Brainscape's Knowledge GenomeTM

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


See full index

CVS > Review Q's Week 6 > Flashcards

Review Q's Week 6 Flashcards

1. patho: vasculitis (1-33) 2. pharma dyslipidemia control (34-59) 3. patho lab: vascular diseases (60-68) 4. biochem: energy utilization (69-100) 5. patho lab: lipid disorders (101-114) 6. clinical medicine: choronic myocardial ischemia (115-152)

1
Q

T/F: in vasculitis, the ability of the vessel to hold more blood is increased due to the thickening of blood vessels

A

false, the elastic property of the vessels is lost so it’s blood holding capabilities are hindered

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

Which of the following occur in small vessels?

a. Giant Cell Arteritis
b. Kawasaki Disease
c. Leukocytoclastic Vasculitis
d. Takayasu Arteritis

A

c. Leukocytoclastic Vasculitis

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

60 year-old women comes in complaining of headaches, joint and facial pain, fever, and difficulties with vision. Whats the diagnosis?

A

Giant cell arteritis

(other symptoms include jaw and tongue claudication- pain when eating or chewing)

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

What are different names of giant cell arteritis?

A

Granulomatous arteritis

arteritis cranialis

Horton disease

arteritis of the aged

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

Mechanism of giant cell arteritis. What findings are used to diagnose (4)?

A

Autoimmune reaction to elastic fibers in vessel wall

Panartheritis, aka inflammation involving all layers of an artery

Multinucleated giant cells

thick wall due to infiltrates (neutrophils, etc.)

Fragmented IEL (black coil in picture)

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

In Panartheritis, where does the inflammation start.

A

The inflammation starts in the media, and then spreads to the intima and adventitia- ending up in all the layers

media ⇨ intima & adventitia

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

A 30 year-old women comes in with painful, cool, and pale extremities, dizziness, headaches, chest pain, hypertension, and abdominal pain. Her renin levels are high and angiography is shown below. Diagnosis?

A

takayasu arteritis

(low perfusion to kidneys caused high renin, which increased BP)

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

What is characteristic of Takayasu arteritis?

A

Aneurysm (formation in the coronary vessels)

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

takayasu arteritis is also known as pulseless disease. Why?

A

When it affects the subclavian branch of the aorta, you won’t be able to feel a pulse due to the thickening of the wall, hence the name

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the vessels of takayasu arteritis

A

thick sclerosing vessels with a narrow lumen

Sclerosing arteritis of media ⇨ adventitia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Target population of

giant cell arteritis VS Takayasu arteritis

A

giant cell arteritis= older women (50+)

Takayasu arteritis= younger women (50-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Polyarteritis Nodosa is

a. Granulomas
b. Necrotizing

A

b. Necrotizing

(giant cell arteritis and Takayasu arteritis are A)

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

What causes the inflammation in Polyarteritis Nodosa?

A

its immune (complex) mediated inflammation

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

polyarteritis nodosa affects which parts of the vessel wall?

A

Affects the whole vessel wall; transmural necrotizing arteritis

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

What causes the microaneurisms in polyarteritis nodosa?

A

Segmental inflammation & necrosis ⇨ macrophages clean the necrosis ⇨ healing occurs (fibrin mesh, platelets, collagen) ⇨ the scar tissue is not as flexible/elastic ⇨ microaneurysmsor ruptures ⇨ nodules

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

Whats a characteristic of polyarteritis nodosa?

A

Mural fibrinoid necrosis

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

A four year olf child comes in with conjunctivits, lymphadenopathy, and a strawberry looking toungue + cracked lips. Diagnosis?

A

Kawasaki Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

A biopsy of a 2 year old girl shows bulges on the heart. diagnose and explain.

A

multiple coronary aneurysms formed the bulges on the heart

kawasaki disease

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

Necrotizing arteritis with VS without mucocutaneous lymph node (MCLN)

A

with MCLN= kawasaki disease

without MCLN= Polyarteritis nodosa

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

Symptoms of Kawasaki disease

(+ how do diagnose?)

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

What does Wegener granulomatosis affect?

A

upper/lower respireatory tract

lungs

ear, nose, throat

kidney

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

Patient comes in with nasal passage inflammation, numbness, weakness, scarrying on the foot, and a history of asthma. After further investigation, eosinophil count is high and the scar tissue contains granulomas. Diagnose.

A

Churg Strauss Syndrome

(patients often misdiagnosed with allergies)

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

Antineutrophil Cytoplasmic Antibodies (ANCA) are used to diagnose which types of vasculitis?

A

Wegener granulomatosis

Churg Strauss Syndrome

Leukocytoclastic Vasculitis

Microscopic polyangiitis

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

Patient comes in with palpable purpura. Further tests reveal high ANCA levels. diagnose.

A

Leukocytoclastic Vasculitis

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

vasculitis + respiratory granuloma + no eosinophils=

A

wegner granulomaotosis

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

vasculitis + respiratory granuloma + eosinophils+ asthma=

A

churg strauss syndrome

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

vasculitis + no respiratory symptoms + skin purpura

A

Leukocytoclastic vasculitis

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

T/F: Buerger Disease (Thromboangiitis Obliterans) only affects arteries and veins

A

false, its called “angiitis” and not Arteritis because it affects all kinds of blood vessels, arteries, veins, nerves. the pain is due to the nerve inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Who does Buerger Disease (Thromboangiitis Obliterans) most likely affect? Where?

A

Heavy smokers + young males

affects hands and legs (blood flow blocked due to inflammation, may be blocked to the point of gangrene and amputation)

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

T/F: Thromboangiitis Obliterans is reversible at early stages of the disease if the smokers quit

A

true

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

T/F: Raynaud’s cannot cause ischemia

A

false, secondary Raynaud’s or Raynaud’s Phenomenon can because its accompanied by other conditions

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

Diagnose

A

Buerger Disease

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

Why does Raynaud’s Disease occur?

A

overreaction to cold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

When is endogenous cholesterol synthesis highest?

A

at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Mechanism of action of Statins.

A

Inhibitors of Cholesterol Biosynthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

the rate-limiting enzyme in cholesterol biosynthesis is …

A

HMG-COA reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How do statins cause a decrease in LDL?

A

they stop cholesterol synthesis and the body compensates by making more LDL receptors so they can utilize the LDL’s of the circulation (higher LDL uptake)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When are statins contraindicated?

(adverse side effects=2)

A

in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What’s the most pronounced effect of fibrates?

A

decrease in plasma triglyceride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

first line treatment of primary hypertriglyceridemia.

A

Fibrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

T/F: Fibrates affect both LDL and HDL concentrations

A

true, decrease LDL and increase HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Fibrates are agonists of which receptors? What are these receptors?

A

α peroxisomal-proliferator activator receptors (PPARα), which are nuclear transcription factors that play a role in lipid metabolism

(+ PPARα= + lipid metabolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

3 side-effects of fibrates

A
  1. Cholelithiasis (formation of gallstones),
  2. weight gain
  3. alopecia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Mechanism of action of bile acid-binding resins.

A

Bile acid binding agents are large polymers of hydrocarbons that can bind bile salts and block intestinal absorbtion. (decrease bils salt reabsorbtion)

This causes the liver to start to convert cholesterol into bile acids to compensate, thus decreasing hepatic cholesterol. (LDL is taken from the circulation by the liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

bile acid-binding resins mostly affect which of the following?

a. HDL
b. LDL

A

b. LDL

(May raise HDL levels slightly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Side effects of Cholestyramine + Colestipol

A

GI disturbances such as constipation and bloating

Interfere with absorption of some drugs like warfarin and digitalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Mechanism of action of Ezetimibe

A

inhibit Cholesterol Absorption in the brush border of enterocytes in the duodenum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does Nicotinic Acid reduce plasma levels of VLDL?

A

by inhibiting the synthesis of fatty acids in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How does Nicotinic Acid reduce plasma TG levels?

A

By reducing lipolysis in adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What’s the most effective agent for increasing HDL?

A

Nicotinic Acid (Niacin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

2 side effects of Nicotinic Acid (Niacin)

A

Weight gain due to inhibition of lipolysis

Hyperuricemia precipitates gout.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Mechanism of action of Omega-3-fatty acids

A

Inhibit VLDL and TG synthesis in the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9)?

A

a serine protease involved in cholesterol homeostasis- reducing serum LDL clearance.

(PCSK9 is a serine protease that reduces both hepatic and extrahepatic LDL receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Mechanism of action of Evolocumab

A

Monoclonal antibodies that inhibit PCSK9 have emerged as a new class of drugs that very effectively lower LDL cholesterol levels (by stopping what inhibits the LDL clearance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Which of the following most effectively lowers LDL?

a. Evolocumab
b. Simvastatin
c. Clofibrate
d. Nicotinic Acid (Niacin)
e. Lovastatin
f. Ezetimibe
g. Cholestyramine

A

b. Simvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Which of the following most effectively lowers HDL?

a. Evolocumab
b. Simvastatin
c. Clofibrate
d. Nicotinic Acid (Niacin)
e. Lovastatin
f. Ezetimibe
g. Cholestyramine

A

d. Nicotinic Acid (Niacin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Which of the following most effectively lowers triglycerides?

a. Evolocumab
b. Simvastatin
c. Clofibrate
d. Nicotinic Acid (Niacin)
e. Lovastatin
f. Ezetimibe
g. Cholestyramine

A

c. Clofibrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Which of the following is used to treat combined hyperlipidemia?

a. Evolocumab
b. Simvastatin
c. Clofibrate
d. Nicotinic Acid (Niacin)
e. Lovastatin
f. Ezetimibe
g. Cholestyramine

A

d. Nicotinic Acid (Niacin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

When should Simvastatin be taken and why?

A

at night because that when the endogenous cholesterol synthesis is highest

(they inhibits cholesterol synthesis)

60
Q

Describe the shown coronary lesion

a. a predominantly fibrous plaque
b. a central lipid core covered with a thin fibrous cap
c. a mural thrombus incorporated in a plaque
d. inflammatory infiltrate with giant cells
e. fibrinoid necrosis

A

b. a central lipid core covered with a thin fibrous cap

61
Q

What is the pathological process
in this lesion?

a. Inflammation
b. Edema
c. Congestion
d. Neoplasia
e. Infarction

A

e. Infarction

62
Q

How old is this MI?

a. 1 day
b. 5 days
c. 10 days
d. 30 days

A

c. 10 days

63
Q

What is the lesion pointed to by the arrows?

a. Cardiac hypertrophy
b. Cardiac metastases
c. Cardiac aneurysm and thrombosis
d. Myocarditis
e. Myocardial infarction

A

c.Cardiac aneurysm and thrombosis

64
Q

What is the lesion shown in this coronary section?

a. Intramural thrombus
b. ruptured plaque and occlusive thrombus
c. hemorrhage in a plaque
d. calcified plaque
e. fibro-fatty plaque

A

b.ruptured plaque and occlusive thrombus

65
Q

A patient came in with squeezing chest pain and a first angiogram showed a severe occlusion. A couple of minutes later the pain was gone and a second angiography showed no occlusion. How is this possible?

A

Prinzmetal Angina (Variant Angina)

66
Q

Describe the lesion?

A

largely fibrous atheromatous lesion

67
Q

describe the lesion

A

fatty atheromatous lesion

68
Q

What is Creatine kinase? When does CK increase after an MI?

A

an enzyme found primarily in heart muscle cells

increases in serum within 3 to 6 hours; the peak levels occur between 16 and 30 hours.

69
Q

What precent of the bodies oxygen is used up by the heart?

A

10% of body oxygen consumption

70
Q

Which of the following cardiac energy stores are short-term?
– phosphocreatine
– glycogen
– triacylglycerols

A

– phosphocreatine

keep the heart going for 5 to 10 sec.

71
Q

Which becomes an important energy source in heart failure?

a–Glucose
b–Fatty acids
c– Lactate and Pyruvate
d– Amino acids
e– Ketone bodies

A

e– Ketone bodies

72
Q

What are two heart functions that cause it to need high amounts of energy?

A

ions pumps

+
contractile apparatus

73
Q

Which is insulin insensitive?

GLUT 1 or GLUT 4

A

GLUT 1

74
Q

T/F: lactate is a waste product that’s produced when the heart uses glucose to make ATP

A

false, it’s not a waste product because the heart has O2 and can oxidize lactate to pyruvate, then make more ATP from it via to kerbs cycle

(its a waste product in muscle)

75
Q

How does glucose enter cardiac cells?

A

via GLUT1/4 receptors

they go from high to low concentrations so no energy is needed

76
Q

Low does lactate enter cardiac cells?

A

vis monocarboxylate transporters

77
Q

What’s the main way of cardiac cells to make ATP?

A

oxidative phosphorylation

78
Q

How can the heart utilize triacylglycerol?

A

via lipoprotein lipase activity (has high levels of this enzyme)

79
Q

Which of the following needs oxygen to be able to be converted into ATP?

a. glucose
b. fatty acids

A

b. fatty acids

(A=produce some ATP without using O2)

80
Q

On average, how does the heart produce most of the energy it uses (which method)? Where does it get the energy come from mostly?

A

90% of total myocardial energy produced by oxidative phosphorylation (mitochondria)

20% of energy from glucose and the remainder of energy from fatty acids

81
Q

T/F: as a fetus develops, his heart relies less on fatty acids and more on glucose

A

false, the opposite is true. In fetal life the circulatory load is low and the heart uses glucose (limited oxygen availability), but then with development, the heart load increases and fatty acids are used for energy.

82
Q

Explain what causes the heart to use more glucose as fuel when we’re fed.

A

higher insulin causes GLUT4 (glucose transporters) to bring more glucose into cardiac tissue

the insulin also decreases free fatty acid release from adipose tissue

the insulin also activates ↑ acetyl-CoA carboxylation and thus ↑ malonyl-CoA- this inhibits CPT-1 (which is used to transport fatty acids into the mitochondria for beta oxidization)

83
Q

Explain how the heart uses more fatty acids for fuel when patient is exercising.

A

Exercise uses up ATP→AMP levels increase→that increases AMPK→AMPK inhibits acetyl-CoA carboxylase (which makes acetyl CoA into malonyl CoA)→malonyl CoA decreases (malonyl CoA inhibits CPT-1, which helps fatty acids get into mitochondria)→CPT-1 is more acitve→ more fatty acid beta-oxidation

84
Q

T/F: CPT-1 in the heart is much more sensitive to inhibition by malonyl CoA than liver isoform

A

true

85
Q

What two things activate VS what two things inhibit

Pyruvate dehydrogenase (PDH)

A

activate= Ca + Mg

inhibit= Acetyl-CoA + NADH

86
Q

Pyruvate dehydrogenase (PDH) controls the hearts oxidization of two things.

A

oxidation of glucose and lactate by the TCA cycle in the myocardium

87
Q

Which amino acid gives us pyruvate?

a. aspartate
b. glutamine
c. alanine

A

c. alanine

88
Q

Which type of fuel does the heart work best while using?

A

the heart works best when using a mixture of metabolic fuels

89
Q

Which amino acid gives us fumarate?

a. aspartate
b. glutamine
c. alanine

A

a. aspartate

90
Q

Does oxidative phosphorylation need oxygen?

A

yes

(oxygen is the electron acceptor of complex IV of the electron transport chain…)

91
Q

Which amino acid gives us alpha-ketoglutarate?

a. aspartate
b. glutamine
c. alanine

A

b. glutamine

(glutamine/ glutamate give us alpha ketoglutarate)

92
Q

How does cardiac ischemia cause calcium overload?

A

when oxygen supply drops, we cannot use fatty acid oxidization for fuel, so we use glycolysis (which doesn’t use oxygen and doesn’t produce as much ATP)

Glycolysis produces NADH, which we then re-oxidize into NAD+ by making lactate. The problem starts when lactate (which is acidic) build-up and affects the ion pumps, which then lead to Ca overload.

The pumps that aid in Ca efflux (Na-Ca exchange) also don’t get enough energy to function, so that causes the Ca to stay in the cell and accumulate.

93
Q

Explain reperfusion damage.

(ROS involvement)

A

oxygenated cardiac cells produce antioxidants to protect itself from the free radicals (which damage the cell membrane). But if a patient has an MI (example), the cardiac cells are unable to keep producing the antioxidants- which causes the free radicals (O2) to damage the cell membrane.

When reperfusion occurs and the cells get highly oxygenated blood, free radicals are formed (O2) and they end up damaging the cell membrane even more (no antioxidants to balance out the high oxygen-the antioxidants don’t have time ti be made)

94
Q

T/F: during ischemia, the surrounding cardiac tissue uses fatty acid as fuel

A

true; Fatty acids dominate as a substrate for residual oxidative metabolism due to increased plasma levels of fatty acids

95
Q

During reperfusion which acts as a fuel

a. fatty acid oxidation
b. glucose oxidation

A

a. fatty acid oxidation

The dominance of fatty acid oxidation during reperfusion inhibits glucose oxidation

96
Q

in heart failure, which is the cardiac fuel source?

a. glycolysis
b. fatty acid oxidation

A

a. glycolysis

(due to decreased oxygen availability)

97
Q

Describe the fetal heart metabolic profile.

A

high glycolytic capacity

low mitochondrial oxidation capacity

98
Q

What two conditions copy the fetal heart’s metabolic profile.

A

cardiac hypertrophy and cardiac failure

(high glycolytic capacity+ low mitochondrial oxidation capacity)

99
Q

How is shifting oxidative metabolism from fatty acids to glucose beneficial?

A

– Reduced oxygen requirements

– Reduced accumulation of fatty acids and toxic fatty acid metabolites (in a failing heart, the mitochondria is damaged and cannot oxidize FA, the FA intermediates build up. We switch to glucose use so we stop this build-up)

100
Q

What lifestyle choices may help preserve the heart activity of patients with heart failure?

A

ketogenic diet

(heart then uses ketone oxidization for energy)

** not clear if this is beneficial yet- its in a tafreeg so just ignore this I guess

101
Q

What is this? What does it indicate?

A

arcus senilis

may be a sign of hyperlipidemia

102
Q

What is this?

A

Xanthelasma

(sign of hyperlipidemia)

103
Q
A

Xanthoma

104
Q

How do you calculate the LDL of a fasting patient with triglycerides less than 4.5mM?

A
105
Q

How do you calculate the LDL of a fasting patient with triglycerides more than than 4.5mM?

A
106
Q

Primary VS Secondary dyslipidemia

A

Primary= a genetic defect in the lipid metabolism as a cause of the problem

Secondary= due to another condition (ex/ diabetes)

107
Q

What are the three ways to diagnose acute coronary syndrome?

A

history

ECG

clinical biochemistry

108
Q

What are the three cardiac biomarkers that are important for diagnosing MI?

A

Creatine Kinase (CK)

Aspartate transaminase (AST)

Lactate dehydrogenase (LDH)

109
Q

Which of the following cardiac markers are the first to increase after MI?

a. Creatine Kinase (CK)
b. Aspartate transaminase (AST)
c. Lactate dehydrogenase (LDH)

A

a. Creatine Kinase (CK)

3-8 hours after MI

110
Q

Which of the following cardiac markers is the last to get back to normal after an MI?

a. Creatine Kinase (CK)
b. Aspartate transaminase (AST)
c. Lactate dehydrogenase (LDH)

A

c. Lactate dehydrogenase (LDH)

8-14 days

111
Q

Which Lactate dehydrogenase (LDH) isoform is cardiospecific?

A

LDH1

112
Q

When does AST increase after an MI?

A

6-10 hours

113
Q

Which cardiac biomarkers are used for ACS diagnosis?

A

CK-MB

Troponins

114
Q

When is a troponin test most sensitive?

A

A Troponin T or I taken at 12 hrs post-onset of chest pain is very sensitive

115
Q

stable coronary artery disease vs. acute coronary syndrome

which one has a demand and supply mismatch?

A

both!

but in stable coronary artery disease, the mismatch occurs slowly while in ACS it happens suddenly

116
Q

How do each of these plaque features affect vulnerability?

thickness of fibrous cap

lipid pool size

amount of inflammatory cells

A

fibrous cap= thinner the cap, more vulnerable to rupture

lipid pool size= bigger pool size, more vulnerable to rupture

more inflammatory cells, the more vulnerable to rupture

117
Q

How does mitral regurgitation affect supply/demand of the heart?

A

mitral regurgitation→ increase contractility→ increases the hearts demand for blood

118
Q

How does hypertension affect supply/demand of the heart?

A

hypertension → increasing systolic wall tension→ increases demand

119
Q

How long does the angina have to last for it to be labeled as chronic?

A

2 months

120
Q

What’s the best evaluation method of stable CAD?

A

history!

“It is possible to make a confident diagnosis on the basis of history alone”

121
Q

Typical duration fo ischemic chest pain

A

1-5 minutes

122
Q

What are the three characteristics of typical angina?

(if patient meets all three then definite angina)

A
  1. substernal chest pain (quality= heavy, duration=1-5min)
  2. provoked by exertion
  3. relieved by rest or nitroglycerin
123
Q

What two cardiovascular conditions mimic angina? why?

A

Aortic Stenosis + Hypertrophic Cardiomyopathy
both cause obstruction of flow to outside of the ventricle, causing non CAD angina

124
Q

How do you diagnose patients with stable CAD? What are some obstacles?

A

patients with stable CAD often have normal physical exams and ECG’s

That’s why we do functional tests- to provoke cardiac ischemia by stressing the patient.

We also have anatomical tests (ex/angiography) so we can see the arteries

125
Q

What’s the strongest predictor of long-term survival?

A

LVEF is the strongest predictor of long-term survival as LVEF declines, mortality increases

(Patient with an LVEF <50% is already at high risk for CV death)

126
Q

What patients are recommended for ECG exercise testing?

A
  1. Patients with an intermediate pretest probability of IHD (not a high probability- if high then we don’t need the test)
  2. No major ECG changes or LBBB
  3. Are able to exercise
127
Q

blood pressure changes before and after exercise

in normal patients VS in patients with ischemic heart

A

in normal patients= after exercise BP increase

ischemic heart= BP decreases because heart doesn’t have strength to contract and raise BP

128
Q

You suspect patient of having stable CAD. When do you use…

Coronary computed tomography angiography

VS.

Catheterization & Coronary Angiography

A

CT angiography= its less invasive, so its done for patients with low/intermediate likelihood of CAD- when you’re not certain

Catheter coronary angiography= more invasive and involves catheterization, do it when patient has high CAD risk or taking optimal medical therapy (OMT) fails

129
Q

Which of the following are more sensitive at detecting ischemia?

a. imaging techniques
b. ECG
c. symptoms (ex/angina)

A

a. imaging techniques

(imaging techniques based on perfusion, metabolism or wall motion are more sensitive)

130
Q

patient comes in with substernal chest pain (quality= heavy, duration=1-5min) that is provoked by exertion but NOT relieved by rest. diagnose.

A

atypical angina (2/3 of the three characteristics)

131
Q

calssify the severity of the angina:

patient has marked limitation when climbing one flight of stairs

A

class III

135
Q

Patient does a Stress Radionuclide Imaging and most of the anterior heart tissue appears red. What does this mean?

A

heart muscle tissue with a good blood flow will emit more gamma rays than areas with a poor blood flow or damaged tissue. So his heart has a good blood supply.

136
Q

Stress Radionuclide Image. diagnose.

A

with rest all areas get O2= complete horseshoe

with stress= the apex isn’t getting enough blood

137
Q

How does Stress Echocardiography work?

A

areas of the heart are given numbers (divided into segments), and when patient is exercising we see how each segment moves. (bad movement means ishemia)

hypokinetic means not moving well

akinetic means not moving at all

138
Q

Risk stratification (of CAD) is done by evaluating 4 factors. What are they? how are they tested?

A

1-Risk stratification by clinical evaluation.

2-Risk stratification by ventricular function. (echocardiogram)

3-Risk stratification by response to stress testing.

4-Risk stratification by coronary anatomy. (angiography)

139
Q

Patient has ECG abnormalities, which is a preferred test?

stress imaging OR exercise ECG test

A

stress imaging

St ress Imaging has advantages over conventional Exercise ECG Test because it can be done even if there are resting ECG abnormalities

(exercise ECG test is done if ECG is normal****)

140
Q

Four ways stress imaging is better than exercise ECG

A
  1. can be done even with ECG abnormalities
  2. can be used if patient can’t exercise
  3. better sensitivity and specificity
  4. can quantify and localise ischemia areas
142
Q

Coronary artery bypass surgery uses which two vessels to bypass the blockage?

A

internal mammary artery

saphenous vein

145
Q

Which of the following relief of anginal symptoms by increasing blood supply? How?
• Beta-blockers
• Calcium antagonists
• Nitrates

A

• Nitrates

by decreasing systemic will tension

146
Q

How does each of the following relief angina symptoms?
• Beta-blockers
• Calcium antagonists

A

they both decrease demand of blood by increasing heart rate and contractility

147
Q

first step to treating chronic angina? What happens if patient is resistant?

A

give OMT (optimal medical therapy)

if resistant, revascularize by PCI or CABG

148
Q

can revascularization therapy be used as first line treatment of CAD? if yes, when?

A

As first-line treatment in patients with :

Left main coronary artery disease (50% stenosis or more ).

Multivessel disease with severe or extensive ischemia.

Left ventricular dysfunction with EF of 35–50

150
Q

Why do people suffer silent ischemia? (3 reasons)

A

higher pain threshold

silent episodes reflect less severe ischmia

defect in pain preception

151
Q

How should silent ischemia be managed?

A

managed as angina

152
Q

T/F: Silent ischemia reflects less severe ischemia.

A

true

CVS (13 decks)

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