Cardio Flashcards
1
Q
Angiotensin ultimately originates in what organ?
A
The liver
2
Q
Which apoprotein is responsible for the assembly of VLDL in the liver?
A
ApoB-100
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)
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.
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
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
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)
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
9
Q
What are the location/boundaries of the pericardium?
A
Lies within the mediastinum; inferior wall of fibrous pericardium attaches to diaphragm
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
11
Q
What nerve innervates the pericardium?
A
Phrenic nerve
12
Q
What is the most posterior part of the heart?
A
Left atrium
13
Q
What is the most anterior part of the heart?
A
Right ventricle
14
Q
What is the most commonly injured part of the heart in trauma?
A
Right ventricle
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)
16
Q
Where is the best place to listen to the mitral valve?
A
5th L ICS MCL (apex)
17
Q
Where is the best place to listen to the tricuspid valve?
A
5th L ICS
18
Q
Where is the best place to listen to the pulmonic valve?
A
2nd L ICS
19
Q
Where is the best place to listen to the aortic valve?
A
2nd R ICS
20
Q
Where is Erb’s point?
A
3rd L ICS
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)
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)
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
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)
25
What pathology are associated with the erb’s point? For murmurs, know systolic vs diastolic.
Aortic regurgitation (diastolic)
Pulmonic regurgitation (diastolic)
Hypertrophic cardiomyopathy (systolic)
At erb's Point we get High
26
What pathology are associated with S3?
EARLY diastolic pathology
Mitral regurgitation
HF
Volume overload
Can be normal
27
What pathology are associated with S4?
LATE diastolic pathology
Hypertrophy
Pressure overload
Extreme HTN
ALWAYS ABNORMAL
S4 Dose Have Pretty Extreme Appetite
28
What causes the sound you hear for S1?
What part of the heart cycle occurs after S1 and before S2?
Where is it loudest?
Mitral and tricuspid valves closing
Systole
Mitral area
29
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?
Aortic and pulmonic valves closing
Diastole
L upper sternal area
30
Explain the pathway of conduction throughout the heart
SA node > atria > AV node > IV septum/Bundle of His > L+R bundle branches > purkinje fibers > ventricles
31
Explain how contraction of the heart is stimulated
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
32
Where in the heart conduction pathway does the signal slightly delay? Why?
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!
33
How does the cardiac conduction pathway begin?
Self excitation of SA node; caused by leaky sodium and calcium ions inward and rising resting membrane potential
34
How are purkinje fibers able to instantaneously transmit cardiac impulse through ALL of ventricular muscle?
Higher permeability of gap junctions at intercalated discs
35
What would you call a pacemaker anywhere else besides SA node?
Ectopic pacemaker
36
Explain the effect parasympathetic stimulation on the heart conduction pathway
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
37
Explain the effect sympathetic stimulation on the heart conduction pathway
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
38
What does the P wave of the cardiac cycle represent?
Atrial depolarization; followed by atrial contraction
39
What does the QRS complex of the cardiac cycle represent?
Ventricular depolarization; followed by ventricular contraction
40
What does the T wave of the cardiac cycle represent?
Ventricular repolarization; slightly before isovolumic relaxation, ventricles remain contracted until end of T wave
41
What does the R-R interval of the cardiac cycle represent?
Rate of one single cardiac cycle/heartbeat
42
What does the P-R/P-Q interval of the cardiac cycle represent?
Depolarization of atria to start of ventricle contraction
43
What does the Q-T interval of the cardiac cycle represent?
Depolarization and repolarization of ventricles
44
What would inversion of a T wave on an EKG indicate?
Ischemia or recent MI
45
What would a pathological U wave on an EKG indicate?
Hypokalemia
46
What does a long QTI predispose pts to? What is it caused by?
Torsades de pointes VTACH (wide QRS) > caused by drugs, low K or Mg, congenital abnormalities
47
Compare AV node fibers vs sinus nodal fibers
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
48
Where does the myocardial action potential occur?
All cardiac myocytes, except those in SA and AV nodes
49
Briefly explain overview of myocardial action potential?
Depolarization (more positive membrane) > AP plateaus > repolarization (more negative membrane)
50
Describe phase 0 of the myocardial action potential
Depolarization
Fast Na channels open
Slow Ca channels open
51
Describe phase 1 of the myocardial action potential
Initial repolarization
Fast Na channels close
Fast K channels open
Slow Ca channels still open
52
Describe phase 2 of the myocardial action potential
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
53
Describe phase 3 of the myocardial action potential
Rapid repolarization
Slow Ca channels close
Slow K channels open
54
Describe phase 4 of the myocardial action potential
Resting membrane potential
High potassium permeability through leaky potassium channels
NaK ATPase and NaCa (Na in Ca out) exchanger at work
55
Where does the pacemaker action potential occur?
SA and AV nodes
56
Describe phase 0 of the pacemaker action potential
Opening of Ca channels causes upstroke
fVNaC permanently inactivated > slow conduction velocity used by AV node to prolong transmission from A > V
57
Describe phase 3 of the pacemaker action potential
Inactivation of Ca channels
Activation of K channels
> K efflux
58
Describe phase 4 of the pacemaker action potential
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
59
What system controls HR and strength?
ANS
60
What is the basis of regulation of the cardiac cycle?
Intrinsic cardiac pumping regulation in response to changes in volume of blood flowing into the heart
61
What determines the amount of blood pumped into the heart each minute?
Venous return
62
What is the Frank-Starling Mechanism?
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
63
Explain sympathetic stimulation and its role in ANS control of the heart
Increased CO > increases HR and force of contraction > increases volume of blood pumped and ejection pressure
64
Explain parasympathetic stimulation and its role in ANS control of the heart
Deceased CO >
minor decrease of contraction strength
major decrease of HR
vagal nerve fibers distributed more to atria than ventricles
65
Explain the effect of potassium ions on heart function
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
66
Explain the effect of calcium ions on heart function
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
67
Where do the coronary arteries lie and where do they supply blood to?
CA and their branches lie in the epicardium and supply blood to the myocardium
68
During which heart phase do the coronary arteries fill?
Diastole
69
Describe the branching pattern of the coronary arteries
Aortic root > RCA + LCA
RCA > R marginal
RCA + LCA > PDA
LCA > LAD (widow)
LCA > circumflex > L marginal
70
What CA supplies blood to the SA node?
RCA
71
What CA supplies blood to the right ventricle?
RMA
72
Where does the LAD artery supply blood to?
Anterior 2/3 IV septum, anterior LV
73
Where does the circumflex artery supply blood to?
LA and posterior walls of LV
74
Where does the PDA supply blood to?
AV node, posterior 1/3 AV septum
75
Explain the branching of the aorta below the diaphragm
Inferior phrenic, celiac trunk (foregut), middle suprarenal arteries, renal arteries, SMA (midgut), testicular arteries, IMA (hind gut), lumbar arteries, common iliac arteries
76
What are the major lower extremity veins?
Anterior tibial, posterior tibial, peroneal veins, lower popliteal fossa, popliteal vein, superficial femoral vein
77
Explain the anatomy of the femoral and saphenous veins
Deep femoral v is lateral, joins superficial femoral and great saphenous in femoral canal, common femoral vein
78
In what pathologies would a high pulse pressure be present?
Hyperthyroid, aortic regurgitation, aortic stiffening, OSA, exercise
79
In what pathologies would a low pulse pressure be present?
Aortic stenosis, cardiogenic shock, cardiac tamponade, HF
80
What would cause high contractility?
B1R stim, increased intracellular Na/Ca
81
What would cause low contracility?
B1 blocker, HF, acidosis, hypoxia, NDHPCCB
82
What medication class would decrease preload?
Venous vasodilator (nitroglycerin, ACEis, ARBs)
83
What determines the amount cardiac muscles can contract in preload?
End diastolic volume
84
What determines afterload?
End systolic volume
85
What blood vessels have the highest total cross sectional area and lowest velocity?
Capillaries
86
Explain capillary fluid exchange
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
87
What are starling forces and what do they determine?
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
88
Explain the acute effects of early exercise on the CV system.
CO maintained by increased HR and SV
89
Explain the adaptive effects of late exercise on the CV system.
CO maintained by HR only (as SV plateaus)
As HR increases > less filling time > decreased CO > diastole is shortened
90
Explain the function and biochem of atrial natiuretic peptide
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
91
Explain the function and biochem of brain natriuretic peptide
Released from ventricular myocytes in response to increased tension
Longer half life than ANP
Used to Dx HF
92
Explain the function and biochem oF LDL
Transports cholesterol made in the liver to the tissues
93
Explain the function and biochem of HDL
Scavenges cholesterol from tissues and back to liver for disposal
94
Explain the unique relationship between the cardiovascular and pulmonary system
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
95
What is pulmonary HTN?
Increased pressure in pulmonary vasculature ONLY; elevated mean pulmonary artery pressure > 20 mmHg at rest
96
Explain the pathogenesis of pulmonary HTN and what it can lead to
Increased pulmonary vascular resistance > increased right ventricular pressure > increased right ventricular hypertrophy > right HF
97
What are the different possible causes of pulmonary HTN?
Idiopathic, inherited, drug induced, connective tissue disease
HD/HF (most common)
Lung disease and/or hypoxemia
Chronic thromboembolism
98
RF for pulmonary HTN
CHF, MI, chronic anemia, COPD/lung disease, chronic thromboembolism, pulmonary arterial HTN (genetic, idiopathic), lung fibrosis
99
Complications of pulmonary HTN
Arteriosclerosis, medial hypertrophy, intimal fibrous of pulmonary arteries, right HF
100
Clinical characteristics of pulmonary HTN
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
101
What is the most common type of systemic HTN and its causes?
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
102
What is the most common cause of second degree systemic HTN?
Renal/renovascular disease
103
What is seen microscopically in pulmonary HTN?
Smooth muscle proliferation occurs due to decreased apoptosis; genetic connection to BMPR2 gene
104
RF for systemic HTN
Increased age, obesity, DM, physical inactivity, excess salt, excess alcohol, smoking, fhx
AA > caucasians > Asian
105
Complications of systemic HTN
CAD, HF, left ventricular hypertrophy, a fib, aortic dissection, aortic aneurysm, stroke, CKD, retinopathy
106
What defines a hypertensive crisis, hypertensive urgency, and hypertensive emergency?
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)
107
Sx of systemic HTN
Commonly asymp
Fundoscopic exam showing hypertensive retinopathy (not required for dx)
108
What is congestive heart failure?
Cardiac pump dysfunction leads to congestion of the heart, decreased CO, and low perfusion
109
Types of left sided CHF
Systolic dysfunction: HF with reduced EF, increased EDV, decreased contractility
Diastolic dysfunction: HF with preserved EF, normal EDV, decreased compliance (increased EDP)
110
Etiology/causes of L CHF
Ischemic HD
HTN
Aortic and mitral valvular diseases
Myocardial disease
111
Common causes of R CHF
Left HF
Pulmonary HTN
Cor pulmonale - isolated right HF due to pulmonary causes
112
RF for CHF
Old age, CAD, HTN, DM, valvular heart disease, tobacco, obesity
113
Complications of L CHF
A fib, stroke/thrombosis, hypoxic encephalopathy, coma, death, right HF
114
Shared clinical characteristics of both types of CHF
S3 heart sounds, rales, JVD, pitting edema
115
L CHF clinical characteristics
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
116
R CHF clinical characteristics
S3, rales, JVD, pitting edema
Congestive hepatomegaly (increased central venous pressure > increased resistance to portal flow) > NUTMEG LIVER on cadaver exam
Dyspnea, orthopnea, fatigue
117
what is angina pectoris?
Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm, no myocyte necrosis
118
Different types of angina pectoris
Stable angina
Vasospastic/variant
Unstable angina
119
Stable angina definition
most common
usually secondary to atherosclerosis (>70% occlusion)
triggered by: atherosclerosis, activity, BP, HR
120
Vasospastic/variant angina definition
occurs at rest secondary to CA spasm
triggered by: cocaine, alcohol, triptans
121
Unstable angina definition
Thrombosis with incomplete coronary artery occlusion
Triggered by: atherosclerosis, activity, BP, HR
122
RF for stable and unstable angina
HTN, HLD, tobacco, MI RF
123
RF for vasospastic/variant angina
Tobacco use
124
Clinical characteristics of stable angina
Pain on exertion, resolves with rest
No ECG changes
125
Are troponin levels elevated in any forms of angina?
No
126
Clinical characteristics of vasospastic angina
Pain at rest secondary to coronary artery spasm
Transient ST elevation on ECG
127
Clinical characteristics of chronic ischemic heart disease
Enlarged heavy heart with L ventricular hypertrophy and dilation
Obstructive ordinary atherosclerosis
Scars from healed infarcts
128
Complications of chronic ischemic heart disease
Leading cause of death worldwide
Progressive CHF leading to heart transplant
129
Clinical characteristics of unstable angina
Pain on mild extortion or at rest
Possible ST depression/T-wave inversion on ECG
130
What is chronic ischemic heart disease
Progressive onset of HF over many years due to chronic ischemic myocardial damage
131
What is myocardial ischemia
Imbalance between supply (perfusion) and demand of heart for oxygenated blood
132
Etiology of chronic ischemic heart disease
Reduced blood flow to obstructive atherosclerotic lesions in coronary artery, usually preceded by MI
Progression of CAD
133
Pathogenesis of chronic ischemic heart disease
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
134
RF of chronic ischemic heart disease
HLD, HTN, MI, tobacco use, alcohol use, sedentary lifestyle, age, SAD diet
135
What is a myocardial infarction
Death of cardiac muscle due to prolonged severe ischemia
136
Most common cause of myocardial infarction
Rupture of coronary artery atherosclerotic plaque
137
Commonly occluded arteries with MIs
LAD > RCA > circumflex
138
Pathogenesis of MI
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
139
Biochem of MI
Loss of blood flow > cessation of aerobic metabolism within seconds
Inadequate production of ATP > accumulation of lactic acid
140
STEMI characteristics
Transmural
Full thickness
ST elevation, pathological Q waves
141
NSTEMI characteristics
Subendothelial
Subendocardium (inner 1/3)
ST depression
142
What is seen on microscopy at 0-24 hours, 1-3 days, 3-14 days, and 14+ days post MI
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
143
RF for MI
Age, genetics, males, post menopausal women (drop in estrogen), atherosclerosis
144
Complications of MI
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
145
Complications of MI by time frame (0-24 hours, 1-3 days, 3-14 days, 2+ weeks)
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
146
Clinical characteristics MI
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
Aortic stenosis - S or D?
S
148
Aortic regurgitation / insufficiency - S or D?
D
149
Mitral stenosis - S or D?
D
150
Mitral insufficiency - S or D?
S
151
Mitral valve prolapse - S or D?
S
152
Etiology of aortic stenosis
Age-related calcification, bicuspid aortic valve
153
RF aortic stenosis
Age, atherosclerosis, bicuspid aortic valve
154
complications of aortic stenosis
SAD (syncope, angina, DOE), LV pressure is less than aortic pressure during systole
155
Clinical characteristics aortic stenosis
Cresc-decresc ejection murmur
Pulses parvus et tartus (weak pulse)
Soft S2 and ejection click
156
Etiology aortic regurgitation
BEAR (bicuspid aortic valve, endocarditis, aortic root dilation, rheumatic fever
157
Complications aortic regurgitation
L CHF
158
Clinical characteristics aortic regurgitation
Early diastolic decrescnedo
High, blowing murmur
Wide PP
Pistol shot femoral pulse
Pushing nail bed
159
Mitral stenosis etiology
Rheumatic fever
160
Mitral stenosis pathogenesis
L atrial pressure > ventricular pressure
161
Mitral stenosis complications
Left atrial dilation, pulmonary congestion, a fib, ortner syndrome, hemopytsis, RCHF
162
Mitral stenosis clinical characteristics
Follows opening snap, delayed rumbling mid-late murmur
163
Mitral insufficiency etiology
Ischemic heart disease (post MI), MVP, LV dilation, rheumatic fever, infective endocarditis
164
Mitral insufficiency clinical characteristics and sound
asymptomatic to shortness of breath, fatigue, and inability to exercise may arise (later in disease)
Holosystolic, high pitched blowing murmur
165
Types of endocarditis
Infective/bacterial
No bacterial thrombotic endocarditis
166
Etiology infective endocarditis
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
Pathogenesis infective endocarditis
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
Non bacterial thrombotic endocarditis etiology
Marantic endocarditis; rare
Vegetations arise on mitral or aortic valve, consists of sterile, platelet-rich thrombi that dislodge easily
169
RF of infectious endocarditis
Subacute: dental procedure
RF by bacteria;
Prosthetic valves - s epidermis
GI/GU procedure - enterococcus
IV drug use - S aureus, pseudomonas, candida
170
RF nonbacterial endocarditis
Hypercoagulable state from advanced malignancy (pancreatic adenocarcinoma) or SLE (Libman sacks endocarditis)
171
Complications of bacterial endocarditis
Leads to valve regurgitation, septic embolism
172
Complications of nonbacterial endocarditis
Embolism
173
Clinical characteristics of infectious endocarditis
```
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
Nonbacterial endocarditis clinical characteristics
Asymptomatic
175
Mitral valve prolapse etiology
Rheumatic fever, chordae rupture, myxomatous degeneration (primary or secondary due to connective tissue disease)
176
Mitral valve prolapse complications
Typically benign, can predispose to infective endocarditis
177
Mitral valve prolapse clinical characteristics
Late crescendo murmur with midsystolic click occurring after carotid pulse
178
Rheumatic heart disease definition
Immune mediated (type II hypersensitivity)
Antibodies react to M protein, cross-react with self-antigens (often myosin)
179
Rheumatic heart disease etiology
Pharyngeal infection with group A B-hemolytic strep
Not direct effect of bacteria
180
Pathogenesis rheumatic heart disease
Affects heart disease mitral > aortic > tricuspid (MAT)
181
Complications rheumatic heart disease
Early valvular regurgitation
Late valvular stenosis
182
Clinical characteristics rheumatic heart disease
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
Carcinoid heart disease definition
Cardiac manifestation of systemic syndrome caused by carcinoid tumors (occurs in 50% of people)
184
Carcinoid heart disease etiology
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
Carcinoid heart disease complications
Tricuspid insufficiency then pulmonary valve insufficiency
186
Carcinoid heart disease clinical characteristics
Flushing of skin, cramps, N/V, diarrhea
187
Types of cardiomyopathies
Dilated, Hypertrophic, Restrictive
188
Dilated cardiomyopathy etiology
Most common, dilation of cardiac chambers (ventricles)
Idiopathic, genetic, drugs, infxn, ischemia, systemic
189
Hypertropic cardiomyopathy etiology
Second most common; enlargement of cardiac muscle surrounding ventricles
Familial, autosomal dominant, chronic HTN, friedrich ataxia
190
Restrictive cardiomyopathy etiology
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
Dilated cardiomyopathy complications
Systolic dysfunction
| Clot formation
192
Hypertrophic cardiomyopathy complications
Diastolic dysfunction
Sudden death in young athletes
Arrhythmias
193
Restrictive cardiomyopathy complications
Diastolic dysfunction
194
Dilated cardiomyopathy clinical characteristics
CHF, S3, systolic regurgitation murmur, dilated heart on echo
BALLOON APPEARANCE OF HEART ON CXR, ECCENTRIC HYPERTROPHY IN VENTRICLE, sarcomeres added in series
195
Hypertrophied cardiomyopathy clinical characteristics
S4, systolic murmur, mitral regurgitation, dyspnea, syncope
VENTRICULAR CONCENTRIC HYPERTROPHY, MUSCLE TISSUE ENLARGED, sarcomeres added in parallel
196
Restrictive cardiomyopathy clinical characteristics
Low voltage ECG
MUSCLE LESS COMPLIANT, LESS CONTRACTILE
197
Myocarditis etiology
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
Complications of myocarditis
SCD (Major cause in adults >40)
Arrhythmias, heart block, dilated cardiomyopathy, CHF, mural thrombus with systemic emboli
199
Myocarditis clinical characteristics
Dyspnea, chest pain, fever, arrhythmias (persistent tachycardia out of proportion to fever)
If viral in etiology: lymphocytic infiltrate with focal necrosis
200
Pericarditis definition
Inflammation of pericardium, fluid accumulates around heart
201
Pericarditis etiology
Primary and secondary
SCCARR IIN pericardium
```
Surgery
Connective tissue disorder
CV events
Autoimmune
Radiation
Renal failure
Idiopathic (most common)
Infection (coxsackie B)
Neoplasm
```
202
Pericarditis complications
Pericardial effusion
203
Pericarditis clinical characteristics
Sharp pain, WORSE BY INSPIRATION, BETTER SITTING UP AND LEANING FORWARD
Friction rub
Diffuse ST elevation or depression
204
Patent ductus arteriosis definition
Ductus arteriosis failes to close after birth; allows blood to flow back to lungs
205
Patent ductus arteriosis etiology
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
Patent ductus arteriosis complications
Late cyanosis in lower extremities
207
Patent ductus arteriosis clinical characteristics
No symptoms or cyanosis, fatigue, tachycardia
Continuous machine-like murmur
PDA is normal in utero, and normally closes after birth
208
Tetralogy of fallot etiology
Anterosuperior displacement of infundibular septum
Most common cause of early childhood cyanosis
209
Tetralogy of fallot complications
Pulmonary stenosis forces R to L flow across VSD > RVH
210
Tetralogy of fallot clinical characteristics
Pulmonary infundibular stenosis
RVH - boot heaped heart on xray
Overriding aorta
VSD
“Tet spells” often caused by crying, fever, exercise
211
Aneurysm definition
Dilation of aorta
212
Types of aneurysm
Abdominal aortic
| Thoracic aortci
213
Abdominal aortic aneurysm pathogenesis
Transmural (all 3 layers)
Inflammation and extracellular matrix degradation
214
Abdominal aortic aneurysm RF
Tobacco, age, males, Fhx
215
thoracic aortic aneurysm pathogenesis
Aortic root dilation due to high pressure could lead to aortic valve regurgitation
216
Thoracic aortic aneurysm RF
HTN, bicuspid aortic valve, connective tissue disease (Marfan), tertiary syphilis
217
Abdominal aortic aneurysm Complications
Aortic dissection
218
thoracic aortic aneurysm
Aortic dissection
219
Abdominal aortic aneurysm clinical characteristics
Abdominal/back pain as sign of leaking, dissection, imminent rupture
Palpable pulsatilla abdominal mass
220
Abdominal aortic aneurysm clinical characteristics
Abdominal/back pain as sign of leaking, dissection, imminent rupture
221
Aortic dissection definition
Longitudinal intimal tear forming a false lumen
222
Types of aortic dissection
Stanford type A: proximal, ascending aorta
Stanford type B: distal, descending aorta, below L subclavian artery
223
Aortic dissection RF
HTN, bicuspid aortic valve, inherited CT disorders (Marfan syndrome)
224
Aortic dissection complications
Organ ischemia, aortic rupture, death
Aortic regurgitation, cardiac tamponade
225
Aortic dissection clinical characteristics
Tearing, sudden-onset chest pain radiating to back
Unequal BP in arms
CXR: mediastinal widening
226
Arteriosclerosis definition
Hardening of arteries, arterial wall thickening, loss of elasticity
227
How dose Arteriosclerosis affect blood vessels and which ones?
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
Atherosclerosis definition
Form of arteriosclerosis
Build up of cholesterol plaques in tunica intima
Elastic arteries and medium/large size muscular arteries
229
Atherosclerosis Etiology
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
Atherosclerosis complication
Atherosclerosis of CA (CAD) is #1 killer of M +F in US
CAD, MI
231
Atherosclerosis RF
HTN, tobacco, HLD, DM
Age, males, postmenopausal status, Fhx
232
Atherosclerosis clinical characteristics
Angina, claudication, asymptomatic
233
Familial hypercholesterolemia definition
Receptor disease from mutation in gene encoding for LDL
234
Familial hypercholesterolemia Pathophysiology
Loss of feedback > increased cholesterol levels
Premature atherosclerosis
Increased risk of MI
235
Familial hypercholesterolemia RF
Fhx
236
Familial hypercholesterolemia Complications
MI, CAD
237
Familial hypercholesterolemia clinical characteristics
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
Giant cell (temporal) arteritis etiology
Focal granulomatous inflammation
Increased ESR, IL-6 levels correlate with disease activity
Affects branches of carotid artery
239
Giant cell (temporal) arteritis RF
Females, over 50, polymyalgia rheumatica
240
Giant cell (temporal) arteritis complications
Irreversible blindness due to anterior ischemic optic neuropathy
241
Giant cell (temporal) arteritis clinical characteristics
UL HD, temporal artery tenderness, jaw claudication
242
Peripheral arterial disease (PAD) definition
Insufficient tissue perfusion due to narrowing or occlusion of aorta or peripheral branches
243
Peripheral arterial disease (PAD) Etiology
Narrow arteries reduce blood flow to arms/legs
Buildup of fatty, cholesterol-containing deposits on artery walls (atherosclerosis), reduces blood flow through arteries
244
Peripheral arterial disease (PAD) RF
Fhx, HTN, HLD, age, obesity, CAD
245
Peripheral arterial disease (PAD) Complications
Critical limb ischemia, stroke, MI
246
Peripheral arterial disease (PAD) clinical characteristics
```
Coldness in LE or foot
LE numbness
Weakness
Loss of peripheral pulses
Cramping
Skin color change
Sores that wont heal
ED
Hair loss
```
247
Pulmonary embolism definition
Obstruction of pulmonary artery or one of its branches by thrombus
248
Pulmonary embolism Etiology
Affected alveoli are ventilated but not perfused (V/Q mismatch)
249
Pulmonary embolism RF
```
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
Pulmonary embolism Complications
Sudden death due to clot preventing blood from filling LV
Hypotension, shock, recurrent thromboembolism, pulmonary infarction, RHF
251
Pulmonary embolism Clinical characteristics
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
Raynaud phenomenon definition
Color changes of skin due to decreased blood flow
253
Raynaud phenomenon Etiology
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
Raynaud phenomenon complications
Secondary: Digital ulceration
255
Raynaud phenomenon clinical characteristics
Color change from white (ischemia) to blue (hypoxia) to red (reperfusion)
Most often to fingers/toes
256
Thromboangitis Obliterans / Buerger disease definition
segmental, thrombosis, acute and chronic inflammation of medium sized and small arteries (tibial and radial)
257
Thromboangitis Obliterans / Buerger disease Etiology
Direct endothelial cell toxicity by tobacco or immune response to the same agents
258
Thromboangitis Obliterans / Buerger disease RF
Heavy cigarette smokers before age of 35
259
Thromboangitis Obliterans / Buerger disease Complications
Vascular insufficiency
260
Thromboangitis Obliterans / Buerger disease Clinical characteristics
Superficial nodular phlebitis, severe pain at rest, chronic ulceration of toes, fingers, feet
261
Deep vein thrombosis definition
Blood clot within a deep vein (proximal LE veins - iliac, femoral, popliteal)
262
DVT etiology
```
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
DVT RF
Obesity, contraceptives, pregnancy, fhx, previous venous thromboembolism, HRT
Inherited thrombophlebitis:
Factor V Leiden mutation
Protein C deficiency
Protein S deficiency
264
DVT complication
PE
265
DVT clinical characteristics
Leg swelling, pain, warmth, redness
Unilateral pitting edema in leg
D-dimer: rule OUT DVT
Wells criteria for DVT
266
Varicose veins etiology
Prolonged increased intraluminal pressure and loss of vessel wall support
Superficial veins of LE
267
Varicose veins RF
Obesity, FHx, females
268
Varicose veins complications
Increased venous pressure, venous stasis, pedal edema, stasis dermatitis, ulcerations
269
Varicose veins definition
Abnormally dilated, tortuous veins
270
Vasculitis definition
Vessel wall inflammation
271
Large vessel Vasculitis Etiology
aorta and large branches to extremities, head, neck
giant cell (temporal arteritis
Takayasu arteritis: granulomatous inflammation occurring in pts under 50
272
Types of Vasculitis
Large vessel, medium vessel, small vessel
273
Medium vessel Vasculitis etiology
Main visceral arteries and branches
Kawasaki disease: arteritis with mucocutaneous lymph node syndrome, in children. Coronary arteries involved with aneurysm or thrombosis
274
Small vessel Vasculitis etiology
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
Viral myocarditis etiology
Adenovirus, coxsackie B, parvovirus B19, HIV, HHV-6
276
Viral myocarditis clinical characteristics
Lymphocytes infiltrate with focal necrosis is highly indicative
277
The truncus arteriosis gives rise to…
Asc aorta + pulmonary trunk
278
Bulbus cordis gives rise to…
Outflow tract of LV and RV
279
Primitive ventricle/aorta gives rise to…
Trabeculated part f R + L ventricles/aorta
280
L horn of sinus venosus gives rise to…
Coronary sinus
281
R horn of sinus venosus gives rise to…
Smooth part of R atrium (sinus venarum)
282
When does the foremen ovale close? What causes this closure?
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
What is patent foramen ovale
Failure of septum primum and secundum to fuse after birth
284
What eventually develops into the arterial system?
Aortic arch derivatives
285
1st aortic arch derivative
Maxillary arteries - branch of ext carotid
1st arch is max
286
2nd aortic arch derivative
Stapedial and hyoid arteries
second stapedial
287
3rd aortic arch derivative
Common carotid artery and proximal part of internal carotid artery
288
4th aortic arch derivative
Aortic arch and proximal right subclavian artery
289
6th aortic arch derivative
Proximal part of pulmonary arteries and ductus arteriosus (left)
290
Endocardial cushion gives rise to…
Atrial septum, membranous IV septum, AV + semilunar valves
291
R common cardinal + R anterior cardinal vein gives rise to…
SCV
292
Posterior, subcardinal + supracardinal veins give rise to…
IVC
293
Primitive pulm vein gives rise to…
Smooth part of LA
294
What are the three roles of the lymphatic system
Returns interstitial fluid from tissues back to heart
Helps large molecules like hormones and lipids enter the blood
Helps with immune surveillance
295
When does interstitial fluid become lymph?
Once in the lymphatic vessels
296
Where is all of the collected lymph dumped?
Veins
297
When do the one way mini valves of lymphatic capillary walls open?
When pressure in interstitial space is greater than pressure in lymphatic capillary, endothelial mini valves open
298
Lymph vessel flow
Capillaries > bigger vessels > trunks > ducts
299
What “pushes” lymph through the lymphatic system?
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
What are the lymphatic trunks? What are they named after?
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
what places does lymph go from the trunks?
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
Where does the right lymphatic duct dump lymph into?
The junction of the right jugular vein and right subclavian vein
303
Where does the thoracic duct dump lymph into?
The junction of the left jugular vein and left subclavian vein
Same junction as right duct but on L side of body
304
Why do lymph ducts dump into the junction of jugular and subclavian veins?
Because the pressure is very low, easier for lymph to flow in
305
What are lymph nodes in the intestinal wall called?
Peyer’s patches
306
What types of cells detect pathogen in lymph nodes?
Dendritic cells
307
Pathway of infection in lymph
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
What are the three MAIN groups of lymph nodes?
Inguinal
Axillary
Cervical
309
What group of lymph nodes drained abdominal wall below umbilicus, lower extremities, and genitalia
Inguinal
310
What group of lymph nodes drains the posterior pharynx, tonsils, thyroid, and throat?
Anterior cervical
311
What group of lymph nodes drains the scalp, neck, thorax, cervical, and axillary lymph nodes?
Posterior cervical
312
What group of lymph nodes drains the Mediastinum, lungs, esophagus, and abdomen
Supraclavicular via thoracic duct
313
What group of lymph nodes drains the Majority of the breast?
Axillary
314
What are the great arteries of the heart that carry blood away from the heart?
Aorta + pulmonary arteries
315
Describe the flow of blood to and from the heart, including when it is oxygenated and not.
LV pumps oxygenated blood > aorta > rest of body > deoxygenated loop comes back via RA > RV > to lungs via pulmonary artery > LA > LV
316
What are the lymphaitc organs?
Diffuse lymphoid tissue, nodes/peyers patches, Thymus, spleen, tonsils
317
Lymphatic function of tonsils
Form ring of lymphoid tissue around throat, trap pathogens from food eaten and air inhaled
318
Lymphatic function of thymus
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
Lymphatic function and location of spleen
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
What is the major relationship between the cardio and pulmonary systems?
They work together to circulate blood and oxygen throughout the body.
321
What are the starling forces that affect lymph?
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
What is the most common etiology of metastatic disease?
Lung tumors
323
What is pericardial effusion?
Any fluid above normal 30-50mL found in pericardial space
324
Pericardial effusion etiology
Typically due to hydrostatic or oncotic forces
325
What is a hemopericardium? What causes it and what can it lead to?
Blood in pericardial sac
MI with rupture, traumatic perforation
Cases cardiac tamponade, death may occur
326
Complications pleural effusion
Cardiac tamponade (fluid compresses heart, decreased CO)
327
Pleural effusion clinical characteristics
Alternans on ECG, QRS alternating due to moving around in fluid
CXR-water bottle appearance
Echo- heart dancing in pericardium
328
Bicuspid aortic valve etiology
Usually R + L coronary cusps are fused (common)
329
Bicuspid aortic valve definition
2 instead of 3 lobes
330
Complications bicuspid aortic valve
Ascending aortic aneurysm
331
Bicuspid aortic valve clinical characteristics
Aortic stenosis and aortic regurgitation
| Systolic ejection click just after S1
332
Patent ductus arteriosis (PDA) RF
Prematurity
| Rubella
333
What is the most common septal congenital defect?
Interventricular septal defects
334
Interventricular septal defects Complications
Increased risk of endocarditis
335
Interventricular septal defects clinical characteristics
Asymptomatic holosystolic murmur
| CHF
336
What is the tetralogy in tetralogy of fallot
VSD
Pulmonic stenosis
RVH
Dextroposed aorta overriding VSD
337
What are the four types of shock?
Hypovolemic, cardiogenic, obstructive, distributive
338
What are causes of hypovolemic shock?
Hemorrhage, dehydration, burns
339
What are causes of cardiogenic shock?
Acute MI, HF, valvular dysfunction, arrhythmia
340
What are causes of obstructive shock?
Cardiac tamponade, PE, tension pneumothorax
341
What are causes of distributive shock?
Sepsis, anaphylaxis, CNS injury
342
What are sx of hypovolemic shock?
Cold, clammy skin
343
What are sx of cardiogenic shock?
Cold, clammy skin
344
What are sx of obstructive shock?
Cold, clammy skin
345
What are sx of distributive shock?
Warm, dry skin
346
What are hemangiomas?
Common vascular birthmarks made of extra blood vessels in the skin, benign
347
What is kaposi sarcoma?
Endothelial malignancy most commonly affecting skin, mouth, GI tract, respiratory tract
Metastatic, dangerous
HHV-8, HIV
348
RF kaposi sarcoma?
Old Eastern European males, AIDS, organ transplant, lindau von hipple disease (cavernous type)
349
complications kaposi sarcoma
Pericardial effusion
| Cardiac tamponade
350
kaposi sarcoma clinical characteristics
Purple/black papules that may scale
351
What is Chagas’ disease?
Parasite (trypanosoma cruzi)
“Kissing bug”
352
What is the leading cause of infectious myocarditis worldwide?
Chagas’ disease
353
RF Chagas’ disease
Central American, Mexico, southern US (rare)
354
Complications Chagas’ disease
Dilated cardiomyopathy, HF, reduced EF, arrhythmias, heart block
Cardiac arrest
Enlarged esophagus
Enlarged colon
355
Chagas’ disease clinical characteristics
```
Swelling at bite sitefever
Fatigue
Rash
Body aches
Headache
```
356
What is the etiology of Lyme disease?
Borrelia burgdorferi
Deer tick bite
357
RF Lyme disease
NE US
358
Lyme disease complications
```
AV block
Carditis
Bell’s palsy
Migratory myalgia
Encephalopathy
Chronic arthritis
```
359
Lyme disease clinical characteristics
Erythema migrans rash - bullseye rash
| Flu like sx
360
Rocky Mountain spotted fever etiology
Rickettsia rickettsii
| Tick vector
361
Rocky Mountain spotted fever clinical characteristics
Headache, fever, rash (vasculitis)
| Rash starts at wrists and ankles and spreads to trunk, palms, soles
362
What are the three types of viral hemorrhagic fever?
Yellow fever, dengue fever, filoviruses
363
Yellow fever (viral hemorrhagic fever) clinical characteristics
High fever, black vomitus, jaundice
| May see councilman bodies on liver biopsy
364
a deficiency B1 can lead to what
B1 deficiency (wet beriberi) can lead to high output cardiac failure (dilated cardiomyopathy)
