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B2 > The end > Flashcards

The end Flashcards

1
Q

What is happening to the ventricles, atria, valves and on EKG strip during the first heart sound (S1)?

A

AV valves close because ventricular pressure exceeds atrial pressure.
Isovolumic contraction occurs due to rapid increase in ventricular pressure.
Occurs during QRS complex

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2
Q

What is happening to the ventricles, atria, valves and EKG strip during the second heart sound (S2)?

A

Ventricular depolarization (T wave), closing of semi-lunar valves [due to ventricular pressure falling below aortic], isovolumic relaxation, ventricular pressure declines until exceeded by atrial P

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3
Q

What happens during the ventricular filling phase to the atria, valves, and on EKG strip?

A

AV valves are open, aorta and pulmonic valves are closed, atrial contraction, P wave

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4
Q

What happens during the ventricular ejection phase to the atria, valves, and on EKG strip?

A

AV valves closed, aorta and pulmonary valves open, ventricular pressure rises suddenly and then declines once rate of evacuation of blood is greater than rate of ejection.
Towards end marks beginning of T wave.

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5
Q

What produces the S3 sound?

A

ventricular filling - seen in young and some pathologies

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6
Q

What produces the S4 sound?

A

atrial contraction get last bit of blood out

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7
Q

________ have ATPase activity and ______ are made up of monomer G-actin

A

thick filaments, thin filaments

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8
Q

Regulatory proteins are tightly bound to ______ on ____ filaments and are responsible for coupling of intracellular Ca++ transient to acto-myosin bridge cycling

A

actin, on thin filaments

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9
Q

Tropomyosin are two non-identical chains that lie in one of 2 groove formed by 2 actin polypeptide chains. What is their function?

A

allow or prevent interaction of actin and myosin

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10
Q

What three proteins make up the troponin complex and what is their function?

A

1) Troponin C = bind Ca++; contain 4 binding sites, I and II are specific for Ca++ and II and III bind both Ca++ and Mg++ and stablizing the troponin complex
2) Troponin I = inhibits interaction between actin and myosin [weaker than tropomyosin]
3) Troponin T = maintains the troponin complex by binding the other two

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11
Q

What enhances troponin I activity?

A

PKA phosphorylation –> inhibits cross-bridge cycling during diastole

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12
Q

PKA modulates EC coupling by phosphorylating 4 main target proteins? How?
How is PKA activated?

A

Ca++ channels, Ryr in SR, phospholamban (PLB), troponin

1) Ca++ channels = enhance open probability
2) Ryr in SR = stimulates Ca++ influx to increase Ryr channel activity which improves Ca++ release
3) Phospholamban(PLB) = normally represses activity of Ca++ ATPase pump and inhibits relaxation of Ca++ transient; once phosphorylated, repression removed.
4) Reduces affinity of troponin complex for Ca++ –> relaxation

PKA is activated by sympathetic stimulation by NE

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13
Q

The _____ of the sarcomere is the space where actin is absent

A

H zone

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14
Q

The sarcomere is the area between each ____ and poses a physical constraint on max myofibril shortening

A

Z line

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15
Q

The I band are thin, light areas that contain ______ and ______

A

Z lines, actin filaments

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16
Q

The ________ are opaque, dark areas consisting of ordered overlap between thick filaments, mainly ______

A

A bands, myosin

[also contain actin]

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17
Q

Describe what happens during sarcomere contraction

A

During contraction, actin and myosin filaments interact and actins are pulled toward center of each myosin myofilament.. The H zones disappear and the I band becomes very narrow.

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18
Q

Describe parasympathetic effect on heart rate and conduction velocity

A

Ach binds muscarinic receptors on the SA node, atria and AV node –>

  • decrease heart rate (via dec in rate of phase 4 depol via dec If)
  • decreased conduction velocity through AV node –> inc PR interval (dec inward ca++ current)
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19
Q

Describe sympathetic effect on heart rate and conduction velocity

A
  • Norepinephrine acts on beta receptors.
  • Increased HR by inc rate of phase 4 depol (inc If)
  • Inc conduction velocity through AV node, dec PR interval (inc inward Ca++ current)
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20
Q

True/False: In an EKG, the signal travels from positive to negative leads

A

FALSE - negative to positive

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21
Q

Describe the arrangement of bipolar lead I

A

Left arm + and right arm negative [0]

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22
Q

Describe the arrangement of bipolar lead II

A

left foot + and right arm - [60]

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23
Q

Describe the arrangement of bipolar lead III

A

left foot + left arm - [120]

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24
Q

Describe the arrangement of avF

A

left foot positive, right and left arms have indiff electrode [90]

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25
Q

Describe the arrangement of avL

A

left arm +, indiff electrode by right arm and left foot [330]

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26
Q

Describe the arrangement of avR

A

right arm +, indiff electrodes on left foot and eft arm [210]

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27
Q

Describe the location and attachments to fibrous skeleton of the heart

A
  • in the coronary sulcus
  • all muscles and ventricles sweep up in a circular or oblique fashion and attach to the fibrous skeleton
  • All valves of the heart are embedded in the same plane of fibrous skeleton
  • The fibrous skeleton provides for attachment of the cardiac muscle fibers of atria and ventricles and acts as an insulator
  • penetrated by AV bundle that is the only connecting link between atrial and ventricular muscle
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28
Q

Pain sensations from the heart are carried on _______ fibers whose cell bodies are found in the ______

A

sympathetic, dorsal root ganglia

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29
Q

The inferior vena cava is derived from the ______

A

right vitelline vein

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30
Q

The superior vena cava is derived from the _______

A

right anterior cardinal vein

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31
Q

The coronary sinus and oblique vein of the left atrium are derived from the ____

A

left sinus horn

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32
Q

The sinus venarum is derived from the _______

A

right sinus horn

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33
Q

What remains of the umbilical arteries in the adult human?

A

internal iliac arteries and medial umbilical ligaments

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34
Q

What remains of the umbilical vein?

A

ligamentum teres of liver

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35
Q

What remains of the ductus venosus?

A

ligamentum venosum

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36
Q

Describe cross-bridge cycling in smooth muscle

A

A rise in cytoplasmic Ca++ binds to Ca++ binding protein calmodulin and activates MLCK. MLCK phosphorylates MLC20 and facilitates actin binding and cross-bridge cycling.

Phosphorylation of MLC20 is balanced by MLCP.

MLCP dephosphorylates MLC20 –> reduces cross-bridging cycling –> muscle relaxation

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37
Q

Describe the hydrostatic and osmotic pressures along the skeletal muscle capillary

A

The capillary osmotic pressure stays constant.
The hydrostatic pressure is higher at the beginning of the capillary [pushing fluid out - net filtration] then becomes lower than osmotic pressure towards the end [bringing fluid back in - net reabsorption]

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38
Q

Describe the hydrostatic pressure and plasma oncotic pressure in the glomerular capillary. How does this compare to the tubular hydrostatic P?

A

The glomerular hydrostatic P is constant and stays high
The tubular hydrostatic P is constant and states low.
The plasma oncotic P falls in the middle and rises to a max that is below glomerular hydrostatic P.

As a consequence, high capillary filtration and low reabsorption.

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39
Q

What keeps glomerular capillary hydrostatic pressure high?

A

efferent arteriole

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40
Q

What are the three main systems that regulate systemic arterial pressure?

A

1) sympathetic nervous system
2) RAS
3) renal sodium handling

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41
Q

True/False: Pulmonary circulation has a considerable effect on systemic arterial pressure

A

FALSE FALSE FALSE

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42
Q

Describe norepinephrine’s effect on a) pulse pressure b) systolic blood pressure c) diastolic blood pressure d) mean arterial P e) heart rate

A

increases PP, DP, SP, MAP

dec HR

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43
Q

Describe isoproternol’s effect on a) pulse pressure b) systolic blood pressure c) diastolic blood pressure d) mean arterial pressure e) heart rate

A

dec DP, MAP
inc HR, PP
mixed effect on systolic bp

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44
Q

True/False: Blood flow to the coronary vessels increases during exercise

A

true

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45
Q

What is the difference between noreepinephrine and epinephrine at high doses? at low doses?

A

at high doses, epinephrine increases PP more and increases HR
at low doses, epi decreases diastolic P

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46
Q

What are dopamines effects on a) renal blood flow, b) cardiac output, c) TPR, MAP

A

a) at low doses, inc renal blood flow via D1
b) at medium doses, increases cardiac output via B
c) at high doses, increases TPR and MAP via alpha

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47
Q

True/False: Resistance vessels are regulated by parasympathetic innervation

A

FALSE - receive very little parasympathetic innervation

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48
Q

At rest, what two organs receive greater portions of cardiac output than heart?

A

liver and skeletal muscle

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49
Q

Autoregulation is well developed in renal, coronary and cerebral systems. In what system is it not well developed?

A

The skin

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50
Q

How can NSAIDs lead to renal failure?

A

Normally, if there is a real or perceived decrease in extracellular fluid volume entering the kidney then there is an increase in angiotensin II and sympathetic activity.
There is a balance between contraction of renal arterioles and dilation of arterioles [via release of prostaglandins] to optimize RBF. When NSAIDS block release of prostaglandins - arteriole dilation inhibited so renal blood flow sinks and ta-da renal failure

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51
Q

What are the three factors that regulate renin release?

A

decrease in stretch of afferent arteriole
decrease in macula densa NaCl activity
increase in sympathetic nerve activity

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52
Q

Describe autoregulation of renal blood flow

A

a) myogenic mechanism= renal afferent arterioles contract in response to stretch - increased renal arterial pressure stretches the arterioles which contract and increase resistance to maintain constant blood flow
b) tuberoglomerular feedback = increased renal arterial pressure –> inc delivery of fluid to macula densa –> constriction of nearby afferent arteriole –> inc R to maintain constant blood flow

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53
Q

Describe tuberoglomerular feedback in detail.

A

A decrease in arterial P leads to a decrease in glomerular hydrostatic pressure and dec in GFR.

Ascending limb reabsorbs more NaCl due to decreased flow.

When flow reaches macula densa in distal tubule, sense decrease in NaCl.

Macula densa cells have a Na/K/Cl ATPase that produces a certain amount of adenosine at normal [NaCl] levels. This adenosine stimulates receptors on mesangial cells which leads to contraction of the afferent arteriole.

In low [NaCl], not much adenosine being made, so decreased contraction of afferent arterioles.

There is an increase in renin release which leads to increase efferent arteriole contraction [R]

Therefore, system adjusts itself to increase GFR

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54
Q

Describe the change in ICF/ECF in response to careless admin of saline.

A

Overhydration.
Isotonic
There is no change in osmolarity that would allow H2O to flow in and out of cells. ECF increases with no change in ICF.

Overall, expansion of ECF only

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55
Q

Describe the change in ICF/ECF in response to compulsive water drinking

A

Hypotonic [have to drink mass quant]

Dec in estracell osm –> expands ECF –> higher intracellular particle concn –> water goes into cells –> expands ICF. Cells swell.

Overall, expansion of both ICF and ECF

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56
Q

Describe the change in ECF/ICF in response to drinking sea water.

A

Hypertonic

Inc in extracell osmolarity –> extra particles will draw H2O out of cell –> cells and ICF shrink –> ECF expands –> leads to xs thirst and dry tongue

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57
Q

Describe the change in ECF/ICF in response to hemorrhage.

A

Isotonic

Contracts ECF compartment

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58
Q

Describe the change in ECF/ICF in response to adrenocortical insufficiency [Addison’s dz]

A

Hypotonic.

Aldosterone normally stimulates Na+/K+ pump. When absent, Na+ enters urine –> saline diuresis. Salt loss in xs of H2O.

Therefore, osm in ECF decreases –> causes intracell osm to increase –> water enters cells –> ICF expands.

Overall, ECF contracts and ICF expands.

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59
Q

Describe the change in ECF/ICF with diabetes insipidus.

A

With diabetes insipidus, dec in ADH, therefore lose water.
Increases extracellular osmolarity so water shifts out of cells BUT you’re continually losing water because you don’t have ADH so hahaha doesnt matter

ECF and ICF decrease.

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60
Q

What is the primary place for water reabsorption in the kidney?

A

papillary/medullary collecting duct

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61
Q

Blood vessels control their diameter via smooth muscle except for in what instance?

A

capillaries - single layer of endothelial cells

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62
Q

Why do AV valves close during filling of atria?

A

lack of P gradient

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63
Q

Pressure in what part of the cardiovascular system directly measures blood pressure?

A

aorta

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64
Q

Describe the normal delays in conduction of electrical impulse in the heart.

A

AV node delays activation of ventricles by 120ms.

Bundle of his has a 30-120ms delay in receiving signal from AV node.

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65
Q

What happens in the case of LBBB as far as conduction of electrical impulse?

A

Right ventricle has to excite left so pattern of excitation shifted to the right [signal normally transmitted to bundle of his down to purkinje fibers]

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66
Q

List in order from highest to lowest for impulse generation:

AV node, purkinje, SA node, His bundle branch

A

SA node, AV node, His bundle branches, Purkinje Fibers

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67
Q

Why does tetanus not occur in cardiac muscle cells?

A

effective refractory period is too long

[even if it wasn’t - cells would die because wouldn’t refill enough]

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68
Q

True/False: SA and AV node cells generate an upstroke that is slower than atrial, purkinje and ventricular cells

A

TRUE

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69
Q

Conductance of what ion determines RMP?

A

K+

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70
Q

The resting membrane potential of ventricular, atrial and purkinje cells is -80 to -90. Why is this slightly more positive than the K+ equilibrium potential if K+ matters so damn much?

A

Na+ permeability

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71
Q

Describe the action potential in ventricular, atrial and purkinje cells

A

Phase 0 = upstroke, increase in Na+ conductance, increase in Na+ inflow, depolarization
Phase 1 = brief repol due to K+ out [Ito channels active at 30mV]
Phase 2 = plateau caused by in Ca++ conductance and K+ conductance [via delayed rectifier, 20mV] canceling each other out
Phase 3 = repolarization due to dec Ca++ conductance and inc K+ conductance [dominates]. Lrg outward K+ current [Ik1 - neg 20mV]
Phase 4 = RMP. Stable MP due to perm across IK1 channels.

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72
Q

The duration and potential of which phase of action potential in ventricular, atrial and purkinje cells determines amount of force by muscle?

A

Phase 2

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73
Q

Describe action potential in the SA node.

A

Phase 0= inc Ca++ conductance
Phase 3=repolarization. Phases 1+2 skipped bc of activation of Ica w/ progressive activn of Ik leads to rapidly repol.
Phase 4=diastolic depol. Ik declines and If increases until threshold potential hit.

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74
Q

How does Na+ play a role in SA node action potential?

A

In phase 4, Ifunny channels allow increase in Na+ conductance. They are turned on by hyperpolarization to -40mV of membrane during axn potential.

Na+ DOES NOT PLAY A ROLE IN PHASE 0.

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75
Q

The _____ is the most negative membrane potential during diastole

A

maximum diastolic potential, -55 to -60mV

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76
Q

The conduction velocity is inversely proportional to __________. KNOW DIS.

Also, where is conduction velocity quickest and slowest?

A

resting membrane potential

Quickest in purkinje, slowest in AV node.

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77
Q

Describe the absolute, effective, and relative refractory periods of cardiac action potential.

A

ARP begins with upstroke and ends after plateau.
ERP lasts a bit longer than ARP.
RRP begins immediately after ARP.

78
Q

What three changes alter pacemaker activity?

A

change of phase 4 slope
change in threshold potential
change in max diastolic potential

79
Q

How is SA node activity altered in vagal response?

A

dec in max diastolic potential
dec in phase 4 slope
lead to slowed pacemaker

[via Ach channels activating K+ channels –> hyperpol]

80
Q

How are atria and ventricles affected by vagal response?

A

Axn potential duration in atria dec

In ventricles, antagonization of beta adrenergic stimulation

81
Q

How is AV node altered in vagal response?

A

decreased excitability which leads to decreased transmission through ventricles –> ventricular escape

82
Q

How does sympathetic stimulation alter SA node activity?

AV node?

A

SA node - inc pacemaker firing, inc slope of phase 0, inc If, Ic and Ik

Av node - increase conduction velocity

83
Q

How does hyperkalemia affect

a) ventricular, atrial and purkinje fibers
b) SA node

A

a) dec action potential amplitude, inc conduction velocity, increased repol in phase 3
b) dec automacity

84
Q

How does hypokalemia affect

a) ventricular, atrial and purkinje
b) SA node

A

a) increase in action potential duration

b) inc automacity

85
Q

Describe what each wave in the QRS corresponds to.

A

Q wave = depol of septum
R wave = activation of most ventricular mass
S wave = depol of base

86
Q

The QT interval signifies

A

depol of ventricles

87
Q

True/False: The heart can be viewed as a dipole with asymmetric distribution of electrical changes within a volume conductor

A

True

88
Q

Which leads are considered “bipolar”?

Fun fact - the advantages of unipolar is that you can determine the direction of propagation and conduction velocity.

A

I, II, and III

the rest are unipolar

89
Q

_____ are useful for obtaining patterns of ventricular activation in transverse or horizontal plate

A

precordial leads

90
Q

Name 4 arrhythmias of junctional origin

A

AV block, PJC’s, junctional escape rhythm, junctional tachy

91
Q

What can axis deviations be a sign of?

A

hypertrophy

RAD - obstructive lung dz, pulm HTN
LAD - phys or patho due to inc afterload

92
Q

What leads constitute the frontal and horizontal planes on EKG?

A

frontal - I-III and the a’s

transverse - v1-v6

93
Q

______ are common in myocardial infarction, anesthesia, digitalis admin

A

arrhythmias

94
Q

Describe early after depolarizations

A

delayed repolarizations that favor re-opening of Ca++ channels

Long QT –> Torsades de pointes

Can be caused by long axn potential, dec in K+/Na/Ca channels

95
Q

Describe delayed after depolarizations

A

abnormal Ca++ release event includes transient membrane depolarization AFTER final phase of repolarization

Can be caused by cardiac glycosides, inc HR, caffeine

96
Q

Re-entry arrhythmias require what three things?

A

1) long reentrant pathway
2) slow conduction
3) short ERP

97
Q

Circus movement re-entry arrhythmias can be caused by an anatomical or non-anatomical block. What are the three types?

A

leading circle, figure 8, spiral wave

98
Q

The size of the action potential determines the size of the Ca++ transient. What two things enhance the Ca++ transient?

A

action potential duration increase, plateau level increase

99
Q

Describe ryanodine receptors (Ryr) and their role in Ca++ induced Ca++ release

A

Ryr are Ca++ channels in t-tubules that are juxtaposed with Ca++ channels in dyad regions.

Ryr are activated when Ca++ enters the cell through t-tubule Ca++ channel. They open and Ca++ enters cytoplasm down concn gradient.

100
Q

Describe relaxation of Ca++ transient.

A

Ca++ ATPASE IS A BIG DEAL KNOW THIS.
Drives Ca++ into the SR.

3Na+/Ca++ exchanger in sarcolemma and t-tubules pumps Ca++ out. MAJOR MECHSM FOR BALANCE OF Ca++ ENTRY. KNOW THIS TOO.

101
Q

Describe actin-myosin cross-bridge cycling

A
  • Myosin head is activated via ATP binding hydrolyzation to ADP and Pi.
  • Activated head binds actin and then Pi released which strengthens bond
  • Actin completes a power stroke and ADP dissociates and myosin head pivets, thin myofilaments slide towards center [this can form rigor complex]
  • Another ATP binds myosin head –> myosin head detaches from actin
  • ATP hydrolyzed which reactivates myosin head
102
Q

Describe how sarcomere length and tension contribute to force of the muscle contraction

A

If there is a large sarcomere length, there is no overlap between actin and myosin, so shortening is impossible
At short lengths, there is almost a complete overlap, shortening and force development are maximal.

[Once filaments overlap, tension fails]

103
Q

How does heart failure lead to increased wall stress?

A

There is enlargement of the ventricular chamber (inc radius) and thinning of the ventricular wall (dec thickness)

Wall stress = PxR / wall thickness

Therefore increased stress

104
Q

Describe the difference between isotonic and isometric contraction and their normal order in the heart cycle.

What happens if a load is removed near end of isotonic contraction?

A

Isotonic - tension changes, length unchanged
Isometric - tension unchanged, length changes

Isometric contraction –> isotonic contraction –> isotonic relaxation –> isometric relaxation

If load removed - isometric relaxation occurs before isotonic

105
Q

What is the pre-load?

A

Pressure/Volume that heart begins ventricular contraction with [EDV/P]

106
Q

What is the after-load?

A

Pressure/Volume at which aortic valve opens. Reflects force against which heart fights to pump blood into circulation.

107
Q

What is the end systolic P/V

A

pressure/volume when aortic valve closes - good index of contractility

108
Q

What does the diastolic P/V tell you

A

defines properties of relaxed heart and forces from circulation that fill heart

109
Q

What is pulse pressure equal to on the pressure-volume loop?

A

The afterload pressure [pressure when aortic valve opens] - the peak of the loop during systole

110
Q

How can the ejection fraction be calculated from the pressure volume loop?

A

SV/peak

[SV is the max volume - min volume on PV loop]

111
Q

What happens to the compliance of the heart at very high ejection volumes?

A

Compliance dec

Heart becomes more stiff affecting its performance

112
Q

Describe the atrial kick

A

Atrial contraction that occurs right before ventricular systole to inc preload and increase efficient of ventricular ejection

113
Q

_______ is ejecting blood into circulation under pressure

A

stroke work

114
Q

______ is accelerating blood from ventricles to aorta or pulmonary artery

A

kinetic work

115
Q

______ is stretching and deformation of visceroelastic matrix and muscle bundles during contraction

A

internal work

dissipated as heat which dec mechanical performance
and inc wall tension
this worsens if afterload increases

116
Q

What are the effects of increased preload on:

end systolic volume, stroke volume, peak systolic P, ejection fraction, cardiac output

A

increases all

117
Q

What are the effects of increased afterload on:

end systolic volume, stroke volume, peak systolic P, ejection fraction, cardiac output

A
  • increases end systolic volume
  • decreases stroke volume and cardiac output
  • increases peak systolic P
  • decreases ejection fraction
118
Q

What are the effects of increased contractility on:

end systolic volume, stroke volume, peak systolic P, ejection fraction, cardiac output

A
  • increases all except end systolic volume [more efficient pumping]
119
Q

What are the affects of sympathetic stimulation and cardiac hypertrophy on cardiac output?

A

increases

120
Q

How does intrapleural pressure effect heart function and venous return?

A

Determines pressure in right atrium and thus P gradient between venous system and heart which impacts venous return

121
Q

How does inspiration increase cardiac output?

A

Upon inspiration, chest wall expands. This decreases intrapleural Pressure which increases abdominal pressure.
This creates a pressure gradient within inferior vena cava that pulls blood into the heart, increasing right atrial P and venous return

122
Q

Would increasing or decreasing the resistance to venous return increase cardiac output?

A

Decreasing resistance

[2/3 total RVR comes from large arteries]

123
Q

How do increases and decreases in contractility impact cardiac output and venous return?

A

Go in same direction.

An increase in contractility increases cardiac output and venous return bc large ejection volumes tend to decrease left atrial P and thus inc pressure gradient for venous return.

A dec in contractility means poor emptying so blood accumulates on venous side and there is reduced venous return.

124
Q

How does exercise impact cardiac output?

A

increases because of inc in HR [CO=SVXHR]

125
Q

If cardiac output is proportional to heart rate, which does it decline with very high rates?

A

Incomplete diastolic phase which leads to dec SV

126
Q

Describe the Frank-Starling Law of the Heart

A

The Frank–Starling law of the heart states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant. In other words, as a larger volume of blood flows into the ventricle, the blood will stretch the walls of the heart, causing a greater expansion during diastole, which in turn increases the force of the contraction and thus the quantity of blood that is pumped into the aorta during systole.

127
Q

Describe the layers that filtrate travels through from the glomerulus to the bowman’s capsule

A

First goes through fenestrated endothelial layer outside glomerulus, which allows AAs and glucose to leak through.
Then enters basement membrane which stops large molecules.
Then enters epithelial cell layer [tubule cell layer] which contains tight junctions whose expression pattern determines the ability of particles to move paracellularly

Finally enter bowman’s capsule afterward.

128
Q

True/False: Most nephrons are cortical

A

true 85% cortical, 15% juxtamedullary

129
Q

True/False: The nephron includes the collecting tubules

A

FALSE, everything but

130
Q

How does ADH increase water reabsorption?

A

Normally, only proximal convoluted tubule to ascending loop of henle perm to water

There are AQP2 channels in the collecting duct that are modulated by ADH - water reabsorbed in presence of ADH

[w/o ADH water perm is very low in late nephron and 0 in inner medulla]

131
Q

Describe the function of the vasa recta in relation to the loop of Henle

A

Loop of Henle reabsorbs water on descending loop of henle and reabsorbs NaCl and urea on ascending loop

Vasa recta follows loop and does the opposite

132
Q

What does decrease in [NaCl] entering macula densa cells of the distal convoluted tubule lead to overall in terms of arteriole R?

A

Increase in resistance of efferent arteriole [DUE TO RAS]
Decrease in resistance in afferent arteriole [due to dec contraction due to dec adenosine production due to dec Na/K activity at MD]

133
Q

True/False: In renal circulation, the pressure in the afferent arteriole is much higher than efferent

A

true

134
Q

What is filtration fraction equal to?

A

FF=GFR/renal plasma flow

135
Q

Under basal conditions, sympathetic nervous system doesn’t do much. When does it play a role in modifying renal blood flow?

A

during hemorrhage - there is constriction of blood vessels and JMA is innervated and can affect renin release

136
Q

Describe the two main outcomes of ATII release

A

inc na+ retention, inc water retention

137
Q

Describe the impact of ATII on the following:

a) adrenal gland
b) sympathetic nerves
c) brain
d) proximal tubule
e) aterioles

A

a) adrenal gland releases aldosterone, NE, and epi which inc Na+ retention
b) sympathetic nerves release Ne
c) brain inc thirst and inc ADH –> water retention
d) proximal tubule inc Na+ and H2O reabsorption
e) arterioles contract

138
Q

How can ACE inhibitors lead to acute renal failure in a patient whose GFR is compromised?

A

If the pressure in the afferent arteriole is dec [ie renal artery stenosis], the body increases renin release which produces Ang II and aldosterone.
AT II increases resistance in the efferent arteriole which increases glomerular pressure and thus GFR.

If ACE inhibitor taken, renin pathway does not occur. There is a dec in GFR that leads to acute renal failure.

139
Q

True/False: O2 consumption and GFR are proportional

A

true

If filtering more Na+ need more O2 because Na/K pump uses O2

140
Q

______ blocks Na/K pump and decreases O2 consumption of the kidneys

A

Ouabain

141
Q

The starling equation can be used to determine _________

A

GFR

142
Q

What happens to pressure in the tubules in urinary tract obstruction and accordingly to net filtration?

A

Pt increases so net filtration going to dec [not as much pull of water into tubules]

143
Q

What happens to net filtration in hypoalbuminemia?

A

Dec oncotic pressure in capillaries so increased net filtration

144
Q

What happens to net filtration in diabetic nephropathy?

A

There is increased permeability of albumin into the glomerulus –> proteinuria and inc GFR

[until nephrons die]

145
Q

What happens to a) hydrostatic P, b) GFR, c) oncotic P

A

hydrostatic P dec
GFR inc
oncotic P inc

146
Q

Why is inulin clearance used to determine GFR?

A

it is freely filtered
NOT reabsorbed
NOT secreted

147
Q

True/False: Plasma creatinine is used to plasma creatinine concentration.

A

True

overestimates bc secretion but pcr overstimated bc of lab chem so cancel each other out

148
Q

In what part of the proximal convoluted tubule is urea passively reabsorbed?

A

urea

149
Q

Describe the location of the

a) Na+/H+ antiporter
b) Na+/Cl- symporter
c) Na/K/Cl symporter
d) Na+ conductance

What substances/drugs target these areas?

A

a) Na+/H+ antiporter found in the proximal convoluted tububle
b) Na+/Cl- sym in the distal convoluted tubule. blocked by thiazide.
c) Na/K/Cl sym in the thick ascending limb - blocked by loop diuretics
d) Na+ conductance - in cortical collecting duct - blocked by amilorid.
- Enhanced by aldosterone

150
Q

67% of sodium reabsorption occurs in what part of the nephron?
How much occurs in the cortical collecting duct?

A

PCT

3% occurs in aldosterone sensitive zone of cortical collecting duct

151
Q

How and where is Cl- reabsorbed from the kidney?

A

Cl- either needs an antiporter or paracellular mechsm via following-
As H2o leaves during Na+ reabs, Cl- gets more concentrated and lumen becomes more negative. Compels Cl- to get back paracellularly into peritubular space.

There is no Cl- movement in the collecting duct

152
Q

What triggers urea reabsorption in the kidney?

A

Na+ reabs –> H2o reabs –> inc in luminal concentration which leads to passive reabs

153
Q

___% of total body K+ is intracellular

A

98

154
Q

Which of the following DOES NOT increase K+ excretion?

a) insulin
b) metabolic alkalosis
c) beta-agonists
d) beta-antagonists
e) aldosterone

A

D

155
Q

Which of the following DOES NOT cause K+ shift out of the cell?

a) hyperosmolarity
b) hypoosmolarity
c) exercise
d) cell lysis
e) acidosis

A

b

156
Q

_____% is normal fractional excretion of K+

A

10-20

157
Q

What two mechanisms cause aldosterone secretion from adrenal gland?

A

angiotensin II production

increase in extracell K+ [directly stimulates adrenal gland]

158
Q

Describe the mechanism of Amiloride

A

Amiloride mades collecting duct membrane more negative [blocks Na+ conductance]. Since membrane hyperpolarized, K+ doesn’t want to leave tubule cell and therefore doesn’t enter the tubular lumen. Spares K+.

159
Q

Describe which pumps are affected in Bartter’s syndrome and Gittelman’s syndrome

A

a) Bartter’s syndrome - Na/K/Cl in thick ascending loop

b) Gittelman’s- NaCl in dct

160
Q

Why does Liddle’s syndrome (pseudohyperaldosteronemia) cause HTN?

A

too much aldosterone stimulating Na/K –> too much Na reabs –> too much fluid

161
Q

Which sodium glucose linked transporters are responsible for glucose transport

A

SGLT2 (90%) and SGLT1 (10%)

162
Q

True/False: Glucose is secreted into the nephron

A

FALSE ONLY ENTERS VIA GLOMERULUS

163
Q

The _____ is the plasma concentration at which transporters are working at max

A

splay point

164
Q

When can glucose be used to estimate GFR?

A

When Na+ reabsorprtion is blocked - such as by phlorzin

165
Q

What can you infer from a substance that has

a) greater clearance than inulin
b) lesser clearance than inulin

A

Inulin clearance = GFR

a) if greater clearance, then secreted
b) if lesser clearance, then reabsorbed

166
Q

True/False: PAH is only filtered into the nephron

A

FALSE it is also secreted into the PCT

167
Q

What is PAH clearance used to estimate in the kidney?

A

RBF

168
Q

_______ prevents uric acid reabsorption in the kidney and therefore is used to treat gout

A

Probenecid

169
Q

Unlike inulin, the clearance of urea is dependent on ______

A

tubular flow; inc with inc flow

170
Q

Describe why an overdose in a weak acid like phenobarbital would get treated by a base (such as bicarb)

A

Bicarb would take the H+ from the weak acid and leave it in its charged form.
Charged Pb- will be trapped in lumen and excreted.

171
Q

True/False: The fractional excretion of creatinine is over 100% and PAH is about 500%

A

SI TRUE TRUE TRUE

172
Q

What drives water reabsorption in descending limb?

A

All of the Na+, Cl- and K+ reabsorbed by the ascending limb that leaves the medulla salty

173
Q

Where do H2O and urea reabsorption happen in the collecting duct?

A

H2O in cortex

urea deep in medulla [kidneys hold on to inc osm in medulla and drive h2o reab in loop of henle]

174
Q

Plasma flow exiting from glomerular capillaries is approximately ___% less than that entering glomerular capillaries

A

20, bc 20% filtered

175
Q

True/False: ADH inc both H2O and urea permeability in cortical and outer medullary collecting ducts

A

FALSE

increase both in innermedullary ducts

176
Q

Why is urea clearance over 100%?

A

because it can return to LOH from the vasa recta

then distal tubule impermeable so it gets stuck

177
Q

Paraventricular and supraoptic neurons of the hypothalamus produce _____ which bind to V2 receptors

A

ADH

178
Q

Does mannitol cause diuresis or anti-diuresis and how

A

causes osmotic diuresis because gets stuck in tubule and holds water in

179
Q 
What happens to
a) urine volume
b) urine osmolarity
c) urine urea
d) clearance of urea
in high ADH states
A

antidiuresis

a) dec volume
b) inc osmol
c) inc urea concn [less liquid[
d) dec clearance of urea [pours into interstitial fluid due to adh]

180
Q

The osmotic gradient in the medullary/papillary duct is essential for excretion of a ______ urine

A

hypotonic

181
Q

______ is the predominant electrolyte found in urine

A

urea

182
Q

What is needed to determine H2o content in ECF?

A

need IV tracer

183
Q

In men, ____ of water content in ICF and ____ in ECF

A

2/3, 1/3

184
Q

T/F= Furosemide diminishes free water clearance

A

False

185
Q

Glomerotubular balance (GTB) stabilizes _____ while tubuloglomerular feedback stabilizes ____

A

sodium reabsorption, GFR

186
Q

What are the two primary regulators of aldosterone?

A

angiotension II and increased plasma K

187
Q

Aldosterone leads to increased H+ _______ in medullary collecting duct

A

secretion

188
Q

ANP acts via membrane receptors coupled to GC to DECREASE Na+ reabs in ________ and increases GFR at glomerulus [acts like NO]

A

medullary/papillary collecting duct

ANP IS ANTI ALDOSTERONE

189
Q

ADH, Aldosterone, ATII affecrts Na+ and H2o reabsorption in what parts of the kidney?

A

ADH affects all collecting duct and late distal tubule[ h2o reabs]
Aldosterone affects latter part of distal tubule and cortical collecting duct [inc Na reabs]
ATII contracts efferent arteriole and enhances Na+ reabs in proximal tubule
ANP diminishes Na+ reabs in latter collecting duct and enhances GFR

190
Q

Why do pt’s with heart failure develop edema?

A

Increased volume is predominantly on venous side
Body sensing mechanisms on arterial side
Body thinks volume depleted
Baroreceptors save Na+ which inc plasma osm and inc ADH –> edema

191
Q

How do sodium consumption and excretion remain in balance with progressive nephron loss?

A

inc fractional excretion

192
Q

How does Creatinine maintain a balance in renal failure?

A

if only 1/10 nephrons, then creatinine builds up from 1 to 10 –> 1/10 of GFR has 10X creatinine and an equal filtered load is found

B2 (15 decks)

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