Mini 1 - Cardio + Respiratory Flashcards

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1
Q

What increases Hb affinity for oxygen?

A

Increased pH/decreased acidity, decreased PCO2, decreased temperature, decreased 2,3 BPG.

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2
Q

How can Respiratory System compliance be calculated?

A

1/C(RS) = 1/C(lung) + 1/C(CW)

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3
Q

When is pulmonary vessel resistance the lowest?

A

At FRC.

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4
Q

What formula is used to find RV with the use of a spirometer?

A

VL = Vs (F0-F1)/F1 *F1 being the new lower [He]

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5
Q

What is a distinguishing feature of large veins?

A

Valves, vasa vasorum, and smooth muscle in tunica adventitia for peristalsis (much moreso than in tunica media).

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6
Q

What is Expiratory Reserve Volume (ERV)?

A

The volume that can be expired after normal expiration.

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7
Q

When is a diastolic murmur heard?

A

Aortic/pulmonic regurgitation, mitral/tricuspid stenosis.

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8
Q

How do you calculate resistance of the air way knowing partial pressures?

A

Alveolar - airway opening pressure / volume of air out

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9
Q

What is the normal length of a QRS complex?

A

0.08-0.1s

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10
Q

What are the normal anatomical R to L shunts?

A

Thebesian veins, bronchial veins into PV. Reduces PO2.

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11
Q

What is the function of Tamm-Horsfall Protein (THP)?

A

It and IgAs inhibit attachment of urogenic E. coli to epithelium.

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12
Q

How does 3rd degree AV block present on an ECG?

A

Broad QRS, no relation between P-P and R-R.

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13
Q

What are the inferior axis ECG leads?

A

II, avF, III

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14
Q

What vessels have the largest cross-sectional area?

A

The capillary network.

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15
Q

What is Inspiratory Capacity?

A

TV+IRV

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16
Q

What is the normal PO2 and PCO2 of inspired air?

A

PO2 = 150mmHg PCO2 = 0mmHg

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17
Q

When is the S2 sound heard?

A

When the aortic/pulmonic valves close, during slow isovolumetric relaxation.

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18
Q

What are macrophages in the respiratory system called? How do they leave?

A

Dust cells. Some migrate to the bronchioles to use the mucociliary elevator, some exit via lymph, some stay in the interalveolar septum for months-years.

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19
Q

What is the diffusion capacity?

A

V/PA

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20
Q

What is reactive hyperemia?

A

Short interruption of blood flow causes vasodilation and then increased flow.

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21
Q

What are the risks of beta blockers?

A

Bradycardia, hypotension, bronchospasm.

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22
Q

What can increase diffusion capacity?

A

Exercise, supine position, body size.

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23
Q

What are the effects of carboxyhemoglobin/CO?

A

Occupies binding sites on Hb so reduces the saturation of O2. It also increases the affinity of Hb for oxygen so it cannot deliver it as easily to tissues. High pressure oxygen must be delivered to overcome it. Venous blood will be bright red as opposed to dark red.

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24
Q

What are the PaCO2s of all the causes of arterial hypoxemia?

A

Increased in hypoventilation, decreased in low PiO2. Unchanged in VQ heterogeneity increases, R to L shunt,

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25
Q

How do you calculate the driving pressure of pulmonary circulation?

A

MPAP of pulmonary artery - LA pressure

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26
Q

What is normal cardiad index?

A

2-6-4.2L/min/m^2. <1.8=cardiogenic shock.

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27
Q

What are the stages of the transtheoretical model of change?

A

Precontemplation, contemplation, preparation, action, maintenance, relapse.

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28
Q

What are P75 and P98?

A

P75 = 40mmHg, P98 = 100mmHg

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29
Q

What is the formula for ejection fraction?

A

SV/EDV

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30
Q

What is a metabolic rate? What is the base metabolic rate?

A

Demand for oxygen uptake. BMR is about 300mL/min at 37C. Changes about 30mL with every 1C change.

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31
Q

What is stage I hypertension?

A

Greater or equal to 140-159 systolic and/or 90-99 diastolic

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32
Q

What is the normal PO2 and PCO2 of Alveoli?

A

PAO2 = 100mmHg PACO2 = 40mmHg

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33
Q

In aortic/pulmonic regurgitation, how is blood pressure altered? What sounds/murmurs are heard?

A

Systolic is increased, diastolic is reduced. S3, diastolic murmur.

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34
Q

In aortic/pulmonic stenosis, how is blood pressure altered? What sounds/murmurs are heard?

A

Systolic and diastolic are reduced. S4, systolic murmur.

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35
Q

What is the normal mean electrical axis?

A

-30 to +90 degrees

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36
Q

What cells is mucus made of and what does it contain?

A

Goblet cells, mucins (glycoproteins), salts, sIgA

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37
Q

What characterizes asthma? How is it best treated?

A

Bronchial and mucosal hypersensitivty and hyperreactivity - early phase is better treated with bronchodilators, late phase is better treated with antiinflammatories.

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38
Q

How can pulmonary circulation pressure be approximated?

A

With wedge pressure.

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39
Q

How do you treat atrial fibrillation?

A

With an anticoagulant.

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40
Q

Describe phase II of the valsalva maneuver.

A

High pressure reduces venous return and reduces stroke volume and pulse pressure, so arterial BP and MAP fall. Over the next 5-10s, reflex sympathetic activity causes an increase in heart rate and constriction (halting drop in MAP).

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41
Q

Where are continuous/somatic capillaries found? What’s special about them?

A

Muscle, CT, lung, nervous tissue, exocrine glands. A special type makes up the BBB. Some have pericytes/rouget cells.

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42
Q

What is arterial hypoxemia/hypoxia and what are the causes?

A

PaO2 is reduced. Low inspired PO2, diffusion limitation, hypoventilateion, VQ mismatch, L-to-R venous shunt.

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43
Q

How do you find a corrected QT interval in long QT syndrome?

A

Bazett’s formula: QT/root(R-R)

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44
Q

What is Tidal Volume (TV)?

A

The volume inhaled in normal inspiration.

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45
Q

What is the Bohr Equation?

A

Vd/Vt = [Fe-Fa/Fi-Fa]O2 = [Fa/Fe/Fa] CO2 Or partial pressures.

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46
Q

What is the threshold for Calcium T type and L type channels?

A

T: -55mV, L: -40mV

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47
Q

Where is the pericardial cavity?

A

Between the visceral and parietal serous epicardium. Fibrous pericardium is on the outside.

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48
Q

What gas are alveoli filled with at the end of expiration?

A

Alveolar gas (used).

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49
Q

What are the types of capillaries?

A

Continuous/somatic, fenestrated/visceral, sinusoid/discontinuous.

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50
Q

What are the effects of pulmonary surfactant?

A

Reduces surface tension, increases compliance, reduces fluid accumulation in alveolar space, equalizes ventilation among alveoli/keeps their size relatively uniform.

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51
Q

At what point is the respiratory system most compliant?

A

FRC (around 3L).

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52
Q

What is the change in blood pressure when moving away from the heart?

A

0.78mmHg/cm

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53
Q

What are the effects of aortic/pulmonic regurgitation on EDV, ESV, and SV?

A

Increased, Unchanged, Increased,

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54
Q

What is Hb saturation dependent on?

A

It’s dependent on PO2, not oxygen concentration in the blood.

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55
Q

What are the cells in the heart that can be pacemakers besides the SA node?

A

AV node and Purkinje fibers.

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56
Q

What does ACh do to the heart?

A

Increases K+ permeability of SA node cells which hyperpolarizes maximum diastolic potential.

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57
Q

What is regression to the mean?

A

A statistical phenomenon that occurs with repeated measurements.

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58
Q

What side of the heart is the cardiac cycle graph showing?

A

Left.

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59
Q

What are the effects of verapamil and diltiazem/Ca++ blockers?

A

Decreased conduction/Increased refractoriness (only in slow fibers or ones that fire frequently and are incompletely repolarized at rest), decreased automaticity.

Peripheral vasodilation (mainly arteriolar), decreased heart rate, decreased contractility.

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60
Q

What are the lateral ECG leads?

A

I, avL, V5, V6

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61
Q

How does increased contractiliity affect the cardiac function curve?

A

Moves it up and to the left.

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62
Q

What parameters change in exercise?

A

Decreased ESV, increased EDV, SV, BPs.

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63
Q

What are the effects of metoprolol/beta blockers?

A

SA node: decreases If (pacemaker current), less frequent firing. AV node: decrease of calcium and potassium channels, increased refractoriness. In conclusion, there is (insignificant) reduction of contractility, and a marked heart rate decrease.

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64
Q

How do you tell apart the three unchanged PaCO2 arterial hypoxemia conditions?

A

Give 100% pure oxygen - only increased venous shunt will have a PaO2 <400. Then measure CO diffusion capacity - VQ mismatch will have normal, diffusion problems will show reduced capacity.

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65
Q

What is standard deviation?

A

Square root of variance.

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66
Q

In mitral/tricuspid stenosis, how is blood pressure altered? What sounds/murmurs are heard?

A

Systolic and diastolic are decreased. There is no sounds but a diastolic murmur.

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67
Q

What is theophylline?

A

A methylxanthine (type of bronchodilator). Also includes caffeine and theobromine. It has three proposed mechs of action - inhibition of PDE, blockade of adenosine receptos, antiinflammatory (possibly enhances HDAC/decreases cytokine release).

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68
Q

What’s the difference between pulmonary and systemic hypoxia?

A

Pulmonary causes vasoconstriction, systemic causes vasodilation.

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69
Q

What is tissue hypoxemia and what are the causes?

A

PaO2 is normal. Stagnant hypoxia (reduced blood flow/volume), anemic hypoxia (reduced Hb), histotoxic hypoxia (cannot make ATP).

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70
Q

How does lung volume affect pulmonary blood vessels - both extraalveolar and intraalveolar?

A

Increased lung volume reduces resistance on the extraalveolar vessels anre increases it on the intraalverolar vessels.

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71
Q

What are the effects of left sided heart failure?

A

Pulmonary edema, pleural effusion.

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72
Q

What kind of drug is amiodarone?

A

Class III, K+ blocker.

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73
Q

What is mean systemic filling pressure?

A

The point where venous return = 0

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74
Q

What is the optimum inhaled drug size?

A

2-5um

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75
Q

How does 2nd degree AV block present on an ECG?

A

Mobitz type I (Wenchebach) is regularly irregular, PR interval lengthens until QRS is dropped and then it repears. Type II just has a dropped QRS without sequential PR lengthening.

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76
Q

What is Poisseuille’s Law?

A

R = 8(viscosity)L/pir^4

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77
Q

What is ATPS?

A

Ambient TP Saturated. T=Tspirometer PB=760mmHg PH2O=Ts saturation pressure

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78
Q

Is the tunica media thinner or thicker than the tunica adventitia?

A

Thicker in arteries, thinner in veins.

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79
Q

What are the ECG effects of amiodarone / K+ blockers?

A

Mild PR interval increase, QT increase.

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80
Q

What does hypocapnia cause?

A

Airway constriction reflex.

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81
Q

What is Total Lung Capacity (TLC)?

A

ERV+TV+IRV+RV

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82
Q

What is a distinguishing feature of post-capillary venules?

A

Pericytes/Rouget cells in tunica media.

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83
Q

What is Sjogren Syndrome?

A

Dry eyes, dry mouth.

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84
Q

What protein is responsible for most of cardiac muscle passive tension?

A

Titin.

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85
Q

What receptors provide negative feedback to the respiratory system?

A

Mechanoreceptors in the lung and thorax, chemoreceptors.

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86
Q

What is the difference between type I and type II pneumocytes?

A

I is simple squamous, not dividing. II are bulgy, lamellar bodies exocytose surfactant, have mitotic activity, can become type I.

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87
Q

How can O2 transport be limited?

A

By perfusion or diffusion.

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88
Q

What effects does tolerance have in mucosal immunity/GI?

A

Recruitment and activation of T regulatory cells, increased production of IL-10, TGF-beta, TOLLIP, decreased costimulatory molecules (B7, CD80/CD86), TLR, CD14 (on intestinal macrophages).

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89
Q

At what point are the majority of people diagnosed with COPD?

A

When they have lost half their lung function.

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90
Q

When is the blood flow velocity highest?

A

After aortic ejection.

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91
Q

Which phases of the valsalva maneuver can be fatal to heart failure patients?

A

I and IV because of the increased MAP.

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92
Q

What is Zileuton?

A

A leukotriene pathway inhibitor that blocks 5-lipozygenase (involved in LT synthesis).

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93
Q

How does 1st degree AV block present on an ECG?

A

Prolonged PR interval.

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94
Q

How is pulmonary vessel resistance regulated?

A

Not by autonomic nervous system, increased CO decreases resistance.

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95
Q

What is special about GALT intraepithelial lymphocytes?

A

They may secrete gammadeltaTCR, require no priming (considered ‘innate’ T cells), respond spontaneously to challenge and release cytokines.

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96
Q

What are the cells in the heart that can be pacemakers besides the SA node?

A

AV node and Purkinje fibers.

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97
Q

In inhalation, about how much fresh gas reaches the alveolar region?

A

~350mL

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98
Q

What kind of drug is lidocaine?

A

Class Ib, Na+ channel blocker.

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99
Q

Where are fenestrated/visceral capillaries found?

A

Where rapid exchange between tissues takes place - kidney, intestine, pancreas.

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100
Q

What is central venous pressure/CVP?

A

Pressure in the thoracic vena cava near the RA. change in volume/Cv

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101
Q

Do you see any hypertrophy in aortic/pulmonic regurgitation?

A

Eccentric.

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102
Q

What does phospholambam do?

A

It helps SR calcium uptake when it is phosphorylated and unbinds.

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103
Q

What cells in the stomach secrete gastrin?

A

G cells.

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104
Q

Knowing volume and transmural pressure, how can compliance be calculated?

A

The derivative of volume/pressure.

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105
Q

What are the most common causes of death after a myocardial infarction?

A

Arrhythmias after 24 hours, LV wall rupture within 4-7 days.

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106
Q

What is the LQTS2 mutation?

A

Loss of function IKr

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107
Q

What is irreversible shock?

A

Decompensated shock without treatment or blood loss >20%. Results in organ damage and death.

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108
Q

What is Laplace’s law?

A

P = 2ST/r

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109
Q

What ‘generation’ of alveoli are the respiratory zone?

A

17-23.

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110
Q

What are vocal cord nodules?

A

A subepithelial hemorrhage which over time results in subepithelial scarring.

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111
Q

What is x-descent on the jugular venous pressure graph?

A

Right atrial relaxation.

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112
Q

Which way do the lung and chest recoil?

A

The lung always wants to recoil in, and the chest wall outward.

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113
Q

How can you see ventricular enlargement on an ECG?

A

Add the highest peak of V1 to the highest peak of V5 or V6, and if its over 7 big boxes it’s ventricular enlargement.

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114
Q

What is standard error?

A

Measure of dispersal or variability of the sample means relative to the true population mean. SD/sqrt(n)

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115
Q

Does heart depolarization and repolarization go outward or in?

A

Depol goes out (endo to epicardium), repol goes in (epi to endocardium).

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116
Q

What is TOLLIP?

A

It inhibits TLR in the PAMP/PRR interaction/cascade.

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117
Q

What cells in the stomach secrete HCl?

A

Parietal cells.

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118
Q

What is y-descent on the jugular venous pressure graph?

A

Right atrial pressure drop as blood flows into the ventricle.

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119
Q

What is the ultimate formula for flow?

A

(P1-P2)Xpir^4/8(viscosity)L

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120
Q

What are the GI antigen sampling pathways?

A

Enterocyte pathway (no B7, no activation), DC pathway, M cell pathway (transcytosis, antigen presentation to APC).

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121
Q

How is CO2 found in blood?

A

HCO3- (2/3) or carbamate (binds amino acids or Hb), and also physically dissolved.

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122
Q

What is ipratropium?

A

An antimuscarinic drug (type of bronchodilator). It blocks M3 receptors.

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123
Q

Does blood oxygen and CO2 always equal alveolar oxygen and CO2?

A

Oxygen no ( is always slightly lower and can be problems that lower it), CO2 always.

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124
Q

What happens to the FEV1/FVC ratio in obstructive and restrictive lung disease?

A

Obstructive it decreases, restrictive it stays the same or increases.

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125
Q

How are medicare and medicaid funded?

A

Both federal, medicaid can be state.

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126
Q

How do you calculate alveolar ventilation?

A

CO2 output / CO2 alveolar pressure X 863

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127
Q

What fraction of tidal volume goes into the dead space?

A

1/3

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128
Q

What is the average left atrial pressure?

A

6-12

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129
Q

Does the baroreceptor reflex affect stroke volume?

A

No

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130
Q

What is FVC?

A

Forced vital capacity (amount of air exhaled in forceful maximal exhalation).

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131
Q

What is the vestibule and nasal fossa?

A

The vestibule is the external part (lined by keratinized stratified squamous epithelium) and the internal part is the nasal fossa (lined by respiratory epithelium).

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132
Q

What is typical microcirculation?

A

Arteriole to metarteriole to capillary to venule.

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133
Q

What is FEV1?

A

The amount of air exhaled in the first second of forceful exhalation after maximal inspiration.

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134
Q

What is the effect of pH on CO2 binding?

A

Decreased pH (increased H+) causes CO2 release from the binding site.

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135
Q

What does the NCX channel do?

A

Brings in 3 sodiums in exchange for 1 calcium.

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136
Q

What can decrease diffusion capacity?

A

Increased thickness or lower surface area of the alveolo-capillary membrane, or a decrease in capillary volume.

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137
Q

What cells in the stomach secrete pepsinogen?

A

Chief cells.

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138
Q

What are the effects of right sided heart failure?

A

Accumulation of blood in venous/systemic circuit - distension of jugular veins, ascites, peripheral edema, visceral organ changes “nutmeg liver”.

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139
Q

What is the effect of emphysema on VQ mismatch?

A

Increased.

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140
Q

What is a confidence interval?

A

The chance that a value falls within a range. If the odds ratio 1 falls within the CI, then it’s not significant.

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141
Q

When is surfactant made?

A

By the 24th week of gestation. By the 35th there’s enough to cover the alveoli and reduce surface tension.

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142
Q

What are the effects of an effective therapy that prolongs life but offers no disease cure to the prevalence in a population?

A

Goes up.

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143
Q

What are the layers of the endocardium?

A

Inner thin endothelial layer, middle myoelastic layer, deep subendocardial layer (merges with myocardium, has Purkinje fibers).

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144
Q

What is the Cardioinhibitory center?

A

The Nucleus Ambiguous and the Dorsal Motor Nerve of the Vagus). They slow heart rate and decrease cAMP.

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145
Q

What are the false and true vocal cords lined by?

A

False vocal cords by respiratory epithelium, true vocal cords by nonkeratinized stratified squamous epithelium.

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146
Q

When is VQ = infinity?

A

Alveolar dead space.

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147
Q

What is the normal PO2 and PCO2 of veins?

A

PvO2 = 40mmHg PvCO2 = 45mmHg

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148
Q

What are some personality characteristics associated with tobacco use?

A

Extraversion, neuroticism, lower conscientiousness, sensation seeking, impulsivity, externalizing traits associated with smokers.

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149
Q

What are metarterioles?

A

Connect arterioles to capillaries. No true tunica media. They have a precapillary sphincter - a single SMC regulating blood flow.

150
Q

What are the anterolateral precordial leads?

A

V5, V6

151
Q

What is a Chi-square test?

A

Can be used to compare groups of nominal variables and assess if they’re independent.

152
Q

What does it mean when lead I is neg and avF is positive?

A

Right axis deviation.

153
Q

What are the effects of acute and chronic hypercapnia on ventilation?

A

Goes up, then during the days falls to a higher end steady state as the kidney corrects pH levels and the CCRs stop stimulating.

154
Q

How does the heart compensate with significant aerobic training?

A

Increase in PNS tone, decreased heart rate, increased stroke volume (CO is same), increased ventricular mass, increased angiogenesis in skeletal/heart muscles.

155
Q

What effects does metoprolol/beta blockers have on an ECG?

A

Increased PR interval.

156
Q

What does the dead space do then if it’s not for actual gas exchange?

A

Produces mucus, has macrophages, warms gas.

157
Q

What is STPD?

A

Standard TP Dry: T= 0C PB=760mmHg PH20=0

158
Q

Are S3 and S4 always pathological? When are they heard relative to the normal sounds?

A

S4 yes, S3 can be normal. S4 - S1 - S2 - S3

159
Q

What is the relationship between resistance and generation of airway branching?

A

It increases and peaks around generation 4, then decreases.

160
Q

What are the effects of aortic/pulmonic regurgitation on EDV, ESV, and SV?

A

Increased, Unchanged, Increased.

161
Q

How do you calculate what PAO2 of a gas should be?

A

Fx (of inspired gas)X(PB-PH2O)

162
Q

What are the types of heart failure when it can’t properly eject and fill with blood?

A

Forward failure and backward failure respectively.

163
Q

What is zafirlukast?

A

A leukotriene pathway inhibitor that blocks leukotriene B4 receptors.

164
Q

How do perfusion and ventilation vary throughout the lung when standing?

A

Both higher in lower lung, but perfusion more significantly increases.

165
Q

What is variance?

A

How far a set of numbers are spread from the mean. The sum squared of each value subtracted from the mean, over n-1

166
Q

What are antitussives?

A

Anti-cough drugs, block reflex in receptors in tracheobronchial passages. Includes codeine (activates mu receptors in medullary cough center) which is an addictive opioid, and dextrometorphan which activates different receptors and is a non-addictive opioid (also has no analgesic properties).

167
Q

Describe the structure of the trachea.

A

Bifurcates at T4, has 16-20 C rings of hyaline cartilage connected by trachealis smooth muscle. Has 3 layers, mucosa, submucosa, adventitia.

168
Q

What are the effects of aortic/pulmonic stenosis on EDV, ESV, and SV?

A

Unchanged, Increased, Decreased.

169
Q

What is normoventilation?

A

Arterial O2 pressure = 40mmHg

170
Q

Describe rapidly adapting stretch receptors.

A

Located in airway epithelium, innervated by myelinated vagal fibers. Activated by lung distension, irritants. Produce cough and bronchoconstriction.

171
Q

What is better at buffering H+, erythrocytes or plasma?

A

Erythrocytes. They produce lots of HCO3-, and it’s transported out in exchanged for chloride.

172
Q

How do antimuscarinics compare to b2 agonists?

A

Bronchodilation is less intense in asthma but equal/more in COPD. It is not used as much for COPD now because it had too much effect on secretions.

173
Q

How are cardiac glycosides (e.g. digitalis) positive inotropic agents?

A

Inhibit the Na+/K+ pump so there’s a rise of IC Na+, meaning the Ca++ efflux is reduced.

174
Q

Do you see any hypertrophy in mitral/tricuspid regurgitation?

A

Eccentric.

175
Q

What are the effects on ventilation with a drop in pH?

A

Increased. Increase faster at constant PaCO2 (slower if it also falls).

176
Q

What are the risks of calcium channel blockers?

A

Bradycardia, hypotension, worsening heart failure (should be avoided in heart failure).

177
Q

How do emphysema patients find some relief?

A

By exhaling through a mostly closed mouth to increase the pressure leading to the airway, preventin airway collapse.

178
Q

What is physiological dead space?

A

Anatomical dead space (conducting zone) + regions ventilated but not perfused with blood.

179
Q

What is the formula for cardiac output?

A

CO = SV X HR

180
Q

What cardiovascular diseases lead in crude mortality?

A

Ischemic heart disease.

181
Q

What is risk? What is the difference between relative risk and absolute risk?

A

Risk is # new cases / pop initially at risk to be a case. Relative risk = incidence in exposed / incidence in unexposed. Absolute risk = incidence in exposed - incidence in unexposed.

182
Q

What are the formulae for prevalence?

A

Incidence X duration. Total # of cases / # examined

183
Q

What is the normal length of a QT interval?

A

<400ms

184
Q

What drops in orthostasis?

A

Venous return, stroke volume, cardiac output, MAP.

185
Q

How is cardiac index calculated?

A

CI=CO/BSA

186
Q

Using a box plot how do you figure out which values are outliers?

A

If they are more than 1.5XIQR bigger than the minimum or smaller than the maximum.

187
Q

What is the most common cardiovascular disease?

A

Hypertension.

188
Q

What are Paneth cells?

A

Essential intestinal scavengers, produce antimicrobial defensins.

189
Q

When is the S1 sound heard?

A

In closing of mitral/tricuspid valves, during isovolumetric contraction.

190
Q

What is O2 capacity?

A

The maximal chemically bound O2.

191
Q

How do you treat atrial fibrillation?

A

With an anticoagulant.

192
Q

What is methemoglobin?

A

Hemoglobin with Fe 3+, cannot bind oxygen. Needs MetHb reductase.

193
Q

Describe olfactory epithelium.

A

Pseudostratified columnar, has olfactory receptor cells, suporting/sustenacular cells (yellow-brown, have an ovoid nuclei, broader apex, microvilli on apical surface), and basal cells. Dendritic processes of olfactory receptor cells forms a dilation extending above the surface, has nonmotile cilia that possess chemoreceptors. to recognize odorants. There are also Bowman’s glands in the CT deep to the olfactory epithelium.

194
Q

What are the effects of lidocaine / Na+ channel blockers. How is it given? Where is it distributed? What’s it’s half life.

A

Given intravenously. Only dysfunctional myocardium is affected. It’s distributed everywhere, it’s half life is ~20 mins. Great for arrhythmias associated with membrane depolarization. Decreased automaticity (mainly in ventricles), increased refractoriness in depolarized cells, slight decreased refractoriness in normal cells. Slows heart rate.

195
Q

What changes will increase both venous return and cardiac output?

A

Increased blood volume, decreased venous compliance, decreased arteriolar resistance. BUT arteriolar resistance will not alter mean systemic filing pressure.

196
Q

How is the heart cycle altered in exercise?

A

The cardiac cycle is shortened, systole is reduced, diastasis is gotten rid of, APs are more frequent, propagated faster, shorter in duration, strength of contraction with each AP is greater, rate of development of ventricular pressure and relaxation is increased (positive lusitropic effect).

197
Q

What arteries does atherosclerosis typically involve?

A

aorta and major branches, coronary artery, cerebral artery, femoral/popliteal arteries.

198
Q

What is the effect on increased inotropic activity (sympathetic stimulation) on Fmax and Vmax?

A

Both increase.

199
Q

What are the three core functions of public health?

A

Assessment, policy development, assurance.

200
Q

What are the different kinds of cells in respiratory epithelium?

A

Brush cells (microvilli, chemoreceptors), Basal cells, Small granule/DNES cells (release hormones, thought to regulate airway/vascular caliber, thought to be cells that give rise to small cell carcinoma).

201
Q

What are glucocorticoids?

A

A type of antiinflammatory. Also potentiate beta adrenergic responsiveness to agonists (possibly by increasing E synthesis). Proposed mechs of action: alteration of concentration of peripheral leukocytes/macrophages, altering transcription of pro/antiinflammatory cytokines, inhibition of prostaglandin and leukotriene synthesis by blocking PLA2.

202
Q

What are the oro, naso, and laryngopharynx lined by?

A

Oropharunx and laryngopharynx by nonkeratinized stratified squamous epithelium, nasopharynx by respiratory epithelium.

203
Q

What is Residual Volume (RV)?

A

The volume remaining in the lungs after maximum expiration. Generally about 1.5L.

204
Q

List antiinflammatory cytokines.

A

IL-10, TGF-beta

205
Q

At about what voltage does the fast VG sodium channel open?

A

-70mV

206
Q

What kind of vessels to WBCs migrate into?

A

Venules.

207
Q

Where are the low pressure baroreceptors?

A

Vene cavae, RA, PT. They are more volume detectors (detect venous return increase).

208
Q

What is the normal length of a PR interval?

A

0.12-0.2s

209
Q

Do you see any hypertrophy in mitral/tricuspid stenosis?

A

Atrial eccentric.

210
Q

What is the relationship between RAP and VR at a constant CVP?

A

Inversely proportional

211
Q

What is active hyperemia?

A

Increase in blood flow (in active muscles) due to the increase in metabolism. This uses the metabolic theory of control.

212
Q

What are the effects of mitral/tricuspid stenosis on EDV, ESV, and SV?

A

Decreased, Unchanged, Decreased.

213
Q

How do you calculate the driving pressure of systemic circulation?

A

MAP of aortic blood pressure - RA pressure

214
Q

What mucosal immunity things to epithelial cells secrete?

A

Cytokines, antimicrobial peptides/proteins, they transcytose Igs.

215
Q

What is stage II hypertension?

A

Greater or equal to 160 systolic and/or 100 diastolic

216
Q

What kind of drug is metoprolol?

A

Class II, beta blocker.

217
Q

Do transplant patients keep their pulmonary reflexes?

A

No.

218
Q

What is the epiglottis lined by?

A

Anterior (lingual) surface and upper 1/2 of posterior (respiratory) surface by stratified squamous epithelium, lower 1/2 of posterior surface by respiratory epithelium.

219
Q

Are there any RBCs in lymph? Are there valved?

A

No. Yes.

220
Q

What side of the heart is the jugular venous pressure graph showing?

A

Right.

221
Q

What is the relative pleural pressure in end inspiration and end expiration? And during expiration/inspiration.

A

-10 and -5 respectively. During expiration/inspiration it’s -8.

222
Q

What vessels do starling forces relate to?

A

Capillaries.

223
Q

What is Vital Capacity (VC)?

A

ERV+TV+IRV

224
Q

What happens to TLC and RV in obstructive lung disease?

A

They both increase, but RV increases more so RV/TLC ration increases.

225
Q

Where are sinusoidal capillaries found? What is special about them?

A

Liver, BM, spleen. They are often torturous and have the slowest blood circulation.

226
Q

What does ‘electrogenic’ mean?

A

Generates a current.

227
Q

What are the most important metabolites in the muscle, heart, brain?

A

Muscle: adenosine, K+ Heart: adenosine, NO Brain: CO2

228
Q

Which vessels have vasa vasorum?

A

Large veins (>1cm), large/elastic arteries (>1cm), medium/muscular arteries (2-10mm).

229
Q

What are the surfaces of the heart valves?

A

Spongiosa (LCT, auricularis or arteriolis), Fibrosa, Ventricularis (DCT, extends as chordae tendinae into ventricles).

230
Q

What is the optimal thickness of a capillary membrane that both allows for diffusion and mechanical stability?

A

1-1.5um.

231
Q

How do you differentiate stable angina pectoris from acute coronary syndrome?

A

Pain 2-5 min and alleviated with nitroglycerin in stable angina. <20 min in ACS and not alleviated with nitroglycerin.

232
Q

How is MAP calculated?

A

MAP = CO X TPR MAP = diasBP + 1/3PP

233
Q

What is the alveolar wall/interalveolar septum made of?

A

CT, elastic fibers, capillaries. They have interalveolar pores of Kohn.

234
Q

What does the v wave mean on the pressure trace?

A

Atrial filling and mitral valve opening.

235
Q

What is the myogenic theory of control of CO?

A

Increased flow results in vessel stretch which results in depol via Ca++ L, resulting in vasoconstriction. EC calcium is needed for this reflex. NO is also autosynthesized by endothelial cells from arginine (stimulated by paracrine agents e.g. histamine, shear stress). NO catalyzed GTP to cGMP, resulting in vasodilation.

236
Q

Do you see any hypertrophy in aortic/pulmonic stenosis?

A

Concentric.

237
Q

What is decompensated shock?

A

Compensation mechanisms are maxed out, metabolic demands are not met, there is cellular ischemia happening. Hypotension, dyspnea, acidosis, cool and pale skin, mental confusion.

238
Q

What sounds/murmurs are present in a VSD? What can happen if it’s untreated?

A

S2 split, holosystolic murmur. If it’s untreated, there will be irreversible RV hypertrophy and pulmonary hypertension that can reverse the L-to-R shunt (Eisenmenger syndrome).

239
Q

What is the circle of Willis?

A

Helps provide blood flow to the brain, is made up of the basilar artery and internal carotids.

240
Q

List proinflammatory cytokines.

A

IL-1, IL-6, TNF-alpha, IL-15

241
Q

What is compensated shock?

A

Blood loss is 10-20%, reflex and compensation can usually return MAP to close to normal and maintain adequate vital organ perfusion and oxygenation. Fluids must be administered. Even is blood pressure is normal, CO may be reduced.

242
Q

What is the respiratory exchange rate?

A

R=CO2 output/O2 uptake

243
Q

What are the factors affecting airway resistance?

A

Density and viscosity of the gas, partial pressure of CO2, autonomic innervation, lung volume, agents (histamine, ACh, TxA2, prostaglandin F2, leukotrienes (LTB4, C4, D4)).

244
Q

How far does the lumen have to be occluded to have stable angina?

A

70%

245
Q

What does the c wave mean on the pressure trace?

A

The flaps bulge into the atria.

246
Q

Describe the RAAS system.

A

BP falls, renin is released which catalyzes angiotensinogen into angiotensin I. ACE (released from the lungs) converts ATI into ATII. ATII constricts vessels via ATI receptors, stimulates ADH release from the posterior pituitary, stimulates aldosterone (salt retention) release from the adrenal cortex.

247
Q

What is the LQTS1 mutation?

A

Loss of function IKs

248
Q

How are E and NorE positive inotropic agents?

A

Stimulate beta1, PKA phosphorylates things involved in calcium metabolism (e.g. Ca++ L, RyR).

249
Q

What are the effects of verapamil and diltiazem/Ca++ blockers on an ECG?

A

Increased PR interval.

250
Q

What does the a wave mean on the pressure trace?

A

Atrial contraction.

251
Q

What is a normal ejection fraction?

A

0.55-0.65 at rest.

252
Q

Describe the rhythm generator.

A

Found in the medulla, VRG and DRG (within NTS) which are interconnected, also the pneumotaxic center in the pons. VRG mainly involved with cardio, autonoic coupling, basic bronchial muscle cells, extra drive. DRG mainly involved with integration of input from the periphery via CN IX and X. Pneumotaxic center turns off breathing, controls respiratory frequency.

253
Q

What type of receptor are olfactory receptors?

A

GPCRs.

254
Q

What is the olfactory region of the nose?

A

The roof, superior lateral walls, and septum including superior concha. It is lined by olfactory epithelium.

255
Q

What is prehypertension?

A

120-139 systolic and/or 80-89 diastolic

256
Q

What does the symbol c’ mean?

A

End of capillary.

257
Q

When is the chest wall most compliant?

A

At around 60-70% total lung capacity.

258
Q

In what conditions is a systolic murmur heard?

A

Aortic/pulmonic stenosis, mitral/tricuspid regurgitation, ASD, VSD.

259
Q

What effects on the heart does sympathetic stimulation have?

A

IKr, IKs are increased more at positive voltages but deactivate more at negative ones, increasing HR. Ca++L increased so the upstroke is faster - increasing HR. Speed of AP conduction through AV node is increased. Rate of ventricular relaxation is increased (positive lusitropic effect). The strength of contraction with each action potential is greater.

260
Q

Which veins have valves?

A

Medium (1-10mm) and large (>1cm).

261
Q

What does a myocardial infarction look like under the microscope?

A

Absence of cardiomyocyte nuclei.

262
Q

What are the anteroseptal precordial leads?

A

V1, V2

263
Q

What happens to lung volumes after age 60?

A

TLC stays the same but RV increases.

264
Q

What is BTPS?

A

Body TP Saturated: T=37C PB=760mmHg PH2O=47mmHg

265
Q

In mitral/tricuspid regurgitation, how is blood pressure altered? What sounds/murmurs are heard?

A

Systolic and diastolic are reduced. S3, systolic murmur.

266
Q

How does pulmonary hypoxia affect vessels?

A

Increased vasoconstriction - hypoxia inhibits Kv channels and opens Ca++ channels.

267
Q

What channels are involved in slow response APs?

A

Funny channel, Calcium T-type channel, Calcium L-type channel, IKr and IKs (rapid and slow rectifier channels).

268
Q

What are the effects of hypoxia on ventilation?

A

It goes up then at day 4/5 it reaches maximum and stays. It takes a while for the ventilation to rise to the maximum for the first few days because alkalosis from CCR hyperventilation inhibits the response.

269
Q

What layers of the heart are the Purkinje fibers between?

A

Endocardium and myocardium.

270
Q

What is infant mortality rate?

A

deaths in kids <1y/o / # live births in same period in a specified pop

271
Q

What do cross-presenting Dendritic Cells do in mucosal immunity?

A

They present peptides via MHCI to CD8 T cells.

272
Q

What are the possible effects of hypertension?

A

Heart failure, LV hypertrophy, risk for ischemic heart disease, renal failure (contracted, granular kidneys), stroke, vascular dementia, vision problems.

273
Q

What is an outbreak or an epidemic?

A

Sudden occurrence in community either never experienced before or in greater numbers than normally expected in that time/area.

274
Q

What is albuterol?

A

A beta2 agonist (type of bronchodilator). It increases cAMP synthesis (resulting in activation of cAMP dependent kinase / inactivation of MLCK) and ultimately resulting in bronchodilation.

275
Q

What is the definiton of ischemia?

A

When oxygen demand > oxygen supply

276
Q

Describe emphysema.

A

Stimulus increases macrophages which atract neutrophils that release elastase. Eventually it is too much elastase for the a1AT to overcome.

277
Q

How is cardiac output calculated with the Fick Principle?

A

CO = VO2/(Ca-Cv) VO2 = the rate of oxygen consumption in mL/min. Ca is blood O2/mL from a peripheral artery. Cv is blood O2/mL from mixed venous blood (RA, RV, or PT)

278
Q

What is the LQTS3 mutation?

A

Gain of function INa

279
Q

What is the difference between epicardial and endocardial APs?

A

Epicardial APs are shorter in duration - more Ito expression.

280
Q

Using a box plot how do you figure out which values are outliers?

A

If they are more than 1.5XIQR bigger than the minimum or smaller than the maximum.

281
Q

What kind of drugs are verapamil and diltiazem?

A

Class IV, calcium channel blockers.

282
Q

How can you see ischemia on an ECG?

A

ST segment not on the isoelectric line.

283
Q

Describe phase I of the valsalva maneuver.

A

Increase in intrathoracic pressure compresses thoracic aorta - blood pressure rises. Heart rate lowers due to baroreceptor activation.

284
Q

Describe phase IV of the valsalva maneuver.

A

Blood surges into the thorax, so venous return, and therefore cardiac output, pulse pressure, and MAP all go up. Baroreceptor reflex is triggered, resulting in transient bradycardia.

285
Q

In exercise, why doesn’t the baroreceptor overcome the increased MAP?

A

The MAP is reset to a new reversible setpoint.

286
Q

Describe the central chemoreceptors.

A

Mitchell (rostral area), Schlafke (intermediate area), Loeschcke (caudal area). Located in the brainstem, are sensitive to changes in pH. Provide 80% of ventilation effects.

287
Q

Which sex is more likely to get COPD?

A

Women

288
Q

What is ANOVA?

A

Compare means and standard deviations of more than two groups. One way analysis compares the mean difference in one variable, two way analysis compares the mean difference in two variables.

289
Q

What are the anteroapical precordial leads?

A

V3, V4

290
Q

What is the normal PO2 and PCO2 of arteries?

A

PaO2 = 90mmHg PaCO2 = 40mmHg

291
Q

What sounds/murmurs are present in an ASD?

A

S2 split, mid-systolic murmur.

292
Q

Are inspiration/expiration active or passive?

A

Inspiration is active, exhalation is passive.

293
Q

What are the functions of intestinal microbiota?

A

Competitive inhibition of pathogens, vitamin synthesis, involved in normal immune development, deconjugation of bile salts, production of antimicrobials.

294
Q

What is the relationship between lung volume and the distance fro airway opening.

A

There is less volume the further we go from the airway opening, until we reach the conducting zone where it is constant.

295
Q

What does it mean when lead I is pos and avF is neg?

A

Left axis deviation

296
Q

Where does autoregulation occur and via which theory of control?

A

Mainly in the brain, heart, kidneys - and myogenic.

297
Q

Are terminal bronchioles respiratory zone or conducting zone?

A

The last of the conducting zone.

298
Q

What happens to TLC and RV in restrictive lung disease?

A

They both decrease but proportionately so the RV/TLC ratio stays the same.

299
Q

At FRC, is intrapleural pressure positive or negative?

A

Negative.

300
Q

What is the average pulmonary artery pressure?

A

25/8mmHg

301
Q

What are the effects of mitral/tricuspid regurgitation on EDV, ESV, and SV?

A

Increased, Decreased, Increased (decreased effective).

302
Q

What channels are involved in fast response APs?

A

Fast VG sodium channel, Ito (transient outward potassium), Calcium L-type channel, IKr and IKs (inward rectifiers).

303
Q

What is most of health spending in the US on?

A

Health insurance.

304
Q

Where do T-tubules enter cells in cardiac muscle?

A

At the Z line.

305
Q

Describe C-fibers/J-receptors.

A

Near capillaries, innervated by unmyelinated vagal fibers. Activated in increase in interstitial fluid and pulmonary embolism. Produces rapid shallow breathing, bronchoconstriction, cardiovascular depression.

306
Q

What is Functional Residual Capacity (FRC)?

A

ERV+RV

307
Q

What kind of proteins do respiratory epithelial cells secrete that aid in mucosal immunity?

A

Beta-defensins (promote lysis, chemotactic, promote phagocytosis), Cathelicidins, surfactant proteins A & D, lysozyme/muraminidase (can cleave gram + cell walls).

308
Q

What is the volume of the respiratory and conducting zones?

A

Respiratory zone volume is variable, conducting zone volume is constant at around 150mL.

309
Q

What is the normal length of an ST segment?

A

About 120ms.

310
Q

Where is 80% of the lung resistance found?

A

Up to generation 7.

311
Q

What is Darcy’s Law regarding flow, pressure, radius?

A

F=(P1-P2)/r

312
Q

What’s an endemic?

A

A condition in a defined area normally found in a certain percentage.

313
Q

Describe the peripheral chemoreceptors.

A

Sense PCO2 (also sensitive to pH and PO2). Provdide 20% of effect to ventilation. Carotid body, made up of type I chemosensitive cells, type II support cells, capillary, carotid sinus nerve. Decrease of pH inside the cell inhibits a K+ channel - leads to cell depolarization, calcium influx, a release of a neurotransmitter to the sinus nerve.

314
Q

What is the difference between exudate and transudate?

A

Exudate contains proteins, transudate doesn’t (ultrafiltrate).

315
Q

What is Henry’s Law?

A

O2 concentration = solubility X partial pressure.

316
Q

What are the risk factors for atherosclerosis?

A

Dyslipidemia (increased cholesterol/LDL, decreased HDL), smoking (endothelial injury), hypertension, diabetes mellitus, also others. Interestingly enough, premenopausal women are less at risk.

317
Q

In the PV loop, where is EDV and ESV?

A

B and D.

318
Q

What is respiratory epithelium?

A

Ciliated pseudostratified columnar epithelium with goblet cells (produce mucus).

319
Q

What’s the difference between cardiac and skeletal DHPRs and RyRs?

A

Cardiac ones aren’t mechanically coupled, and it has less DHPRs and less well ordered RyRs.

320
Q

Describe the series of neuron interactions once the Nucleur Tractus Solitarius is signalled by high pressure baroreceptor increased firing rate (MAP).

A

Glutaminergic afferents synapse in the medulla where the NTS is. Another glutaminergic interneuron synapses at the Caudal Ventrolateral Medulla. A GABAergic neuron goes to the vasomotor cortex (which has tonic output via the bulbospinal pathway).

Normally a glutaminergic neuron goes to the preganglioni sympathetic fibers, then another one into the adrenal medulla. The adrenal medulla sends out E and NorE.

321
Q

Do arteries or veins have external or internal laminae?

A

Arteries.

322
Q

What does wedge pressure approximate?

A

LA pressure.

323
Q

Describe Club Cells.

A

Replace goblet cells in bronchioles. Nonciliated, dome-shaped, lots of SER (cyt P450), secretes some surfactant components, secretes some antimicrobial peptides, some act as stem cells.

324
Q

What does the symbol v with a dash over it mean?

A

Mixed venous.

325
Q

How do lymphatic vessels differ for veins?

A

Blind ending, thinner walls, no distinct tunics, no RBCs, more valves, can be dilated with lymph, also enters right atrium.

326
Q

What is the average right atrial pressure?

A

-4 to 4 mmHg

327
Q

What is the epiglottis made of?

A

Elastic cartilage core and hyaline cartilage elsewhere.

328
Q

What % of total delivered drug is delivered to the lower airways using a pMDI (conventional pressurized metered dose inhaler).

A

10-20%

329
Q

What is the formula for incidence?

A

new cases / # at risk to be a new case (in a time frame)

330
Q

What is the effect of increased preload on Fmax and Vmax?

A

Fmax is increased.

331
Q

What is the sea level PO2?

A

~147mmHg

332
Q

What is a type II error?

A

When you reject a correct null hypothesis.

333
Q

Describe phase III of the valsalva maneuver.

A

Glottis opens BP falls transiently so heart rate transiently rises.

334
Q

What kind of hyperemia is prominent in phasic and occlusive activity?

A

Active and reactive primarily.

335
Q

Why is there a physiological S2 split on inspiration?

A

Decrease of intrathoracic pressure increases venous return, pulmonic valve is delayed.

336
Q

In the PV loop where is there systolic and diastolic aortic blood pressure?

A

Systolic is the peak, diastolic is C.

337
Q

What activates the Funny Channel?

A

Hyperpolarization and cAMP.

338
Q

What is MERS?

A

Middle Eastern Respiratory Syndrome? Pandemic

339
Q

What is crude rate? What is specific and standardized rate?

A

Mortality from all causes in a specific pop over a time period. Specific is only concerned with one subgroup. Standardized is to ensure differences in rates are not due simply to age distribution differences.

340
Q

What vessels hold the majority of blood?

A

Veins (capacitance vessels).

341
Q

What’s a t-test?

A

It evaluates the difference between means of two sets of values. Can be independent (samples on one occasion) or paired.

342
Q

What is acute coronary syndrome?

A

Unstable angina + acute myocardial infarction.

343
Q

What is transmural BP?

A

Pressure inside - pressure outside. (Pi-PoXr

344
Q

Describe the Slowly adapting stretch receptors (Hering-Breuer).

A

Located in airway smooth muscle, innervated by large myelinated fibers. Activated in lung distension, breath holding, deflation below FRC. Stops inspiration, prevents over-exhale.

345
Q

What is the difference between eccentric and concentric hypertrophy?

A

Eccentric results from a volume overload and increases chamber volume, it’s also reversible. Concentric results from an afterload overload and reduces chamber volume as well as ventricular compliance.`

346
Q

What is the effect of amiodarone / K+ blockers?

A

Ventricular AP has prolonged repolarization so is prolonged. It also somewhat blocks funny channels, alpha and beta channels, calcium. Conduction decreased, markedly increased refractoriness, strongly decreases abnormal automaticity.

347
Q

What is a normal FEV1/FVC?

A

80%

348
Q

What is a P-value?

A

The probability of rejecting the null hypothesis.

349
Q

Where are the high pressure baroreceptors?

A

Carotid sinus, aortic arch, renal afferent arterioles. Detect CO increase.

350
Q

What is the metabolic theory of control of CO?

A

Arterioles are sensitive to metabolites/paracrine agents and they cause local dilation/constriction.

351
Q

What is the ‘normal point’?

A

The RAP where CO = venous return.

352
Q

What are the effects on ventilation with a drop in PaO2?

A

Increased. Increase faster at constant PaCO2 (slower if it also falls).

353
Q

Why does standing motionless for a long time cause syncope?

A

Increased blood pressure in lower extremities, increased of Venous Pc, net filtration, decrease in venous blood pressure, decrease in central venous pressure, decrease in venous return and cardiac output, decreased blood to brain.

354
Q

What is bronchiolar epithelium like in chronic asthma?

A

Thick, has increased goblet cells, thick basement membrane due to deposition of collagen fibers.

355
Q

What is the z-score?

A

The difference between a score and the population mean in terms of units of standard deviation.

356
Q

What is the max diastolic membrane potential of slow response nodal cells?

A

-60mV

357
Q

What is a type I error?

A

When you accept a wrong null hypothesis.

358
Q

Where is smooth muscle in alveoli?

A

Around ducts but not sacs.

359
Q

When is the lung most compliant?

A

At low volumes.

360
Q

What is Inspiratory Reserve Volume (IRV)?

A

The volume that can be inspired after maximal inspiration.

361
Q

When is VQ = 0

A

Venous shunt (no air)

362
Q

What percentage of lung cancer and COPD deaths is smoking directly responsible for?

A

90%

363
Q

Describe bronchioles.

A

<1mm, no cartilage, no glands. Epithelium becomes ciliated simple columnar or cuboidal, goblet cells replaced by Club Cells.

364
Q

What is P50?

A

The partial pressure at which 1/2 the Hb binding sites are bound. 27mmHg.

365
Q

What has higher compliance, pulmonary or systemic circulation?

A

Pulmonary

366
Q

What is the solubility of oxygen?

A

0.003

367
Q

How much O2 does hemoglobin bind?

A

Each gram of hemoglobin binds 1.34mL O2

368
Q

Where is the slowest conduction through the heart?

A

In the AV node.

369
Q

How many cigarettes are in a pack?

A

20

370
Q

What percent of the air is oxygen?

A

21%

371
Q

What happens to diastolic pressure in exercise?

A

Nothing or a slight decrease - due to TPR

372
Q

What slow wave AP channel do Purkinje fibers lack?

A

Ca T type.