Brainscape's Knowledge GenomeTM

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


See full index

NPLEX I (2022) > Cardio > Flashcards

Cardio Flashcards

1
Q

Angiotensin ultimately originates in what organ?

A

The liver

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

Which apoprotein is responsible for the assembly of VLDL in the liver?

A

ApoB-100

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

A 54-year-old Hispanic woman is following up after recent blood work. Her cholesterol panel reveals elevated triglycerides and VLDL. She would prefer to avoid pharmaceutical treatment if possible but is worried about her risk of atherosclerosis.

Which Fredrickson hyperlipoproteinemia (HLP) type represents this patient based on her elevated lab values?

A

HPL type 4

Type 1 = TG + CM
(Type 3= TC, TG, and IDL)

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

HDL is denser than VLDL and LDL since it contains more _______

A

Protein

Although HDL is the smallest lipoprotein, it has the highest ratio of proteins to lipids making it the densest.

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

What is the outermost layer of blood vessels? Explain its microscopic anatomy.

A

Tunica adventitia/externa - contains blood and lymph vessels and nerves that supply the artery

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

What is the middle layer of blood vessels? Explain its microscopic anatomy.

A

Tunica media - made of smooth muscle, collagen, reticular and elastic fibers

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

What is the innermost layer of blood vessels? Explain its microscopic anatomy.

A

Tunica intima - simple squamous endothelial cells supported by a similarly thin layer of connective tissue, includes endothelium and internal elastic lamina (in muscular arteries)

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

What is the microscopic anatomical difference between layers of elastic and muscular arteries?

A

elastic arteries contain MORE elastic tissue in the tunica media than muscular arteries

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

What are the location/boundaries of the pericardium?

A

Lies within the mediastinum; inferior wall of fibrous pericardium attaches to diaphragm

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

What is the structure of the pericardium?

A

3 layers (outermost to inner):

  • Fibrous pericardium
  • Parietal layer of serous pericardium
  • Pericardial cavity
  • Visceral layer of serous pericardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What nerve innervates the pericardium?

A

Phrenic nerve

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

What is the most posterior part of the heart?

A

Left atrium

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

What is the most anterior part of the heart?

A

Right ventricle

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

What is the most commonly injured part of the heart in trauma?

A

Right ventricle

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

Enlargement of the left atrium can cause what pathologies?

A

Mitral stenosis; compression of esophagus (dysphagia), compression of L laryngeal nerve causing hoarseness (Ortner syndrome)

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

Where is the best place to listen to the mitral valve?

A

5th L ICS MCL (apex)

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

Where is the best place to listen to the tricuspid valve?

A

5th L ICS

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

Where is the best place to listen to the pulmonic valve?

A

2nd L ICS

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

Where is the best place to listen to the aortic valve?

A

2nd R ICS

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

Where is Erb’s point?

A

3rd L ICS

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

What are the murmurs associated with the mitral valve and how do they sound?

A

Mitral regurgitation (holosystolic)

Mitral valve prolapse - systolic (midsystolic click)

Mitral stenosis (diastolic)

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

What pathology are associated with the tricuspid valve? For murmurs, know systolic vs diastolic.

A

Tricuspid regurgitation (holosystolic)

Ventricular septal defect (holosystolic)

Tricuspid stenosis (diastolic)

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

What pathology are associated with the pulmonic valve? For murmurs, know systolic vs diastolic.

A

All systolic ejection murmurs

Pulmonic stenosis
Atrial septal defect
Flow murmur

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

What pathology are associated with the aortic valve? For murmurs, know systolic vs diastolic.

A

All systolic murmurs

Aortic stenosis

Flow murmur (physiologic murmur)

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

What pathology are associated with the erb’s point? For murmurs, know systolic vs diastolic.

A

Aortic regurgitation (diastolic)

Pulmonic regurgitation (diastolic)

Hypertrophic cardiomyopathy (systolic)

At erb’s Point we get High

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

What pathology are associated with S3?

A

EARLY diastolic pathology

Mitral regurgitation
HF
Volume overload

Can be normal

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

What pathology are associated with S4?

A

LATE diastolic pathology

Hypertrophy
Pressure overload
Extreme HTN

ALWAYS ABNORMAL

S4 Dose Have Pretty Extreme Appetite

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

What causes the sound you hear for S1?

What part of the heart cycle occurs after S1 and before S2?

Where is it loudest?

A

Mitral and tricuspid valves closing

Systole

Mitral area

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

What causes the sound you hear for S2?

What part of the heart cycle occurs after S2 and before the next S1?

Where is it loudest?

A

Aortic and pulmonic valves closing

Diastole

L upper sternal area

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

Explain the pathway of conduction throughout the heart

A

SA node > atria > AV node > IV septum/Bundle of His > L+R bundle branches > purkinje fibers > ventricles

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

Explain how contraction of the heart is stimulated

A

Contraction stimulated by conduction system; ion flow across cardiac muscle cells initiates action potent ion and leads to contraction

Then, heart resets and returns to baseline and it all repeats

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

Where in the heart conduction pathway does the signal slightly delay? Why?

A

AV node; this is the only place there is no fibrous barrier between atria and ventricles, less gap junctions; allows time for atria to empty blood into ventricles prior to contraction

Control of the conduction pathway!

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

How does the cardiac conduction pathway begin?

A

Self excitation of SA node; caused by leaky sodium and calcium ions inward and rising resting membrane potential

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

How are purkinje fibers able to instantaneously transmit cardiac impulse through ALL of ventricular muscle?

A

Higher permeability of gap junctions at intercalated discs

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

What would you call a pacemaker anywhere else besides SA node?

A

Ectopic pacemaker

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

Explain the effect parasympathetic stimulation on the heart conduction pathway

A

Vagal n stimulation at SA/AV nodes > releases Ach at vagal endings, increasing permeability of membrane to K+ ions > increases membrane negativity (hyperpolarization) > tissue less excitable

Decreased SA node rhythm > decreased HR

Decreased excitability of AV junctional fibers b/w atrial muscle and AV node > slows transmission of cardiac impulses to ventricles

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

Explain the effect sympathetic stimulation on the heart conduction pathway

A

Sympathetic nerves most concentrated in ventricular muscle

NE released at nerve endings > stimulate beta-1 adrenergic receptors > increases cardiac rhythmicity and conduction > increased rate of SA node > increased rate of conduction and level of excitability throughout heart > increased force of contraction (esp ventricles)

Increased heart force + HR

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

What does the P wave of the cardiac cycle represent?

A

Atrial depolarization; followed by atrial contraction

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

What does the QRS complex of the cardiac cycle represent?

A

Ventricular depolarization; followed by ventricular contraction

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

What does the T wave of the cardiac cycle represent?

A

Ventricular repolarization; slightly before isovolumic relaxation, ventricles remain contracted until end of T wave

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

What does the R-R interval of the cardiac cycle represent?

A

Rate of one single cardiac cycle/heartbeat

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

What does the P-R/P-Q interval of the cardiac cycle represent?

A

Depolarization of atria to start of ventricle contraction

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

What does the Q-T interval of the cardiac cycle represent?

A

Depolarization and repolarization of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What would inversion of a T wave on an EKG indicate?

A

Ischemia or recent MI

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

What would a pathological U wave on an EKG indicate?

A

Hypokalemia

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

What does a long QTI predispose pts to? What is it caused by?

A

Torsades de pointes VTACH (wide QRS) > caused by drugs, low K or Mg, congenital abnormalities

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

Compare AV node fibers vs sinus nodal fibers

A

SA node fibers have less negative resting membrane potential, caused by leaky sodium and calcium ions > fast sodium channels blocking from opening due to higher resting membrane potential > slower action potential overall

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

Where does the myocardial action potential occur?

A

All cardiac myocytes, except those in SA and AV nodes

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

Briefly explain overview of myocardial action potential?

A

Depolarization (more positive membrane) > AP plateaus > repolarization (more negative membrane)

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

Describe phase 0 of the myocardial action potential

A

Depolarization

Fast Na channels open

Slow Ca channels open

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

Describe phase 1 of the myocardial action potential

A

Initial repolarization

Fast Na channels close
Fast K channels open

Slow Ca channels still open

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

Describe phase 2 of the myocardial action potential

A

Plateau

Fast K channels close

Slow Ca channels still open, increasing influx balance leaving K more and more

Calcium influx triggers: Ca release from sarcoplasmic reticulum + myocyte contraction via excitation-contraction coupling

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

Describe phase 3 of the myocardial action potential

A

Rapid repolarization

Slow Ca channels close
Slow K channels open

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

Describe phase 4 of the myocardial action potential

A

Resting membrane potential

High potassium permeability through leaky potassium channels

NaK ATPase and NaCa (Na in Ca out) exchanger at work

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

Where does the pacemaker action potential occur?

A

SA and AV nodes

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

Describe phase 0 of the pacemaker action potential

A

Opening of Ca channels causes upstroke

fVNaC permanently inactivated > slow conduction velocity used by AV node to prolong transmission from A > V

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

Describe phase 3 of the pacemaker action potential

A

Inactivation of Ca channels
Activation of K channels

> K efflux

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

Describe phase 4 of the pacemaker action potential

A

Slow spontaneous diastolic depolarization from funny current

Slow/mixed Na/K influx > accounts for automaticity of SA and AV nodes (slope determines HR) > Ach/adenosine will decrease HR, catecholamines will increase HR

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

What system controls HR and strength?

A

ANS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the basis of regulation of the cardiac cycle?

A

Intrinsic cardiac pumping regulation in response to changes in volume of blood flowing into the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What determines the amount of blood pumped into the heart each minute?

A

Venous return

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the Frank-Starling Mechanism?

A

Ability for the heart to adapt to increasing volumes of blood

More heart muscle is stretched during filling > greater contraction force > greater quantity of blood pumped into aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Explain sympathetic stimulation and its role in ANS control of the heart

A

Increased CO > increases HR and force of contraction > increases volume of blood pumped and ejection pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Explain parasympathetic stimulation and its role in ANS control of the heart

A

Deceased CO >

minor decrease of contraction strength

major decrease of HR

vagal nerve fibers distributed more to atria than ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Explain the effect of potassium ions on heart function

A

Excess extracellular K > dilated, flaccid heart > slow HR

Excess K could also block conduction of electrical impulse from atria to ventricle

Why?
Decreases resting membrane potential (less neg), decreases intensity of AP, decreased heart muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Explain the effect of calcium ions on heart function

A

Excess intracellular Ca causes opposite effects of potassium

Excess leads to spastic contraction

Why?
Ca initiates the cardiac contractile process
Decreased Ca leads to cardiac weakness like the effects of high K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Where do the coronary arteries lie and where do they supply blood to?

A

CA and their branches lie in the epicardium and supply blood to the myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

During which heart phase do the coronary arteries fill?

A

Diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Describe the branching pattern of the coronary arteries

A

Aortic root > RCA + LCA

RCA > R marginal
RCA + LCA > PDA
LCA > LAD (widow)
LCA > circumflex > L marginal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What CA supplies blood to the SA node?

A

RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What CA supplies blood to the right ventricle?

A

RMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Where does the LAD artery supply blood to?

A

Anterior 2/3 IV septum, anterior LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Where does the circumflex artery supply blood to?

A

LA and posterior walls of LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Where does the PDA supply blood to?

A

AV node, posterior 1/3 AV septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Explain the branching of the aorta below the diaphragm

A

Inferior phrenic, celiac trunk (foregut), middle suprarenal arteries, renal arteries, SMA (midgut), testicular arteries, IMA (hind gut), lumbar arteries, common iliac arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are the major lower extremity veins?

A

Anterior tibial, posterior tibial, peroneal veins, lower popliteal fossa, popliteal vein, superficial femoral vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Explain the anatomy of the femoral and saphenous veins

A

Deep femoral v is lateral, joins superficial femoral and great saphenous in femoral canal, common femoral vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

In what pathologies would a high pulse pressure be present?

A

Hyperthyroid, aortic regurgitation, aortic stiffening, OSA, exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

In what pathologies would a low pulse pressure be present?

A

Aortic stenosis, cardiogenic shock, cardiac tamponade, HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What would cause high contractility?

A

B1R stim, increased intracellular Na/Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What would cause low contracility?

A

B1 blocker, HF, acidosis, hypoxia, NDHPCCB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What medication class would decrease preload?

A

Venous vasodilator (nitroglycerin, ACEis, ARBs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What determines the amount cardiac muscles can contract in preload?

A

End diastolic volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What determines afterload?

A

End systolic volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What blood vessels have the highest total cross sectional area and lowest velocity?

A

Capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Explain capillary fluid exchange

A

Cap pressure pushes fluids out, interstitial pressure pushes fluid in

Plasma osmotic and oncotic pressure pulls fluid in, interstitial fluid osmotic pressure pulls fluid out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are starling forces and what do they determine?

A

Contraction force is proportional to preload; hearts ability to change contractions and SV in response to venous return. SV increase with increase in amount of blood that fills ventricles (EDV)

Starling forces determine fluid movement through cap membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Explain the acute effects of early exercise on the CV system.

A

CO maintained by increased HR and SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Explain the adaptive effects of late exercise on the CV system.

A

CO maintained by HR only (as SV plateaus)

As HR increases > less filling time > decreased CO > diastole is shortened

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Explain the function and biochem of atrial natiuretic peptide

A

Released from atrial myocytes in response to increased blood volume and atrial pressure

Caused vasodilation and decreased Na in the renal/medullary collecting duct

Dilates afferent renal arterioles and constricts efferent arterioles to promote diuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Explain the function and biochem of brain natriuretic peptide

A

Released from ventricular myocytes in response to increased tension

Longer half life than ANP

Used to Dx HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Explain the function and biochem oF LDL

A

Transports cholesterol made in the liver to the tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Explain the function and biochem of HDL

A

Scavenges cholesterol from tissues and back to liver for disposal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Explain the unique relationship between the cardiovascular and pulmonary system

A

Pulmonary vasculature is the only one that vasoconstriction under hypoxia, so the well ventilated areas are perfused

Other areas of the body, hypoxia causes vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is pulmonary HTN?

A

Increased pressure in pulmonary vasculature ONLY; elevated mean pulmonary artery pressure > 20 mmHg at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Explain the pathogenesis of pulmonary HTN and what it can lead to

A

Increased pulmonary vascular resistance > increased right ventricular pressure > increased right ventricular hypertrophy > right HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What are the different possible causes of pulmonary HTN?

A

Idiopathic, inherited, drug induced, connective tissue disease

HD/HF (most common)

Lung disease and/or hypoxemia

Chronic thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

RF for pulmonary HTN

A

CHF, MI, chronic anemia, COPD/lung disease, chronic thromboembolism, pulmonary arterial HTN (genetic, idiopathic), lung fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Complications of pulmonary HTN

A

Arteriosclerosis, medial hypertrophy, intimal fibrous of pulmonary arteries, right HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Clinical characteristics of pulmonary HTN

A

PLEXIFORM LESIONS (complex vascular formations originating from remodeled pulmonary arteries, like a spider vein in the lungs)

Fatigue, dyspnea, syncope, peripheral edema, palpitations, chest pain on exertion

Medial hypertrophy of muscular and elastic arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is the most common type of systemic HTN and its causes?

A

1st degree: multi factorial

Increased CO: increased HR, contractility (exercise, anxiety), increased preload (amount of blood filling heart), decreased afterload

Increased TPR: amount of blood circulating and diameter of BVs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the most common cause of second degree systemic HTN?

A

Renal/renovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is seen microscopically in pulmonary HTN?

A

Smooth muscle proliferation occurs due to decreased apoptosis; genetic connection to BMPR2 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

RF for systemic HTN

A

Increased age, obesity, DM, physical inactivity, excess salt, excess alcohol, smoking, fhx

AA > caucasians > Asian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Complications of systemic HTN

A

CAD, HF, left ventricular hypertrophy, a fib, aortic dissection, aortic aneurysm, stroke, CKD, retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What defines a hypertensive crisis, hypertensive urgency, and hypertensive emergency?

A

Crisis: 180/110

Urgency: 180/120+ with NO sx end organ damage

Emergency: 180/120+ with evidence of end organ damage (encephalopathy, stroke, retinal hemorrhage, MI, HF, kidney injury)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Sx of systemic HTN

A

Commonly asymp

Fundoscopic exam showing hypertensive retinopathy (not required for dx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is congestive heart failure?

A

Cardiac pump dysfunction leads to congestion of the heart, decreased CO, and low perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Types of left sided CHF

A

Systolic dysfunction: HF with reduced EF, increased EDV, decreased contractility

Diastolic dysfunction: HF with preserved EF, normal EDV, decreased compliance (increased EDP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Etiology/causes of L CHF

A

Ischemic HD
HTN
Aortic and mitral valvular diseases
Myocardial disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Common causes of R CHF

A

Left HF
Pulmonary HTN

Cor pulmonale - isolated right HF due to pulmonary causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

RF for CHF

A

Old age, CAD, HTN, DM, valvular heart disease, tobacco, obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Complications of L CHF

A

A fib, stroke/thrombosis, hypoxic encephalopathy, coma, death, right HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Shared clinical characteristics of both types of CHF

A

S3 heart sounds, rales, JVD, pitting edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

L CHF clinical characteristics

A

S3, rales, JVD, pitting edema

pulmonary edema (increased pulmonary venous pressure > pulmonary venous distention and transduction of fluid) > HF CELLS IN LUNGS

Orthopnea (SOB when supine)

Paroxysmal nocturnal dyspnea

Dyspnea, orthopnea, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

R CHF clinical characteristics

A

S3, rales, JVD, pitting edema

Congestive hepatomegaly (increased central venous pressure > increased resistance to portal flow) > NUTMEG LIVER on cadaver exam

Dyspnea, orthopnea, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

what is angina pectoris?

A

Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm, no myocyte necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Different types of angina pectoris

A

Stable angina

Vasospastic/variant

Unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Stable angina definition

A

most common

usually secondary to atherosclerosis (>70% occlusion)

triggered by: atherosclerosis, activity, BP, HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Vasospastic/variant angina definition

A

occurs at rest secondary to CA spasm

triggered by: cocaine, alcohol, triptans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Unstable angina definition

A

Thrombosis with incomplete coronary artery occlusion

Triggered by: atherosclerosis, activity, BP, HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

RF for stable and unstable angina

A

HTN, HLD, tobacco, MI RF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

RF for vasospastic/variant angina

A

Tobacco use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Clinical characteristics of stable angina

A

Pain on exertion, resolves with rest

No ECG changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Are troponin levels elevated in any forms of angina?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Clinical characteristics of vasospastic angina

A

Pain at rest secondary to coronary artery spasm

Transient ST elevation on ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Clinical characteristics of chronic ischemic heart disease

A

Enlarged heavy heart with L ventricular hypertrophy and dilation

Obstructive ordinary atherosclerosis

Scars from healed infarcts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Complications of chronic ischemic heart disease

A

Leading cause of death worldwide

Progressive CHF leading to heart transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Clinical characteristics of unstable angina

A

Pain on mild extortion or at rest

Possible ST depression/T-wave inversion on ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What is chronic ischemic heart disease

A

Progressive onset of HF over many years due to chronic ischemic myocardial damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is myocardial ischemia

A

Imbalance between supply (perfusion) and demand of heart for oxygenated blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Etiology of chronic ischemic heart disease

A

Reduced blood flow to obstructive atherosclerotic lesions in coronary artery, usually preceded by MI

Progression of CAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Pathogenesis of chronic ischemic heart disease

A

Long and slow onset w/o sx

Syndrome of ischemic heart disease are late manifestations of coronary atherosclerosis

Appears post infarction due to functional decompensation of hypertrophied non infarcted myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

RF of chronic ischemic heart disease

A

HLD, HTN, MI, tobacco use, alcohol use, sedentary lifestyle, age, SAD diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What is a myocardial infarction

A

Death of cardiac muscle due to prolonged severe ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Most common cause of myocardial infarction

A

Rupture of coronary artery atherosclerotic plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Commonly occluded arteries with MIs

A

LAD > RCA > circumflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Pathogenesis of MI

A

Initial event > sudden change in plaque > intraplaque hemorrhage, erosion, ulceration, rupture, fissuring

When exposed to subendothelial collagen and necrotic plaque contents, platelets adhere, become active, release granule contents, and aggregate to form microthrombi

Vasospasm is stimulated by mediators released from platelets

TF activates, activates coagulation pathway, increases bulk of thrombus, occludes complete lumen > leads to ischemia and myocyte death occurring at the location of the anatomical region supplied by artery in question

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Biochem of MI

A

Loss of blood flow > cessation of aerobic metabolism within seconds

Inadequate production of ATP > accumulation of lactic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

STEMI characteristics

A

Transmural

Full thickness

ST elevation, pathological Q waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

NSTEMI characteristics

A

Subendothelial

Subendocardium (inner 1/3)

ST depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What is seen on microscopy at 0-24 hours, 1-3 days, 3-14 days, and 14+ days post MI

A

0-24 hrs: wavy fibers, coagulative necrosis, dark eosinophilic stripes

1-3 days: coagulative necrosis, neutrophils showing acute inflammation

3-14 days: macrophages, granulation tissue

14+ days: scar complete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

RF for MI

A

Age, genetics, males, post menopausal women (drop in estrogen), atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Complications of MI

A

If caught late: necrosis of cardiac myocytes > chronic IHD, CHF, death

DARTH VADER: death, arrhythmia, rupture, tamponade, HF, valve disease, aneurysm, dressers, embolism, recurrence/regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Complications of MI by time frame (0-24 hours, 1-3 days, 3-14 days, 2+ weeks)

A

0-24 hours: ventricular arrhythmia, HF, cardiogenic shock
Vinny has constipation for 24 hours

1-3 days: postinfarction fibrinous pericarditis

3-14 days: cardiac tamponade, mitral regurgitation, LV, pseudoaneurysm

2+ weeks: dressier syndrome, HF, arrhythmia, ventricular aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Clinical characteristics MI

A

Elevated bio markers (CK-MB, troponins)

Chest/arm/back/neck/jaw pain

Trouble breathing

Lightheadedness

Diaphoresis/cold sweats

N/V

Severe chest pain

Malaise, fatigue

147
Q

Aortic stenosis - S or D?

A

S

148
Q

Aortic regurgitation / insufficiency - S or D?

A

D

149
Q

Mitral stenosis - S or D?

A

D

150
Q

Mitral insufficiency - S or D?

A

S

151
Q

Mitral valve prolapse - S or D?

A

S

152
Q

Etiology of aortic stenosis

A

Age-related calcification, bicuspid aortic valve

153
Q

RF aortic stenosis

A

Age, atherosclerosis, bicuspid aortic valve

154
Q

complications of aortic stenosis

A

SAD (syncope, angina, DOE), LV pressure is less than aortic pressure during systole

155
Q

Clinical characteristics aortic stenosis

A

Cresc-decresc ejection murmur

Pulses parvus et tartus (weak pulse)

Soft S2 and ejection click

156
Q

Etiology aortic regurgitation

A

BEAR (bicuspid aortic valve, endocarditis, aortic root dilation, rheumatic fever

157
Q

Complications aortic regurgitation

A

L CHF

158
Q

Clinical characteristics aortic regurgitation

A

Early diastolic decrescnedo

High, blowing murmur

Wide PP

Pistol shot femoral pulse

Pushing nail bed

159
Q

Mitral stenosis etiology

A

Rheumatic fever

160
Q

Mitral stenosis pathogenesis

A

L atrial pressure > ventricular pressure

161
Q

Mitral stenosis complications

A

Left atrial dilation, pulmonary congestion, a fib, ortner syndrome, hemopytsis, RCHF

162
Q

Mitral stenosis clinical characteristics

A

Follows opening snap, delayed rumbling mid-late murmur

163
Q

Mitral insufficiency etiology

A

Ischemic heart disease (post MI), MVP, LV dilation, rheumatic fever, infective endocarditis

164
Q

Mitral insufficiency clinical characteristics and sound

A

asymptomatic to shortness of breath, fatigue, and inability to exercise may arise (later in disease)

Holosystolic, high pitched blowing murmur

165
Q

Types of endocarditis

A

Infective/bacterial

No bacterial thrombotic endocarditis

166
Q

Etiology infective endocarditis

A

Infection of endocardial surface of heart, typically involves 1+ heart valves

Bacteria > fungi

Acute: S aureus; large destructive vegetation’s on normal valves; rapid onset

Subacute: strep Viridans; small vegetations on congenitally abnormal or diseased valves; gradual onset

167
Q

Pathogenesis infective endocarditis

A

Mitral valve affected more often than aortic

Tricuspid valve associated with IV drug use (Don’t Tri Drugs)

Endothelial injury > formation of vegetation’s consisting of platelets, fibrin, and microbes on heart valves

168
Q

Non bacterial thrombotic endocarditis etiology

A

Marantic endocarditis; rare

Vegetations arise on mitral or aortic valve, consists of sterile, platelet-rich thrombi that dislodge easily

169
Q

RF of infectious endocarditis

A

Subacute: dental procedure

RF by bacteria;
Prosthetic valves - s epidermis

GI/GU procedure - enterococcus

IV drug use - S aureus, pseudomonas, candida

170
Q

RF nonbacterial endocarditis

A

Hypercoagulable state from advanced malignancy (pancreatic adenocarcinoma) or SLE (Libman sacks endocarditis)

171
Q

Complications of bacterial endocarditis

A

Leads to valve regurgitation, septic embolism

172
Q

Complications of nonbacterial endocarditis

A

Embolism

173
Q

Clinical characteristics of infectious endocarditis

A 
FROM JANE
Fever
Roth spots
Osler nodes
Murmur
Jane way lesions
Anemia
Nail bed hemorrhages
Emboli

Vascular phenomena: septic embolism, petechiae, splinter hemorrhages, Jane way lesions

Immune phenomena: immune complex deposition, glomerulonephritis, Osler nodes, Roth spots

Modified duke criteria

174
Q

Nonbacterial endocarditis clinical characteristics

A

Asymptomatic

175
Q

Mitral valve prolapse etiology

A

Rheumatic fever, chordae rupture, myxomatous degeneration (primary or secondary due to connective tissue disease)

176
Q

Mitral valve prolapse complications

A

Typically benign, can predispose to infective endocarditis

177
Q

Mitral valve prolapse clinical characteristics

A

Late crescendo murmur with midsystolic click occurring after carotid pulse

178
Q

Rheumatic heart disease definition

A

Immune mediated (type II hypersensitivity)

Antibodies react to M protein, cross-react with self-antigens (often myosin)

179
Q

Rheumatic heart disease etiology

A

Pharyngeal infection with group A B-hemolytic strep

Not direct effect of bacteria

180
Q

Pathogenesis rheumatic heart disease

A

Affects heart disease mitral > aortic > tricuspid (MAT)

181
Q

Complications rheumatic heart disease

A

Early valvular regurgitation

Late valvular stenosis

182
Q

Clinical characteristics rheumatic heart disease

A

Aschoff bodies: granuloma with giant cells

Anitschkow cells: enlarged macrophages with ovoid, wavy, rod-like nucleus

J<3NES (major criteria):

Joint (migratory arthritis)

<3 carditis

Nodules in skin (subcutaneous)

Erythema marginatum (evansecent rash with ring margin)

Sydenham chorea (involuntary irregular movements of limbs/face)

183
Q

Carcinoid heart disease definition

A

Cardiac manifestation of systemic syndrome caused by carcinoid tumors (occurs in 50% of people)

184
Q

Carcinoid heart disease etiology

A

Involves endocardium and valves of right heart

Cardiac lesions: firm, plaque like endocardial fibrous thickening inside tricuspid and pulmonary valves (contain smooth muscle cells and collagen fibers)

185
Q

Carcinoid heart disease complications

A

Tricuspid insufficiency then pulmonary valve insufficiency

186
Q

Carcinoid heart disease clinical characteristics

A

Flushing of skin, cramps, N/V, diarrhea

187
Q

Types of cardiomyopathies

A

Dilated, Hypertrophic, Restrictive

188
Q

Dilated cardiomyopathy etiology

A

Most common, dilation of cardiac chambers (ventricles)

Idiopathic, genetic, drugs, infxn, ischemia, systemic

189
Q

Hypertropic cardiomyopathy etiology

A

Second most common; enlargement of cardiac muscle surrounding ventricles

Familial, autosomal dominant, chronic HTN, friedrich ataxia

190
Q

Restrictive cardiomyopathy etiology

A

Known as infiltrative, decreased ventricular compliance

PLEASe Help:
P: postradiation fibrosis
L: Loeffler endocarditis
E: endocardial fibroelastosis (kids)
A: amyloidosis
Se: sarcoidosis
Help: hemochromatosis
191
Q

Dilated cardiomyopathy complications

A

Systolic dysfunction

Clot formation

192
Q

Hypertrophic cardiomyopathy complications

A

Diastolic dysfunction
Sudden death in young athletes
Arrhythmias

193
Q

Restrictive cardiomyopathy complications

A

Diastolic dysfunction

194
Q

Dilated cardiomyopathy clinical characteristics

A

CHF, S3, systolic regurgitation murmur, dilated heart on echo

BALLOON APPEARANCE OF HEART ON CXR, ECCENTRIC HYPERTROPHY IN VENTRICLE, sarcomeres added in series

195
Q

Hypertrophied cardiomyopathy clinical characteristics

A

S4, systolic murmur, mitral regurgitation, dyspnea, syncope

VENTRICULAR CONCENTRIC HYPERTROPHY, MUSCLE TISSUE ENLARGED, sarcomeres added in parallel

196
Q

Restrictive cardiomyopathy clinical characteristics

A

Low voltage ECG

MUSCLE LESS COMPLIANT, LESS CONTRACTILE

197
Q

Myocarditis etiology

A

Inflammation of myocardium > global enlargement of heart and dilation of all chambers

Viral: coxsackie A and B virus

Parasitic; trypanosoma cruzi, toxoplasma gondii

Bacterial: borrelia burgdorferi, myoplasma pnemoniae, diphtheriae

Toxins: CO, black widow venom

Rheumatic fever

Drugs (cocaine)

Autoimmune disease

198
Q

Complications of myocarditis

A

SCD (Major cause in adults >40)

Arrhythmias, heart block, dilated cardiomyopathy, CHF, mural thrombus with systemic emboli

199
Q

Myocarditis clinical characteristics

A

Dyspnea, chest pain, fever, arrhythmias (persistent tachycardia out of proportion to fever)

If viral in etiology: lymphocytic infiltrate with focal necrosis

200
Q

Pericarditis definition

A

Inflammation of pericardium, fluid accumulates around heart

201
Q

Pericarditis etiology

A

Primary and secondary

SCCARR IIN pericardium

Surgery
Connective tissue disorder
CV events 
Autoimmune 
Radiation
Renal failure
Idiopathic (most common)
Infection (coxsackie B)
Neoplasm
202
Q

Pericarditis complications

A

Pericardial effusion

203
Q

Pericarditis clinical characteristics

A

Sharp pain, WORSE BY INSPIRATION, BETTER SITTING UP AND LEANING FORWARD

Friction rub
Diffuse ST elevation or depression

204
Q

Patent ductus arteriosis definition

A

Ductus arteriosis failes to close after birth; allows blood to flow back to lungs

205
Q

Patent ductus arteriosis etiology

A

Fetal period: normal (R to L) shunt

Neonatal period: decreased vascular resistance, shunt becomes L to R

Leads to RVH and/or LVH and HF

206
Q

Patent ductus arteriosis complications

A

Late cyanosis in lower extremities

207
Q

Patent ductus arteriosis clinical characteristics

A

No symptoms or cyanosis, fatigue, tachycardia

Continuous machine-like murmur

PDA is normal in utero, and normally closes after birth

208
Q

Tetralogy of fallot etiology

A

Anterosuperior displacement of infundibular septum

Most common cause of early childhood cyanosis

209
Q

Tetralogy of fallot complications

A

Pulmonary stenosis forces R to L flow across VSD > RVH

210
Q

Tetralogy of fallot clinical characteristics

A

Pulmonary infundibular stenosis

RVH - boot heaped heart on xray

Overriding aorta

VSD

“Tet spells” often caused by crying, fever, exercise

211
Q

Aneurysm definition

A

Dilation of aorta

212
Q

Types of aneurysm

A

Abdominal aortic

Thoracic aortci

213
Q

Abdominal aortic aneurysm pathogenesis

A

Transmural (all 3 layers)

Inflammation and extracellular matrix degradation

214
Q

Abdominal aortic aneurysm RF

A

Tobacco, age, males, Fhx

215
Q

thoracic aortic aneurysm pathogenesis

A

Aortic root dilation due to high pressure could lead to aortic valve regurgitation

216
Q

Thoracic aortic aneurysm RF

A

HTN, bicuspid aortic valve, connective tissue disease (Marfan), tertiary syphilis

217
Q

Abdominal aortic aneurysm Complications

A

Aortic dissection

218
Q

thoracic aortic aneurysm

A

Aortic dissection

219
Q

Abdominal aortic aneurysm clinical characteristics

A

Abdominal/back pain as sign of leaking, dissection, imminent rupture

Palpable pulsatilla abdominal mass

220
Q

Abdominal aortic aneurysm clinical characteristics

A

Abdominal/back pain as sign of leaking, dissection, imminent rupture

221
Q

Aortic dissection definition

A

Longitudinal intimal tear forming a false lumen

222
Q

Types of aortic dissection

A

Stanford type A: proximal, ascending aorta

Stanford type B: distal, descending aorta, below L subclavian artery

223
Q

Aortic dissection RF

A

HTN, bicuspid aortic valve, inherited CT disorders (Marfan syndrome)

224
Q

Aortic dissection complications

A

Organ ischemia, aortic rupture, death

Aortic regurgitation, cardiac tamponade

225
Q

Aortic dissection clinical characteristics

A

Tearing, sudden-onset chest pain radiating to back

Unequal BP in arms

CXR: mediastinal widening

226
Q

Arteriosclerosis definition

A

Hardening of arteries, arterial wall thickening, loss of elasticity

227
Q

How dose Arteriosclerosis affect blood vessels and which ones?

A

Affects small arteries and arterioles

Hyaline: thickening of vessel walls secondary to plasma protein leak into endothelium in essential HTN ad DM

Hyperplastic: onion skinning in severe HTN with proliferation of smooth muscle cells

228
Q

Atherosclerosis definition

A

Form of arteriosclerosis

Build up of cholesterol plaques in tunica intima

Elastic arteries and medium/large size muscular arteries

229
Q

Atherosclerosis Etiology

A

Location: A copy cat named Willis: abdominal aorta > coronary artery > popliteal artery > carotid artery > circle of Willis

Inflammation > endothelial cell dysfunction > macrophage and LDL accumulation > foam cell formation > fatty streaks > smooth muscle cell migration > proliferation and ECM deposition > fibrous plaque > complex atheromas > calcification

230
Q

Atherosclerosis complication

A

Atherosclerosis of CA (CAD) is #1 killer of M +F in US

CAD, MI

231
Q

Atherosclerosis RF

A

HTN, tobacco, HLD, DM

Age, males, postmenopausal status, Fhx

232
Q

Atherosclerosis clinical characteristics

A

Angina, claudication, asymptomatic

233
Q

Familial hypercholesterolemia definition

A

Receptor disease from mutation in gene encoding for LDL

234
Q

Familial hypercholesterolemia Pathophysiology

A

Loss of feedback > increased cholesterol levels

Premature atherosclerosis

Increased risk of MI

235
Q

Familial hypercholesterolemia RF

A

Fhx

236
Q

Familial hypercholesterolemia Complications

A

MI, CAD

237
Q

Familial hypercholesterolemia clinical characteristics

A

Very high LDL at young age

Nodules or raised bumps on skin, tendons, eyelids

White ring around cornea

Medications do not work for LDL

238
Q

Giant cell (temporal) arteritis etiology

A

Focal granulomatous inflammation

Increased ESR, IL-6 levels correlate with disease activity

Affects branches of carotid artery

239
Q

Giant cell (temporal) arteritis RF

A

Females, over 50, polymyalgia rheumatica

240
Q

Giant cell (temporal) arteritis complications

A

Irreversible blindness due to anterior ischemic optic neuropathy

241
Q

Giant cell (temporal) arteritis clinical characteristics

A

UL HD, temporal artery tenderness, jaw claudication

242
Q

Peripheral arterial disease (PAD) definition

A

Insufficient tissue perfusion due to narrowing or occlusion of aorta or peripheral branches

243
Q

Peripheral arterial disease (PAD) Etiology

A

Narrow arteries reduce blood flow to arms/legs

Buildup of fatty, cholesterol-containing deposits on artery walls (atherosclerosis), reduces blood flow through arteries

244
Q

Peripheral arterial disease (PAD) RF

A

Fhx, HTN, HLD, age, obesity, CAD

245
Q

Peripheral arterial disease (PAD) Complications

A

Critical limb ischemia, stroke, MI

246
Q

Peripheral arterial disease (PAD) clinical characteristics

A 
Coldness in LE or foot
LE numbness
Weakness
Loss of peripheral pulses 
Cramping
Skin color change
Sores that wont heal
ED
Hair loss
247
Q

Pulmonary embolism definition

A

Obstruction of pulmonary artery or one of its branches by thrombus

248
Q

Pulmonary embolism Etiology

A

Affected alveoli are ventilated but not perfused (V/Q mismatch)

249
Q

Pulmonary embolism RF

A 
THROMBOSIS
T: trauma, travel, thrombophilia
H: hypercoagulable state, hormone replacement 
R: rec drugs/IV drugs
O: old age
M: malignancy
B: birth control pills/patches
O: obesity, obstetrical (pregnancy- 6 wk postpartum)
S: surgery
I: immobilization, iatrogenic (CVC)
S: serious illness
250
Q

Pulmonary embolism Complications

A

Sudden death due to clot preventing blood from filling LV

Hypotension, shock, recurrent thromboembolism, pulmonary infarction, RHF

251
Q

Pulmonary embolism Clinical characteristics

A

Sudden onset dyspnea, pleuritic chest pain, cough, hemoptysis, tachyon ear, tachycardia, syncope, hypoxemia, respiratory alkalosis, sx of DVT,

Wells criteria for PE

ECG: R heart strain - S wave in 1, Q wave in 3, inverted T wave in 3

252
Q

Raynaud phenomenon definition

A

Color changes of skin due to decreased blood flow

253
Q

Raynaud phenomenon Etiology

A

Decreased blood flow to skin due to arteriolar (small vessel) vasospasm in response to cold or stress

Primary: idiopathic

Secondary: mixed connective tissue disease, SLE, CREST syndrome

254
Q

Raynaud phenomenon complications

A

Secondary: Digital ulceration

255
Q

Raynaud phenomenon clinical characteristics

A

Color change from white (ischemia) to blue (hypoxia) to red (reperfusion)

Most often to fingers/toes

256
Q

Thromboangitis Obliterans / Buerger disease definition

A

segmental, thrombosis, acute and chronic inflammation of medium sized and small arteries (tibial and radial)

257
Q

Thromboangitis Obliterans / Buerger disease Etiology

A

Direct endothelial cell toxicity by tobacco or immune response to the same agents

258
Q

Thromboangitis Obliterans / Buerger disease RF

A

Heavy cigarette smokers before age of 35

259
Q

Thromboangitis Obliterans / Buerger disease Complications

A

Vascular insufficiency

260
Q

Thromboangitis Obliterans / Buerger disease Clinical characteristics

A

Superficial nodular phlebitis, severe pain at rest, chronic ulceration of toes, fingers, feet

261
Q

Deep vein thrombosis definition

A

Blood clot within a deep vein (proximal LE veins - iliac, femoral, popliteal)

262
Q

DVT etiology

A 
Virchow triad (SHE)
Status - post op, long drive/flight 
Hypercoagulability - defect in coagulation cascade proteins, OCPs, pregnancy
Endothelial damage - exposed collagen triggers clotting cascade
263
Q

DVT RF

A

Obesity, contraceptives, pregnancy, fhx, previous venous thromboembolism, HRT

Inherited thrombophlebitis:
Factor V Leiden mutation
Protein C deficiency
Protein S deficiency

264
Q

DVT complication

A

PE

265
Q

DVT clinical characteristics

A

Leg swelling, pain, warmth, redness

Unilateral pitting edema in leg

D-dimer: rule OUT DVT

Wells criteria for DVT

266
Q

Varicose veins etiology

A

Prolonged increased intraluminal pressure and loss of vessel wall support

Superficial veins of LE

267
Q

Varicose veins RF

A

Obesity, FHx, females

268
Q

Varicose veins complications

A

Increased venous pressure, venous stasis, pedal edema, stasis dermatitis, ulcerations

269
Q

Varicose veins definition

A

Abnormally dilated, tortuous veins

270
Q

Vasculitis definition

A

Vessel wall inflammation

271
Q

Large vessel Vasculitis Etiology

A

aorta and large branches to extremities, head, neck

giant cell (temporal arteritis

Takayasu arteritis: granulomatous inflammation occurring in pts under 50

272
Q

Types of Vasculitis

A

Large vessel, medium vessel, small vessel

273
Q

Medium vessel Vasculitis etiology

A

Main visceral arteries and branches

Kawasaki disease: arteritis with mucocutaneous lymph node syndrome, in children. Coronary arteries involved with aneurysm or thrombosis

274
Q

Small vessel Vasculitis etiology

A

Arterioles, venues, capillaries, small arteries

Westerns granulomatosis: granulomatous inflammation involving respiratory tract and necrotizing vasculitis affecting small vessles

Churg-Strauss syndrome: same as wegeners but associated with asthma and blood eosinophilia

Microscopic polyangitis: necrotizing small vessel vasculitis with few or no immune deposits

275
Q

Viral myocarditis etiology

A

Adenovirus, coxsackie B, parvovirus B19, HIV, HHV-6

276
Q

Viral myocarditis clinical characteristics

A

Lymphocytes infiltrate with focal necrosis is highly indicative

277
Q

The truncus arteriosis gives rise to…

A

Asc aorta + pulmonary trunk

278
Q

Bulbus cordis gives rise to…

A

Outflow tract of LV and RV

279
Q

Primitive ventricle/aorta gives rise to…

A

Trabeculated part f R + L ventricles/aorta

280
Q

L horn of sinus venosus gives rise to…

A

Coronary sinus

281
Q

R horn of sinus venosus gives rise to…

A

Smooth part of R atrium (sinus venarum)

282
Q

When does the foremen ovale close? What causes this closure?

A

Immediately after birth, due to increased LA pressure

Breath > decreased pulm vasc resistance > increased LA pressure > fossa oval is > increase in O2 > decrease in PGEs > closure of ductus arteriosus

283
Q

What is patent foramen ovale

A

Failure of septum primum and secundum to fuse after birth

284
Q

What eventually develops into the arterial system?

A

Aortic arch derivatives

285
Q

1st aortic arch derivative

A

Maxillary arteries - branch of ext carotid

1st arch is max

286
Q

2nd aortic arch derivative

A

Stapedial and hyoid arteries

second stapedial

287
Q

3rd aortic arch derivative

A

Common carotid artery and proximal part of internal carotid artery

288
Q

4th aortic arch derivative

A

Aortic arch and proximal right subclavian artery

289
Q

6th aortic arch derivative

A

Proximal part of pulmonary arteries and ductus arteriosus (left)

290
Q

Endocardial cushion gives rise to…

A

Atrial septum, membranous IV septum, AV + semilunar valves

291
Q

R common cardinal + R anterior cardinal vein gives rise to…

A

SCV

292
Q

Posterior, subcardinal + supracardinal veins give rise to…

A

IVC

293
Q

Primitive pulm vein gives rise to…

A

Smooth part of LA

294
Q

What are the three roles of the lymphatic system

A

Returns interstitial fluid from tissues back to heart

Helps large molecules like hormones and lipids enter the blood

Helps with immune surveillance

295
Q

When does interstitial fluid become lymph?

A

Once in the lymphatic vessels

296
Q

Where is all of the collected lymph dumped?

A

Veins

297
Q

When do the one way mini valves of lymphatic capillary walls open?

A

When pressure in interstitial space is greater than pressure in lymphatic capillary, endothelial mini valves open

298
Q

Lymph vessel flow

A

Capillaries > bigger vessels > trunks > ducts

299
Q

What “pushes” lymph through the lymphatic system?

A

Smooth muscle in the lymph vessels react to pulsing of nearby arteries, then the squeezing of skeletal muscles exerts external pressure to keep lymph moving and reaching a lymphatic trunk

300
Q

What are the lymphatic trunks? What are they named after?

A

The lymphatic trunks are named after the regions of the body they drain the lymph into:

Two lumbar trunks
Two bronchomediastinal trunks 
Two subclavian trunks
Two jugular trunks 
One interstitial trunk
301
Q

what places does lymph go from the trunks?

A

Either the right thoracic duct (collects from right arm and right side of head and chest)

OR

Thoracic duct, much bigger (collects from rest of body)

302
Q

Where does the right lymphatic duct dump lymph into?

A

The junction of the right jugular vein and right subclavian vein

303
Q

Where does the thoracic duct dump lymph into?

A

The junction of the left jugular vein and left subclavian vein

Same junction as right duct but on L side of body

304
Q

Why do lymph ducts dump into the junction of jugular and subclavian veins?

A

Because the pressure is very low, easier for lymph to flow in

305
Q

What are lymph nodes in the intestinal wall called?

A

Peyer’s patches

306
Q

What types of cells detect pathogen in lymph nodes?

A

Dendritic cells

307
Q

Pathway of infection in lymph

A

Lymphatic capillary > vessel > node: sensed by dendritic cell and presented to B cells to make antibodies

Circulating T cells look for pathogens tagged with antibodies

308
Q

What are the three MAIN groups of lymph nodes?

A

Inguinal
Axillary
Cervical

309
Q

What group of lymph nodes drained abdominal wall below umbilicus, lower extremities, and genitalia

A

Inguinal

310
Q

What group of lymph nodes drains the posterior pharynx, tonsils, thyroid, and throat?

A

Anterior cervical

311
Q

What group of lymph nodes drains the scalp, neck, thorax, cervical, and axillary lymph nodes?

A

Posterior cervical

312
Q

What group of lymph nodes drains the Mediastinum, lungs, esophagus, and abdomen

A

Supraclavicular via thoracic duct

313
Q

What group of lymph nodes drains the Majority of the breast?

A

Axillary

314
Q

What are the great arteries of the heart that carry blood away from the heart?

A

Aorta + pulmonary arteries

315
Q

Describe the flow of blood to and from the heart, including when it is oxygenated and not.

A

LV pumps oxygenated blood > aorta > rest of body > deoxygenated loop comes back via RA > RV > to lungs via pulmonary artery > LA > LV

316
Q

What are the lymphaitc organs?

A

Diffuse lymphoid tissue, nodes/peyers patches, Thymus, spleen, tonsils

317
Q

Lymphatic function of tonsils

A

Form ring of lymphoid tissue around throat, trap pathogens from food eaten and air inhaled

318
Q

Lymphatic function of thymus

A

Development of T cells, making sure T cells that react to normal antigens are destroyed

Active neonatal and preadolescent then slowly atrophies and is replaced by fat after puberty

319
Q

Lymphatic function and location of spleen

A

L side of body below diaphragm, abovestomach

White pulp: antibodies generated by B cells, antibody coated bacteria filtered out

Red pulp: old and defective blood cells are destroyed, keeps RBC and platelets available

320
Q

What is the major relationship between the cardio and pulmonary systems?

A

They work together to circulate blood and oxygen throughout the body.

321
Q

What are the starling forces that affect lymph?

A

Govern passive exchange of water between capillary microcirculation and interstitial fluid

Determine directionality of net water movement between two compartments and the rate at which water exchange occurs

The direction of water exchange is determined by combo of relative hydrostatic and oncotic pressure of these two compartments, rate is governed by permeability of capillary itself

322
Q

What is the most common etiology of metastatic disease?

A

Lung tumors

323
Q

What is pericardial effusion?

A

Any fluid above normal 30-50mL found in pericardial space

324
Q

Pericardial effusion etiology

A

Typically due to hydrostatic or oncotic forces

325
Q

What is a hemopericardium? What causes it and what can it lead to?

A

Blood in pericardial sac

MI with rupture, traumatic perforation

Cases cardiac tamponade, death may occur

326
Q

Complications pleural effusion

A

Cardiac tamponade (fluid compresses heart, decreased CO)

327
Q

Pleural effusion clinical characteristics

A

Alternans on ECG, QRS alternating due to moving around in fluid

CXR-water bottle appearance
Echo- heart dancing in pericardium

328
Q

Bicuspid aortic valve etiology

A

Usually R + L coronary cusps are fused (common)

329
Q

Bicuspid aortic valve definition

A

2 instead of 3 lobes

330
Q

Complications bicuspid aortic valve

A

Ascending aortic aneurysm

331
Q

Bicuspid aortic valve clinical characteristics

A

Aortic stenosis and aortic regurgitation

Systolic ejection click just after S1

332
Q

Patent ductus arteriosis (PDA) RF

A

Prematurity

Rubella

333
Q

What is the most common septal congenital defect?

A

Interventricular septal defects

334
Q

Interventricular septal defects Complications

A

Increased risk of endocarditis

335
Q

Interventricular septal defects clinical characteristics

A

Asymptomatic holosystolic murmur

CHF

336
Q

What is the tetralogy in tetralogy of fallot

A

VSD
Pulmonic stenosis
RVH
Dextroposed aorta overriding VSD

337
Q

What are the four types of shock?

A

Hypovolemic, cardiogenic, obstructive, distributive

338
Q

What are causes of hypovolemic shock?

A

Hemorrhage, dehydration, burns

339
Q

What are causes of cardiogenic shock?

A

Acute MI, HF, valvular dysfunction, arrhythmia

340
Q

What are causes of obstructive shock?

A

Cardiac tamponade, PE, tension pneumothorax

341
Q

What are causes of distributive shock?

A

Sepsis, anaphylaxis, CNS injury

342
Q

What are sx of hypovolemic shock?

A

Cold, clammy skin

343
Q

What are sx of cardiogenic shock?

A

Cold, clammy skin

344
Q

What are sx of obstructive shock?

A

Cold, clammy skin

345
Q

What are sx of distributive shock?

A

Warm, dry skin

346
Q

What are hemangiomas?

A

Common vascular birthmarks made of extra blood vessels in the skin, benign

347
Q

What is kaposi sarcoma?

A

Endothelial malignancy most commonly affecting skin, mouth, GI tract, respiratory tract

Metastatic, dangerous

HHV-8, HIV

348
Q

RF kaposi sarcoma?

A

Old Eastern European males, AIDS, organ transplant, lindau von hipple disease (cavernous type)

349
Q

complications kaposi sarcoma

A

Pericardial effusion

Cardiac tamponade

350
Q

kaposi sarcoma clinical characteristics

A

Purple/black papules that may scale

351
Q

What is Chagas’ disease?

A

Parasite (trypanosoma cruzi)

“Kissing bug”

352
Q

What is the leading cause of infectious myocarditis worldwide?

A

Chagas’ disease

353
Q

RF Chagas’ disease

A

Central American, Mexico, southern US (rare)

354
Q

Complications Chagas’ disease

A

Dilated cardiomyopathy, HF, reduced EF, arrhythmias, heart block
Cardiac arrest
Enlarged esophagus
Enlarged colon

355
Q

Chagas’ disease clinical characteristics

A 
Swelling at bite sitefever
Fatigue
Rash
Body aches
Headache
356
Q

What is the etiology of Lyme disease?

A

Borrelia burgdorferi

Deer tick bite

357
Q

RF Lyme disease

A

NE US

358
Q

Lyme disease complications

A 
AV block
Carditis 
Bell’s palsy
Migratory myalgia
Encephalopathy
Chronic arthritis
359
Q

Lyme disease clinical characteristics

A

Erythema migrans rash - bullseye rash

Flu like sx

360
Q

Rocky Mountain spotted fever etiology

A

Rickettsia rickettsii

Tick vector

361
Q

Rocky Mountain spotted fever clinical characteristics

A

Headache, fever, rash (vasculitis)

Rash starts at wrists and ankles and spreads to trunk, palms, soles

362
Q

What are the three types of viral hemorrhagic fever?

A

Yellow fever, dengue fever, filoviruses

363
Q

Yellow fever (viral hemorrhagic fever) clinical characteristics

A

High fever, black vomitus, jaundice

May see councilman bodies on liver biopsy

364
Q

a deficiency B1 can lead to what

A

B1 deficiency (wet beriberi) can lead to high output cardiac failure (dilated cardiomyopathy)

NPLEX I (2022) (20 decks)

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