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USMLE step 2 cardiology > cardio 10 > Flashcards

cardio 10 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.

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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.

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3
Q

What are normal SVCO2 and MSVo2 values?

A

SVCo2–60-80

MSVo2–65–75

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4
Q

Svo2 and Scv02 diference?

A

Svo2–Pulmonary artery

Scvo2–Superior venacava

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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..

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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)

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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

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8
Q

In which type of shock have high CVP?

A

Cardiogenic

Obstructive

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9
Q

In which type of shock have low CVP?

A 
Hypovolemic
Distrubitive (all type)
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10
Q

In which type of shock have High PCWP?

A 
Cardiogenic
Obstructive (Onley In case of pericardial effusion)
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11
Q

In which type of shock have Low PCWP?

A 
Hypovolemic
Obstructive(Exept in case of Pericardial temponad)
Distributive all type
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12
Q

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

A

Distributive (Septic or anaphylactic shock)

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13
Q

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

A

Hypovolemic
Cardiogenic
Obstructive
Distributive (In case of neurogenic one)

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14
Q

In which type of shock have a Low Svo2?

A

Hypolumic
Cardiogenic
Obstractive
Distributive(Nurogenic one)?

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15
Q

In which type of shock have a High Svo2?

A

Distributive(exept nurogenic one)

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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.

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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)
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18
Q

all score criteria have a value of 1 except?

A

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

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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

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20
Q

Why NOAC preferred over warfarin?

A

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

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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

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22
Q

Origin of AFib wave?

A

Pulmonary vein

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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.

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24
Q

Why this ectopic cardiac tissue is the common location?

A

They have different properties to that of surrounding cardiac tissue.

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25
The therapeutic value of knowing these foci?
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.
26
AVNRT ECG future?
Narrow QRS interval Regular R-R interval Absent /Retrograde P wave P wave in front or after QRS
27
Pathophysiology?
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.
28
Symptom?
``` The most common SVT Palpitation canon A waves Hypotension Lightheadedness Sudden onset and termination ```
29
Risk of chronic venous stasis?
Obesity Advanced age Previous DVT Varicose vein
30
Pathophysiology?
low well tensile strength and venous hypertension--make valve more incompetent--back ward flow--plasma/protein and RBC leak through capillary--Dermatitis.
31
Clinical manifestation?
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.
32
Management?
Leg elevation Stocking exercise Avoiding of prolonged standing
33
Diagnosis?
usualy clinical | Duplex u/s(not done routinley) specialy unilateral one to d/t from dvt
34
what we see on D U/S?
Venous HTN | Regurgitsnt flow
35
Necrobiosis lipoidica diabeticorum?
Found Inpatient with the diagnosis of DM | May precede DM(screen with HA1C)
36
clinical manifestation?
occur commonly in the pretibial area and maybe multifocal | brown dilated blood vessel with central epidermal atrophy.
37
Common S/E of CCB?
Peripheral edema | common in dihydropyridine one
38
pathophysiology?
precapillary arteriolar dilation---increase hydrostatic pressure
39
management?
ACE inhibitors or ARB(Dilate postcapillary venules)
40
what is the common location of edema that occurs secondary to ace inhibitor?
Lip, Tongue, Upper airway, and face
41
The complication of vasopressor treatment?
Decrease B/F to the periphery - -Symetric extremity gangren - -Renal Failure - -Mesenteric ischemia
42
Does the most common disease occur in the next 5 years with patients having PAD and Have intermittent claudication?
MI and stroke(25%) Death due to CVS event (15-30%) mentioned as Coronary artery disease equivalent
43
Normal prognosis of PAD in 5 years?
70-80 %--remain the same 10-20%--progress to worsening of claudication? 1-2 %--complete ischemia--resting pain, nonhealing ulcer, gangrene--leg amputation
44
High ouput heart failure pathophisiology?
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
Factors that cause high output HF by what mechanism
Decrease S.vascular resistance
46
cause of decrease SVR.
- Increase the quality of pheripherial vesels - Bypass of systemic arteriolar resistance - Vasodilation due to unmet tissue metabolic demand
47
factors Increase the quality of pheripherial vesels?
Morbid obesity | Paget disease
48
factor cause bypass of systemic arteriolar resistance?
Congenital AV fistula | Acquired AV fistula--Trauma, Hemodialysis
49
Do factors cause vasodilation due to unmet tissue metabolic demand?
Anemia Hyperthyroidism Thiamin deficiency
50
Clinical manifestation?
``` Symptom of HF(both right and left) Hyperdynamic circulation(increase PP, brisk carotid puls ```
51
What factor increase mechanical complication occurs after MI?
Delay in-stent placment(>=24 Hr) start from symptom
52
What is mechanical complication occurs after MI and their day?
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
VSR symptom?
HF(R and L) Harsh hollo-systolic murmur and thrill cardiogenic shock chest pain
54
The common cause of MSK pain?
costochondritis
55
clinical manifestation?
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
Management?
Reassurance(self-limited, rarely progress to years) | Local or systemic NSAID
57
cause of MR in MI patient
Acutely--papillary muscle displacement due to LVM hypokinesis Late(3-5 day)--papillary muscle rapture
58
Constrictive pericarditis causes?
Idiopathic/viral surgery/radiation Tuberculosis Tumor/uremia
59
Clinical manifestation
right side HF symptom pericardial knock pulses paradoxus kassmul sighn
60
CXR?
pericardial calcification
61
ECHO?
atrial enlargement abnormal septal movment pericardial thickening
62
ECG?
Non-specific Afib sign Low QRS voltage
63
jugular venous tracing?
rapid x and y decent
64
Laboratory?
hypoalbuminemia (due to intestinal lymphangiectasia due to increased CVP --protein-losing enteropathy)
65
Normal JVP?
<8 cm H2O
66
Normal serum albumin level?
3.4-5.4 mg/dl
67
management of constrictive pericarditis?
Diuretic--temporary relief | Pericardiotomy--definitive management for persistent symptoms
68
ISH definition?
systolic >140 and diastolic <90
69
a common cause of ISH?
Aging due to increasing stiffness in the aortic and arterial wall.
70
Differential for ISH?
Disease cause increase pulse pressure
71
How to d/t?
In disease cause increase PP there will be a sign of hyperdynamic circulation
72
management of ISH?
lifestyle modification | CCB and low dos thiazid
73
Loop diuretics S/E on HF patient.
Hypokalemia and Hypomagnesimia | This electrolyte imbalance also potentiate digoxin toxicity
74
Clinical manifestation of systemic amyloidosis?
Involve many systems
75
Renal?
Heavy proteinuria | pheripherial edema
76
cardiac?
restrictive cardiomyopathy conduction abnormality low voltage
77
CNS?
stroke autonomic neuropathy pheripherial neuropathy
78
GI?
hepatomegaly malabsorption and dysmotility Gi bleeding due to vascular fragility
79
Pulmonary?
pulmonary nodule pleural effusion tracheobronchial infilitration
80
MSK?
Tongue enlargement | Shoulder pad enlargement
81
hematology?
Anemia | Thrombocytopnia
82
skin?
Thickening of skin subcutaneous nodule/plaque ecchymosis periorbital edema

USMLE step 2 cardiology (16 decks)

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