of 1 except?

A

Age >75 and Stroke/TIA/TE which have a value of 2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the preferred treatment for value >=2

A

Non vitamin k dependent oral direct factor X inhibitors(NOAC)–like abixaban,rivaroxaban,dabigatran and endoxaban

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

Why NOAC preferred over warfarin?

A

Same or superior TE preventive effect
Low risk of ICH
Not require follow-Up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ECG future of Atrial Fib?

A

Absent P wave Or replaced by a chaotic fibrillary wave.
Irregular R-R interval
Narrow QRS complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Origin of AFib wave?

A

Pulmonary vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How pulmonary veins act as ectopy despite not have cardiac tissue?

A

Part of left atrial cardiac tissue extends to the pulmonary vein and acts as a spnicter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why this ectopic cardiac tissue is the common location?

A

They have different properties to that of surrounding cardiac tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

The therapeutic value of knowing these foci?

A

In AFib which not respond to medication we do catheter-based radiofrequency ablation–disrupt waves–disconnect the foci area electrical activity from the left atrial myocyte.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

AVNRT ECG future?

A

Narrow QRS interval
Regular R-R interval
Absent /Retrograde P wave
P wave in front or after QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Pathophysiology?

A

Fast (found Superior and posterior to AV node) and slow(found inferior and posterior to AV node, anterior to coronary artery orifice) –form reentrant circuit at the right atrium. But unlike AVRT no pass ventricle by traversing the AV node.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Symptom?

A 
The most common SVT
Palpitation
canon A waves
Hypotension
Lightheadedness
Sudden onset and termination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Risk of chronic venous stasis?

A

Obesity
Advanced age
Previous DVT
Varicose vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pathophysiology?

A

low well tensile strength and venous hypertension–make valve more incompetent–back ward flow–plasma/protein and RBC leak through capillary–Dermatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical manifestation?

A

leg pain(Itchy and achy)
edema(pitting)
venous dilation(varicosities and telegectasis)
ulcer
woody induration and brown discoloration(due to hemosiderin accumulation)?
Ulcer(due to platelet, protein extravasation, and microvascular disease)common in medial malleolus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Management?

A

Leg elevation
Stocking
exercise
Avoiding of prolonged standing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Diagnosis?

A

usualy clinical

Duplex u/s(not done routinley) specialy unilateral one to d/t from dvt

34
Q

what we see on D U/S?

A

Venous HTN

Regurgitsnt flow

35
Q

Necrobiosis lipoidica diabeticorum?

A

Found Inpatient with the diagnosis of DM

May precede DM(screen with HA1C)

36
Q

clinical manifestation?

A

occur commonly in the pretibial area and maybe multifocal

brown dilated blood vessel with central epidermal atrophy.

37
Q

Common S/E of CCB?

A

Peripheral edema

common in dihydropyridine one

38
Q

pathophysiology?

A

precapillary arteriolar dilation—increase hydrostatic pressure

39
Q

management?

A

ACE inhibitors or ARB(Dilate postcapillary venules)

40
Q

what is the common location of edema that occurs secondary to ace inhibitor?

A

Lip, Tongue, Upper airway, and face

41
Q

The complication of vasopressor treatment?

A

Decrease B/F to the periphery

  • -Symetric extremity gangren
  • -Renal Failure
  • -Mesenteric ischemia
42
Q

Does the most common disease occur in the next 5 years with patients having PAD and Have intermittent claudication?

A

MI and stroke(25%)
Death due to CVS event (15-30%)
mentioned as Coronary artery disease equivalent

43
Q

Normal prognosis of PAD in 5 years?

A

70-80 %–remain the same
10-20%–progress to worsening of claudication?
1-2 %–complete ischemia–resting pain, nonhealing ulcer, gangrene–leg amputation

44
Q

High ouput heart failure pathophisiology?

A

Decrease S.vascular resistance—High cardiac output–high venous return–increase preload– LV compensate early by an increased contraction and eccentric hypertrophy latley–LV decompensation lately–peripheral and pulmonary edema.

45
Q

Factors that cause high output HF by what mechanism

A

Decrease S.vascular resistance

46
Q

cause of decrease SVR.

A
  • Increase the quality of pheripherial vesels
  • Bypass of systemic arteriolar resistance
  • Vasodilation due to unmet tissue metabolic demand
47
Q

factors Increase the quality of pheripherial vesels?

A

Morbid obesity

Paget disease

48
Q

factor cause bypass of systemic arteriolar resistance?

A

Congenital AV fistula

Acquired AV fistula–Trauma, Hemodialysis

49
Q

Do factors cause vasodilation due to unmet tissue metabolic demand?

A

Anemia
Hyperthyroidism
Thiamin deficiency

50
Q

Clinical manifestation?

A 
Symptom of HF(both right and left)
Hyperdynamic circulation(increase PP, brisk carotid puls
51
Q

What factor increase mechanical complication occurs after MI?

A

Delay in-stent placment(>=24 Hr) start from symptom

52
Q

What is mechanical complication occurs after MI and their day?

A

Ventricular failure(acute)
Papillary muscle rapture(3-5 day)
Ventricular septum rapture (3 days–5 week)
Fre wall rapture(5-7 day)
Ventricular aneurysm–up to several months

53
Q

VSR symptom?

A

HF(R and L)
Harsh hollo-systolic murmur and thrill
cardiogenic shock
chest pain

54
Q

The common cause of MSK pain?

A

costochondritis

55
Q

clinical manifestation?

A

sharp,localize(CS and CC joint area) pain
aggravated bay movement, cough, and inspiration
localized tenderness and reproduce pain
pain occurs in rest to

56
Q

Management?

A

Reassurance(self-limited, rarely progress to years)

Local or systemic NSAID

57
Q

cause of MR in MI patient

A

Acutely–papillary muscle displacement due to LVM hypokinesis
Late(3-5 day)–papillary muscle rapture

58
Q

Constrictive pericarditis causes?

A

Idiopathic/viral
surgery/radiation
Tuberculosis
Tumor/uremia

59
Q

Clinical manifestation

A

right side HF symptom
pericardial knock
pulses paradoxus
kassmul sighn

60
Q

CXR?

A

pericardial calcification

61
Q

ECHO?

A

atrial enlargement
abnormal septal movment
pericardial thickening

62
Q

ECG?

A

Non-specific
Afib sign
Low QRS voltage

63
Q

jugular venous tracing?

A

rapid x and y decent

64
Q

Laboratory?

A

hypoalbuminemia (due to intestinal lymphangiectasia due to increased CVP –protein-losing enteropathy)

65
Q

Normal JVP?

A

<8 cm H2O

66
Q

Normal serum albumin level?

A

3.4-5.4 mg/dl

67
Q

management of constrictive pericarditis?

A

Diuretic–temporary relief

Pericardiotomy–definitive management for persistent symptoms

68
Q

ISH definition?

A

systolic >140 and diastolic <90

69
Q

a common cause of ISH?

A

Aging due to increasing stiffness in the aortic and arterial wall.

70
Q

Differential for ISH?

A

Disease cause increase pulse pressure

71
Q

How to d/t?

A

In disease cause increase PP there will be a sign of hyperdynamic circulation

72
Q

management of ISH?

A

lifestyle modification

CCB and low dos thiazid

73
Q

Loop diuretics S/E on HF patient.

A

Hypokalemia and Hypomagnesimia

This electrolyte imbalance also potentiate digoxin toxicity

74
Q

Clinical manifestation of systemic amyloidosis?

A

Involve many systems

75
Q

Renal?

A

Heavy proteinuria

pheripherial edema

76
Q

cardiac?

A

restrictive cardiomyopathy
conduction abnormality
low voltage

77
Q

CNS?

A

stroke
autonomic neuropathy
pheripherial neuropathy

78
Q

GI?

A

hepatomegaly
malabsorption and dysmotility
Gi bleeding due to vascular fragility

79
Q

Pulmonary?

A

pulmonary nodule
pleural effusion
tracheobronchial infilitration

80
Q

MSK?

A

Tongue enlargement

Shoulder pad enlargement

81
Q

hematology?

A

Anemia

Thrombocytopnia

82
Q

skin?

A

Thickening of skin
subcutaneous nodule/plaque
ecchymosis
periorbital edema

USMLE step 2 cardiology (16 decks)

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