Cardioresp Flashcards
1
Q
What phase of AP = Automaticity?
A
phase 4
2
Q
What phase of AP = conduction velocity
A
phase 0
3
Q
What phase of AP = refractory period
A
phase 2 & 3
4
Q
what phase of AP’s do BB’s effect?
A
Phase 4 (slows automaticity)- also slows SAN & AVN
5
Q
which node do CCB’s slow more?
A
AVN> SAN
6
Q
Mech of Class I antiarrhythmics
A
Na+ blockers
7
Q
Class Ia anti arrhythmic and mech
A
Procainamide (Quinidine, Disopyramide)Na+ blocker
8
Q
Class Ib anti arrhythmic and mech
A
Lidocaine (IV) and Mexilitine (PO)Na+ blockers
9
Q
Class IC anti arrhythmic and mech
A
Flecainide and PropafenoneNa+ blockers
10
Q
Mech of Class III antiarrhythmics
A
K+ blockers
11
Q
Class III antiarrhythmics
A
AmioSotalol(Ibutilide, Dofetilide, Dronedarone)
12
Q
What phase do class I antiarrhythmics effect mainly?
A
Phase 0 (and 2 & 3)
13
Q
What to watch out for w/ class Ia drugs (procainamide, disopyramide, quinidine)
A
QT prolongingRenal dysfunction
14
Q
Most common use for class Ia drugs
A
VT (monomorphic)[also SVT]
15
Q
are class Ib (lido/mex) use dependent? What does that mean?
A
Yes, better effect at faster HR
16
Q
Do lido/mex effect QT?
A
No!Can use for afterdepolarizations (dig-induced VT) Can use for torsades
17
Q
2 cautions for lido/mex
A
CHFHepatic dysfunction
18
Q
Which antiarrhythmics are the most potent Na+ blockers?
A
Class Ic (flecainide, Propafenone)
19
Q
Because they are the most potent Na+ blockers, what widens on ECG with Propafenone/flec?
A
QRS (not QT)
20
Q
Used for a fib or refractory SVTs (refused ablation, other meds didn’t work)?
A
Class Ic (flec/propafenone)
21
Q
When is mortality increased with Class Ic (flec/propafenone)
A
structural heart dz (LV dysfxn, LVH, MI, ischemia)
22
Q
what is a common/serious pro arrhythmic effect of class Ic? what is the Rx for it?
A
Can slow Aflutter and cause 1:1 AV conduction.Use with AVN blockers
23
Q
which trial showed that class Ic meds (flecainide, propafenone) had increased mortality with structural heart dz?
A
CAST
24
Q
Even thoughts it a Class III (phase 3), what phases of AP does Amio effect?
A
Phase 0, 3, 4.
25
can you get sinus brady with amio?
yes!
26
What is mech of class III? What are its 2 clinical uses?
K+ channel blockersAfibVT
27
**Side effects of Class III drugs? Why?
Long QT/Torsades;, exacerbated by hypo Mg/K. Reverse-use dependence (works at slower HR---> torsades)
28
What to monitor with Class III meds?
Renal dysfxn (contraindicated)QT
29
most effective drug for preventing recurrent AF and for VT/VF?
Amio
30
Cardiac and Neuro side effects of Amio
bradycardiaLong QT/TorsadesHypotensionATAXIA (falling)TREMOR NEUROPATHY
31
Pulm/Thyroid/GI Side effects of Amio
pneumonitis/fibrosishyper/hypothyroidismincreased LFTs/nausea
32
Ocular/Derm side effects of Amio
corneal depositsretinopathyphotosensitivity/blue skin
33
*Important Drug interactions w/ Amio
warfarin, Dig (have to decrease their dosing)statins
34
Dronedarone indications and contraindications
Indication: PAF w/ 1 assoc. risk factor (age, HTN, LA>5cm, EF<40%)Contraindication: Chronic AF- inc. mortality/CVA/HF! Acute/severe CHF cirrhosis
35
Class IV agents, mech
diltiazemverapamilL-type CCB's (phase 0 and 4)
36
what do Class IV CCB's do to AVN?
prolong conduction and refractoriness
37
Dig mech.
1) BLOCKS Na-K ATPase -> increases intracellular Ca-->inotropy2) increases vagal tone in central CNS3) decreases AVN conduction/increases refractoriness
38
Best use for Dig
AF w/ RVR in CHF
39
what arrhythmia can dig overdose cause?
SVTBidirectional VTPAT w/ variable AVB
40
*Adenosine mech
-binds to Adenosine (A1) receptor-causes compete AVB transiently (dec. cAMP--> dec Ca/Na into cells)- reduces automaticity (hyperpolarizes cell men by inc. K+ outward)
41
*what is adenosine's action in the atria? What is Rx?
shortens atrial refractoriness--> propensity for AF (b/c of inc'd outward K+ flow).Do nothing
42
*adenosine contraindication/indication
asthma/diagnose and treat SVT
43
*adenosine response for:AVNRT/AVRTFocal ATAF/Flutter
AVNRT/AVRT - terminatesFocal AT- AV block can inc./doesnt usu. terminateAF/Flutter- unmasks AF/FL/AVB can inc.
44
which patients cannot get adenosine due to hypersensitivity?
OHT
45
Dig tox Rx?
DigibindDo NOT check dig levels after (they will be very high)
46
atropine mech
acetylcholine blocker
47
atropine indications
bradycardiaAVB
48
ocular side effect of atropine
glaucoma
49
which gender is more likely to get a fib?
male
50
A/C protocol for AF DCCV
TEE-guided or 3 weeks w/ INR>2.
51
at CHADS=2, what is annual stroke rate?
4% (start A/C)
52
CHADSVASC score = CHADS of 2?
4
53
what age gets a point in CHADSVASC?
65
54
Dabigatran (Pradaxa) mech/trial/dose/M&M
-direct thrombin inhibitor- RE-LY- 150 BID- superior to warfarin (dec mortality, ICH) but more GIB
55
which NOAG is potentially dialyzable? does it have a reversal agent?
Dabigatran (Pradaxa)No
56
Rivaroxaban (Xarelto) mech/trial/dose/M&M
-Factor Xa Inhibitor- ROCKET-AF- 20 BID- Noninf. to warfarin/dec. ICH
57
how are the NOAGs mainly excreted?
renal and feces
58
Apixaban (Eliquis) mech/trial/dose/M&M
-Factor Xa- ARISTOTLE-5 BID-superioir to warfarin/marked dec. in major bleeding/dec. ICH
59
what type of bleeding do all the NOAGs decrease c/t warfarin?
ICH
60
who do you rhythm control in a fib?
younghighly symptomaticPAFCHF from AF
61
if no cardiac dz, what antiarrhytmics do you use for a fib?
Class III (all but ibutilide: dronedarone/sotalol/amio for refractory AF/dofetilideClass Ic (flecainide/propfenone)
62
if pt. has CAD, best rhythm control strategy for AF?
Class III or ablation(no flecainide/propafenone)
63
If pt. has HTN, best rhythm control strategy for AF?
Class III/Ic drugs**if bad LVH (>1.5cm thick): have to use AMIO or ablation
64
*if pt. has CHF, rhythm control strategy for AF?
AmioDofetilife (not if on HD)ablation
65
contraindicated meds in AF w/ bypass tracts
BBCCBDig
66
Treatment for AF w/ bypass tracts
DCCVPROCAINAMIDEIBUTILIDEsotalolamioablation
67
why ablate AF?
sxs
68
which patients do you never send for AVN ablation?
young
69
AF ablation success rates after 1st and 2nd procesure?
1 procedure: 60-80%2nd procedure: >80%
70
major complication rate s/p AF ablation?
2-12%
71
which pts do best after AF ablation?
young, very symptomatic, PAF, normal EF, LA < 5cm, no pulm dz/OSA.
72
ibutilide use and monitoring protocol?
-acute conversion of afib (better for AFl)- >4hrs of monitoring QT.
73
at what QTc is dofetilide (Tikosyn) contraindicated?
440ms
74
what is the dosing algorithm for dofetilide accoridng to CrCl?
60ml/min: 500 BID
75
what happens if, after 2nd dose of dofetilide, QTc>500ms
D/C dofetilide
76
after checking QTc 2h after dofetilide, what is protocol?
if QTc inc'd >15% or is >500ms, decrease dose
77
Name 3 factors that can make a prolonged QT turn into torsades
Bradycardia HypomagnesemiaHypokalemia
78
Do you treat torsades with IV mag even if Mag level is normal?
Yes
79
Antiarrhythmic to Rx torsades
Lidocaine
80
When is no anticoagulatuon or ASA OK in afib?
Age<60No heart dz
81
HAS-BLED
HTN (uncontrolled)Abnormal liver or kidneys (Cr>2.6)StrokeBleedingLabile INRElderly (>65)drugs or alcohol
82
What HAS-BLED score indicates high risk?
3
83
Which NOAG can actually reduce mortality c/t warfarin?
Apixaban
84
When is Amio a first line agent as an antiarrhythmic in afib?
In CHF or Severe LVH (>1.5cm)
85
If a pt with multiple comorbidities (76y, HTN, DM, etc) comes in to clinic with afib and sxs but stable, what is your initial recommendation ?
Warfarin
86
Are lidocaine or Ibutilide in the algorithm for antiarrhythmic treatment of afib?
No
87
When does the heart first beat in embryological development?
Day 22
88
List the most common congential anamolies.
VSD - 42%ASD - 10%Pulmonary stenosis - 7%PDA - 7%Tertralogy of Fallot - 5%Aortic valve stenosis - 4%Atrioventricular septal (canal) defect - 4%TGA - 4%Persistent truncus arteriosus - 1%
89
At day 20, when the embryo begins to fold both cranially on itself and medially, what structures are being formed?
* Cranial fold starts the formation of the aortic arch
* right and left endocardial tubes start to come towards each other
* endocardial tubes are developing adjacent to fluid filled sack, the pericardial cavity
90
At day 21, the fusion of the right and left endocardial tube in the cardiogenic region leads to the formation of what?
a single heart tube
91
Draw the pericardial sac at day 21-22.Include aortic sac, bulbis cordis, ventricle, atrium, sinus venosus
92
Describe how the pericardial sac twists and folds into the heart structure.
93
At day 22 the heart starts to beat, what are the four layers of the heart at this point?
* Endocardium (primitive endocardium)
* Cardiac jelly (ECM)
* Myocardium (heart muscle)
* Epicardium (visceral pericardium)
94
The breakdown of what structure leads to the formation of the transverse pericardial sinus?
Dorsal mescardium
95
Another image of how the heart tube twists into form.
Typically twist to the left.
96
In what two conditions is the base of the heart directed to the right side of the body as opposed to the left? What differentiates the two conditions?
Dextrocardia (1/12,000 births) - increased risk of additional heart defectsSitus Inversus - all organs are completely reversed (1/7000 births) - only slight increased risk of additional heart defects
97
What helps form the septum intermedium (which helps separate atrium from ventricles)?
Endocardial cushions (posterior and anterior), Day 28
98
Abnormalities in endocardial cushions can lead to what type of defects?
ASD, VSD, AV canal defects, and TGA
99
What type of cells contribute to the cells that form the endocardial cushion?
Neural crest cells
100
People who have a variety of craniofacial defects are at greater risk of having endocardial cushion defects. What condition could lead to increased risk of atrioventricular septal (canal) defects?
Trisomy 21, Downs
101
What is believed to impair/inhibit neural crest cell migration?
Binge drinking alcohol
102
What causes atrioventricular septal (canal) defects? What is true about the four chambers of the heart?
Endocardial cushion defect; no separation of the four chambers
103
What are the main clinical symptoms of the atrioventricular septal (canal) defects?
Tachypnea, poor feeding, growth retardation around 6 weeks of age as pulmonary vascular resistance continues to fall
104
What two structures help to separate the R and L atria? Describe the characteristics of each.
Septum primum and septum secundum. The secundum is stiffer than the primum. The primum is more pliable.
105
The interface b/t the septum primum and septum secundum forms what structure? As an embryo this allows blood to travel in what direction?
Oval ForamenIt allows blood to flow from the R atrium to the L atrium. After birth, the L atrium becomes a higher pressure system stopping this flow.
106
What type of shunt is ASD? What murmur is commonly associated with ASD?
L to R shunt"split" S2
107
What is the most common type of ASD? What is the male to female ratio?
Secundum; 2 females for every male
108
Why is a patent foramen ovale not considered an ASD?
B/c no septal tissue is missing, it is just that the two atrial septa fail to fuse with each other. Interatrial shunting cannot occur as long as L atrial pressure exceeds R atrial pressure.
109
What structure grows into the right atrium? The left atrium?
R atrium: sinus venarumL atrium: pulmonary veins
110
What begins to grow up from the inferior wall of the ventricles towards the septum intermedium during the 4th week?
Muscular interventricular septum
111
Most common heart defect? Type of shunt?
VSD, L to R shunt
112
What is different about the presentation of small VSDs and large VSDs?
Small VSD: systolic murmurs by 48 hrs after birthLarge VSD: present at 3 to 12 wks with tachypnea, grunting respiration, and slow weight gain
113
What ultimately divides into the aorta and pulmonary trunk?
Truncus Arteriosus
114
What is the most common type of interventricular septal defect?
Membranous (thin) portion of interventricular septum
115
What are some possible of congential heart defects that come as a result of failure of the sepetation of the truncus ateriosus outflow tract?
TGAPulmonary stenosisPTATOF
116
What happens in TGA? What is their saving grace?
Aorta sits of the right ventricle and pulmonary artery sits over the left ventricle. The PDA will help the patient get some oxygenated blood until surgery can be done to swap the position of the arteries
117
For newborns w/ TGA to survive, there must be communication between the two sides of the heart. What two structures can help with this communication?
Peristent or patent foramen ovale or PDA
118
What is PTA? How do newborns present and what will happen without surgical intervention?
Persistent truncus arteriosus is a congenital cardiac malformation in which the outflow of the heart is through a single vessel rather than a pulmonary trunk and aorta.Present w/ cyanosis. Most die of CHF unless surgically corrected
119
What is the clinical presentation of TOF?
Newborns can be cyanotic and fail to thriveMost often: detected during well baby checks, months after they leave the hospital. Sudden incidences of cyanosis w/ hyperpnea are common from 2 mo to the 2 y. Surgery is necessary for survival into adulthood.
120
What determines the severity of TOF?
degree of pulmonary stenosis
121
How will more severe pulmonic stenosis affect heart sounds?
More pulmonic stenosis, greater splitting of S2
122
What is aortic stenosis?
Condition in which the leaves (cusps) of the aortic valve become stiff or fuse together, leaving only a smaller opening for blood to leave the L ventricle
123
In adults, aortic valvular stenosis can lead to what?
Enlargement of the aortic arch due to jetting of blood
124
What is coarction of the aorta?
Constriction in the aorta 95% of the time just above or just below the attachment of the ductus arteriosus
125
What is the hallmark that leads to diagnosis of coarction of the aorta in an adult?
HTN in upper extremities and hypotension in the lower limbs, murmur heard posteriorly in the interscapular regions, notching of the under surface of ribs
126
What are III, IV, VI arch of the of the aorta
III - common and part of internal carotid arteryIV - right subclavian artery (R) and arch of the aorta (L)VI (pulmonary arteries)
127
The acyanotic L-R shunt associated with VSD puts patients at increased risk for?
Pulmonary hypertension
128
What is a patent ductus arterosis?
Failure of ductus arteriosus to close. This results in left to right shunt between aorta and the pulmonary artery
129
What are the three main examples of left to right shunt congenital heart diseases?
ASD, VSD and PDA
130
What are the main clinical features of Tetrology of Fallot?
P - Pulmonary StenosisR - Right ventricular hypertrophyO - Overriding of the aortaV - Ventricular Septal defect
131
What is the most common type of ASD?
The septum secundum is a subsequent membranous ingrowth located to the right and anterior of the septum primum.
132
What can induce closure of a PDA?
Indomethacin
133
This "boot shaped" image of the heart is due to what disease?
Tetralogy of fallot - he heart is typically enlarged and is classically “boot-shaped” due to marked right ventricular hypertrophy. The VSD is usually large with the aortic valve at the superior border, thereby overriding the defect and both ventricular chambers. The obstruction to right ventricular outflow is most often due to narrowing of the infundibulum (sub-pulmonic stenosis) but can be accompanied by pulmonary valvular stenosis. Sometimes there is complete atresia of the pulmonary valve and variable portions of the pulmonary arteries, such that blood flow through a PDA, dilated bronchial arteries, or both, is necessary for survival. Aortic valve insufficiency or an ASD may also be present; a right aortic arch is present in about 25% of cases.
134
What is a tetralogy spell?
A sudden increased constriction of the out flow tract to the lungs
135
What disease is this an image of?
Transposition of the Great Vessels
136
What common genetic syndrome tends to be associated with CHD?
Down syndrome
137
When can a diagnosis of Transposition of the Great Vessels be made?
Within the first hours or days of life. This patient will have severe cyanosis due to circulation running in parallel.
138
How will a patient with Tetrology of Fallot present in clinic?
This patient will have a loud murmur in the first few weeks of life or this patient will have cyanosis. These patients may also have rapid breathing in response to low O2 levels.
139
With the normal on the left, explain what the disease is and what is occuring in the image.
This is VSD. Blood from the LV is under higher pressure, so some moves to the RV, which overloads the pulmonary circulation, and may eventually lead to pulmonary hypertension. RV hypertrophy from volume overload, and LV hypertrophy (because it’s pumping more blood than normal, because of the defect)
140
How will coarctation of the Aorta present clinically?
These patients will have hypertension in the upper parts of the body and hypotension in lower parts. Anastomoses will develop between subclavian artery and aorta through the intercostal arteries. Notching of the ribs.
141
What will occur in patients with a Patent Ductus Arteriosus?
These patients will present with clubbing of toes not fingers. This is due to shunting of hypoxemic blood from PA to descending aorta.
142
What is a VSD?
An incomplete closure of the ventricular septum. This accounts for roughly 40% of CHDs.
143
What is this an image of?
Ventricular septal defect, muscular wall of the septum
144
What is this an image of?
A ventricular septal defect (membranous type)
145
When is the most likely age of presentation of ASD?
Patients usually do not present until age 30
146
What is the special murmur associate with PDA?
Machinery murmur
147
What rare syndrome is associated with CHD?
DiGeorge syndrome
148
What might you want to do in regards to the ductus arteriosus in a patient with TOF?
You may not want their ductus arteriosus to close. May want to give these patients prostaglandin to keep it open.
149
In a patient with TOF what will happen if they are given extra oxygen?
This will have little change.
150
When does a PDA tend to close?
It closes functionally within 10-15 hours of birth. Anatomically it closes 2-3 days after (fusion)
151
This image is associated with which CHD?
Tetralogy of fallot
152
Eisenmengers syndrome is a result of?
Pulmonary vascular disease that develops in patients with large unclosed VSDs. This can lead to shunt reversal then cyanosis and eventually death.
153
What provides blood to the lungs and reduces cyanosis in patients with TOF?
PDA
154
What determines the severity of TOF?
Clinical severity of the disease depends on the extent of pulmonary stenosis.
155
With the normal being on the left what is the disease occurring in the right image?
This is an image of a Patent Ductus Arteriosus
156
Patients with a VSD are at increased risk for?
Pulmonary hypertension
157
What is this an image of ?
Notching of the ribs associated with Coarctation of the Aorta.
158
What aortic stenosis caused by?
This tends to be caused by a bicuspid aortic valve instead of a tricuspid valve. This leads to microtrauma to the valve.
159
What is a paradoxical emboli?
This is a emboli that has crossed an ASD
160
What are the main examples of right to left shunt congenital heart diseases?
Tetralogy of fallot and transposition of the great arteries
161
What is coarctation of the Aorta?
This is a narrowing of the aorta. Infantile forms present as lower extremity cyanosis. Adult forms have hypertension in upper extremeties and hypotension in lower.
162
What does conductance (g) refer to?
The ability of the ions to cross the cell membrane
163
At any instant of time, how does the magnitude of electrical force compare b/t ions?
All ions experience the same magnitude of force. The directionality will vary depending on the charge of the ion.
164
What are three factors that influence the conductance of an ion?
of open ion channels# of leak channelsIon [ ] (especially important in hypo- and hyperkalemia)
165
What is the chemical potential (Nernst potential) of sodium? potassium?
Na+: +60 mVK+: = -80 to -90 mV
166
What changes during an action potential?
Fractional K-conductance and Fractional Na-conductance
167
What effect do positive currents have on V (membrane potential)?
Make V more negative
168
How does the range of membrane potential compare to ENa and Ek?
V cannot be more negative than Ek and or more positive than ENa
169
What allows sodium to move across the cell membrane during resting membrane potential?
Leak channels
170
How do flux and current differ? Describe the directionality of current and flux for the movement of anions and cations
Flux: the direction of movement of the ionCurrent: refers to the movement of positive chargesFor anions, Flux and Current in opposite directionsCations: Flux and current in the same direction
171
What is the equation for the conductance of potassium?
gk x Ko , this helps explain how potassium conductance during hyper- and hypokalemia
172
What are some other names for a positive current?
Outward currentRepolarizing current Hyperpolarizing current
173
Compare how the conductance of urea and potassium are effected by extracellular concentration changes?(May be easiest to draw it out and note differences)
174
Describe the same scenario except this time sodium is made permeable.
Since Na+ is high outside of the cell, it will flow in the opposite direction thus moving into the cell. The same forces will be at play just working in opposite directions.
175
What does the resting membrane potential of nerve, cardiac and skeletal muscle(-70 to -80 mV) tell you about the conductances of sodium and potassium?
gK >>>> gNa
176
Be able to interpret the meanings of this graph
This slide again illustrates (more quantitatively than previously) relationships between membrane potential, fractional conductances and electrochemical potentials for a membrane permeable only to potassium and sodium. The situation for a membrane potential of -30 mV is emphasized when EK is -90 mV and ENa is +60 mV. Note that the absolute value of the sodium electrochemical energy is greater than that for potassium electrical energy but the potassium fractional conductance is greater than the sodium fractional conductance.
177
A negative current will make the membrane potential more?
POSITIVE!
178
What will the effect of a negative current be on V?
Negative current will make V more positive
179
What always happens to V when Gion is increased?
V will always move closer to that ion's Nernst potential, Eion
180
Describe the nature of chemical force and its effect of ions.
Each ion has its own chemical force driving its movement
181
What are the equations for fractional conduction (fg) of potassium and sodium?
182
How many gates does a Na+ ion gated channel have and what are their names? Which one remains open during the resting membrane potential?
2; the activation and inactivation gateThe inactivation gate remains open while a cell is at its resting membrane potential. Despite this gate being open, so sodium can't pass through this channel b/c the other gate is closed. (A "somewhat decent but probably terrible" analogy would be a bird trying to fly through a glass window b/c the curtains are open.)
183
What creates the charge seperation across the cell membrane?
Differences in movement of ions
184
The resting potential will be closest the Nernst potential of which ion?
The ion with the highest conductance
185
What happens when V = Eion?
When V = Eion, there is no electrochemical force. This results in no movement of ions (current)
186
What determines the sign of a current?
The sign of (V - Eion) determines the sign of current b/c conductance can only be positive or zero.
187
How does increasing or decreasing fgion affect V movement in relation to that ion's Nernst potential?
Increasing fgion = Closer to ion's Nernst potentialDecreasing fgion = Away from ion's Nernst potential
188
What is the equation for current that includes conductance, membrane potential, and Nernst potential?
Iion = gion x (V - Eion)
189
When V is negative, what type of force (inward/outward) is exerted on cations? anions?
Cations: inward (attraction)Anions: outward (repulsion)
190
Currents are always defined in terms of the movement of what type of molecules?
Cations
191
At RMP,
192
What are two forces involved in driving ion movement?
Electrical (membrane potential)Chemical (due to differences in a single ion concentration of ICF and ECF)
193
What is the equation for Nernst potential (Eion)?
194
A positive current will make the membrane potential more?
NEGATIVE!!!!
195
The magnitude of an ion's current depend on what two factors?
Forces driving movement: electical (membrane potential) and chemical (Nernst potential)Conductance
196
If a cell membrane was made only permeable to potassium (under standard body conditions), describe the movement of potassium ions and how it would effect membrane potential. Also, when would it stop?
Since potassium concentration is high within cells and low outside, the potassium when begin to flow outward due to the chemical force. As the potassium ions flow out of the cell, the membrane potential will steadily become more negative. Since the membrane potential is steadily increasing, the rate of movement of the potassium ions will steadily decrease until both forces equal each other resulting in equilibrium (no net movement).
197
What is true about the currents of sodium and potassium when a cell is at its resting membrane potential?
INa + IK = 0
198
What are the two factors that determine the magnitude of the chemical force?
* Ratio of Extracellular and Intracellular Ion Concentrations
* The valence of the ion
199
What is a current?(I'm pretty sure I've seen this question asked on Are You Smarter Than a Fifth Grader?)
Movement of ions across the cell membrane
200
When both gates are open what will happen to gNa and INa?
When both gates open gNa and INa will both be increased.
201
When threshold is achieved what happens?
At threshold there is a net depolarizing current due to active sodium channels. This will move V more positive - thus opening more Na activation gates (increasing gNa)
202
What conformation are the voltage-gated sodium channels in when at normal resting potential (resting Na+ channel)?
At resting potential the inactivation gate is open and the activation gate is closed
203
What are symptoms of hypercalcemia?
Muscle weakness, tiredness, confusion, etc
204
As membrane potential becomes more positive, what happens to the potassium delayed rectifier channels?
As it becomes more positive, activation gates slowly open on the potassium delayed rectifier channels.
205
Depolarization of Na-gates acts as what kind of feedback loop?
Positive feedback loop
206
At the peak of the action potential, what will cause repolarization (V moving away from ENa)?
Even though all activation gates are opened, Na+ inactivation gates are closed. This will cause a decrease in gNa and thus depolarization.
207
Is the threshold value fixed within a cell?
NO - it depends of the balance between depolarizing and repolarizing currents
208
What is important to not about the kinetics of the activation and inactivation gates? Why might this be important?
The inactivation gate opens and closes slowly and the activation gate opens and closes rapidly. Because of this, if a cell depolarizes quickly enough activation gates can open before inactivation gates have closed completely.
209
What is conduction velocity?
Conduction velocity is how quickly an action potential propogates along a tissue. It is dependent on the magnitude of the depolarzing current during the upstroke of the action potential.
210
Summarize the process of a nerve action potential.
At the resting potential, both Na- and K-voltage gated channels are closed. The status of the Na-channel is in the resting state. The K-channel is also in the resting state. During the upstroke of the action potential, sodium channels move from the closed (resting) state to the open (active) state. At the peak of the action potential, most of the sodium channels are in the open (active) state. The membrane depolarization that occurs during the upstroke phase also cause K-channels to transition from the closed (resting) state to an open (active) state. With time, the membrane depolarization that activated the Na-channels also causes the open (active) state to transition to a closed (inactivated) state. The repolarization phase results from opening of K-channels. During the undershoot, the open voltage-gated K-channels cause K-permeability to be greater than the potassium permeability that occurs at the resting potential and this causes membrane potential to approach the potassium Nernst potential. With time, the open (active) K-channels transition to the closed (resting) state. This causes K-permeability to decrease and membrane potential moves back to the resting potential.
211
The magnitude of the depolarizing current during the upstroke of the action potential will determine?
212
What are the two gates associated with the Voltage-Gated Sodium Channel?
Activation and Inactivation gate
213
What is the relative refractory period?
During the time that inactive channels are being converted to resting channels, the cell can generate AP if a stronger depolarizing stimulus is given than normally required
214
The number of resting Na+ channels is dependent on what?
Having sufficient time during repolarization before the next depolarization stimulus occurs, and repolarizing to a sufficient extent.
215
If resting potential is moved more positive, how will this affect membrane excitability?
216
As membrane potential becomes more positive what will happen to Na-channels?
There will be an increased probability that their activation gates will be open
217
Increasing fgNa will do what to membrane potential? What formula is associated with that?
Increased fgNa will move membrane potential towards the sodium Nernst potential. The image is the associated formula
218
If the magnitude of the Na+ current during depolarization is decreased what will occur?
* Threshold potential is more positive (decreased excitability)
* Amplitude of AP is decreased
* Rate of Rise of AP is decreased
* Conduction velocity is decreased
219
What is the absolute refractory period?
The period where the cell cannot generate an AP regardless of the strength of the depolarizing stimulus (during the upstroke of the AP)
220
What is the effect of hypercalcemia on the sodium activation curve?
Hypercalcemia will reduce excitability by shifting sodium activation curve more positive
221
What is the threshold point determined by?
If enough active Na+ channels are produced to reach a point where INa (depolarizing current) just barely exceeds IK (repolarizing current), the cell has reached threshold
222
When gNa is increased what will this do to V?
V, the membrane potential, will be moved closer to ENa
223
What is the normal resting potential?
-70 to -80 mV
224
What will be the result of decreased number of resting Na+ channels?
This will diminish the cell's ability to generate INa . This is the underlying problem with hypo and hyperkalemia
225
As the cell repolarizes what will occur to the sodium activation gates?
The activation gates will close first, then the inactivation gates will open again.
226
Depolarization of an action potential is caused by what?
Increasing gNa
227
As the membrane potential moves more positive what happens to the inactivation gates?
They begin to slowly close
228
What is an important cellular feature in the conduction of cardiac action potentials?
Gap junctions
229
What effect does sympathetic stimulation have on the calcium window?
Larger calcium window (shifts the activation curve towards more negative potentials, which mean they open sooner during depolarization)
230
What four characteristics does the magnitude of the L-type calcium channel current in the SA and AV nodes determine?
* Threshold potential
* Amplitude of the AP
* Rate of rise of the AP
* Conduction Velocity (CV)
Note: These are the same characteristics affected by the magnitude of sodium channel current in nervous tissue.
231
Increasing If will have what effects on MDP and phase 4?
Maximum diastolic potential (MDP) will be more positivePhase 4 more steep (reaching threshold sooner)
232
Phase 0 depolarization of atrial myocytes is seen as what on the ECG?
P wave
233
Describe the sequence of calcium channel gate configurations as it progresses through a ventricular action potential.
234
What effect does NE have on delayed rectifier K+ current?
Increases K+ current by causing the delayed rectifier K+ channel activation gates to open sooner
235
Increasing SYM firing to the heart will increase ICaL and conduction velocity in the AV node. How will this show up on an ECG?
Decreased P-R interval
236
During what phase of the action potential does the activation gate of the funny sodium channel open?
Repolarization(This is how the funny sodium channel got its name b/c all other voltage-gated channels open during depolarization)
237
How is a CaL channel opened?
Phosphorylation
238
What effect does norepinephrine have on activation curve of funny sodium channels?
It shifts the curve to be more postiive causing the funny sodium channels to open sooner during repolarization
239
What are two ways to possibly introduce a reentrant loop into a ventricle?
Slow CV (conduction velocity)Decreased duration of ARP
240
What does MDP stand for? What is it's significance?
Maximum diastolic potential, most negative potential in the SA node (normally about ~50mV)
241
What structures of the heart have a calcium-dependent action potential? Describe the shape of this AP.
SA node and AV node
242
Compare and contrast the AV and SA node:Type of action potential, ionic currents, RMP, firing rate, slope of phase 4
SameCa-dependent action potentialSame ionic currents at playNo stable resting potentialDifferentAV has lower intrinsic firing ratePhase 4 in the AV node is less steep than SA node
243
What is happening at the following ECG locations:P wavePR intervalQRS complexST segmentT waveQT interval
P wave: atrial depolarizationPR interval: P wave plus PR segment (AV node)QRS complex: ventricular depolarizationST segment: corresponds to phase 2 of ventricular action potentialT wave: ventricular repolarizationQT interval: QRS complex + ST segment + T wave
244
What are the effects of NE (sympathetic) on ionic currents in the SA and AV nodes?
Increased IfIncreased ICaLIncreased IK
245
As membrane potential becomes more negative, what happens to the number of open funny sodium channels?
The number of open funny sodium channels increases
246
What are the effects on HR and duration of the ventricular AP of sympathetic firing?
Increased HRDecreased duration of the ventricular AP
247
What is true about IK and If at maxium diastolic potential?
IK = If
248
Describe the RMP of the SA node?
Doesn't exist. Funny sodium channels and repolarizing potassium channels are always competing against one another.
249
What are the effects of ACh (parasympathetic) on ionic currents in the SA and AV nodes?
Decreased IfDecreased ICaLDecreased IK (low to moderate vagal activity)Increased IKACh (high vagal activity)
250
Describe what happens during phase 4, phase 0, and phase 3 of the SA node action potential.
Phase 4: pacemaker potential where If (funny sodium current) is > IKPhase 0: Upstroke of action potential due to ICaLPhase 3: Repolarizing phase where Ik is > depolarizing currents
251
What is the status of the two gates of a voltage-gated L-type calcium channel at rest?
Activation gate closed, inactivation gate open
252
What structures of the heart use a sodium-dependent action potential? Describe the shape of this type of AP.
Atrial myocytes, Bundle of His, Purkinje Fibers, Ventricular myocytes
253
What causes the calcium window?
The calcium window is due to the overlap of the curves (probability of an open gate)
254
What happens near the end of phase 2 of the ventricular AP that allows the ventricular myocyte to progress into phase 3 (repolarization)?
The Ca++ inactivation gates will close. This allows for repolarization due to IK
255
What contracts during the P wave?
Atrial muscle
256
Describe how different regions of the heart become excited and the pathway of excitation through the heart.
257
Describe the sequence of excitation in the heart including nodes, muscle, and fibers that conduct the action potential.
* SA node
* atrial muscle
* AV node
* common bundle
* bundle branches
* Purkinje fibers
* ventricular muscle
258
When do the FRP, ARP, RRP occur?
259
Sympathetic and parasympathetic control of HR is due the modulation of ionic currents in what part of the heart?
SA node
260
What is occuring at the following phases of ventricular action potential:Phase 4Phase 0Phase 2Phase 3
Phase 4: Stable resting potential (inward rectifier potassium channels)Phase 0: Upstroke due to INaPhase 2: Plateau phase due to balance b/t ICaL and IKPhase 3: Repolarization phase due to IK (delayed rectifier potassium channels)
261
Exercise leads to the stimulation of what receptor results in changes of HR?
ß-Adrenergic
262
How does sympathetic innervation affect atrial and ventricular myocyte AP?
NE, from sympathetic nerves, has no effect on INa but it does increase ICaL and IK. Duration of the ventricular AP is mainly determined by phase 2 and phase 3. If IK is increased, AP duration is decreased as the rate of repolarization is increased (spiked T wave)
263
What are some factors that can increase junction resistance?
Increased intracellular sodiumincreased intracellular calciumintracellular acidosisischemia and hypoxiadecreased intracellular cyclic-AMP
264
Reduced levels of what within myocytes will impair calcium channel current during the AP?
ATP
265
Describe the effects on HR of blocking sympathetic and parasympathetic innervation of the SA node.
266
What normally acts as the pacemaker of the heart?
SA node
267
Decribe the temporal relationship of the major ionic currents responsible for generating phase 4 depolarization, phase 0 depolarization, and phase 3 repolarization.
268
The voltage-gated L-type calcium channel has two gates. What are they and their rates of open and closure?
Activation gate: Open and closes rapidlyInactivation gate: Opens and closes slowly
269
The rate of rise of phase 0 and conduction velocity of the AP through the ventricles and atria are dependent upon what?
Magnitude of INa
270
What is the conduction velocity of electrical impulses in the in the AV node? Bundle of His?
AV node: ~0.05 m/sec (slowest conduction w/in heart)Bundle of His: ~2 m/sec
271
Describe the net effects of beta receptors on cardiac currents [Calcium L-type, Potassium delayed rectifier, Sodium funny (SA)] and the pathway through which it causes those effects.Do the same for M2-muscarinic receptor.
272
Which leads are responsible for capturing the horizontal planes?
Pre-cordial
273
79 y/0 F with severe dyspnea: note the tachycardia.Describe the rate, rhythm, and axis? What could this patient be experiencing?
Rate: just under 150Rhythm: Irregular rhythmAxis: Right axis deviation Representation of Atrial fibrillation
* almost always tachycardia
* w/ irregular rhythm
274
In which lead, is the Q wave normally found?
AVR lead (210 degrees)
275
What type of block?
Complete heart block/3rd degree
276
How would infarction manifest itself on an EKG? Ischemia?
Infarction: ST segment elevationIschemia: ST segment depression
277
Where does phase 2 of the cardiomyocyte AP show up on an EKG?
It forms the separation b/t the S and T wave
278
What is happening in the heart during the QRS complex?
Ventricular depolarization (contraction)
279
Altering phase 3 of the cardiomyocyte AP will affect what on an EKG?
Alter the shape of the T wave
280
What type of axis deviation would be found in a patient that presented with the following EKG readings?
Normal mean electrical axis, two thumbs up
281
Still looking at axis, a R wave that points up is considered what? downward?
Upward: positiveDownward: negative
282
Which leads are responsible for catching the frontal plane?
Limb
283
60 yF with chest pain
Infarction
284
What type of AV block?
2nd degree AV block Mobitz type I
285
What the three possible criteria to use when determining whether the patient has hypertrophy? Describe the sensitivity and specificity of these.
Romhilt Estes, Cornell, No name criteriaAll poorly sensitive but very specific
286
What type of axis deviation would be found in a patient that presented with the following EKG readings?
Right axis deviation
287
Rapid review: What happens during phases 0-4 of a cardiac myocyte action potential?
288
What is occuring in the heart during the P wave?
Atrial depolarization (contraction)
289
What are the four types of AV block? What are their characteristics
290
What is occurring in the cardiac tissue during the ST segment?
Ventricles are the plateau phase of depolarization (phase 2)
291
What is happening in the heart during the T wave?
Ventricular repolarization (relaxation)
292
What is this patient's HR? What else do you notice about this EKG?
300/5 = 60Lack of P wave (not SA node pacing). Could be AV nodal pacing (almost brachycardia)
293
What type of axis deviation would be found in a patient that presented with the following EKG readings?
Extreme right axis deviation
294
36 y/o F with syncopal episodeDescribe rate, rhythm, axis, and hypertrophy.
Rate: Just under 60Rhythm: Sinus (Lead I and II are good for finding p wave due to placement over atria)Axis: NormalHypertrophy: present
295
Describe the placement of the limb leads and the angles of the vectors that they detect?
Einthoven's Triangle
296
When analyzing axis, which leads are you looking at? What is considered normal?
Lead I and AVF; anything between 0 and 90 degrees
297
Which leads are good for looking at ST elevation?
II, III, aVF
298
What is the treatment for A fib/right axis deviation?
Control HR, consider anticoagulation (CHADS2) to reduce the risk of stoke/thromboembolism
299
What are the 6 steps in the clinical approach to reading an EKG?
* Rate
* Rhythm
* Axis
* Intervals
* Hypertrophy
* Ischemia/Infarction
300
What is occurring the cardiac tissue when the QRS complex begins?
Conduction through the His-Purkinje system and ventricular system
301
When looking at rhythm, what is the first question to ask yourself?
Is it sinus or not? (presence of the P wave?)
302
What is the Cornell calculation for ventricular hypertrophy?
RAVL + SV3 = 20 (in females)RAVL + SV3 = 28 (in males)Gender bias is due to the fact that female breast tissue doesn't conduct electrical impulses as well as muscle
303
Describe the four possible axial scenarios and the direction of the R wave in leads I and aVF.
Normal: positive R wave for bothRight axis deviation (R.A.D.): positive aVF and negative Lead ILeft axis deviation (L.A.D.): negative aVF and positive Lead IExtreme R.A.D: negative aVF and Lead I (in healthy individual, possibly situs inversus)
304
How does one determine the rate when looking at an EKG?
Each big box is 300.So, find two consecutive R-R peaks and count the number of boxes between them. Then, take 300 and divided by the number of boxes that you just counted.
305
What is the most common cause of L ventricular hypertrophy? What are some other possible causes?
Chronic HTNOther causes: aortic stenosis, HOCM
306
An obstruction (due to MI or surgical cut) of the left bundle branch will have what effect on the QRS complex?
Wider due to slower propogation through the ventricle
| * Called a left bundle branch block
307
What type of axis deviation would be found in a patient that presented with the following EKG readings?
Left axis deviation
308
What is responsible for the P-R interval found on an EKG?
The pause in the AV node
309
What is the mechanism by which hypoxia will affect an action potential in the tissue?
Insufficient O2 will decrease ATP formation. L-type Ca++ must be phosphorylated during each action potential to allow Ca++ through. Decreased ATP will impair the Ca++ current which will decrease the duration of the action potential.
310
Long QT syndrome can be cause by?
Decreased Na or K current
311
Why is V (membrane potential) being pushed towards ENa during hypokalemia?
The decreased gK is increasing the fgNa. Increasing the conductance to an ion moves the membrane potential to the Nernest potential of that ion.
312
How does the conductance of potassium relate to the concentration of potassium outside the cell?
It is directly related. As potassium concentration increases outside the cell so does the conductance
313
Why are M cells more susceptible to problems with action potentials?
Action potential prolongs disproportionately relative to the action potential of other ventricular myocardial cells in response to slowing of rate and or in response to action potential prolonging agents. Less potassium current - less repolarizing current that prolongs phase 2Larger Na-Ca exchange current - provides inward current to prolong phase 2
314
What is the Nernst potential formula?
315
What is the mechanism by which calcium corrects hyperkalemia?
Increased calcium produces a positive shift in the Na channel inactivation curve. Calcium also produces a positive shift in the Na channel inactivation curve. This shift can be utilized to recover some excitability by converting inactive sodium channels back to the resting state and increasing the current of sodium.
316
How will insulin act as a regulator of potassium?
Direct stimulation of the Na-K pump by insulin will also act to move potassium into the cell.
317
In regards to a reentrant loop, what will cause a reduce in duration of the AP?
Increase of IK or decrease in ICaL
318
What is a normal extracellular potassium concentration?
3.5 to 5 mEq/liter
319
What are the terms for increased and decreased extracellular potassium levels?
Hypokalemia - decreasedHyperkalemia - increased
320
What causes the resting depolarization associated with hyperkalemia?
A less negative EK than normal
321
What is the mechanism by which hypokalemia will produce a depolarizing resting membrane potential?
Hypokalemia reduces K conductance. Apparently, the effect on membrane potential produced by the reduction of K conductance more than offsets the effect of the more negative Nernst potential produced by hypokalemia. The depolarized resting potential in hypokalemia depresses membrane excitability similar to that occurring in hyperkalemia. The decreased K conductance slows phase 3 repolarization causing the T-wave to flatten and a U wave may appear.
322
What is the mechanism by which EADs can occur?
EAD production occurs via conversion of inactive L-type calcium channels back to the active state during phase 2 or early phase 3 of the action potential. This reactivation can occur because there is a potential region where the Ca-channel activation and inactivation curves overlap. Decreased rate of repolarization (low IK) markedly increases the chances of these because there is more time in the "calcium window". This can allow Ca++ to move into the cell through those channels and create a depolarizing current and move V more positive.
323
What effect will hypokalemia have on gK, IK, and action potential? What will hyperkalemia do?
324
What two conditions make reentrant loops more likely?
Conduction velocity in decreased and duration of the AP is decreased.
325
As potassium outside the cell increases what happens to EK? What happens to EK when potassium outside the cell decreases?
As K outside the cell increases, EK becomes less negative and moves toward zero.As K outside the cell decreases, EK becomes more negative.
326
What effect will hyper and hypokalemia have on the T wave of an ECG?
The T wave is the repolarization of the ventricles. This is largely dependent on potassium. Hypokalemia will have a reduced current thus causing the T wave to look flat and prolonged. Hyperkalemia will have the opposite effect and the T wave will appear shorter and spiked.
327
How will ischemia affect action potential generation?
Ischemia (insufficient blood flow) will lower O2 levels in the heart and decrease ATP formation. The mechanism is similar to hypoxia, but the decreased blood flow will allow K+ to accumulate which will result in local hyperkalemia. This will cause a depolarization of resting membrane potential, phase 4 of resting membrane potential will be more positive.
328
What would be the effect of hyperkalemia on EK in a cell?
There would be a reduced chemical force driving K+ out of the cell as compared to normal. The electrical force needed to balance the reduced chemical force will be less than under normal conditions. Therefore, the Nernst potential will be less negative or more positive than under normal conditions
329
Increasing the membrane potential would have what effect on the number of sodium activation gate needed to open to hit the threshold value?
There would need to be and increased number of activation gates open in order to achieve the threshold value. This is due to the threshold value being more positive.
330
What is the formula for changes in potassium current?
331
What can occur due to a suppression of K+ current?
Early after depolarizations
332
The negative shift in MDP acts to do what on the heart?
This negative shift in MDP acts to slow heart rate by increasing the potential difference between MDP and the threshold for activation of the L-type calcium current
333
What are the mechanisms by which decreased potassium current will speed up the heart?
The decreased conductance causes MDP to become more positive even though EK becomes more negative. In addition, the decreased K conductance allows the funny sodium current to be more effective at driving phase 4 depolarization which results in a faster phase 4 depolarization.
334
How do treat hypokalemia? While treating hypokalemia what will you notice on a patients ECG?
Slow infusion of potassium in order to not overshoot the needed K level. While correcting the hypokalemia you would notice the T wave become shorter and the U wave would disappear.
335
Why do normal people tend to not have problems with EADs?
Normally the ventricle repolarizes quickly enough through the calcium window that activation gates close before there is enough time for inactivation gates to open.
336
What are the three things required for a reentrant loop?
337
Is a U wave characteristic of hyper of hypokalemia?
Hypokalemia
338
How can cocaine increase a person's chances for an EAD?
Cocaine blocks delayed rectifier K channels, slowing the rate of repolarization, and impairs the reuptake of norepinephrine by SYM nerves (increases Ca++ window)
339
What are four important outcomes when INa is decreased?
Threshold potential becomes more positive - decreased excitabilityRate of rise in an action potential would be decreasedAmplitude of action potential will be decreased (diminished height of QRS complex on ECG)Decreased conduction velocity (Resulting in wide P wave and wide QRS complex on ECG)
340
Hyper and hypokalemia both cause depolarization of resting membrane potential. What would this effect be on the number of resting Na+ channels and the INa?
This would decrease the number of resting Na channels thus decreasing the INa during the upstroke of the action potential
341
In regards to a reentrant loop what will cause a decrease in conduction velocity?
Decrease INa
342
How can Beta-adrenergic blockers treat Torsades de Pointes?
Potassium current would be decreased throughout the ventricles action potential would be prolonged and that could affect the reentrant loop.
343
Why in this graph might the line for EK be trending upwards?
Because as KO increases EK becomes less negative and moves towards zero.
344
How does resting depolariztion of cardiac muscle during hyperkalemia affect resting calcium channels?
345
What will the effect of hypo and hyperkalemia be on MDP (maxiumum diastolic potential)?
Hyper - decrease make more negative; phase 4 will be less steep; decreased rate of firing of the SA nodeHypo - increase make more positive; phase 4 more steep; Tachycardia Phase 4 is in reference to an action potential
346
What is flaccid paralysis and what is it a result of?
Potassium disturbances will reduce voltage-gated sodium current in nerve and skeletal muscle. This will result in a person experiencing difficulty contracting their limbs.
347
How does sodium bicarbonate affect potassium regulation?
An increase in extracellular pH (as produced by infusing sodium bicarbonate) will enhance the movement of Na into the cell by the Na-H exchanger. This is an indirect effect.
348
In hypokalemia, what is the major cause of resting depolarization?
Decreased gK. This will lead to an increase fgNa
349
Short QT syndrome can be caused by?
Increased potassium current
350
What is the mechanism by which DADs can occur?
Elevated heart rates can cause an accumulation of calcium within the myocytes (because there is insufficient time to pump all Ca++ out of cell). sarcoplasmic reticulum. Normally these calcium sparks are of no consequence. However, when the sarcoplasmic reticulum becomes overloaded with calcium the intracellular calcium (most likely in microenvironments) can increase to the level that activates a non-selective cation channel in the cell membrane. At negative membrane potentials, sodium ions will enter the cell providing an inward ionic current that can depolarize the cell. Also, the increased calcium level will favor the movement of calcium out of the cell via the Na-Ca exchanger. Since the movement of a calcium ion out of the cell via the exchange also moves 3 sodium ions into the cell, a net inward current is produced by the exchanger. The inward current carried by the Na-Ca exchanger also contributes to DAD production.
351
What will an increase in extracellular Ca levels do to excitability of nerve, skeletal muscle, and cardiac muscle in a person with normal extracellular K+ level?
This would shift Na inactivation and activation curves more positive. Since the person has normal K+ levels the positive shift in Na inactivation channels would have little effect on the number of resting Na+ channels. The positive shift in the Na+ activation curve would shift the threshold to a more positive value and thus would cause reduced excitability in the person.
352
If enough myocytes are generating EADs or DADs, the depolarizing current could be sufficient enough to trigger what?
Reentrant loop
353
How does succinyl choline affect potassium regulation?
The increased intracellular sodium will stimulate the Na-K pump and move potassium into the cell
354
Absence of apoB-100 would result in?
mutation in apoB-100 leads to decreased affinity to LDL-receptor
355
Capillaries with continuous endothelium are best characterized by which of the following?ability to contract and redirect blood flowleakiness to leukocytesprevalence of small endocytic vesicles and caveolae within the endotheliumstructure similar to small lymphatic vessels
prevalence of small endocytic vesicles and caveolae within the endotheliumCapillaries have no vascular smooth muscle, so they cannot contract and redirect blood flow. Leukocytes emigrate across postcapillary venules.
356
What bind to desmosomes?
Intermediate filaments
357
Assume that a red blood cell has an intracellular concentration of 290 mOsm of impermeable solutes. The red blood cell is placed in a solution in a beaker. The osmolality of the solution is 580 mOsm. At equilibrium, the volume of the red blood cell is not changed. Which of the following best describes the solution?All solutes in the solution are impermeable.hypotonic solutionhypertonic solution0.9% NaCl plus 290 mOsm urea1.8% NaCl
A - Incorrect: If all solutes in the solution were impermeable with an osmolality of 580 mosM, cell volume would decrease.B - Incorrect: Cell volume would be increased in a hypotonic solution.C - Incorrect: Cell volume would be decreased in a hypertonic solution.D - Correct: This solution has an osmolality of 580 mOsm and the concentration of impermeable solute is 290 mOsm. Urea is a permeable solute.E - Incorrect: A solution of 1.8% NaCl would cause cell volume to be decreased.
358
How are T-tubules and sarcoplasmic reticulum predominantly arranged?
As a diad
359
A 37-year-old male patient presents to you in your office with complaints of shortness of breath and dizziness. The patient is an avid bodybuilder, and is quite muscular. The patient denies the use of anabolic steroids. All bloodwork is normal, and there are no abnormal valvular sounds. A cardiac ultrasound reveals a marked increase in the size of the heart, particularly in the right ventricle. Which of the following physiological mechanisms may lead to this condition?
* The increased volume of blood passing through the heart triggers the insertion of sarcomeres into the myofibrils. This lengthens each myofibril and allows the heart to pump more blood. This explains the enlarged ventricle.
* There is a large increase in the vasculature surrounding the skeletal muscles. Because of this increased vascular bed there is a decrease in the peripheral resistance to blood flow. Hence his blood pressure will drop leading to the dizziness.
* The increased muscle mass restricts the flow of blood through the muscles by constricting the blood vessels. This increases the diastolic load on the heart. The increase in diastolic load leads the cardiac muscle cells to add myofibrils. The increased myofibrils result in a stiffening of the ventricle due to an increased level of Titan. This leads to stiffening of the ventricle. The heart therefore cannot pump blood efficiently.
* The increased mass of the ventricles lead to an increase in the number and density of gap junctions. These gap junctions result in electrical changes in the heart so that the action potentials will echo throughout the ventricle. This leads to ventricular fibrillation.
The increased muscle mass restricts the flow of blood through the muscles by constricting the blood vessels. This increases the diastolic load on the heart. The increase in diastolic load leads the cardiac muscle cells to add myofibrils. The increased myofibrils result in a stiffening of the ventricle due to an increased level of Titan. This leads to stiffening of the ventricle. The heart therefore cannot pump blood efficiently.A - Not the best answer. This is true, but it occurs following Aerobic exercise. The enlarged ventricle following aerobic exercise results in a heart that pumps blood more efficiently. The addition of sarcomeres in series does not increase the stiffness of the ventricle. This would not explain the shortness of breath or dizziness.B - Not the best answer. There is indeed an increase in the vasculature surrounding the muscles. This actually places more resistance on the flow of blood and leads to an increase in blood pressure. C - This is the best answer.D - Not the best answer. This would lead to death, not dizziness.
360
Which one of the following congenital heart diseases is characterized by early cyanosis and a right-to-left shunt?Aortic stenosis, isolatedPatent ductus arteriosusTetralogy of FallotAtrial septal defect, sinus venosus typeAtrial septal defect, septum primum type
Tetralogy of FallotAmong the congenital heart defects listed, tetralogy of Fallot is the only one that has a right to left shunt early in life. This shunt causes early cyanosis.
361
Absence of apoB-48 would result in?
would result in the absence of chylomicrons
362
At the peak of a normal action potential the sodium electrochemical energy approaches _________ and the potassium electrochemical energy becomes _________.zero, greater than 100 mVthe sodium Nernst potential, greater than 100 mV+60 mV, zero-100 mV, zero
zero, greater than 100 mVAn ion’s electrochemical energy is the difference between the membrane potential and the ion’s Nernst potential. At the peak of the action potential the membrane potential approaches the sodium Nernst potential (between +40 and +60 mV). Accordingly, Na electrochemical energy approaches zero. Since EK is about -90 mV, the potassium electrochemical energy is greater than 100 mV at the peak of the action potential.
363
Concentration = Mass / VolumeMannitol is a large molecule that is largely confined to the intravascular space after i.v. injection. Assume that 10 gm of mannitol was injected i.v. to a person and that blood was withdrawn a short time later. The plasma concentration of mannitol was 0.005 gm per ml. If all mannitol remained within the vasculature and none was excreted, which of the following is the best estimate of the plasma volume in this person?0.5 liter1 liter2 liters5 liters10 liters
2 litersThe concentration of mannitol in plasma equals 0.005 gm/ml. This concentration equals the mass of mannitol injected (10 gm) divided by the volume of plasma.Plasma volume = Mass / Plasma concentration = 10 gm / 0.005 gm/ml = 2000 ml = 2 liters
364
The liver plays an important role in the metabolism and elimination of cholesterol from the body. The transport of free cholesterol from peripheral tissues to the liver (reverse cholesterol transport) is dependent on which of the following?chylomicronsHDLIDLLDLVLDL
HDLReverse Cholesterol Transport: Free cholesterol is removed from tissues by plasma high-density lipoprotein (HDL). It is esterified by LCAT associated with HDL and transported to the liver, where it is eliminated from the body primarily after conversion to bile acids or bile salts.
365
Intravenous infusion of isotonic saline (0.9% NaCl) can be used to correct the sodium deficit associated with dilutional hyponatremia. In this situation, excess water intake decreases plasma sodium below normal levels. Assume that plasma sodium is 110 mEq/liter in a person with dilutional hyponatremia. Which of the following will occur in this person following intravenous infusion of isotonic saline?decrease in capillary pressuredecrease in intracellular osmolalitydecrease in intracellular volumehypotonic expansionisotonic contraction
decrease in intracellular volumeDilutional hyponatremia can occur by excess intake of water, which will initially reduce plasma sodium concentration, decrease ECF osmolality, and increase ECF volume. The decrease in ECF osmolality will cause water to move into cells, increasing ICF volume and decreasing ICF osmolality. I.v. infusion of isotonic saline (290 mOsm) will raise extracellular osmolality towards normal in a person with dilutional hyponatremia. This change will cause water to move out of the ICF. A - Incorrect: Capillary pressure will be increased due to the increased volume of the ECF.B - Incorrect: As water moves out of cells, intracellular osmolality will increase towards normal.C - Correct: ICF volume will decrease.D - Incorrect: A hypotonic change would increase ICF volume. Infusion of isotonic saline to a person with dilutional hyponatremia will cause ICF volume to decrease.E - Incorrect: ICF volume is decreased in this situation due to the rise in ECF osmolality following infusion of isotonic saline to a person with dilutional hyponatremia.
366
A 36-year-old male bartender is brought by ambulance to your emergency room because a patron jumped over the bar, grabbed an ice pick, and stabbed him in the chest rather than pay his bar tab at the end of the night. The ice pick entered the chest about 2 cm to the left of the sternum in between the fourth and fifth rib. Upon examining the bartender, you note very little blood is coming from the puncture wound and normal lung sounds from both the right and left lung. However, his heart is beating rapidly at 100 beats per minute, his external jugular veins are bulging, and you have difficulty hearing his heart sounds. You order a PA and lateral chest film because you suspect which of the following?HemothoraxPneumothoraxCardiac tamponadeAortic valve stenosisDeep venous thrombosis
The answer is C. Cardiac tamponade. (Moore and Dalley, pp 140-141.) The ice pick likely penetrated the left ventricle of the heart, causing blood to leak into the pericardial sac. The rapid filling of the pericardial space does not allow the heart to fully expand between contractions leading to increased venous hypertension, thus the filling of the external jugular veins. Since the heart can only pump small quantities of the blood with each beat, it speeds up (tachycardia). The heart sounds and apical heartbeat soften because the blood surrounding the heart absorbs the sounds. A hemothorax (answers a) and pneumothorax (answer b) are unlikely since both right and left lungs sounds are normal and because of the location of the ice pick injury. Aortic valve stenosis (answer d) would not result from a puncture wound. Deep venous thrombosis (answer e) generally occurs in the lower extremity and results in leg pain and is not caused by a puncture wound.
367
In the same image there are specific cellular structures. The cellular structures indicated by the arrows would best be described as:A BandsContraction BandsI BandsIntercalated DiscsZ Discs
Contraction BandsA - A Bands. This is incorrect. The A bands are the Dark bands in the sarcomeres. The A bands are visible in the image, as are the striations. The A bands are composed of the myosin filaments.B - This is the correct answer. These contraction bands form within cardiac tissue about 12 to 48 hours after injury.C - I Bands. This is incorrect. The I bands are the light bands in the sarcomeres. They are composed of the Z disk and the actin filaments.D - Intercalated Discs. This is incorrect. The intercalated discs are the connections between the adjacent cardiac myocytes. There is a distinct possibility that one of the structures may be an intercalated disc (far left arrow), but this is more likely a contraction band forming at the intercalated disc. The other two arrows clearly point to contraction bands.E - Z Discs. The Z discs are not present in this tissue at this magnification. They are found in the middle of the I bands in the sarcomeres. They are the site where the actin filaments attach.
368
Following the upstroke of the action potential in a nerve, membrane potential moves toward the potassium Nernst potential during repolarization. Which of the following is occurring at this time?decreasing potassium electrochemical energydecreasing sodium electrochemical energyincreasing sodium conductancemore negative potassium chemical energysodium current is greater than potassium current
decreasing potassium electrochemical energyCorrect answer is A.A - The potassium electrochemical energy is equal to V – EK. As membrane potential moves more negative during repolarization, V – EK becomes smaller.B - As V moves more negative during repolarization, the difference between V and ENa becomes greater over time, and so the sodium electrochemical energy increases during repolarization.C - Sodium conductance increases during the upstroke of the action potential and is responsible for increased sodium current during depolarization.D - Potassium chemical energy is equal to the potassium Nernst potential. Under normal conditions, an insignificant change occurs in intracellular and extracellular concentrations of sodium and potassium during an action potential, so the Nernst potentials to both ions remain constant. Membrane potential changes during the action potential because of changes in conductance to ions.E - Sodium current is greater than potassium current during depolarization, and the reverse is true during repolarization.
369
A 16-year-old boy is brought to the ER with dyspnea. His past medical history is significant for an unrepaired atrial septal defect. Physical examination reveals cyanosis, distended jugular veins, hepatosplenomegaly, and a systolic ejection murmur. This patient has most likely developed which of the following complications of congenital heart disease?aortic aneurysmmyocardial infarctionparadoxical embolismpneumoniapulmonary hypertension
pulmonary hypertensionAnswer: E Pulmonary hypertensionPatients with uncorrected ASDs may develop narrowing of the pulmonary vasculature, in which case the flow of blood through the defect may be reversed thereby creating a right-to-left shunt. The increase in pulmonary capillary pressure is transmitted to the pulmonary arteries, called pulmonary hypertension, resulting in right-sided heart failure. Complications of ASDs include cyanosis, right ventricular hypertrophy, right heart failure and paradoxical emboli.This patient's diagnosis is Eisenmenger syndrome due to atrial septal defect.
370
A mother brings her 2-year-old son to the pediatrician. She states he occasionally appears to be short of breath after running or wrestling with his brother. Also, his preschool teacher notes that she sees him squatting down on the playground. On physical exam you hear a holosystolic murmur. A CXR in your office reveals right ventricular hypertrophy of the heart (giving a vague boot-like appearance). You refer the patient to a pediatric cardiologist. The single greatest factor that determines the clinical outcome associated with the most likely congenital heart defect in this patient is:The severity of rotation of the overriding aortaPositioning of the aortic archDegree of pulmonary stenosisAge of patient at diagnosisPresence of left ventricular hypertrophy
Degree of pulmonary stenosisCorrect answer is C. The clinical outcome of Tetrology of Fallot depends primarily on the severity of the pulmonic stenosis, as this determines the direction of blood flow. If the pulmonary stenosis is mild, the abnormality resembles an isolated VSD and the shunt may be left to right without cyanosis. As the obstruction increased in severity, there is greater resistance to right ventricular outflow. As right sided pressures approach or exceed left sided pressures, right to left shunting develops, producing cyanosis.
371
What will cause myosin to bind?
Myosin will bind whenever the troponin complex does not cover the actin binding site. Activation of myosin by myosin light chain kinase is important in smooth muscle contraction.
372
For a nerve, shifting the sodium channel activation curve toward a more positive potential would be expected to ______________ the rate of depolarization during the upstroke phase of the action potential and __________ the number of resting sodium channels.decrease, not affectdecrease, increaseincrease, decreaseincrease, not affect
decrease, not affectA depolarizing shift in the sodium channel activation curve would not affect the number of resting channels (determined by the position of the inactivation curve in relation to the resting potential) but would reduce the number of sodium channels activated during the upstroke of the action potential. This reduction in active sodium channels would reduce the magnitude of the inward sodium current thereby reducing the rate of depolarization during the upstroke.
373
A burn patient under your care has a plasma osmolarity of 280 mOsm. The osmolarity of the interstitial fluid in the burn area is 279 mOsm compared to 277 mOsm in non-burn areas. Which of the following best completes the following statement? In the Burn Area the osmotic pressure difference across the capillary wall acts to drive fluid __________ across the capillary wall and provides a driving force of __________ mm Hg.from interstitial to plasma; 20from plasma to interstitial; 20from interstitial to plasma; 60from plasma to interstitial; 60
from interstitial to plasma; 20Correct answer is A. The fluid osmotic pressure inside the capillary is greater than outside for both the burn area and normal area. Accordingly, the osmotic pressure difference will act to drive fluid inward across the capillary wall in the burn area as well as in the normal area. In the burn area the 1 mOsm concentration difference produces a osmotic pressure difference of about 20 mm Hg.
374
A person with chronic obstructive pulmonary disease had bilateral edema of the lower extremities. Assume that interstitial fluid pressure of the lower extremities is 10 mm Hg, plasma osmolality is 290 mOsm, and interstitial osmolality is 289 mOsm. If the extent of edema is staying constant (i.e., no net fluid movement across the capillary), which of the following is the best estimate of capillary pressure within the lower legs of this person?10 mm Hg15 mm Hg20 mm Hg30 mm Hg40 mm Hg
30 mm HgCorrect answer is D. The difference in solute concentration between plasma and interstitial fluid is 1 mosm/liter. Since each 1 mosm/liter diffence in concentration generates a force equal to 20 mm Hg, the solute difference creates a force for reabsorbtion of water into the capillary of 20 mm Hg. The diffusion of water is from low solute concentration (interstitial fluid) to high solute concentration (plasma within capillaries). For no net movement of water to occur, capillary pressure must be greater than interstitial fluid pressure by 20 mm Hg, so capillary pressure equals 30 mm Hg.
375
A 63-year-old woman is hyponatremic with a plasma sodium concentration of 120 mEq/liter. This person weighs 60 kg and has 17% body fat. Assuming that the desired plasma sodium concentration is 140 mEq/liter, which of the following is the best estimate of this person's sodium deficit?685 mEq700 mEq715 mEq730 mEq745 mEq
Na+ deficit = TBW x (desired [Na+] – present [Na+])Na+ deficit = (LBM x 0.72) x (desired [Na+] – present [Na+])Na+ deficit = (60 – 0.17 x 60) x 0.72) x (140 mEq/L – 120 mEq/liter) = 717 mEq
376
A 21 year old woman is hyponatremic with a plasma sodium concentration of 115 mEq/liter. This person weighs 50 kg and has 15% body fat. Assuming that the desired plasma sodium concentration is 140 mEq/liter, which of the following is the best estimate of this person's sodium deficit?850 mEq900 mEq950 mEq1000 mEq1050 mEq
850 mEq
377
An electrode is inserted into a nerve cell to record membrane potential. A drug is added to fluid surrounding the nerve cell, and resting membrane potential changes from -70 mV to -60 mV and remains stable at this value. There is no change in intracellular or extracellular concentrations of sodium or potassium following addition of the drug. Which of the following could account for this effect of the drug?decrease in fractional conductance to potassiumdecrease in sodium conductance of leak channelsincreased flux of chloride anion into the nerve cellincrease in the magnitude of repolarizing currentsmore negative potassium Nernst potential
decrease in fractional conductance to potassiumCorrect answer is A. The drug has caused membrane potential to move to a less negative potential. This could be caused by an increase in magnitude of a depolarizing current or a decrease in the magnitude of a repolarizing current. A - This is correct because decreased fractional conductance to potassium would cause resting membrane potential to move away from the potassium Nernst potential and towards the sodium Nernst potential.B - A decrease in sodium conductance of leak channels would cause resting membrane potential to move more negative.C - An increased flux of an anion into the cell would make resting membrane potential more negative.D - An increase in the magnitude of repolarizing currents would make resting membrane potential more negative.E - There was no change in the intracellular or extracellular concentration of potassium, so the potassium Nernst potential did not change.
378
A 25-year-old male has been referred to your clinic by the nurse practitioner at the local CVX pharmacy because of periods of severe chest and arm pain. He also states that he is frequently short of breath and that the symptoms have been getting worse. You have ordered a cardiac stress test and subsequently, a coronary artery perfusion and imaging which reveals significant coronary disease resulting in the placement of 3 stents. Your physical exam of the patient is unremarkable with the exception of the presence of what appear to be xanthomas present on the extensor tendons of both hands. His family history reveals that his father died of a heart attack at the age of 26 and his mother is alive and healthy at age 57. Routine lab work reveals a plasma cholesterol level of close to 700 mg/dL in a fasting blood sample.Which of the following conditions is the likely underlying cause of this young man’s heart disease?Familial hyperchylomycronemiaFamilial hypercholesterolemiaFamilial hypertriglyceridemiaTangier DiseaseA diet high in cholesterol
Correct answer is B, familial hypercholesterolemia or Type II familial hyperlipoproteinemia, is the clear best answer here. In addition to his own high cholesterol levels and cardiovascular disease at such an early age, this young man has a family history on his father’s side of early cardiovascular disease but not on his mother’s side which suggests an autosomal dominant inheritance pattern. Answer A is not consistent with this patient’s lab work or the properties of Type I hyperlipoproteinemia or lipoprotein lipase deficiency which does not lead to early cardiovascular disease. Answer C is also not consistent with the patient as there is no history of diabetes, obesity, or alcoholism, etc. noted or increase in VLDL production. While hypercholesterolemia is seen in these patients, cardiovascular disease generally does not manifest itself at such a young age in this condition. Answer D, Tangier’s Disease or Familial alpha lipoprotein deficiency refers to a lipoprotein deficiency or hypolipoproteinemia and it is characterized by a significant deficiency of HDL which is not noted in this patient. This disease is also characterized by unusual ophthalmic symptoms or appearance and is sometimes referred to as fisheye disease. It is associated with clear and dangerous symptoms in childhood due to lipid soluble vitamin malabsorption and a variety of issues not seen in this patient.Answer E could be a cause of elevated cholesterol levels but given the family history of this patient, it is clear that an autosomal dominant, condition is the most likely in this case and so this would not be a likely cause.
379
If capillary osmolality is 290 and interstitial fluid is 288, where will fluid flow?
From interstitial fluid to capillary
380
A 34-year-old woman gave birth to her third child; a full term 7 lb 2 oz baby girl. At the second well baby checkup at 3 months the mother reported that the baby girl was more frail than her other children at this age, and seems to have more difficulty breast feeding. The 3-month-old baby girl has a machine like murmur between S1 and S2 heart sounds, best heard in the left suprasternal notch. Additionally, her toes were slightly bluish. Blood pressure taken in both right and left arms and legs were normal for a 3-month-old. A chest plain film showed normal heart size and aortic knob. The physician would order an echocardiogram to mostly likely diagnose which of the following conditions in this 3-month-old girl?aortic stenosiscoarctation of the aortatransposition of the great arteriespersistent truncus arteriosuspatent ductus arteriosus
patent ductus arteriosusCorrect answer is E: patent ductus arteriosus which caused both a machine like murmur that is best heard at the left suprasternal notch or in the back between the scapulae, and cyanosis of the toes but not the fingers. Aortic stenosis (answer A) would tend to cause enlargement of the aortic knob (arch due to jetting of blood) and left ventricular hypertrophy (her aortic knob and heart size was normal). Coarctation of the aorta (answer B) would cause hypertension in the upper extremities and hypotension in the legs. A baby girl with transposition of the great arteries (answer C) or persistent truncus arteriosus (answer D) would have symptoms (cyanosis) so severe that she would unlikely live to the 3rd month without medical intervention.
381
A 61-year-old man weighs 80 kg and is determined to have 20% body fat. He receives an i.v. infusion of 3 liters of 5% dextrose. Assume that no fluid losses occur by any route. Which of the following is the best estimate of extracellular fluid volume in this person several hours later when dextrose has been completely metabolized?15.4 liters16.4 liters17.4 liters30.7 liters46.1 liters
16.4 liters
382
In a nerve cell, the Nernst potential is found to be -90 mV for potassium, +60 mV for sodium, and -60 mV for chloride. The resting potential is -70 mV. Based on this information, you conclude that at resting potential:chemical energy for chloride is -70 mV.chloride current is negative.electrical energy for potassium is +20 mV.electrochemical energy for sodium is +60 mV.there is a net repolarizing current.
chloride current is negative.
383
A 78-year old female presents to her primary care physician due to decreased endurance and increased difficulty sleeping at night. She coughs a lot at night if she sleeps flat on her back, but she can sleep when elevated by several pillows. Her lungs sound congested and her external jugular vein is distended. The heart valves sounds immediately adjacent to both sides of her sternum are normal, but there is a mid-systolic click immediately followed by a “whooshing” sound heard at the apex of her heart inferior to her left breast. During cardiac ultrasound the papillary muscles of the left ventricle appeared ruptured. What is the working diagnosis?aortic valve stenosisaortic valve regurgitationmitral valve stenosismitral valve regurgitationtetralogy of Fallot
Answer is D) mitral valve regurgitation. The mid-systolic click immediately followed by a “whooshing” sound at the apex of her heart inferior to her left breast suggests a problem with the mitral valve. The rupture of the papillary muscles of the left ventricle is associated with mitral valve regurgitation rather than C) mitral stenosis. Aortic valve stenosis a. presents as a systolic murmur just to the right of the second intercostal space (location for ausculation of the aortic valve.) If B) aortic valve regurgitation were present, generally there would be a diastolic murmur, which is not present. Aortic valve stenosis is associated with enlargement of the left ventricle (due to increased resistance), which presents as enlargement of the left wall of the heart. In severe cases aortic valve stenosis causes enlargement of the aortic knob due to turbulence created downstream of the stenosis. C) Mitral valve stenosis would be heard as a diastolic murmur at the 4th or 5th intercostal space on the left side of the chest at the midclavicular line. E) Tetralogy of Fallot is unlikely to go undiagnosed in a 78-year old and would present with holosystolic murmur with right ventricular enlargement.
384
A 39-year-old female patient showed marked elevation of plasma triglycerides (~2,500 mg/dl; normal < 150 mg/dl) and chylomicrons. Upon injections with a peptide fragment of which of the following proteins was the hypertriglyceridemia corrected in this patient?apoA-1apoC-IIapoEapoB-100apoB-48
apoC-IIA. apoA-1 activates lecithin:cholesterol acyltransferase which esterifies cholesterol in HDLB. apoC-II activates lipoprotein lipase to be able to break down triglyceridesC. apoE LDL receptor ligand; helps to remove lipoproteins from the circulationD. apoB-100 LDL receptor ligand; major protein of LDLE. apoB-48 exclusively found in chylomicrons; does not bind to LDL receptor
385
Actin binds to what at the intercalated disc?
Actin binds to adherens at the intercalated discs.
386
During the upstroke of the action potential in a nerve, membrane potential moves toward the sodium Nernst potential. Which of the following is occurring at this time during this upstroke phase?decrease in potassium chemical energydecrease in sodium electrochemical energymore positive sodium chemical energynet repolarizing current across the membraneopening of inactivation gates on sodium channels
decrease in sodium electrochemical energyA. Incorrect: Chemical energy for ions (Nernst potentials) does not change during the action potential. The Na/K ATPase rapidly pumps any sodium ions that enter the cell back out, and pump potassium ions back into the cell. Ion concentrations remain nearly constant during an action potential.B. Correct: As membrane potential moves closer to ENa during the upstroke of the action potential, the electrochemical potential for sodium (V – ENa) will decrease.C. Incorrect: The Nernst potential for sodium does not change during the action potential.D. Incorrect: There is a net depolarizing current during the upstroke of the action potential.E. Inactivation gates are slowly closing during the upstroke of the action potential.
387
A 100 kg man with 10% body fat receives an i.v. infusion of 3 liters of fluid which is 5% dextrose in 0.9% NaCl. Which of the following is the best estimate of the extracellular fluid volume at equilibrium in this person after the infusion?15 liters18 liters22 liters25 liters48 liters
Total body water = Lean body mass x 0.72 = (100 kg – (10% x 100 kg)) x 0.72 = 64.8 litersICF volume = (2/3) x TBW = 43.2 litersECF volume = (1/3) x TBW = 21.6 liters The solution infused i.v. is 0.5% dextrose and 0.9% NaCl. At equilibrium, the dextrose will be metabolized so this will be equivalent to infusing 3 liters of 0.9% NaCl. The 3 liters will remain in the ECF, so ECF volume will be 21.6 liters + 3 liters, or 24.6 liters.
388
A 63-year-old man is brought to the emergency department due to weakness in moving his limbs. Earlier in the day, he had eaten a pufferfish which is known to contain tetrodotoxin, a substance which blocks voltage-gated sodium channels. Tests reveal that plasma sodium levels are normal. Which of the following effects in nerves could be caused by tetrodotoxin to account for his symptoms?decreased rate of rise during depolarization of the action potentialincreased chemical energy for sodiumincreased conduction velocity of the action potentialincreased number of resting sodium channelsmore negative threshold
decreased rate of rise during depolarization of the action potentialSince tetrodotoxin blocks voltage-gated sodium channels, sodium current would be reduced during the upstroke of the action potential.A - Correct: The reduced sodium current will slow the rate of rise of the action potential.B - Incorrect: Chemical energy for sodium is determined by the ratio of extracellular and intracellular sodium concentrations, and the valence of sodium. These will not be affected by tetrodotoxin.C - Incorrect: The decreased sodium current will decrease conduction velocity of the action potential.D - Incorrect: If the number of resting sodium channels was increased, sodium current would be increased. Tetrodotoxin decreases sodium current.E - Incorrect: By decreasing sodium current, tetrodotoxin would make threshold less negative (more positive), and decrease excitability.
389
Excess water intake decreases plasma sodium below normal levels resulting in dilutional hyponatremia. Isotonic saline (0.9% NaCl) can be used to correct the sodium deficit in this situation. Assume that plasma sodium is 110 mEq/liter in a person with dilutional hyponatremia. Which of the following will occur in this person following intravenous infusion of isotonic saline?decrease in extracellular osmolalityincrease in intracellular osmolalityincrease in intracellular volumehypotonic contractionisotonic expansion
increase in intracellular osmolalityAlthough 0.9% NaCl is normally an isotonic solution, it is a hypertonic to this person with dilutional hyponatremia (which decreases osmolality of the extracellular and intracellular fluid). The plasma sodium concentration is 110 mEq/liter, which is about half of the plasma osmolality (which would be about 220 mEq/liter, lower than normal).A - Infusion of 0.9% saline will raise extracellular osmolality.B - The increase in extracellular osmolality after the saline infusion will cause water to diffuse out of the cells, causing intracellular osmolality to increase.C - As water diffuses out of cells, intracellular volume will decrease.D - The saline infusion expands the volume of the extracellular space.E - The osmolality of body fluids is still lower than normal.
390
Absence in apoE would result in?
would result in increased levels of VLDL because apoE helps in receptor binding
391
During the 4th though the 7th week of embryonic development the initially single ventricular chamber is being subdivided into right and left ventricles by a muscular ventricular septum. The final growth of the interventricular septum is linked to which other event in embryonic heart development?growth of the septum primumformation of the ostium secundum in the septum primumfinal septation of the truncus arteriosusincorporation of the four pulmonary veins into the left atriumfusion of the superior/anterior and inferior/posterior endocardial cushions
final septation of the truncus arteriosusAnswer is C) final septation of the truncus arteriosus. Thus, as the ventricles are becoming completely separate chambers the outflow of the heart is separating into aortic and pulmonic outflow. This occurs at about the 8th week of development. Growth of the septum primum a. occurs earlier during heart development in the 4th to 6th week of development. The formation of the ostium secundum in the septum primum b. occurs in about the 6th week of development. The incorporation of the four pulmonary veins into the left atrium d. occurs at about the 5th week of development. Fusion of the superior/anterior and inferior/posterior endocardial cushions e. occurs in about the 4th week of development.
392
Leukocyte diapedesis typically occurs where?across lymphatics exclusivelyacross post-capillary venulesanywhere in the systemic vasculaturemost frequently across fenestrated capillary beds, and occasionally through continuous capillaries
During inflammation, movement of leukocytes from blood into the interstitial space (diapedesis) occurs mainly in post-capillary venules.
393
A pediatrician detects a harsh murmur along the left sternal border in a 3 week old boy. The parents report that the baby gets 'bluish' when he cries or drinks from his bottle. Echocardiogram reveals pulmonary stenosis and right ventricular hypertrophy. What is the best diagnosis?atrial septal defectcoarctation of the aortatetrology of Fallottruncus arteriosus
Answer: C Tetrology of FallotTetrology of Fallot includes 4 anatomic changes: pulmonary stenosis, ventricular septal defect, dextroposition of the aorta, and right ventricular hypertrophy. It is the most common cyanotic congenital heart disease, accounting for 10% of all congenital heart defects. Cyanosis appears shortly after birth or early in infancy due to right-to-left shunting of venous blood from the right ventricle into the dextroposed aorta. Narrowing of the pulmonary artery impedes the entry of blood into the lung, thereby increasing the pressure in the right ventricle.
394
In the eLearning Case, the person with chronic obstructive pulmonary disease had bilateral edema of the lower extremities. Assume that capillary pressure within the lower legs of this person is 30 mm Hg, pressure in interstitial fluid is 0 mm Hg, and plasma osmolality is 290 mOsm. If the extent of edema is staying constant (i.e., no net fluid movement across the capillary), which of the following is the best estimate of osmolality of intracellular fluid?288 mOsm288.5 mOsm290 mOsm291.5 mOsm292 mOsm
288.5 mOsmIf the extent of edema is remaining constant, the movement of fluid into the interstitial space from capillaries must be exactly balanced by movement of fluid from the interstitial space into capillaries. Capillary pressure is 30 mm Hg, which drives fluid out of the capillary. Therefore, the force for reabsorbtion of fluid into capillaries must be equal to 30 mm Hg. Each one mOsm difference in between plasma and interstitial fluid develops a force of 20 mm Hg driving water movement. Since capillary pressure is 30 mm Hg, a difference in osmolality of 1.5 mOsm will develop a force of 30 mm Hg. Solute concentration in interstitial fluid must be 1.5 mOsm lower than plasma osmolality, or 288.5 mOsm. Interstitial osmolality will be equal to intracellular osmolality.
395
What would apo-CII absence result in?
would result in elevated chylomicron levels
396
A 42 year old woman weighing 60 kg with 10% body fat has a plasma osmolality of 290 mOsm. She receives an i.v. infusion of 2 liters of 0.45% NaCl. Which of the following best describes the resulting change in body fluids in this person?hypertonic contractionhypertonic expansionhypotonic contractionhypotonic expansionisotonic contractionisotonic expansion
hypotonic expansionA solution of 0.45% NaCl has an osmolality of 145 mOsm. The intitial effect of infusion of this solution would be to increase the volume of the ECF and to decrease the osmolality of the ECF. The latter effect will cause water to diffuse into cells, reducing osmolality of the ICF and increasing its volume. As water moves out of the ECF, its volume will decrease back towards normal but its volume will still be greater than normal at equilibrium. This infusion will result in a hypotonic expansion resulting in decreased osmolality of the ICF and ECF, as well as an increase in ECF volume.
397
A 47-year old male arrives by ambulance to the emergency department due to left-sided chest pain. He refused to lie down on the ambulance gurney because it made the chest pain worse. He has no other pain. While his heart rate is elevated, his blood pressure is 127 / 82, and all his heart valves sound normal. There does appear to be a diffuse squeaky leather sound, which worsens when the patient is asked to forcefully expel air. His lungs sound normal. What is the working diagnosis?cardiac tamponadecoarctation of the aortacongestive heart failurepatent ductus arteriosuspericarditis
Answer is E) pericarditis. The pain is localized to the left chest and does not radiate to his left arm. The patient’s chest pain is worse when lying flat and when the diaphragm is forced upward during forced expiration both suggest pericarditis. The diffuse squeaky leather sound also suggests pericarditis. All heart valve sounds would be diminished during A) cardiac tampanade (fluid in the pericardial sac). If the patient had B) coarctation of the aorta the upper extremity blood pressure would be elevated, which it is not. If the patient has C) congestive heart failure his lung sounds would not be normal. If the patient had a D) patent ductus arteriosus, then there would be a “machine-like” holosystolic murmur best hear on the upper left sternal border, which is not present.
398
Tests reveal that a 37 year old man is hypernatremic as his plasma sodium concentration is 160 mEq/liter. This person’s total body water is 42 L. If the desired plasma sodium concentration is 140 mEq/liter, which of the following values is closest to the water deficit in this person?3 liters4 liters5 liters6 liters7 liters
6 litersThe correct answer is D. H2O Deficit = Present TBW x { ( Current [Na+] / Normal [Na+]) -1} H2O Deficit = 42 liters x { (160 mEq/L / 140 mEq/L) -1} = 6 liters
399
You deliver a 6 lbs, 6 oz full term baby girl. Her breathing rate is slightly elevated, and when she cries her lips turn blue. Her toes are also bluish. You immediately send for a pediatric cardiologist who orders an echocardiogram. The sonographer who immediately performs the echo study is convinced that the baby girl has transposition of her great vessels. Which of the following is the most likely additional heart defect that the newborn girl also has?overriding aortaventricular septal defectligamentum arteriosumcoarctation of the aortaaortic aneurysm
ventricular septal defectThe answer is B. Ventricular septal defect. (Moore and Dalley p 151; Sadler p 178.) The additional heart defect the newborn girl also has is a ventricular septal defect. Babies born with transposition of the great vessels normally present with symptoms of cyanosis as the ductus arteriosus closes within the first day of birth. Since in this defect the aorta is sitting on top of the right ventricle and the pulmonary trunk is receiving blood from the left ventricle, blood is being pumped mainly just to the body by the right side and mainly just to the lungs by the left side. The only way oxygenated blood is getting to the body is if the two sides are connected, often by a patent ductus arteriosus. Babies with this defect are immediately but on oxygen, and prostaglandins are also given to help keep the ductus arteriosus open longer than normal. About 25% of the time that transposition of the great vessels is present, there is also a ventricular septal defect, which aids in the intermixing of blood from the two sides of the heart. This condition must be treated surgically. Defects of the aortic arch are normally not present. Ligamentum arteriosum (answer C) would make the problem worse. Coarctation of the aorta (answer D) would make the problem worse. An overriding aorta (answer A) is the second best answer. An aortic aneurysm (answer E) is unlikely to be present in a newborn.
400
A 43 year old woman has been lost in the wilderness for one week. She is brought to the Emergency Department after being found, and is conscious and responsive to questions. Her blood pressure is lower than normal and her plasma osmolality is elevated. Based on this information, which statement is correct about this person?Interstitial volume in systemic organs is increased.Intracellular osmolality is decreased.Intracellular volume is increased.The best treatment is i.v. infusion of 5% dextrose.This is an example of an isotonic contraction.
Correct answer is D. This situation is an example of dehydration and this is indicated by the low blood pressure and increased plasma osmolality. Water is lost from the extracellular fluid, which increases it’s osmolality causing water to diffuse out of cells A - Both interstitial volume and plasma volume would be decreased in this person, resulting in a decreased extracellular fluid volume.B - The increase in plasma osmolality indicates that extracellular fluid osmolality is increased, which would cause intracellular fluid volume to decrease and increase intracellular osmolality.C - Water diffuses out of cells when extracellular osmolality is increased, and this would decrease intracellular volume.D - The person has a water deficit and infusing 5% dextrose is the best treatment to restore water to both the extracellular and intracellular fluid compartments (dextrose will be metabolized).E - This is an example of a hypertonic contraction.
401
What would an absence of apoA-1 lead to?
absence of functional apoA-1 results in severely reduced levels of HDL
402
A 82-year-old man went to his family practice physician’s office reporting difficulty sleeping without being propped up on three pillows and shortness of breath. He doesn’t report any unusual chest pain. Using a stethoscope the physician listened to his lungs and heart. The lung sounded relatively normal, but when listening to his heart the first heart sound seemed diminished. Specifically at the left mid-clavicular line at the 5th intercostal space the valve sound at that location was soft and abnormal. All other heart valves sounded normal. The patient’s ECG was normal for a 82-year-old. What is the most likely source of the patient’s problem?cardiac tamponadepericarditisocclusion of the right coronary arteryrupture of pectinate muscle fibersmitral valve prolapse
mitral valve prolapseCorrect answer is E: mitral valve prolapse. The sound of the mitral valve closing is best heard on the left chest wall at the 5th intercostal space at the mid-clavicular line. Of all heart valves the mitral valve is the most frequently damaged. The chordae tendaneae can rupture and cause the valve to flap back into the left atrium during left ventricle systole. Patients with cardiac tamponade (answer A) have shortness of breath (dyspnea), but all of their heart sounds (closure of valves) would be diminished, which was not the case for the 82-year old. Pericarditis (Answer B) often causes a pericardial rub, which was not present in this patient. Occlusion of the right (Answer C) arteries would tend to cause disruption of blood flow, cardiac pain, abnormal ECG, along with shortness of breath, but the patient reports no chest pain, making this unlikely. Rupture of pectinate muscle fibers (answer D) is highly unlikely (they are only present in the atrial chambers) and would have no effect on the mitral valve.
403
Which statement is true for a cardiac muscle cell in the left atria?The T tubules and sarcoplasmic reticulum are arranged in triads.The myosin filament cannot bind actin until it is phosphorylated by myosin light chain kinase.Ca2 -dependent ATPases are present on the sarcoplasmic reticulum.The actin filaments bind to the desmosomes at the intercalated disk.The only source of calcium is the release of calcium from the sarcoplasmic reticulum.
Ca2 -dependent ATPases are present on the sarcoplasmic reticulum.A. The T-tubules and sarcoplasmic reticulum is predominantly arranged as a diad in cardiac muscle. It is a triad in skeletal muscle.B. Myosin will bind whenever the troponin complex does not cover the actin binding site. Activation of myosin by myosin light chain kinase is important in smooth muscle contraction.C. These are required for the return of Ca2+ to the sarcoplasmic reticulum following excitation. They are also found on the sarcolemma. D. Actin binds to the adherens complex at the intercalated disk. Intermediate filaments bind to desmosomes.E. Calcium also enters through voltage gated calcium channels.
404
During the partitioning of the embryonic atrium from a single chamber into right and left atria, there are two septae that form and three openings. Which is the last opening to form and in which septum does it form?ostium primum in septum primumostium primum in septum secundumostium secundum in septum primumforamen ovale in septum primumforamen ovale in septum secundum
foramen ovale in septum secundumAnswer is E) foramen ovale in the septum secundum. There is no foramen ovale in the septum primum d.. There also is no ostium primum in the septum secundum b.. The ostium primum in the septum primum a. forms first. The ostium secundum in the septum primum c. is the second opening to form.
405
What are the two sources of calcium release in a cell?
Calcium enters through voltage gated calcium channels and is released by the sarcoplasmic reticulum.
406
Capillary pressure is referring to pressure driving fluid in which direction? What about interstitial fluid pressure?
Driving fluid out of the capillary into the the interstitial space.Driving fluid from the interstitium to the capillary
407
Assume that a cell has an intracellular potassium concentration of 150 mM and an intracellular sodium concentration of 14 mM. The cell is placed in a solution with a potassium concentration of 15 mM and a sodium concentration of 140 mM. The cell is permeable to only potassium and sodium, and potassium conductance is 20 times higher than sodium conductance. Which of the following is the best estimate of resting membrane potential in this cell?-42 mV-51 mV-54 mV-58 mV-60 mV
-54 mV
408
What is arterial pressure determined by?
Arterial pressure is proportional to the volume of blood within the arterial system. During ejection when inflow is greater than outflow of blood from arteries to veins, arterial pressure increases.
409
What is occurring during atrial contraction?
It is initiated near the end of diastole once atrial depolarization occurs. Atrial contraction only increases atrial pressure slightly and increases ventricular volume by about 10-20%.
410
What do each of these arrow stand for?
411
What is wide splitting of S2? What are some things that can cause it?
412
What do the heart sounds of S1, S2, S3 and S4 indicatie?
413
What are some causes of increased pressure in the right atria?
Tricuspid stenosis, RV failure, and Cardiac Tamponade
414
What causes the physiological splitting of S2 during inspiration?
Venous return to the right heart is a flow, and therefore it is dependent on the pressure gradient driving the flow and resistance. pressure is increased then venous return to the right ventricle will increase. During inspiration, decreased right atrial pressure increases venous return to the right heart. Filling of the right ventricle is increased which causes a greater stroke volume on the next beat (Starling’s Law). The pulmonic valve remains open longer than normal during ejection of this greater stroke volume and so pulmonic valve closure is delayed relative to aortic valve closure on inspiration.
415
What is the formula for Ejection Fraction and what are the normal ranges in humans?
EF = Stroke volume / EDVNormal range is 0.5 to 0.7 and this is an index of contractility of the heart
416
How does the cardiac cycle compare between the right and left heart?
417
What is occurring during the isovolumic ventricular relaxation phase of the cardiac cycle?
This period when the aortic valve is closing and ventricular pressure is falling rapidly. Ventricular volume cannot change since mitral valve is also closed. S2 signals the onset of diastole. Calcium levels in myocytes are decreasing.
418
When does systemic arterial diastolic pressure occur?
During systole
419
What is ESV and what does it represent?
End-systolic volume - the ventricular volume at the end of ejection
420
What are the events that occur when the QRS complex occurs?
Mitral and tricuspid valves close (S1)Pulmonic and Aortic valves opening
421
A cardiac cycle is defined as?
One complete sequence of contraction and relaxation of the heart
422
What is paradoxical splitting of S2 and what are some causes?
423
Since the right and left heart are in series what does this mean for the amount of blood they must pump over a minute?
They must pump the same amount - cardiac output must equal pulmonary blood flow
424
What do the red and blue shaded areas represent respectfully?
Red - Ventricular diastole - begins at the time of aortic valve closure and lasts until mitral valve closureBlue - Ventricular systole - begins at the time of mitral valve closure and lasts until aortic valve closure
425
When ventricular contraction occurs, what happens to the pressure in the ventricles compared to the pressure in the artia? How does this affect the mitral and tricuspid valves?
When the ventricles contract the pressure within them increases and becomes greater than atrial pressure. This results in the closing of the mitral and tricuspid valves to keep blood from flowing back to the atria.
426
Since there is a much lower pressure difference in the right side of the heart, how can it achieve the same level of vascular flow as the left side of the heart?
The level in resistance in the right side of the heart is substantially less than the left side.
427
What is indicated by the pressure in the ventricle and the corresponding artery being the same during ejection?
This indicates that the aortic and pulmonic valves have very little resistance to blood flow
428
What is occurring during the process of ventricular filling?
When ventricular pressure falls below atrial pressure the mitral valve opens and blood flows from the atrium to the ventricle. Rapid filling occurs in the ventricle as blood flows from atrium to ventricle, causing atrial pressure to drop. Most of the filling is due to the pressure gradient being higher in the atrium than the ventricle.
429
When are the tricuspid and mitral valves open?
When atrial pressures are greater than ventricular pressures - allowing the blood to flow from the atria to the ventricles.
430
What are some causes of reduced pressure in the Right Atria?
Hypovolemia and impaired venous return to the heart
431
When can the distinct sound of the aortic valve closing before the pulmonic valve closing be heard?
Upon inspiration by the patient
432
When would atrial contraction become more important for ventricular filling?
During high heart rate, because there is a reduced diastolic filling time
433
How can you determine stroke volume from ESV and EDV?
SV = EDV - ESV
434
How does arterial diastolic pressure compare to ventricular end diastolic pressure?
DP: This is the pressure in the aorta at the time right before the opening of the aortic valve - tends to be roughly 80mmHgEDP: This is the pressure in the ventricle at the end of diastole - normally 0-10 mmHg
435
Explain what the venous waves indicate.
436
What is occurring during isovolumic ventricular contraction?
This is the onset of ventricular systole. This begins once an action potential passes through the AV node and initiates ventricular depolarization; triggered by QRS complex. Contraction causes intraventricular pressure to rise above atrial pressure causing the mitral valve to close. Since the aortic valve is also closed, pressure rises rapidly without a change in volume.
437
What is EDV and what does it represent?
End-diastolic volume - the ventricular volume at the end of filling
438
What accounts for the slight differences is the openings of the pulmonic vs aortic valves? What accounts for this in the closing of the mitral and tricuspid valves?
Upon depolarization of the ventricles, the pressure in the left ventricle will rise much faster (due to larger muscle) than the right ventricle. This will cause the mitral valve to close slightly before the tricuspid valve.The pulmonic valve will open at a much lower pressure than the aortic valve so the pulmonic valve will open slightly before the aortic.
439
What is occurring during the ventricular ejection phase of the cardiac cycle?
Ejection begins when ventricular pressure rises above the aortic pressure - opening the aortic valve. There are two phases.Rapid ejection phase - Immediately after the aortic valve opens, blood rapidly enters the aorta and causes arterial pressure to rise.Slow ejection phase - after ventricular and aortic pressures reach maxium the rate of ejection and both pressures decrease. The peak systolic pressure is nearly the same in the ventricle and aorta because there is little resistance to flow in the aortic valve. Pressure declines throughout the slow ejection phase because the force of contraction is decreasing as ventricular volume gets smaller and due to ventricular repolarization (signified by the onset of the T wave). Eventually intraventricular pressure falls below aortic pressure, which results in aortic valve closure.
440
What is stroke volume?
The volume ejected in a single beat
441
Other than statins, what is a promising therapy to reduce LDL levels?
PCSK9 Inhibitors
442
What are the two epidemics of the US addressed in this lecture?
Obesity and HF
443
Are statins created equal?
No, statins have different levels of efficacy.
444
Which aldosterone blockade has an estrogenic effect that can lead to gynecomastia?
Spironolactone
445
Two examples of PCSK9 inhibitors. Why aren't these as commonly used?
Alirocumab and evolocumabStill awaiting results of outcome trials
446
What is the one well studied method to reduce relative risk for coronary heart disease?
Lipid lowering therapy
447
What are some of the causes of HF?
CADHTNValve dysfunctionIdopathicInfection (Chagas disease)Toxins (alcohol or cytotoxic drugs)Valvular diseaseProlonged dysrhythmias
448
What are the primary effects of PCSK9 inhibitors?
LDL lowering
449
What is angina pectoris? What triggers it? Location? When is it considered stable?
Discomfort (not pain) in chest and related areasTypically retrosternal in location brought on by exertion or emotional stressCan orginate/radiate to jaw, neck, throat, shoulders, back, or arms"Stable" when no change in frequency, duration, precipitating, or relieving factors in past 60 days
450
What is ischemia?
Supply/demand mismatch, most often due to severe CAD
451
What is used to treat bradydysrhythmias (SA node dysfunction, AV node dysfunction, complete AV block)?
Pacemakers
452
List the statins in order of relative potency (low to high).
Lovastatin, Pravastatin, Simvastatin, Fluvastatin, Atorvastatin, Rosuvastatin
453
What are the primary effects of statins?
LDL lowering, modest HDL raising and triglyceride lowering
454
In what patient population does CABG have an especially better mortality reduction in than PCI?
Diabetes mellitus
455
What are medical therapies are known to reduce mortality in HF?
Beta blockers (carvedilol, metoprolol succinate, and bisoprolol)ACE Inhibitors/ ARBs (Lisinopril)Neprilysin inhibitor/ ARB (sacubitril/valsartan) Vasodilators (Hydralazine/isosorbide dinitrate combo)Diuretics - Aldosterone antagonists (spironolactone, eplerenone)Loop diuretic - furosemideSinus node inhibitor (ivabradine)
456
What is the normal function of PCSK9?
PCSK9 binds LDLRs and facilitates their degradation, which ultimately results in lower LDLRs and increased blood cholesterol
457
What is commonly used to in CABG of the LAD?
Left internal mammary artery
458
What do statins inhibit?
HMG-CoA Reductase
459
In patients with STEMI w/o contraindications (asthma, COPD, bradycardia, advanced heart block), what should be administered? Hint: Common side effect = fatigue
Beta blocker
460
When are nitrates indicated? Effect on CAD mortality? Common side effect?
Patients with refractory symptoms despite beta blockers (or intolerant to beta blockers)Effect on CAD mortality: no mortality benefitCommon side effect: headache
461
What treatments are used for symptom management in HF?THESE DO NOT REDUCE MORTALITY.
VasodilatorsLoop diuretics (furosemide)NitratesDigoxinInotropes/infusion therapy (refractory HF)
462
What is the lifetime risk of developing symptomatic CAD after age 40 in men and women?
Men: 49%Women: 32%
463
What are some other terms for coronary artery disease (CAD)?
Ischemic heart disease (IHD)Atherosclerotic heart disease (ASHD)ArteriosclerosisAtherosclerotic cardiovascular disease (ASCVD)
464
What anticoagulant can be used as ancillary therapy to fibrinolytic therapy?
Heparin (UFH)Can be used in both STEMI and NSTEMI
465
ACE Inhibitors are especially good for what type of post-MI patients?What is the most common side effect? A severe side effect?
MI-patients with LV systolic dysfunction (EF < or = 40%)Most common side effect is cough, angioedema is uncommon but serious
466
What does PCI stand for?
Percutaneous coronary intervention (PCI)
467
What is the most common side effect of statins?
Muscles pains (myalgias). It can cause patients to stop taking the medications Statins have been indicated to possibly raise blood sugar resulting in memory impairment
468
What did the Framingham Heart Study establish as a relationship between BMI and HF risk?
For every unit increase in BMI, risk of HF increased by 5% in males and 7% in females
469
What are some possible medical therapies for CAD?
Aspirin (ASA)Thienopyridines (clopidogrel, prasugrel)P2Y12 inhibitor (ticagrelor)Beta blockersACEI/Angiotensin Receptor Blockers (ARB)Nitrates (NTG, isosorbide)Aldosterone antagonistsLipid lowering agentsFibrinolytics (for STEMI)
470
What is important about the stages, phenotypes, and treatment of HF?
HF is a progressive disease. Everyone starts in stage A. This is where we can best try to prevent progression into the other stages of HF. By the time patients get to stage D, there aren't many proven beneficial therapies. Treatment may shift over to palliative comfort care.
471
Why must platelet counts be monitored daily for a patient on heparin?
HIT, heparin-induced thrombocytopenia
472
How does the half-life of LMW heparins (enoxaparin, dalteparin, tinzaparin) compare to heparin?
Longer half-life, less commonly used
473
What is the failure rate of fibrinolytics in the treatment of STEMIs?
~20-40%
474
When are implantable cardioverter defibrillators (ICDs) preferred over pacemakers?
Patients with persistently low EF (
475
What is CABG?
Coronary artery bypass grafting
476
What is used to treat angina?
Nitroglycerin (NTG)
477
What are the 4 "statin benefit groups"?
Known ASCVDLDL > or = 190DiabeticsAdults w/ 10-yr ASCVD risk of >/= 7.5%
478
What is the most common antiplatelet therapy given for CAD (post-MI and maintenance therapy indefinitely)?
Aspirin (ASA)
479
What are the two types of left ventricular dysfunction in HF?
Systolic: impaired contractilityDiastolic: impaired filling, relaxation, or compliance
480
Fibrinolytics are indicated in what type of MI? Examples?
STEMI onlyAtleplase, reteplase, tenecteplase, streptokinase
481
When a patient is allergic to ASA, what are some alternatives?
Clopidogrel, Prasugrel, Ticagrelor
482
What symptom is associated with acute ischemic syndromes/acute coronary syndromes? What are the two possible types of MI
Unstable anginaNon-ST segment elevation MI (NSTEMI) or ST segment elevation MI (STEMI)
483
CAD is commonly asymptomatic. When it is symptomatic, what are the main symptoms?
Chronic stable angina or unstable angina
484
What are the primary effects of niacin? What side effect causes patients to discontinue taking it?
LDL lowering, good HDL and trig effectsFlushing
485
What are two conditions (other than DM) that indicate CABG over PCI?
3 vessel disease and L ventricular dysfunction
486
What are fibrates and what are they used for?
These have an effect on raising HDL, triglyceride loweing and modest LDL lowering
487
What are common side effects of fibrates?
myopathy - especially in individuals with decreased creatinine clearance
488
What are bile acid resins?
These have modest LDL lowering ability
489
What are the current guidelines for prevention of CHD?
Focus on primary prevention. Less focus on achievement of a specific goal and use of non statin. Put them on a drug that will lower their risk
490
When would you use fibrinolytics?
Use in acute ST elevation MI - these convert plasminogen to plasmin to break up a clot
491
When would you not want to use an aldosterone blockade?
Because of its potassium raising effects, avoid using in patient with advanced renal disease or elevated serum potassium
492
Hydralazine/isosorbide combo can have what side effect at high doses?
Lupus-like symptoms
493
What are your survival promoting drugs therapies in heart failure patients?
Beta blockersACE inhibitors or ARBsAldosterone antagonistsHydralazine/isosorbide dinitrate combo
494
When would a patient need biventricular pacing (CRT)?
This is beneficial to patients with symptomatic HF and bundle branch block. This is intended to restor synchronous right and left ventricular conduction.Low ejection fraction, significant HF symptoms despite optimal medical therapy, delayed intraventricular conduction
495
When would you prescribe ICDs?
Low ejection fraction patients, or have hypertrophic cardiomyopathyUse for resuscitated sudden cardiac arrest not associated with acute MI
496
How will left vagal stimulation differ from right?
497
But wait!!! The cross sectional area of a capillary is so so small.... How could this account for the blood flowing so slowly in the capillaries?
Because! The total cross-sectional area of all the capillaries in the system is much greater than all other systemic vessels.
498
Why is turbulent flow important when measuring blood pressure with a sphygmomanometer?
The flow you are hearing between the systolic pressures and diastolic pressures is a turbulent flow.
499
How will Isoproterenol if it primarily affects Beta 2 activation receptors affect MAP, and what will the baroreflex response be?
500
What is Runoff and what is something that can increase it?
Runoff is the rate at which blood leaves the arteriesVasodilation can increase runoff
501
An increased HR will do what to preload?
Decreased preload
502
What will be the baroreflex response be to carotid massage?
503
What are two alternative ways to calculate vascular resistance?
504
How does venoconstriction result in increased venous return to the heart?
Venoconstriction decreases venous compliance, which causes pressure within veins to increase which increases pressure difference between peripherial veins and right atrium. The pressure gradient increases venous return to the heart.
505
Increased firing of what autonomic nerved would cause venoconstriction?
Increased firing of sympathetic nerves would cause venoconstriction. Which would stiffen the wall and decrease venous compliance, thus resulting in increased venous pressure.
506
What can be altered to affect the rate of runoff?
Systemic arteriolar dilation (decreased TPR) results in a lower resistance to flow and a higher rate of runoff. This will result in lower arterial diastolic pressure.
Systemic arteriolar constriction (increased TPR) results in a higher resistance and so a lower rate of runoff. This will increases arterial diastolic pressure.
507
How can gravity effect blood pressures?
Upon standing, the pressure in the veins below the heart increases while venous pressure decreases above the heart.
508
What systemic vessel has the lowest velocity of blood in them? Why might this be important?
Capillaries - The slow flow through capillaries facilitates solute exchange between blood and the surrounding tissue by increasing the time available for exchange.
509
What is Poiseuille's Law and how does it relate to resistance in the body?
Poiseulle's law describes flow through a tube. It states that resistance to flow in a tube is most determined by the radius of the tube.
510
How does ejection rate determine arterial systolic pressure?
The rate of ejection from the left ventricle determines how quickly blood volume in arterial system increases, which influences the peak systolic pressure attained.In aortic stenosis, arterial pulse pressure is reduced because the rate of ejection of blood is decreased due to the high resistance of the aortic valve. Resulting in the pressure rising slower.
511
How does stroke volume affect arterial systolic pressure?
The rise in arterial pressure during ejection is directly proportional to the volume of blood added to the arterial system.
512
What systemic vessel accounts for the majority of TPR?
Arterioles
513
How will expiration be different in its effects on the left and right heart?
514
Since pressure in systemic veins is low and venous return is the same as arterial flow, what does this say for the resistance in veins?
It is very low
515
Because arterioles have the largest drop in systemic pressure, what can be said about their resistance?
The arterioles are the site of highest vascular resistance.
516
What is the formula for compliance of the arterial system?
517
What is the equation for MAP using systolic pressure and diastolic pressure?
MAP = Diastolic Pressure + 1/3 (Systolic Pressure - Diastolic Pressure)MAP = Diastolic Pressure + 1/3 Pulse pressure
518
As a person ages, what happens to the Volume % increase vs pressure? (Hint the slope of the line is compliance)
The compliance decreases. This graph is delta V/ delta P which is the formula for compliance.
519
What is the effect of skeletal muscle pump on venous return?
The veins in the legs contain one way valves which direct blood to the heart. Contraction of skeletal muscles compresses veins in the leg, which forces blood toward the heart. When the skeletal muscles relax, the venous valves prevent backward flow of blood.
520
What is tubulent flow? How can it cause bruits?
Turbulent flow is a disruption of laminar flow. Turbulent flow causes vibrations of the blood vessel wall which are transmitted through the tissue and can be heard through the stethescope as bruits.
521
Calculate TPR assuming that MAP = 100mmHg, RAP = 0mmHg, and CO is 6 liters/minute.
522
How will nitroglycerine affect CO and TPR? What will the baroreflex response be?
523
Answer this!
The highest flow will be in tube C since it has the lowest resistance.
524
What would cause arterial pressure to rise?
This occurs when inflow is greater than outflow - during the rapid ejection phase of ventricular systole
525
What can happen to runoff time if heart rate in increased/decreased?
Decreasing heart rate increases runoff time, so arterial diastolic pressure will decrease.Increasing heart rate decreases runoff time, so arterial diastolic pressure will increase
526
What accounts for the series and parallel resistance in the body?
Series - blood flow from aorta to arteriole to capillaries to veins account for the seriesParallel - the systemic organs
527
How does cross sectional area determine velocity?
The velocity of flow is inversely proportional to the cross-sectional area
528
What is the pathways by which venous pooling upon standing can occur? How will the affect CO?
Because veins are compliant, the increase in venous pressure upon standing will cause veins to distend - minimizing the increase in venous pressure. Venous return to the right heart will decrease upon standing, reducing EDV, decreasing stroke volume and thus reduce CO
529
How does arterial compliance affect arterial systolic pressure?
The aorta and large arteries stretch to some extent as blood is ejected from the left ventricle. This elasticity reduces the rise in arterial pressure during ejection.
530
Where is the major dropping point for pressure in the systemic vessels?
Arterioles - the drop decreases from 80-35mmHg
531
What will the baroreflex response be to carotid occlusion?
532
What are the two factors that determine arterial diastolic pressure?
Rate of runoff - how fast blood flows from arterial to venous system Runoff time - runoff occurs during diastole (while ventricle is filling)
533
How will isoproterenol affect CO if it is selective for Beta 1 activation and what will the baroreflex response be?
534
What is the major determinant of runoff time?
Heart rate
535
What is the famous mnemonic for the effect of breathing on venous return to the heart?
536
How can expiration affect heart rate?
537
Decreased arterial compliance associated with aging can have what affect on systolic pressure?
With aging arterial compliance is reduced which results in a greater increase in arterial pressure during ejection compared to a younger person. As a result an older person will have higher arterial systolic pressure than that of a younger person during ejection of the same stroke volume.The decreased arterial compliance will reduce elastic recoil during diastole, resulting in a faster decrease in arterial pressure during diastole and a lower arterial diastolic pressure than seen in a young person.
538
How can you determine central venous pressure?
Lay patient in a semi-supine position, and the distance in cm of the manubriosternal angle to the point of collapse of the external jugular vein is detemined. Then take this value and add 5 to determine the value.
539
What is the process that occurs after inspiration to account for the delayed closure of the pulmonic valve?
There is an increase in venous return to the right heart. Which will increase the ejection time. Leading to the splitting of the second heart sound.
540
What do each of the numbers designate?
1 - Systolic Pressure2 - Diastolic Pressure3 - Ejection4 - Runoff
541
What is polycythemia?
This relates to people living at higher altitude. The response to having lower oxygen content is an increased production of red blood cells, resulting in increased blood viscosity and therefore greater resistance to blood flow.
542
How does blood viscosity relate to resistance to flow?
Blood viscoscity directly relates to resistance to blood flow.
543
Answer this!
Each tube will receive the same flow since resistance is the same, so each tube will receive 2 liters/minutes
544
What is the equation for venous return to the heart?
(Psystemic veins - Pright atrium) / Resistanceveins
545
How will adding resistance in series differ from resistance in parallel?
546
How does compliance compare between veins and arteries?
Arteries and arterioles have low compliance due to their thick musclar walls. A small increase in blood volume will increase their arterial pressure.In contrast, venules and veins are highly compliant in relation. Large increases in venous blood volume creates a small increase in venous pressure.
547
How will inspiration affect the stroke volume in the left ventricle?
It will increase intrathoracic pressure leading to decreased pressure in pulmonary veins and decreased blood flow to left atrium and decreased LV EDV.
548
How will phenlyephine affect MAP and what will the baroreflex response be?
549
What would cause arterial pressure to fall?
When inflow is less than outflow (during diastole)
550
Patient is given thiopental and succinyl choline, and developes hyerkalemia. Where did the potassium come from that produced the increased plasma potassium concentration in this patient?
Succinylcholine binds to and activates acetylcholine (ACh) receptors at muscle neuromuscular junctions. Accordingly, it depolarizes the subsynaptic membrane. Since succinylcholine resists hydrolysis by acetylcholine esterase, the depolarization of the subsynaptic membrane is prolonged leading to inactivation of sodium channels in the vicinity of the subsynaptic membrane. By this mechanism, the muscle becomes unexcitable inducing a relaxed muscle state. However, increased K-loss from the muscle will occur since potassium efflux through open K-channels increases as membrane potential moves more positive; difference between membrane potential and potassium Nernst potential increases. Succinylcholine produces some Kloss from normal individuals but the effect is blunted by the fact that this loss is confined to K-channels near the endplate. The hypersensitivity of some individuals to succinylcholine is due to the existence of ACh receptors in extrajunctional areas. The extrajunctional receptors increase the area of depolarized membrane and K-efflux though open K-channels. In some rare cases, succinylcholine induces rhabdomyolysis (i.e., breakdown of the muscle membrane).
551
With regards to SA-node cells, what effect does hyperkalemia have on 1) maximum diastolic potential, 2) rate of phase 4 depolarization, 3) rate of phase 0 depolarization, and 4) rate of phase 3 repolarization? Which of these would contribute to the production of a bradycardia?
Maximum diastolic potential becomes more negative, rate of phase 4 depolarization is decreased, rate of phase 0 depolarization is decreased, and rate of phase 3 repolarization is increased. Bradycardia is related to the more negative maximum diastolic potential and decreased rate of phase 4 depolarization.
552
In regards to question 2, by what mechanism(s) does hyperkalemia produce each of the effects on SA-node cells?
All of these effects are produced by the increase in potassium conductance that occurs in hyperkalemia.
553
What effects does hyperkalemia to have on 1) PR interval, 2) RT interval, and 3) T-wave?
PR interval is increased, RT interval is decreased, and T-wave is increased in magnitude.
554
With regards to question 4, by what mechanism does hyperkalemia produce each of the effects on the ECG?
The increase in PR interval results from slowed conduction velocity of both atrial and AV-node action potentials. Enhanced K-conductance contributes to both events. In the atrium, increased sodium channel inactivation due to membrane depolarization also acts to slow conduction. The decrease in RT-interval reflects the decrease in ventricular action potential duration caused by increased K-current due to increased Kconductance. The increased magnitude of the T-wave reflects faster phase 3 repolarization caused by increased K-current due to increased K-conductance.
555
Calcium, insulin, bicarbonate and epinephrine were administered to this patient in an attempt to abort the deleterious cardiac effects of the hyperkalemia? By what mechanism(s) does each of these produce a beneficial effect?
Increased extracellular calcium, in the presence of hyperkalemia, returns excitability related to Na-dependent action potentials towards normal. Extracellular calcium affects the voltage-dependency of sodium channel inactivation (i.e., the position of the inactivation curve on the voltage axis). By increasing extracellular calcium, some sodium channels that were inactivated by the hyperkalemia-induced depolarized state 4 of the membrane are converted to the resting state. The recovery of resting sodium channels acts to return excitability toward normal. Increased calcium produces this effect by shifting the sodium channel inactivation curve toward more depolarized potentials.Bicarbonate acts to return excitability towards normal by shifting potassium into the cell from the ECF thereby shifting resting potential more negative. By reducing extracellular hydrogen ion concentration, bicarbonate enhances sodium transport into the cell via the Na-H exchanger. The increased Na-influx acts to increase intracellular sodium ion concentration. In turn this enhances Na-K pump thereby moving potassium into the cell.By stimulating the Na-K pump, insulin also acts to move potassium into the cell.Epinephrine acts to restore heart rate and AV-node conduction towards normal. It does this by increasing the funny sodium current responsible for phase 4 depolarization in SA-node cells. It also increases L-type calcium current thereby increasing the rate of phase 0 depolarization in AV-node cells (also in SA-node cells). This increases action potential conduction velocity of these cells
556
Within about a 10 min period, this patient’s plasma potassium concentration decreased from 9.8 to 4.1 mEq/L. This represents a loss of how many moles of potassium from the plasma? Where did this potassium go?
Since interstitial and plasma potassium concentration are in equilibrium, the concentration of potassium in the ECF must be reduced by 5.7 mEq/L in order to reduce plasma potassium concentration from 9.8 mEq/L to 4.1 mEq/L.ECF volume is about 20% (i.e., body weight x 0.6 x 0.33) of total body weight. For the patient in this case this would be about 23 liters. A loss of about 131 mEq (23 x 5.7) from the ECF would be required to reduce ECF potassium concentration by 5.7 mEq/L. Since the kidneys cannot excrete this much potassium in 10 minutes (daily excretion of potassium by the kidneys is about 95 mEq), it seems reasonable to conclude that the potassium went into cells.
557
With regards to question 7, does the potassium loss from the plasma account for all of the potassium loss from the extracellular compartment? Explain you answer.
Since the interstitial compartment, rather the plasma compartment, is contiguous to cell membranes, the movement of potassium into cells requires the movement of potassium out of the interstitial compartment and into the cell. The reduction of plasma potassium from 9.8 to 4.1 mEq/L requires that interstitial potassium concentration be reduced by a similar amount. Since the interstitial compartment is about 3-fold larger than the plasma 5 compartment, K-loss from plasma accounts for only about 25% of the K-loss from the extracellular compartment.
558
What are the ideal characteristics of a biomarker for the detection and management of myocardial infarction?
(1)very specific to cardiac muscle and absent from nonmyocardial tissue(2)released quickly into the peripheral blood after onset of injury and reflect quantitatively the magnitude of necrosis(3)easy to use, quick to measure, cheap to measure, and stable in vitro.”
559
What are some good biomarkers for an MI?
Of the cardiac biomarkers listed in the table from Hurst’s The Heart, cTn and CK-MB offer the best match to the optimal properties. Their normal biological properties are not related to their use as biomarkers; they are simply released from cells that died from necrosis. cTn and CK-MB are complementary markers, since troponins are able to detect old MI and CK-MB levels can reflect reinfarction.
560
How does the use of cardiac-specific isoforms of troponin and CK (CK-MB) increase their utility as cardiac biomarkers?
Tissue specificity of a marker makes it far more useful for specific diagnosis. A widely expressed protein that is released upon damage of any tissue would not allow the specific diagnosis of myocardial infarction. For example, myoglobin (as well as non-cardiac specific CK) is released following skeletal muscle injury, which would result in a false positive for MI. Other conditions also cause elevated CK and Mb.
561
Why is skeletal muscle damage a confounding issue for the use of myoglobin?
myoglobin (as well as non-cardiac specific CK) is released following skeletal muscle injury, which would result in a false positive for MI. Other conditions also cause elevated CK and Mb.
562
How might different isoforms of a protein be produced by different cells?
Different isoforms of a protein can arise from several mechanisms, the key is that the mechanisms must show tissue specificity (i.e. occurs in one specific tissue). The potential mechanisms include: (1) multiple genes that have tissue-specific expression (2) alternative mRNA splicing that is tissue specific (3) post-translational processing or modification that is tissue specific (4) tissue specific quaternary structures. The cardiac troponins arise from specific genes expressed only in the heart. There are two different CK genes, CK-M and CK-B. The proteins dimerize to create three different isozymes: CKMB, CKMM, CKBB. So it is the relative expression of two genes that determines the tissue specificity of the isozymes. CKMB is found at high levels in cardiac tissue, CKMM in muscle, and CKBB in brain and lung. Additional isoforms of CKMB can be created by cleavage of the Cterminal lysine by carboxypeptidase (no need to discuss in detail).
563
What type of assay would most likely be used to differentiate between two isoforms that differ by relatively few amino acids
For proteins that have limited amino acid differences, mass spectroscopy is the “gold standard”for their identification. Additionally, if monoclonal antibodies can be raised against uniqueepitopes of the isoforms, they can be used in ELISA or RIA.
564
An experimental biomarker for AMI is copeptin. Based on the data in Figure 4 [shown here; taken from European Heart Journal (2014) 35, 552–556] assess the utility of copeptin and explain how it differs biochemically from currently used biomarkers.
Unlike the other biomarkers, copeptin is not released from necrosed cardiomyocytes. Copeptin is the C-terminal domain of the vasopressin prohormone that is cleaved off during processing. Endogenous stress occurring with the onset of AMI results in the rapid release of active vasopressin and thus elevation of copeptin.It does not work nearly as well as the others
565
The following is an ECG recording in the frontal plane leads from a 61-year-old man. His chief complaint upon arrival at the Emergency Department was severe chest pain. Compared to a normal ECG recording, what is the significant finding on this man’s ECG recording? Explain the mechanism responsible for this change in his ECG recording.
ST segment elevations are prominent in leads II, III, and aVF. This indicates myocardial ischemia within an area of the ventricles. The decreased flow to this region results in local hyperkalemia as potassium accumulates in extracellular fluid (normally some potassium is removed from the tissue by the blood, and ischemia reduces the removal of potassium). Local hyperkalemia depolarizes resting potential in the ischemic region and is evidenced by a shift in the ST segment from the isoelectric baseline.
566
How can ST elevation in different leads on an EKG allow you to figure out where an MI occurred?
567
If blood flow is significantly reduced to an area of the ventricles, myocytes in this region swell. Explain the mechanism responsible for increased size of myocytes in this situation.
Decreased blood flow to a region of the ventricle will reduce oxygen delivery to this tissue and result in decreased ATP generation. The activity of the sodium/potassium pump is dependent on ATP levels, and so pump activity will be reduced in the ischemic zone. The sodium/potassium ATPase extrudes 3 sodium ions from the cell while bringing 2 potassium ions into the cell. Decreased pump activity will cause intracellular solute concentration to rise and so water will move into the cell, causing myocytes to swell.
568
The mean electrical axis reflects the average direction and magnitude during ventricular depolarization. If a significant number of myocytes are lost from the left ventricle, how would this affect the mean electrical axis? How would the recordings of the QRS complex in lead I and aVF change after loss of functional tissue in the left ventricle?
The mean electrical axis reflects the balance between depolarizing currents (phase 0 voltage-gated sodium current) between the right and left ventricles. A severe myocardial infarction in the left ventricle would decrease the number of functional myocytes in the left ventricle and so decrease the magnitude of the sodium current during depolarization of the left ventricle. As a result, the direction of the mean electrical axis would be shifted towards the right ventricle (greater than +90 degrees). The net QRS complex would be positive in lead aVF (as in normal conditions) but the net QRS complex would be negative in lead I (normally net positive) as shown in the above diagram for right axis deviation.
569
What is the most common cause of Right axis deviation?
Right ventricular hypertrophy
570
What are the most common causes of left axis deviation?
Left ventricular hypertrophy or inferior MI
571
What could lead to extreme right axis deviation?
Right ventricular hypertrophy and loss of tissue in the lead ventricle
572
Differentiate b/t Osler's nodes and Janeway Lesions, both of which are associated with embolic complications of infectious endocarditis?
Osler's nodes - tender, red, raised punctate lesions of the hands and feet (painful - Ouch, Ouch, Osler)Janeway lesions - painless hemorrhagic raised areas on the palms and soles
573
What is this and what is it caused by?(hint: bacterial culture is negative)
Non-bacterial thrombotic endocarditisCaused by pro-coagulatory state like pregnancy
574
What is this an image of? When is the typical onset of this condition?
Calcific Aortic StenosisOccurs in late 50s to early 70s
575
How can infective endocarditis lead to this?
Septic emboli leading to vascular occlusion
576
What is valvular insufficiency (regurg)?
Failure of a valve to close completely, thereby allowing reverse flow
577
What are some risk factors for endocarditis?
Rheumatic heart dz, small VSD, PDA, degerative calcific valvular stenoses, bicuspid aortic valve, artificial valves, drug abuse
578
Rheumatic fever results in fibrinous vegetation. This causes what type of appearance?
579
What is this?
Calcific stenosis of the mitral valve
580
What is this?When might this person require surgical intervention?
Calcific stenosis of congenitally bicuspid aorta valve (most frequent congenital CV malformation in humans)Typically needs replaced around 50, which is when they'll become symptomatic
581
What condition to a click-like murmur?
Mitral valve prolapse
582
What are the fastidious organisms that can cause endocarditis?
HACEK groupHemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
583
What are two unique features found in histologic slides of Rheumatic Fever?
Aschoff bodies: foci of chronic inflammationAnitschow Cells: histiocytes w/ abundant basophilic cytoplasm w/ slender, wavy nuclei
584
What are the pathologic criteria for infective endocarditis?
* Microorganisms demonstrated by blood culture or septic embolus
* Active endocarditis
585
What is the most common bacterial cause of sub-acute bacterial endocarditis (SBE)?
Streptococcus Viridans
586
What are the two types of valvular disorders?
Stenosis and Insufficiency (regurgitation)
587
What is Libman-Sack endocarditis associated with?
SLE
588
What are the major JONES criteria for acute rheumatic fever?
J - Joints (migratory polyarthritis (knee))O - Heart, pancarditisN - Nodules - subcutaneousE - Erythema marginatumS - Sydenham's Chorea
589
What is the most commonly affected valve?
Aortic valve
590
Rheumatic fever can have what effects on the mitral valve leaflets? chordae tendinae?
Mitral valve leaflets: Thickening and fusionChordae tendinae: shortening, thickening, and fusion
591
What is the prevalence of mitral valve prolapse? What is its typical clinical presentation?
20% of women; usually asymptomatic but on rare occasion can lead to sudden death
592
What are some major and minor clinical criteria in identifying infective endocarditis?
593
What condition does this illustrate? What does the blood tissue represent?
Mitral valve prolapseMyxomatous degeneration
594
What do the terms isolated and combined meaned in terms of valvular disorders?
Isolated: 1 valveCombined: > 1 valve
595
What process causes the body to attack the valves (mitral > aortic) rather than the streptococcus? What are some of the bacterial Ag's that the body might try to be targeting?
Molecular mimicryStreptococcal M proteins (streptolysin O and DNAseB)
596
What the terms mixed and pure mean in relation to valvular disorders?
Pure: only stenosis or only insufficiencyMixed: Stenosis w/ regurgitation
597
Describe the virulence of Staph Aureus
High virulence. Leading cause of acute infectious endocarditis
598
What is this?
Infective endocarditis
599
What are some common contaminants of blood cultures?
Coag-neg staphylococcus, Bacillus spp, Corynebacterium spp, Propionibacterium spp
600
What disease preferentially affects the mitral valve?
Rheumatic Fever
601
If a woman is diagnosed with a mitral valve prolapse, what is different about the approach to dental procedures or GI surgery?
Anti-microbial prophylaxis (These procedures are notorious for increasing blood borne microbes)
602
What is valvular stenosis?
Failure of a valve to open completely, thereby impeding forward flow
603
What are the two broad categories of endocarditis?
Acute and sub-acute infectious endocarditis (SABE)
604
What is Churg-Strauss Syndrome?
Systemic vasculitis associated with prominent eosinophilia that occurs in young persons with astham or allergy
605
What is this?
Fibrinoid necrosis associated with polyarteritis nodosa
606
What is this an image of?
Polyarteritis nodosa
607
What is this an image of?
Microscopic Polyangiitis
608
What are the pathological indications of giant cell arteritis?
Multinucleated giant cellsCordlike, nodular vessel with narrow lumenFibrous media and thickened intima
609
In giant cell arteritis what are each of the images?
The image on the left in showing granulmonas while the image on the right is showing mixed inflammation with necrosis
610
Takayasu arteritis is also known as what?
The pulseless disease
611
What is Wegner Granulomatosis?
Systemic necrotizing granulomatous vasculitis of unknown etiology.
612
What are the pathological findings associated with thromboangiitis obliterans?
Thrombosis and infarcts. Gangrene.
613
What are the pathological characteristic of polyarteritis nodosa?
Affecting small to medium vessels. Fibrinoid necrosis. Thrombosis and infarction of an organ
614
How do you treat Takayasu arteritis?
Steroids and surgical reconstruction
615
How would you treat Giant cell arteritis?
Steroids and anti-TNF
616
What is this an image of?
Giant cell arteritis
617
What would the gross and pathological finding be in a person with microscopic polyangiitis?
Localized cutaneous vasculitis - GrossPatho - finrinoid necrosis, acute inflammation, and extravasation of RBCs
618
What are the hallmark characteristic of giant cell ateritis?
Also known as Temporal, Granulomatous Ateritis. It is the most common form of vasculitis. Focal, chronic, granulomatous inflammation of the temporal artery. Multinucleated giant cells
619
How would you treat Churg-Strauss Syndrome?
STEROIDS
620
What are the clinical features of Takayasu arteritis?
Weak or non-existant pulsehigh BPOcular disturbancessyncope and dizziness
621
Is a biopsy diagnostic for giant cell arteritis?
It can be, but it is not in over 40% of cases
622
What is polyarteritis nodosa?
Acute necrotizing vasculitis of medium-sized muscular arteries.Associated with hepatitis B
623
When looking at anti-proteinase-3 (PR3-ANCA and c-ANCA) what disease are you monitoring?
Wegeners granulomatosis
624
Microscopic polyangiitis is also known as ?
Systemic hypersensitivity polyarteritis
625
What is kawasaki disease?
Acute necrotizing vasculitis of infancy and early childhood, w fever, rash, oral lesion and lymphadenitis
626
What is being shown in the image on the left and right?
Vasculitis (L) and Necrotizing granuloma (R)
627
What is the clinical triad of affected organs for Wegener Granulomatosis?
Lungs, Kidney, and Upper Respiratory Tract
628
What is microscopic polyangiitis?
A group of inflammatory vascular lesions affecting small vessels that are thought to represent a response to exogenous substances
629
What disease are these two images assciated with?
Takayasu arteritis
630
What is vasculitis?
Inflammation and necrosis of blood vessels (arteries, veins and capillaries)
631
What is Takayasu arteritis?
Inflammatory disease of unknown etiology, affecting large arteries (aorta and branches)
632
What can happen to patients with giant cell arteritis that goes untreated?
Blindness
633
What looking at MPO-ANCA and p-ANCA (anti-myeloperoxidase), what diseases are you looking for?
Microscopic polyangiitis and Churg-Strauss
634
Summarize all the vasculitis disorders in one image
CAN DO!
635
How would you treat Kawasaki disease?
AKA mucocutaneous lymph node syndrome. IVIG and asprin.
636
What are some clinical features of Wegener Granulomatosis?
Sinusitis, Hematuria and proteinuria
637
What is this gross image associated with?
Wegener Granulomatosis
638
What is this an image of?
Microscopic Polyangiitis
639
What is this an image of?
Polyarteritis nodosa
640
What is this an image of?
Giant cell arteritis
641
What are the microscopic findings associated with microscopic polyangiitis?
Fibrinoid necrosis of blood vessel wallsIntramural neutrophilic infiltratesRBC extravasationEndothelial cell swelling
642
What disease is this gross image associated with?
Microscopic polyangiitis
643
Who is mostly affected by thromboangiitis obliterans?
Smokers and young middle aged men
644
What is this an image of?
Progression of thromboangiitis obliterans. Right is the worst.
645
The left image is normal what is wrong in the right image?
Fragmentation of elastic lamina associated with giant cell arteritis
646
What is this an image of?
Takayasu arteritis
647
What is thromboangiitis obliterans?
Occlusive inflammatory disease of medium and small arteries in the distal arms and legs
648
What are the three clasifications of shock?
HypovolemicDistributiveCardiogenic
649
What are some examples of hypovolemic?
Hemorrhage, Dehydration, Burns, Excessive Fluid Loss
650
What are some examples of distributive shock?
Septic, Anaphylactic, Neurogenic
651
What are some examples of cardiogenic shock?
Cardiac tamponade, heart failure, MI
652
What are the the two common results of shock?
Decreased MAP and impaired organ blood flow
653
What is the main problem in each type of shock?
Hypovolemic: Low blood volumeDistributive: arteriolar problemCardiogenic: pump problem
654
Describe the systemic effects/concept map of hypovolemic shock.
655
How can you distinguish hypovolemic shock due to hemorrhage from dehydration? How do you treat both of these?
Hemorrhage: Isotonic contraction (plasma osmolality is nearly normal), bloodDehydration: Hypertonic contraction (plasma osmolality is greater than normal), 5% dextrose
656
During hemorrhagic shock, the person's pulse would have been described as weak or thready. What is the significance of this finding?
657
How much blood can be lost before aterial pressure changes? CO? What is responsibl for the difference b/t the two values?
Arterial pressure begins to change after 30% of blood is lost.CO begins to change after 20% of blood is lost.The difference is due to the baroreflex. The baroreflex can stimulate arteriolar contraction which will act to sustain MAP as long as possible.
658
What are all of the factors that alter and adjust SV in hemorrhagic shock?
659
Describe the mechanism that leads to septic shock, a form of distributive shock.
660
What happens to the rate of runoff in distributive shock?
Increased!!!
661
What allows for the extravasation of leukocytes from post-capillary venules despite the increased production of NO in septic shock? (This results in increased vascular permeability and edema)
Pro-inflammatory factors outweigh high levels of NO
662
Describe the mechanism leading to decreased MAP in anaphylactic shock.
663
Why is eprinephrine used in the acute treatment of anaphylactic shock rather than norepinephrine?
It's effects on both alpha-1 receptors as well as relax airways via beta-2 receptors
664
Describe the mechanism leading to decreased MAP in neurogenic shock.
665
Describe the mechanism/concept map leading to cardiac tamponade.
666
What curve utilized in P-V loops is affected by cardiac tamponade?
Passive filling curve will be shifted upwards and EDV decreased
667
What would be the major change in a person's ECG recording after development of cardiac tamponade?
Diminish amplitude of waves and reduce heart sounds
668
What are the compensatory responses to shock?
669
What are the effects of SYM activation of Beta-1 receptors? Alpha-1 receptors?
Beta-1: Increase HR and SV (increased inotropic state)Alpha-1: arteriolar constriction (increased TPR) and venoconstriction (increased venous return)
670
What are the intial problems, compensatory responses, and secondary complications in the three types of shock?
671
What is the main way to differentiate b/t hemorrhagic shock and cardiogenic shock?
Hemorrhagic shock: Decreased CVPCardiogenic shock: Increased CVP
672
What are the treatments for each of the types of shock?
673
What is irreversible shock?
674
What are some of the mechanisms that lead to irreversible shock?
675
What is the key feature of aortic insufficiency?
Low diastolic pressureThis is because of back flow of blood from the aorta to LV, blood volume in the arterial system decreases faster than normal during diastole, even though systemic arteriolar resistance is unchanged.
676
What can be a result of chronic mitral insufficiency?
This will lead to elevated atrial pressures which can result in hypertrophy of the LA.
677
How does mitral insufficiency compare to tricuspid insufficiency?
678
What are some chronic problems associated with mitral stenosis?
Pulmonary edema impairs O2 transport and reduces O2 levels in lung tissue.
679
What will happen to the time of left ventricular systole from aortic stenosis?
Aortic pressure rises more slowly than normal and pulse pressure will be reduced. The time for left ventricular systole will be prolonged.
680
How do aortic insufficiency and pulmonic insufficiency compare?
681
What are the four types of murmurs?
682
What determines the murmur characteristic of mitral stenosis?
The pressure gradient is highest across the valve at the beginning of rapid ventricular filling. As blood enters, left atrial pressure falls during diastole. Artial contraction causes the second part of the murmur.
683
What is this an EKG of?
In mitral stenosis the cardiac valve disorder is in the left heart. This will cause right ventricular hypertrophy. Associated with a right axis deviation.
684
What are some consequences of backflow from the aorta to the LV?
This can result in extra filling of the LV - acute and chronic effectsAbnormal runoff of blood from the arterial system.
685
What is mitral insufficiency?
This is failure of the mitral valve leaflets to close.
686
What is the notched P wave from in regards to mitral stenosis?
Elevated atrial pressure can result in hypertrophy of the LA
687
What can be a result of chronic aortic stenosis?
Increased afterload due to high resistance of the stenotic aortic valve will lead to left ventricular hypertrophy over time.
688
What is mitral stenosis?
The mitral valve doesn't open completely. This causes a diastolic murmur.
689
What is the difference between aortic strenosis and pulmonic stenosis?
690
How does mitral stenosis compare to triscuspid stenosis?
691
How will valve dysfunctions of the right heart relate to the left heart?
692
What is aortic stenosis?
The valve leaflets do not open - reducing the size of the opening through which blood is ejected. This increases resistance to LV ejection.
693
What is an important characteristic about stroke volume in aortic insufficieny?
694
What are the two systolic murmurs in the left heart?
Aortic stenosis and mitral regurgitation
695
What happens to pulse pressure in aortic insufficiency? Why does this occur?
Pulse pressure is increased in aortic insufficienyLeft ventricular end diastolic volume is increased, which will increase SV when compared to normal. This will produce a large pulse pressure and higher arterial systolic pressure.
696
How can chronic aortic insufficiency affect the P wave on an EKG?
It can become enlarged
697
Can aortic stenosis affect exercise?
Patients with aortic stenosis will have severely restricted cardiac output thus most likely having exercise intolerance
698
What is the mnemonic to remember for predicting the sounds associated with each problem?
699
What is a diastolic murmur?
Begins with or after the second heart sound and ends before the first heart sound
700
What are the important mnemonics to remember?
701
What causes the murmur associated with mitral insufficiency?
Increased ventricular pressure will be greater than the LA during systole. This will cause a holosystolic murmur
702
What is aortic insufficiency (regurgitation)?
This occurs when the aortic valve leaflets fail to close completely. This leads to a backflow of blood from the aorta to the LV
703
What determines the intensity of a murmur?
It is directly related to the magnitude of the flow across the defective valve, which is dependent on the pressure gradient driving the flow.
704
What is tricuspid stenosis? How will this affect the mean electrical axis for ventricular depolarization?
705
What causes the murmur associated with aortic regurgitation?
This is a result of pressure difference decreasing throughout diastole as aortic pressure decreases and LV pressure increases.Results in a diastolic decrescendo murmur
706
What are the two diastolic murmurs in the left heart?
Aortic regurgitation and mitral stenosis
707
What can be a result of chronic aortic insufficiency?
Chronic overfilling of the ventricle will result in left ventricular hypertrophy.
708
What is the cause of the specific murmur associated with aortic stenosis?
The murmur is dependent on the pressure difference across the valve. Initially the pressure difference is low as ejection begins, and rises as ventricular pressure increases above aortic pressure. As ventricular pressure begins to decrease the pressure difference between the aorta and ventricle becomes. This is the cause of the crescendo-decrescendo
709
What is the hallmark of aortic stenosis?
Large pressure difference between the LV and aorta during ventricular systole.
710
What is a systolic murmur?
Begins with or after the first heart sound and ends at or before the second heart sound (S1 to S2)
711
What is being circled in this image?
Non caseating granulomas
712
What are 4 diseases that can present with myocardial involvement?
Amyloidosis, Sarcoidosis, Storage diseases, and Idiopathic
713
What is cardiomegaly?
Increase in cardiac weight or size
714
What is amyloidosis?
It leads to cardiomegaly, and is an amyloid infiltrate. Typicall presents with right sided failure
715
What is this an image of
Dilated cardiomyopathy
716
What are these stains associated with?
Cardiac amyloidosisLeft - Congo Red StainRIght - Apple Green birefringence
717
What is the gross pathology associated with dilated cardiomyopathy?
Cardiomegaly, dilation of the ventricles, mural thrombi.
718
What is a cardiomyopathy?
Myocardial disease with obscure etiology, often genetic and acquired factors.
719
What are some risk factors associated with dilated cardiomyopathy?
720
What are these images associated with?
Hypertrophic cardiomyopathyLeft - septal wall hypertrophy
721
What are the clinical features of hypertrophic cardiomyopathy
722
What is sarcoidosis?
Generalized granulomatous disease. Presenting with non-caseating granulomas and fibrosis
723
What is restrictive cardiomyopathy?
Group of diseases in which myocardial or endocardial abnorms limit diastolic filling.
724
These are images of microfiber disarray
LOOK AT THEM!
725
What is the difference between endomyocardial fibrosis, Loeffler endocarditis, and endocardial fibroelastosis?
726
What are some of the gross pathological features of hypertrophic cardiomyopathy?
CardiomegalySeptal hypertrophyObstructive patternLV thickened wall
727
How do you treat dilated cardiomyopathy?
Transplant
728
What are some causes of secondary dilated cardiomyopathy?
729
These images are associated with what?
Endomyocardial diseases
730
What is the difference between the image on the left and right?
The left is normal Right is dilated cardiomyopathy - atrophy and fibrosis
731
What is the gross pathology of restrictive cardiomyopathy?
732
If one family member has hypertrophic cardiomyopathies, why would it be important to tell other family members?
This disease has a fairly strong genetic correlation. These include genes encoding sarcomere proteins
733
What will electron microscopy reveal in dilated cardiomyopathy?
Increased mitochondria and loss of sarcomeres.
734
What is dilated cardiomyopathy?
Left or biventricular dilation, impaired contractility and can eventually lead to congestive heart failure.
735
What is this an image of? What is the significance of the area that the arrow is pointing to?
This is dilated cardiomyopathy. It is fibrous. The area the arrow is pointing to is where a mural thrombi would appear.
736
What is a hypertrophic cardiomyopathy?
Left or biventricular hypertrophy. Asymmetric (septal hypertrophy). Can be obstructive.
737
What is the mechanism of action of Sodium Nitroprusside?
Direct action relaxing arterioles and venules via NO
738
What is the physiological effect of Losartan and what is it used to treat?
Lowers TPR, reduces plasma volumeheart failure, diabetic nephropathy
739
What is the drug Quinidine used to treat?
Atrial arrhythmias, PSVT, WPW
740
What is Atenolol used to treat?
Decrease myocardial O2 demand to lessen angina, heart failure
741
What are some side effects of Amiodarone?
Torsades de pointes, pneumonitis, pulmonary fibrosis
742
What is Diltiazem used to treat?
Arrhythmia, Prinzmetal’s angina
743
What are the important side effects associated with Quinidine?
Torsades de pointes, cinchonism, thrombocytopenia, anticholinergic effects
744
What is the mechanism of action of Atenolol?
Beta-receptor antagonist
745
What is the mechanism of action and physiological effect of Nifedipine?
Ca-channel blockerPrevents smooth muscle contraction
746
What class of drug is Procainamide?
Anti-arrhythmic Class IA
747
What is Metoprolol used to treat?
Treatment and prophylaxis of PSVT; prevent recurrent MI in pt recovering from MI; decrease myocardial O2 demand to lessen angina, heart failure
748
What is the mechanism of action of Hydrochlorothiozide?
Inhibits Na reabsorption in distal tubules
749
What class of drug is Lidocaine?
Anti-arrhythmic Class IB
750
What is Lidocaine used to treat?
Acute treatment of ventricular arrhythmia from MI; suppress ventricular tachycardia
751
What are some of the side effects of Lidocaine?
Neurotoxicity including seizures
752
What is the mechanism of action of Metoprolol?
Beta-1 adrenergic receptor antagonist (beta-blocker)
753
What is the mechanism of action of Digoxin?
Inhibits the Na/K-ATPase
754
What class of drug is Esmolol?
Anti-arrhythmic Class II
755
What type of drug is hydrochlorothiozide?
Antihypertensive - diuretic
756
What type of drug is Nifedipine?
Antihypertensive vasodilator
757
What is the mechanism of action of Procainamide?
Na channel blocker; also block K channels. Decreases phase 0 depolarization.
758
Diltiazem is what type of drug?
Antihypertensive vasodilator
759
What is the physiological effect of hydrochlorothiozide and what is it used to treat?
Lowers plasma and ECF volume thus decreasing workload on heart and TPRFirst therapy for managing HTN, heart failure
760
What type of drug is Fenoldopam?
Antihypertensive - Misc
761
What is the physiological effect of Esmolol?
Reduces heart rate, myocardial contraction force; prolongs AV node conduction and refractory period (slows HR and lessens contractility)
762
What is the physiological effect of Lidocaine?
Purkinje fibers: depresses automaticity; higher affinity for ischemic tissue: suppresses spontaneous depolarization in ventricles by blocking reentry
763
What is the physiological effect of Fenoldopam and what is it used to treat?
Decreases TPR with increased renal blood flowAcute treatment of severe HTN
764
What is the physiological effect of Sodium Nitroprusside and what is it used to treat?
Peripheral vasodilation—lowers preload and afterloadHypertensive emergency, acute MI, aortic dissection, heart failure
765
What class of drug is Amiodarone?
Anti-arrhythmic Class III
766
What is the mechanism of action of Amiodarone?
Blocks Na, K, and Ca channels; blocks beta-1 receptors
767
What is the physiological effect of Atenolol?
decreases blood pressure, renin release, and sympathetic outflow from brain
768
What are the side effects associated with Esmolol?
AV block and cardiac arrest
769
What is Procainamide used to treat?
Refractory ventricular fibrillation; pulseless ventricular tachycardia
770
What is Digoxin used to treat?
Atrial fibrillation (first-line with heart failure or sedation); SVT
771
What is the mechanism of action of Diltiazem?
Calcium channel blocker
772
What is the physiological effect of Digoxin?
Increased intracellular Na followed by greater Ca influx; greater contraction
773
What is the physiological effect of Metoprolol?
Reduces heart rate, myocardial contraction force; prolongs AV node conduction and refractory period (slows HR and lessens contractility)
774
What is the mechanism of action of Lidocaine?
Na channel blocker: inhibits influx of Na thru fast Na channels
775
What type of drug is Losartan?
Antihypertensive - Angiotensin Receptor Blocker
776
What class of drug is Quinidine?
Antiarrhythmic Class IA
777
What is Amiodarone used to treat?
Atrial and ventricular arrhythmias
778
What is Esmolol used to treat?
Short-term control of: sinus tachycardia, PSVT, ventricular rate in pt with atrial fibrillation/ flutter
779
What class of drug is Metoprolol?
Anti-arrhythmic Class II
780
What class of drug is Digoxin?
Antiarrhythmic Class Misc
781
What is the mechanism of action of Esmolol?
Beta-1 adrenergic receptor antagonist (beta-blocker)
782
What is the mechanism of Quinidine?
Na channel blocker; also block K channels. Decreases phase 0 depolarization.
783
What type of drug is Atenolol?
Antihypertensive Sympatholitic
784
What type of drug is Sodium Nitroprusside
Antihypertensive Vasodilator
785
What are some of the side effects of Metoprolol?
Fewer CNS effects than nonselective beta blockers, hypotension, bradycardia
786
What are the side effects of Digoxin?
Nausea, vomiting, mental status change, vision color and EKG changes
787
What are the side effects associated with Procainamide?
SLE symptoms
788
What is the physiological effect of Procainamide?
Decreases myocardial CV, excitability and contractility; prolongs duration of AP
789
What are the physiological effects of Amiodarone?
Properties of all 4 classes of Antiarrhythmic drugs
790
What is the mechanism of action of Fenoldopam?
Selective D-1 inhibitor agonist
791
What does nitroglycerine do?
Activates GC which increases cGMP levels and relaxes the vessel. Used in angina and decreases resistance in arteries.
792
What is the physiological effect of Quinidine?
Decreases myocardial CV, excitability and contractility; prolongs duration of AP
793
What is the physiological effect of Diltiazem?
Prevent vascular SM contraction
794
What is hypertension defined as?
Diastolic > 90Systolic > 140
795
What are the causes of hypertension?
Increasd COIncrease TPRor BOTH
796
What are the two classifications of hypertension?
Primary - etiology is unknownSecondary - underlying cause of the increased CO or TPR is known
797
What are some areas of research for primary hypertension?
Abnormal function of the Na/K ATPase resulting in elevated cytosolic Ca2+Microvascular dysfunction - decreased levels of nitric oxide and increased endothelin-1
798
As age increases how does this change the source of hypertension?
799
Why with increasing age does TPR become the main source of hypertension?
Arterioles begin to hypertrophy and there is decrease ventricular compliance
800
What is the pathway by which renal parenchymal disease can increase MAP?
801
How can renovascular hypertension lead to increased MAP?
802
How can pheochromocytoma lead to increased TPR and CO?
803
How can an adrenal glad tumor lead to increased MAP?
804
Does hyper/hypothyroidism lead to hypertension?
THERE IS A STONG ASSOCIATION
805
What is baroreceptor desensitivity?
806
Summarize the development of hypertension
807
Describe the dysfunction in development of hypertension in the heart and blood vessels.
808
Describe dysfunction in development of hypertension in the kidney and baroreceptor desensitization
809
Describe the dysfunction in development of hypertension in the adrenal gland and the central effects
810
How will ventricular hypertrophy shift a pressure volume loop? Why?
811
What kind of damage can occur to the heart and arteries from hypertension?
812
How will heart failure shift a P-V loop?
813
What are the systolic and diastolic dysfunctions in heart failure?
814
What sympatholytic agents can be used to help manage hypertension?
815
What are the main renin-angiotensin medications for managing hypertension?
816
How can calcium channel blockers help manage hypertension?
817
What is hemostasis?
The cellular and noncellular process that prevents blood loss following blood vessel injury
818
What are the three steps in hemostasis?
* Platelet plug formation
* Coagulation
* Fibrinolysis
819
What are the two steps of platelet plug formation?
* Platelet adhesion
| * Platelet aggregation
820
What are the three proteins that play an important role in platelet adhesion? What are their functions?
* Collagen
* Von Willebrand Factor (VWF) - binds subendothelial collagen
* Glycoprotein Ib-V-IX - surface protein of platelets that binds VWF
821
What the two possible sites for synthesis of VWF?
* Endothelial cells (Weibel-Palade bodies) - Constitutive and inducible
* Platelets (stored in alpha granules)
822
Describe the quaternary structure of VWF found in plasma. What enzyme is important in processing VWF in plasma?
Multimers w/ varying MW (600 kD to 20,000 kD) ADAMTS-13: protease that cleaves ultra large VWF multimers into smaller sizes
823
What type of cell is this? What is the green arrow pointing to? What does this structure store?
Platelet, alpha body, stores VWF
824
What the top and bottom arrows pointing to?
Top: plateletBottom: VWF coated surface
825
Aside from platelet adhesion, what is an important function of VWF?
Factor VIII carrier protein (VWF extends the half-life of FVIII from 2 hrs to 12 hrs)
826
What allows monomeric platelets to aggregate?
Platelet agonist
827
What protein is used in platelet cross-linking?
Fibrinogen
828
What are some platelet agonists? (5)
ADP, collagen, thrombin, thromboxane A2, epinephrine
829
What step follows platelet plug formation in hemostasis?
Fibrin clot formation
830
What the three coagulation pathways in-vitro?
Intrinsic, Extrinsic, and Common
831
What are the three contact activation factors?
HMWK, PK (prekallikrein), FXII
832
Which factor is thrombin?
FIIa
833
Which enzyme in the coagulation pathway converts fibrinogen to fibrin?
FIIa (thrombin)
834
Draw the three in-vitro coagulation pathways.
835
What are the four major differences b/t the in-vivo coagulation pathway and the in-vitro coagulation pathway?
* Renamed pathways (Extrinsic to initiation, intrinsic to propagation)
* Removal of the contact activation factors (HMWK, PK, FXII)
* Emphasis on the role of thrombin (goes back to work on the first physiological step in the initiation pathway which is FXI, activates critical allosteric activators)
* Presence of FXIIIa, which is activated by thrombin
836
Map out the propagation and initiation pathways.
837
What are the vitamin K dependent coagulation proteins
Factors II, VII, IX, X (coagulation)Protein C and protein S
838
Vitamin K plays an important role in what process in these proteins?
Post-tln gamma-carboxylation of glutamic acid residues, forming gamma-carboxyglutamic acid (gla)
839
Interaction with what ion with these gla residues allows for a conformational change?
Ca++
840
What happens to PS (phosphatidylserine) during platelet activation?
PS residues flip flops from the inner leaflet to the outerleaflet. The flip flopping of the PS residues allows for the activation fo FX and FII (prothrombin)
841
How does thrombin alter fibrinogen?
It removes fibrinopeptides A and B from the essential domain. The removal of these peptides allows fibrin molecules to polymerize.
842
What factor is involved in the cross linking of fibrin?
Factor XIIIa
843
What are the two enzymes involved in breaking down fibrin polymers?
Tissue plasminogen activator (t-PA) cleaves plasminogen into plasmin. Plasmin is what degrades fibrin.
844
What are the three inhibitors of fibrinolysis and their site of action?
PAI-1 and PAI-2 inhibit t-PAAlpha2-AP inhibits plasma
845
What is used to measure fibrinolysis activity?
Fibrin degradation products
846
What is the number one risk factor for atherosclerosis?
Age
847
What has been proven to be an outstanding biomarker for atherosclerosis?
CRP
848
Decribe the sensitivity of angiography?
The progression of atherosclerosis and the clinical risk of atherosclerotic plaques are underestimated by angiography.Poorly sensitive b/c vessels have compensatory mechanism to maintain the diameter of their lumen
849
Describe the state of the lumen throughout the progression of atherosclerosis?
850
Fill in this chart..........
851
What is a good modality for plaque imaging?
Ultrasound and virual histology
852
What is true about the plaques that rupture leading to atherosclerosis?
Plaques that rupture leading to atherosclerosis are not often the most stenotic by angiography
853
What is Virchow's triad of the pathogenesis of thrombosis?
Injury to endothelium, altered blood flow, and increased coagulability of the blood
854
What are the atheroprone sites?
Areas where turbulence creates low shear stress
855
What can be seen in this thrombus?
Lines of Zahn
856
What is this?
Cholesterol emboliWhen you see cholesterol clefts think about atherotic embolic dz
857
Where is the olfactory area in the nasopharyngeal cavity?
858
Which mitotically active cells produce neuronal cells throughout life?
Basal cells of the olfactory epithelium
859
The axonal projections of olfactory epithelium project from which portion of the cell to what region of the brain?
Basal region and contacts neurons of the olfactory bulb in the brain
860
What protein secreted by olfactory glands binds odorants? What do plasma cells in this region secrete?
Olfactory Binding Protein (OBP); IgA
861
What are the two functional components of the respiratory system?
Conduction SytemRespiratory System
862
What is the conduction system comprised of?
Nasal and oral cavities to terminal bronchioles
863
What is the respiratory system comprised of?
Pulmonary acini consisting of respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli
864
Describe the flow of blood from the R ventricle through the lungs and body until it returns to the R atrium.
865
Describe the positioning of the trachea, larnyx, pharnyx, and bronchi.
Pharnyx, Larnyx, Trachae, Bronchi
866
What structure terminates at the respiratory bronchioles and gives rise to the alveolar capillary plexus?
Pulmonary artery
867
What concentric structures helps keep the trachea open at all times?
Discontinuous rings of hyaline cartilage
868
What do each of the letters represent?
C: Hyaline cartilageM: mucosaT: trachealis muscleL: longitudinal muscle
869
What do each of these letter represent in this cross section of the trachea?
E: Respiratory epitheliumLP: Lamina propriaSM: SubmucosaF: Fibroelastic Tissue
870
Tobacco can have an immobilizing effect on what structure of the respiratory structure?
Cilia
871
Describe the specific components of the respiratory system starting with nasal and oral cavities to the respiratory bronchioles.
872
At what level traveling deeper into the respiratory system, does hyaline cartilage stop playing a role in its structure?
Terminal bronchiole
873
What are the structures numbered 1-3?
874
Describe the orientation of smooth muscle fibers and elastic fibers around the bronchioles.
Smooth muscle fibers are oriented concentricallyElastic fibers are oriented longitudinally
875
What is this a slide of?
Terminal bronchioleNote: the absence of cartilage as well as some smooth muscle still present
876
What do each of the letters represent?
A: alveoliAD: alveoli ductsAS: alveoli sacsR: respiratory bronchioleT: Terminal bronchiole
877
Where are club cells found? What is their former name? What do they produce?
The number of clara cells progressively increases the number of goblet cells decreases. Goblet cells disappear entirely at the level of the terminal bronchiole. Former name: Clara CellsClub cells produce surfactant
878
What are the three types of cells present in the alveolar sac?
Type I pneumocytesType II pneumocytesAlveolar macrophages
879
What type of cells produce surfactant in the alveoli?
Type II pneumocytes
880
Replace each blue dot with these abreviatons: P1, P2, E, M, or C.P1: type 1 pneumocyte, P2: type 2 pneumocyte, E: endothelial, M: macrophage, C: capillary
881
What is being circumscribed in blue in this type II pneumocyte?
Surfactant granule
882
What is the composition of surfactant?
883
What are some common respiratory diseases?
Rhinovirus infections, Influenza, Pneumonia, Emphysema, Cystic Fibrosis, and Asthma
884
Rhinoviruses typically affect which portion of the respiratory system?
The conducting system
885
What are some of the symptoms of the flu?
Fever, sore throat, muscle and head aches, coughing, and fatigue
886
What is the leading cause of death among the elderly?
Pneumonia
887
Identify the structures.
888
Where is the thorax located?
B/t the neck and abdomen
889
What are the key skeletal elements of the thorax?
12 thoracic vertebrae12 ribs and costal cartilages1 sternum
890
What are the components of the sternum?
Manubrium, body, xiphoid process
891
What are the three types of ribs? Which ribs belong to each of these classifications?
True ribs (1-7): attach directly to sternumFalse ribs (8-10 or some say 8-12): costal cartilages do not directly attach to sternum)Floating ribs (11-12): lack costal cartilage
892
Which ribs are included in the typical ribs? What are there four common structures?
3-9Head, tubercle, shaft/body, and angle of rib
893
What is the most frequent site of rib fractures?
Just lateral to the angle of the rib
894
How many facets does the head of true ribs have?
2, a superior and inferior facet
895
What are these components of the ribs?
896
The scalene tubercle in the 1st rib is the site of attachment for which muscle?
anterior scalene m.
897
What is another name for the sternal angle?
Angle of Lewis
898
If which structure is left intact, will it allow for possible regeneration of the rib?
Periosteum
899
Where is the 13th rib usually located?
On C7about 0.5 to 1% of the population has a cervical rib
900
What is circumscribed in green? What is the dense fibrous band connecting it to?
The cervical rib; the dense fibrous band is connecting it to the 1st rib
901
What condition is associated with the presence of the cervical rib?
Venous Thoracic Outlet Syndrome(Fun fact: Your fellow classmate THE Miles Sanderson had this syndrome, which led to a blood clot in his shoulder.)
902
Where do the ribs 1-7 articulate with the stenurm?
903
What 4 bodily landmarks occur at the level of the sternal angle (the junction of the manubrium with body of sternum)?
Attachment of the 2nd ribintervertebral level at disc b/t T4 and T5bifurcation of tracheaazygos veins drains into the SVC
904
Where are the regions of the mediastinum located?
905
What commorbidity is often associated with pectus excavatum?
Mitral valve prolapse
906
What is pectus carinatum?
Ridge projecting anteriorly (more rare than excavatum)
907
In what patient population is pectus carinatum most likely to develop?
11 to 14 y/o pubertal males undergoing a growth spurt
908
What is the name of the joint between the ribs and its corresponding vertabrae?
Costovertebral joint, it's a synovial joint b/t head of rib and body of vertebra at a facet or demifacet
909
The costotranverse joint is a synovial joint b/t what two structures?
tubercle of the rib and the transverse process of the vertebra
910
In which ribs is the costotranverse joint fairly curved? fairly flat?
Curved: 1-7Flat: 8-12
911
What type of joints are the sternocostal joints?
Cartilaginous
912
What is costochondritis? In what population is it most common?
Chest pain due to inflammation of the cartilage and bones in the chest wall.Overuse injury in athletes
913
What the three layers of the intercostal muscles?
External, internal, and innermostThe external runs down and medial on both sides (like putting hands into front pockets), and the internal and innermost run direction 90 degrees to that
914
Where do the intercostal nerves run?
Between the internal and innermost intercostal muscle (b/t I and I)
915
What is different about the subcostal muscles?
They "skip" a ribFound on the posterior portion of thoracic wall
916
Where does the pectoralis major originate and insert? pectoralis minor? serratus anterior muscle?
917
Where are the lateral cutaneous and anterior cutaneous branches given of the intercostal nerves?
918
Which vein seperates the pectoralis major and the deltoid?
Cephalic vein
919
Describe the typical positioning of artery, vein, and nerve from cranial to caudal under the groove of each rib?
VANV: veinA: arteryN: nerve
920
What is shingles?
A reactivation of a latent herpes varicella-zoster viral infection
921
What is a dermatome? Where are dermatomes C5, T4, T7, T10, L1
An area of the skin which receives innervation from a single spinal nerve.C5: clavicleT4: "teat", nippleT7: xiphoid process (pointy)T10: umbilicus (O reminds you of the umbilicus)L1: inguinal ligament
922
~75% of the breast is drained into which lymph nodes?
Axillary lymph nodes
923
What is polythelia? In what population is it most common?
Supernumerary nipple(s) which may appear similar to a mole, anywhere along the mammalian lines (milk lines)Males
924
What is polymastia? When is most liked noticed?
Additonal breast along the milk line b/t the axilla and groin.Rare, most likely noticed at the time of pregnancy due to enlargement and possible production of milk
925
What is gynecomastia?
Excessive development of the male mammary gland
926
What is contained in the mediastinum?
heart, great vessels, trachea, esophagus, and thymus
927
Which muscle acts as the principal muscle of inspiration?
Diaphragm
928
The are two pectoral nerves? Which pectoralis muscles do they innervate?
Lateral and Medial Pectoral NerveMedial pectoral nerve innervates both the major and minor pectoralisLateral pectoral nerve only innervates the pectoralis major
