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USMLE CAARDIOVASCULAR > PATHOLOGY > Flashcards

PATHOLOGY Flashcards

1
Q

What is the arterial structure? and how is it made off?

A
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2
Q

Type of arteries?

A
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3
Q

What are the most affected arteries by atherosclerosis

A
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4
Q

Name the 3 key concept for atherosclerosis formation

A
  1. Endothelial damage
    a. HTA
    b. tabaco
    c. LDL
    d. turbulent flow
  2. Chronic inflammation
    Macrophages release cytokines
  3. Smooth muscle proliferation
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5
Q

What is the key growth factor that make smooth mm proliferate?

A
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6
Q

Types oh hemorrhagic isquemia

A
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7
Q

Pathogenesis of atherosclerosis

A
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8
Q

Name the 5 organs and their regions more affected by isquemia

A
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9
Q

Which section is the most prone to produce isquemia?

A

B. Fibrous cap

Thin fibrous cap with weak connective tissue are prone to produce isquemia.

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10
Q

What are the cells we can find here?

A

Dark blue: fibrous cap
Pale area: Macrophages filled with lipid

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11
Q

% of obstruction of coronary lumen to produce estable angina

A
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12
Q

Why people with coronary aa disease sudden deaths?

A

Arrrythmias

Develop Ventricular taqycardias or AF

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13
Q

Risk factors for developing coronary aa disease?

A

Hypertension
hyperlipidemia
Family history (1 relative, F lees 60 and male less 50)
Smoking
Obesity

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14
Q

What is the extent of the coronary ischemia?

A
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15
Q

Ischemic changes in EKG in NSTEMI

A

T inversions
ST Depressions

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16
Q

What are the gross changes expected in myocardial infarction?

A
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17
Q

What are the acute complications myocardial infarction?

A
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18
Q

What valve is affected in inferior infarcts?

A

Mitral valve because it attaches to the inferior wall if the left ventricle

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19
Q

Complications of stent colocation¨:

A
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20
Q

What are the coronary arteries territories?

A
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21
Q

What are the 2 hallmarks of right ventricular infarction?

A
  1. Elevated jugular venous pressure
  2. Hypotension: decreased preload
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22
Q

What is a special complication of MI infarctions?

A
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23
Q

What does an elevated AVR means?

A
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24
Q

What is the difference between a posterior and a inferior infarction?

A

Posterior: It just affects the Posterior descending artery

Inferior: Affects the dominant artery

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25
Q

Explain the 2 special types of infarctions:

A
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26
Q

Treatment for STEMI

A

Thrombotic problem:
1. Aspirin: reduce platelet agreggation
2. Heparin: inhibit clots

Ischemic problem
1. BB: reduce oxygen demand
2. Nitrates

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27
Q
A
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28
Q
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29
Q
A
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30
Q

Type of angina:

A
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31
Q

Describe the type of pain, biomarkers, ecg changes and infarction:

A
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32
Q

Causes of sudden cardiac death?

A
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33
Q

Diagnosis of miocardial infarction:

A
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34
Q

ECG locations of STEMI

A
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35
Q

What are NSTEMI ECG changes observed?

A
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36
Q

Name the biomarkers in cardiac ischemia and hrs

A
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37
Q

Types of CK? Where we can find them

A
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38
Q

What is a rare myocardial biomarker found?

A
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39
Q

What is the treatment of NSTEMI?

A
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40
Q

What is unstable angina?

A
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41
Q

What is the tx of unstable angina?

A
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42
Q

Complications of myocardial infarction

A
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43
Q

How can we diagnose stable angina?

A
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44
Q

Whats a key feature of stable angina.

A
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45
Q
A
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46
Q

Mechanism of action of nitrates

A
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47
Q

Explain the relationship of nitrates and stable angina

A

Nitrates vasodilate specially vv that helps lower the preload (benefits)

Lesser degree is vasodilate aa supplying more blood to the myocardium.

In complex CAD….

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48
Q

What are the forms of nitrates (4)

A
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49
Q

Adverse effect of nitrates:

A
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50
Q

What is the nitrate withdrawal syndrome?

A
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51
Q

BB and stable angina

A
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52
Q

Name 2 B1 cardioselective drugs

A

Atenolol
Metoprolol

DIOSA ATENEA (MEDUSA) LE METEMOS UN CORAZON!

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53
Q

Types of calcium channel blockers

A
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54
Q
A
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55
Q
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56
Q
A
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57
Q

What is ranolazine?

A
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58
Q

What is the fear effect of ranolazine?

A
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59
Q

Diagnosis of prinzmetal angina

A
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60
Q

Treatment of prinzmetal angina

A
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61
Q

What do we mean by coronary steal?

A
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62
Q

Name the nitrates and onset of effect

A
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63
Q

What is the mechanism of action of nitrates?

A

Mechanism of action: nitrates and phosphodiesterase-5 inhibitors

Exogenous nitrous oxide (NO) activates guanylyl cyclase, resulting in activation of protein kinase G. There is a reduction in intracellular calcium as a result of increased sarcoplasmic reticulum calcium ATPase (SERCA) and an increase in myosin-light-chain-phosphatase (MLCP) activity, resulting in smooth muscle relaxation. The net result of both pathways is vasodilation

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64
Q

Adverse effects of nitrates?

A
  1. Vasodilation
    a. headache
    b. flushing
    c. Reflex tachycardia
  2. Tolerance. To avoid need a min 8 hrs free intervals
  3. Cyanide poisoning. Sodium nitroprusside
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65
Q

What time most it elapses to take PDE 5 inhibitor and nitrates?

A

24 hrs

Cyclic GMP causes smooth muscle relaxation and subsequent vasodilation. Nitrates increase cGMP via increased intracellular NO. PDE-5 inhibitors decrease the metabolism of cGMP to GMP. Taking both medications together leads to significantly increased cGMP-induced vasodilation.

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66
Q

Name 4 cardioselective BB

A
  1. Atenolol
  2. Metoprolol
  3. Bisoprolol
  4. Esmolol

Diosa atenea (medusa) le meten un corazon y luego las servientes se vuelven viejitas y le sale una E en la cabeza.

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67
Q

Name 3 BB no cardioselectives and its adverse effects

A

TIMMY CON UN COHETE EN EL FUNDIO Y LUEGOOO CAE EN EL MAR Y NADA!! SOLO NADA!!

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68
Q

Name 3 uses of propanolol and 1 for timolol

A
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69
Q

Name 2 BB no selective with alpha effect

A
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70
Q

What are the effect B receptor blockage?

A
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71
Q

Classification of calcium channel blockers and agents:

A

Dihidropiridinicos: Ricardo con la esposa y amor rojooooooos

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72
Q

Mechanism of action of calcium channel antagonism

A

CCBs bind to and block L-type calcium channels in cardiac and vascular smooth muscle cells; → decreased frequency of Ca2+ channel opening in response to cell membrane depolarization; → decreased transmembrane Ca2+ current

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73
Q

Verapamil mainly act on ____________

A

VENTRICLES

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74
Q

Adverse effects of calcium channel antagonism

A
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75
Q

In what phase of the myocadiac cells act BB

A
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76
Q

A postural tremor that improves with alcohol consumption is characteristic of _________________.

A

Essential tremor

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77
Q

GLUCAGON
In patients with beta-blocker overdose, intravenous glucagon should be administered when blood pressure and heart rate do not respond sufficiently to IV fluids and atropine alone. Glucagon increases intracellular cAMP by activating adenylate cyclase, which improves cardiac contractility and heart rate while bypassing the beta receptors. It also improves hypoglycemia.

A
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78
Q

Nicardipine belongs to ________________ family.

A

Calcium channel blockage dyhidropyridinicos.

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79
Q

What are the rates of the pacemakers?

A
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80
Q

What is the normal QRS complex?

A
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81
Q

How to read axis in ecg

A
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82
Q

What does a right or left axis deviation means?

A
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83
Q

What causes short PR intervals?

A

Wolf parkinson white?

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84
Q

What causes short and prolonged QT intervals?

A
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85
Q

What is torsade de pointes and causes?

A
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86
Q

What causes the long QT syndrome?

A
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87
Q

Ways to acquire prolonged QT syndrome?

A
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88
Q

When we found T waves?

A

hyperkalemia

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89
Q
A
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90
Q

Explain the myocyte action potential

A
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91
Q

Explain phase 4 myocyte action potential

A
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92
Q

Explain phase 0 myocyte action potential

A
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93
Q

Explain phase 1 myocyte action potential

A
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94
Q

Explain phase 2 myocyte action potential

A
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95
Q

Explain phase 3 myocyte action potential

A
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96
Q

What is the refractory period?

A
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97
Q

Explain the pacemaker action potential

A
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98
Q

What are the 2 family drugs that affect the pacemaker action potential?

A
  1. Calcium channel blocker
  2. BB
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99
Q

Flecainide belongs to ___________________ family

A

Sodium channels blocks…. first antiarrhythmyc class

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100
Q

What gives the property of automaticity in pacemakers action potential?

A

Funny current

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101
Q

Family of epinephrine and mechanism of action?

A

like epinephrine stimulate beta 1 adrenergic receptors in the heart, thereby increasing Ca2+ influx through the sequential opening of T-type calcium channels and L-type calcium channels in the sinoatrial node and atrioventricular node in the late part of phase 4 of the pacemaker action potential (AP). Catecholamines also increase the flow of Na+ through pacemaker channels (funny channels; If). These effects lead to more rapid depolarization, which increases heart rate. Other effects of epinephrine are mediated through beta 2 adrenergic receptors (bronchial relaxation) and alpha 1 adrenergic receptors (vasoconstriction), which ease breathing and stabilize blood pressure in anaphylactic shock, respectively.

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102
Q

Pnemotecnia for pacemakers action potential phase

A

403

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103
Q

Mechanism of action of adrenaline and norepinephrine

A
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104
Q

Uses of BB antiarrhythmics

A
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105
Q

Adverse effects of BB

A
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106
Q

What is the antidote of BB overdose?

A
107
Q
A
108
Q

What is the effect of K channel blockers in ecg?

A
109
Q

Family and mechanism of action of amiodarone

A
110
Q

Side effects of amiodarone

A
111
Q

Family and mechanism of action of dromeradone?

A
112
Q

Family and mechanism of action of sotalol

A
113
Q
A
114
Q

What is the ecg effect of class 4 antiarrhytmics

A
115
Q

Indications of verapamil

A
116
Q

Side effects of calcium channel antagonism

A
117
Q

Name the miscellaneous antiarrhythmics

A
  1. Adenosine
  2. Digoxin
  3. Magnessium
118
Q

What is the mechanism of action of adenosine?

A
119
Q

Indications of magnessium?

A
120
Q

Why there is a straight line in the PR

A

The signal must past throught all the conduction system
AV node, HIZ, bunddle branches and purkinje

121
Q

What are the causes of AV blocks?

A

AV node: disease
HIZ-Purkinje disease

122
Q

Explain the types of AV blocks

A
123
Q

Explain 1st degree AV block

A
124
Q

Explain 2nd degree Mobitz1 AV block

A
125
Q

Explain 2nd degree Mobitz 2 AV block

A
126
Q

Explain 3erd degree block

A
127
Q

Explain AV blocks and lyme disease

A
128
Q
A
129
Q

Causes of AV blocks

A

aging=fibrosis/sclerosis

130
Q

Treatment for AV blocks

A
131
Q
A
132
Q
A
133
Q
A
134
Q
A
135
Q

What determines the heart rate in tachycardias?

A
136
Q

___________ (disease) is associated with FA?

A

Hyperthyroidism

137
Q

Triggers for FA?

A
138
Q

What is the basics in treatment of FA?

A
139
Q
A
140
Q

Talk about cardioversion

A

80% resolves with electrical cardioversion. Quimical cardioversion has too much adverse effects.

141
Q
A
142
Q

Explain the CHADSVASC score

A

Equal or more than 2: anticoagulant
less: aspirin

143
Q

Explain the pulmonary vein isolation procedure, when we do it? and why?

A
144
Q

What is the treatment of atrial flutter?

A
145
Q

Explain the atrial flutter ablation

A

burn

146
Q

Explain the pathways of coagulation cascade

A

JESUS CON SU CORONA DE ESPINAS SANGRANDO MORADO LE OTORGA A MI ABUELO KUBALA EL NUMERO 7 ESTE CON SU RODILLA RASPADA CON LA LETRA E PATEA UNA PELOTA DE SOCCER Y GOLPEA EL 10

147
Q

Why thrombin is said to be like an accelerator?

A
148
Q

Function of antithrombin and where it is produced?

A
149
Q

Types of heparins?

A
150
Q

What is the difference in function of heparins? LMWH and HMWH

A
151
Q

What are the PROS of LMWH?

A
152
Q

Whay is fondaparinux?

A
153
Q

Uses of heparin?

A
154
Q

What is the exam that RUTH was fucked up by in internal medicine? What does it valorates? and what is normal values?

A

aTTP

Activated partial thromboplastin time.

NO SOY KUBALITA! Intrinsic and common pathway!!

less 1 but expected in treatment 1.5 to 2.5

155
Q

_________________ is the antidote for heparin induced bleeding

A

Sulfate protamine

156
Q

Why heparin induce thrombocytopenia?

A
157
Q

When should I expect HIT? (TIME)

A
158
Q

What factors does warfarin affect?

A
159
Q

Hemostasis is classified as?

A
160
Q
A
161
Q
A
162
Q

TP is obtained by adding ____________ to the px plasma

A
163
Q

What is and why does INR exist?

A
164
Q

Indications of warfarin? (3)

A
  1. Deep vein thrombosis
  2. Arrhythmias
  3. Prosthetic valve disease
165
Q

Toxicity of warfarin and what medication increases its leves?

A
166
Q

Can we give warfarin during pregnancy?

A
167
Q

Why can warfarin trigger skin necrolisis?

A
168
Q

What is the heparin bridge?

A
169
Q

What to do with a warfarin overdose with and without bleeding?

A
170
Q

Mnemotechnic for warfarin inducers and inhibitors

A

Inhibitors: Sing this like a cheer (“2, 4, 6, 8 who do
we appreciate…” ) that kind of melody….
“-Navir, -Azole, Erythro,- and Cipro
- Inhibit! Inhibit! They all Inhibit!
Cimitidine, Class Four And Grape-Fruit Juice. Inhibit! Inhibit! They all Inhibit!”
(The P450 inhibitors: All the HIV
Protease inhibitors
(end with suffix- navir), all the “azole” antifungals, Erythromycin
(but none of the other macrolides
), Ciprofloxacin
and all the other fluoroquinolones, Cimitidine, Class IV Anti-arrhythmatics (use-dependent Ca channel blockers
)= Diltiazem
, Verapamil
, and grapefruit juice)

And for the inducers: .. this is a rhyme, like a nursery rhyme…
“Treat TB
and the mind, Induce the P450 enzyme
“
Inducers of P450:TB
drugs: Rifampin
and Isoniazid
“Mind” drugs (really barbiturates
, antiseizure drugs, and herbal antidepressants
): Phenobarbital
, Phenytoin
, Carbamazepine
, and St. John’s Wort (herbal antidepressant
)

171
Q

Effect of TP and TPT of direct thrombin and factor X inhibitors

A
172
Q

Name the Direct Thrombin inh meds:

A

RUDY (ART ATTACK) HAS FRIENDS DESIRE AND VALE TIMES 2 CAUSE SHE IS DOPPED BUT BECAUSE OF THAT BUILDSHIT FRIENDSHIP HE HAS LEPRA.

173
Q

Why does HIT forms?

A
174
Q

Adverse effects of direct thrombin inhibitors

A
175
Q

__________________ Is the only direct thrombin inhibitor that has a reversal agent known as _____________________

A
  1. Dabigatran
  2. IDARUCIZUMAB
176
Q

Name the direct Xa inhibitors

A
  1. Apixaban
  2. Rivaroxaban
  3. Edoxaban
177
Q

_____________________ is the reversal agent of Factor Xa direct inhibitors

A

ANDEXANET

178
Q
A
179
Q

What is the mechanism of action of statins?

A

Harry potter and eMa Guatson are COstArs in LIPIDS secrets.

180
Q
A
181
Q

Function of the 3 types of cholesterol

A
182
Q

How are triglycerides composed?

A
183
Q

Function of lipoprotein lipase?

A
184
Q

Mechanism of action of fibrates?

A

3 simposon ariels with pepe

185
Q

Name the 3 acid bile resines

A
  1. Colestyramine
  2. Colesevelam
  3. Colestipol
186
Q

What is the mechanism of action of acid bile resins

A

Preventing its absorbtion

187
Q
A
188
Q
A
189
Q
A
190
Q

What is the Paroxysmal supraventricular tachycardia? What is the most common cause?

A

Sudden onset of tachycardia originated in the atrium

AVNRT
Atrioventricular nodal reentrant tachycardia

191
Q

What is the retrogrades P waves and where we can find them?

A

AVNRT

192
Q

Treatment of AVNRT

A
  1. Carotid massage
  2. Vagal maneuvers
  3. Adenosine
  4. BB or ant calcium
  5. Surgical ablation
193
Q

What characteristics we find in WPW syndrome in ECG?

A
  1. Delta wave
  2. Short PR syndrome

DELTA WAVE: PREEXITATION OF THE VENTRICLES

194
Q

What is the bunddle of kent?

A
195
Q
A
196
Q

Explain atrial fibrillation and WPW syndrome

A
197
Q

WHY IS IT IMPORTANT TO KNOW WHY IN WPW RAPID FA YOU CANNOT SLOW THE AV NODE CONDUCTION?

A
198
Q

Antiarrhythmic drug that preferably binds to ischemic tissue

A

LIDOCAINE

199
Q

What does USE DEPENDANT means with flecainamide?

A

Flecainide is a class Ic antiarrhythmic that blocks cardiac sodium channels. This drug exhibits “use dependence” meaning drug binding to sodium channels increases at fast heart rates as explained in the video. For this reason, flecainide toxicity is most likely to occur during exercise.

Through blockade of sodium channels, flecainide may prolong the QRS interval. Significant QRS prolongation is an indication to stop the drug due to high risk of toxicity. Patients started on flecainide are usually referred for a cardiac stress test to evaluate the QRS interval during exercise. If the QRS interval prolongs with exercise, the patient is at increased risk for flecainide toxicity.

200
Q

With what 2 class 3 antiarrhytmic drugs we do hospital QT surveillance?

A
  1. Dofetilide
  2. Sotalol
201
Q

_______________ has a class I indication for all patients after myocardial infarction to reduce the risk of sudden death

A

BB

202
Q

Which antiarrhythmic drugs display the ¨reverse use dependence¨ characteristic?

A

SOTALOL

203
Q

What can block adenosine response ?

A

Methylxanthines have a similar chemical structure and can block

(cafeine and theophyline)

204
Q

What is atropine?

A

Is a muscarinic receptor blocker

205
Q

What are the antimuscarinic effect?

A
206
Q

Name the 2 arrhythmias in which we almost everytime use antiarrhythmics

A
207
Q
A
208
Q

Phase 0 in myocyte cells equals ______________________

A

QRS

Depolarization

209
Q

The depolarization and repolarization of ventricles is demostrated in the myocyte action potential by phase __________________ and in the ecg by ________________

A

0, 1, 2 and the end phase 3

ECG: QT interval

210
Q

Explain why K channel blockers prolong QT interval

A

Prolongs phase 1, 2 and 3

211
Q
A
212
Q
A
213
Q
A
214
Q

_______________ is the drug of election in WPW FA

A

PROCAINAMIDE

IV

215
Q

Why class 1B antiarrhythmic drugs prefer ischemic tissue?

A
216
Q

What is the drug of choice in ventricular ischemic tachycardias and why?

A
217
Q

Why lidocaine helps in re-entry arrhythmias?

A
218
Q

In what patients we can use class 3 antiarrhythmic drugs?

A

Arrhythmias with structural normal hearts

219
Q

What antiarrhythmic drugs are use dependance ?

A

All class 1 but mainly Class 1C

220
Q

Mechanism of action of amiodarone and effects in ecg

A
221
Q

Why amiodarone causes adverse effect?

A
222
Q

Classification of murmurs

A
223
Q
A
224
Q

What is the point of maximum impulse in the heart?

A
225
Q
A
226
Q

Causes of diastolic murmurs?

A
227
Q

Causes of systolic murmurs

A
228
Q

Diastolic murmurs are always pathologic and systolic murmurs not always.

A
229
Q
A
230
Q

How can we distinguish a murmur of a stenotic aortic valve from hypertrophic myocardiopathy ?

A
231
Q

How is a aortic regurgitation murmur heard?

A
232
Q

Mitral regurgitation murmur?

A
233
Q

How do we hear a mitral stenosis murmur?

A
234
Q

What is carvallos sign?

A
235
Q

What causes holosystolic murmurs?

A
236
Q

Type of murmur in PDA

A
237
Q

What manuevers can we use to increase or decrease preload?

A
238
Q

Most manuevers increase with preload except:

A
  1. hypertrophic myocardiopathy
  2. mitral valve prolapse
239
Q

What manuever increase or decrease the afterload?

A
240
Q
A
241
Q
A
242
Q
A
243
Q

What 2 pathologies cause a crescendo and decrescendo murmur?

A
  1. Aortic stenosis
  2. Hypertrophic myocardiopathy
244
Q

What clinical manifestations are present in severe aortic stenosis?

A
  1. S2 silent
  2. peak late murmur
  3. Weak carotid upstrokes
245
Q

What is persistent S2 splitting and what pathologies cause it?

A
246
Q

What is fixed S2 splitting and what patologies cause it?

A
247
Q

Explain the types of S2 splitting? 3

A

Corazon con jeanes PEPE

P. PERSISTENT: Inhalation
E. FIXED
P PARADOXYCAL : Exhalation

248
Q
A
249
Q

What is the S2 loud sound ? What causes it?

A
250
Q

Where we found S3 sounds?

A
251
Q

KENTUCKY

A

S3

252
Q

TENESSE

A

S4

253
Q

Bicuspid aortic valve predispose to _______________________

A

Aortic disection

254
Q

What auscultation findings are found during pregnancy? (2)

A

Upper left sternal murmur: Corresponds to pulmonic valve and increase blood flow and volume

S3.

255
Q

Explain physiological splitting?

A
256
Q

What does a persistent splitting means?

A

Splitting during exhalation and inhalation

257
Q

What does splitting means? And a paradoxical splitting?

A

That the pulmonic valve closes latter than the aortic valve.

Aortic valve closes first

258
Q

What is the hallmark of left ventricular failure?

A

Left ventricular end diastolic pressure is elevated

259
Q

What are the heart failure cells in lung biopsy?

A
260
Q

____________________ mmhg is the normal jugular venous pressure

A

6-8

261
Q

What is the hepatojugular reflux and how to obtain it?

A
262
Q

What are the abnormal heart sounds in heart failure?

A
263
Q

What is the opposite of the RAAS

A

Natriuretic peptide

264
Q

Explain the relationship of heart failure and ADH?

A

USMLE CAARDIOVASCULAR (4 decks)

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