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502 Cards in this Set
- Front
- Back
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Myocardial action potential During phase 0 of the myocardial action potential, -------- ------- ------ channels open.
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voltage-gated Na+
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Initial repolarization, or phase 1, is when voltage-gated ---- channels begin to open and when voltage-gated Na+ channels ---- (close OR inactivate?).
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K+ begin to open. Na+ channels inactivate.
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Phase 2 is the plateau, when ------- influx balances ------ efflux.
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Ca++ influx balances K+ efflux.
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Ca++ influx triggers another Ca++ release from the ------- --------, which leads to myocyte ------.
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sarcoplasmic reticulum. contraction
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During what phase do the voltage-gated Ca++ channels close?
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phase 3
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During phase 3, the rapid repolarization phase, there is massive -------- efflux.
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K+
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During resting potential, the myocyte membrane is highly permeable to what ion?
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K+
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Where does the pacemaker action potential normally occur?
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SA and AV nodes.
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The phase 0 stroke of the pacemaker AP differs from that of the ventricular AP in that the pacemaker cells lack fast ------ ------- ------- channels.
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voltage-gated Na+
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By using Ca++ current for phase 0 upstroke, the conduction velocity is slowed compared to the fast Na+ upstroke of the ventricular AP. What purpose does this slowed conduction serve?
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The AV node then prolongs trasmission from the atria to ventricles, allowing for sufficient filling time.
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Which phase of the ventricular AP is absent in the pacemaker AP?
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phase 2, during which there is Ca++ influx in the ventricular AP.
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What ion is responsible for the slow depolarization current in the pacemaker AP? This current accounts for the automaticity of the SA and AV nodes.
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Na+ (this is the If, or the funny current)
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ACh and catecholemines alter the slope of phase 4, which determines the ------- ------.
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heart rate
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Phase 4 depolarization occurs during which phase of the cardiac cycle?
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diastole
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During exercise, cardiac output (CO) INITIALLY increases as a result of an increase in -----.
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Stroke volume
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After prolonged exercise, CO increases as a result of an increase in ------.
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heart rate
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the product of ----- and ----- equals cardiac output.
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stroke volume X heart rate
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Fick principle for cardiac output :
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CO = (rate of O2 consumption) / (arterial O2 content-venous O2 content)
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Formula for mean arterial pressure
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CO X TPR
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What is pulse pressure?
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systolic - diastolic
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Pulse pressure correlates to what other measure?
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stroke volume
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What three entities affect stroke volume? (Mnemonic: SV CAP)
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contractility, afterload, preload
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If afterload is decreased, what happens to stroke volume?
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increased
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What happens to stroke volume in pregnancy?
Name two other conditions that cause a similar change in SV? |
increases
Anxiety and Exercise |
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What does hypoxia/hypercapnea do to contractility?
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decreases
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What does a decrease in extracellular Na+ do to contractility?
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increases
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Digitalis increases intracellular ---- ion.
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Na+, with a resultant increase in IC Ca++
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What does acidosis do to contractility?
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decreases
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Ventricular end diastolic volume is -----.
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preload
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What is afterload?
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diastolic arterial pressure (proportional to peripheral resistance)
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What class of drugs decreases preload?
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venous dilators (nitroglycerine)
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Drugs like hydralazine decrease ------.
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afterload (they are vasodilators)
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Force of contraction is proportional to -------.
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initial length of cardiac muscle fiber (preload)
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Sympathetic stimulation will shift the curve on a graph of CO vs. preload up and toward the ---- (right / left).
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left.
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Ejection fraction is stroke volume divided by -----.
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end diastolic volume
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EF is an index of ventricular -------.
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contractility
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What is normal EF?
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greater than 55%
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Viscosity of blood depends mostly on ------
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hematocrit
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name three conditions in which viscosity increases.
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(1) polycythemia
(2) hyperproteinemic state (e.g. multiple myeloma) (3) hereditary spherocytosis |
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Resistance is proportional to viscosisty and inversely proportional to ---------.
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radius to fourth power.
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Decreasing the volume of blood shifts the venous pressure curve to the ------. (on a graph of venous return vs. RA pressure)
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left
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On a graph of CO vs. EDV, digitalis (positive inotrope) will shift the curve ------.
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up.
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Isovolumetric contraction is the period between ---- valve closure and ----- valve opening.
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between mitral v. closure / aortic v. opening
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During which period is O2 consumption by the heart the highest?
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isovolumetric contraction
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For each heart sound, give the significance:
S1 |
mitral and tricuspid valve closure
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S2
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aortic and pulmonic valve closure
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S3
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at end of rapid ventricular filling
sound is normal in children but indicates disease in adults |
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S4
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high atrial pressure/ stiff ventricle
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For each situation, give the corresponding heart sound.
high atrial pressure/ stiff ventricle |
S4
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aortic and pulmonic valve closure
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S2
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mitral and tricuspid valve closure
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S1
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at end of rapid ventricular filling
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S3
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Dilated CHF is associated with which extra heart sound?
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S3
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S4 is associated with what condition?
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hypertrophic ventricle
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For each wave of the jugular venous pulse, give the corresponding physiologic event.
a wave and elevated (Canon) a wave indicates what |
atrial contraction
AV dissociation |
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c wave
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RV contraction; tricuspid valve bulging into atrium and the beginning of each systole
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x descent and v wave
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relaxation of the right atrium
volume of blood that enters the right atrium during Ventricular systole/increase in atrial pressure due to filling against closed tricuspid valve. |
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What is the function of the T tubule?
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allows depolarization to travel down it, leading to muscle contraction
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This band in a skeltal muscle contains MYOSIN filaments (thick filaments)
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H band/zone
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This band in a skeltal muscle contains only ACTIN filaments (thin filaments)
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I band
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Which band in a muscle remains the same size?
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A band (dark bands)
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During muscle contraction, which bands shrink?
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H, I, and Z bands
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What is the function of the ryanodine receptor?
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voltage-sensing CA+2 channel protein in the sacroplasmic reticulum
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What is the function of the dihydropyridine receptor?
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voltage-sensing CA+2 channel protein in the T-tubule
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Where does the calcium come from that stimulates cardiac muscle contraction?
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extracellular calcium enters the cell during the plateau of the action potential and stimulates release of calcium from the sarcoplasmic reticulum (calcium-induced calcium release)
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Name three ways that cardiac muscle differs from skelatal muscle with regards to its electrophysiolopgy.
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1. action potential has a plateau which is due to Ca++ influx.
2. Cardiac nodal cells spontaneously depolarize, resulting in automaticity. 3. Cardiac myocytes are electrically coupled to each other by gap junctions. |
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How does the action potential in smooth muscle lead to contraction?
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The smooth muscle membrane depolarizes, voltage-gated calcium channels open, calcium rushes into the cell, calcium binds to calmodulin, calcium calmodulin complex activates myosin light chain kinase, MLCK phosphorylates myosin light chain which crosslinks with actin and causes contraction.
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How is myosin light chain phosphatase involved in relaxation.
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It dephosphorylates myosin light chain, making it less able to cross-bridge with actin--allowing relaxation
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Muscle contraction is a result of cross-linking between which two proteins?
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actin and myosin
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____binds to myosin head during a skeletal muscle contraction
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ATP
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Electrocardiogram Identify the significance of each of the following: P wave
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atrial depolarization
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PR segment
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conduction delay through AV node
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QRS complex
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ventricular depolarization
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QT interval
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mechanical contraction of ventricles
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T wave
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ventricular repolarization
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ST segment
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isoelectric, ventricles depolarized
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U wave
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caused by hypocalemia
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What is masked by the QRS complex?
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atrial repolarization
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Where is the pacemaker of the heart?
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SA node in right atrium
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Match the ECG finding with the description of the ECG trace:
1. Progressive lengthening of the PR interval until a beat is "dropped" (a pwave not followed by a QRS complex). Usually asymptomatic. |
B. 2nd degree AV block, (Mobitz type I) (wenckebach)
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2. A rapid succession of identical, back-to-back atrial depolarziation waves. "sawtooth appearance"
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G. Atrial flutter
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3. Dropped beats that are not preceded by a change in the length of the PR interval . These abrupt, nonconducted P waves result in a pathologic condition.
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C. Mobitz Type II
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3. PR interval is prolonged (>200 msec). Asymptomatic
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A. AV block 1st degree
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4. Chaotic and erratic baseline with no discrete p waves in between irregularly spaced QRS complexes
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F. Atrial Fibrillation
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5. The atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate.
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D. 3rd Degree, complete AV block
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6. A completely erratic rhythm with no identifiable waves.
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E. Ventricular Fibrillation
a fatal arrythmia witho immediate defibrillation |
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Name five compensatory mechanisms that are activated when baroreceptors detect low MAP
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1. Heart rate increases (beta1)
2. contractility increases (beta1) 3. venous tone--venous return increases (alpha) 5. TPR increases (alpha) 4. kidneys retain sodium and H20 (renin-angiotensin-aldosterone system) |
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Aortic Arch baroreceptor transmits via what nerve to the medulla?
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vagus (X)
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Carotid Sinus baroreceptor transmits via what nerve to the medulla?
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glossopharyngeal (IX)
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Decreasing the stretch on the baroreceptors leads to: (increased/decreased) efferent sympathetic stimulation
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Increased. Decreased stretch as a result of decreased MAP decreases the afferent signal from the baroreceptor which leads to an increase in the efferent sympathetic signal from the brain
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Hypotension leads to vaso____(constriction/dilation)
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vasoconstriction
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What is the effect of a carotid massage?
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It increases the pressure in the carotid artery, increases the stretch of the baroreceptors, and leads to a decrease in heart rate.
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Which receptor transmits to the medulla, responding only to increase blood pressure
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Aortic arch
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Name three physiological changes that are sensed by peripheral chemoreceptors (carotid and aortic bodies).
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1. decreased pO2 below 60 mmHg;
2. increased pCO2; 3. decreased pH of blood |
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Central chemoreceptors (in brain) respond to ____ and ____ but do not directly respond to _____.
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Respond directly to changes in pH and pCO2, but not pO2
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Which organ has the largest share of systemic cardiac output?
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Liver
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Which organ has the highest blood flow per gram of tissue?
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Kidney
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Which organ has a large arteriovenous O2 difference
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Heart
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Match the normal pressures with a heart chamber or major vessel: A. Right atrium/vena cava, B. Right Ventricle, C. Pulmonary Artery, D. Left Atrium, E. Left Ventricle, F. aorta <150/10
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E. LV
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<25/10
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C. PA
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<25/<5
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B. RV
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<5
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A. RA
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<130/90
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F. aorta
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<12
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D. LA
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What does the PWCP approximate?
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Pulmonary capillary wedge pressure approximates left atrial pressure.
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How is PWCP measured?
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Swan-Ganz catheter
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What factors regulate blood flow to the following tissues? Heart
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local metabolites: O2, adenosine, NO
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Brain
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local metabolites: CO2; H+(pH)
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Kidneys
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myogenic and tubuloglomerular feedback
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Lungs
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hypoxia causes vasoconstriction (only organ in which hypoxia leads to vasoconstriction)
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Skeletal muscle
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local metabolites: lactate, adenosine, K+
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Skin
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sympathetic stimulation in response to changes in body temperature
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Plasma - clotting factors = what?
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serum
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Blood is ___% of body weight
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8%
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Blood is ___% plasma.
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55% The rest is formed elements (hematocrit)
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Plasma is ____% proteins.
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7%
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Plasma proteins are ___% albumin.
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55%
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Plasma proteins are ___% globulins
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38%
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Leukocytes are normally ____% PMNs, ___% lymphocytes, ___% monocytes, ___% eosinophils, ___basophils.
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40-70% PMNs, 20-40% lymphos, 2-10% monos, 1-6% eos, <1% basophils
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What is MAP in terms of systolic and diastolic pressures
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1/3 systolic +2/3 diastolic
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What happens to CO if HR is too high
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diastolic filling decreases and CO decreases
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What is an example of this
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ventricular tachycardia
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What is SV in terms of EDV and ESV
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EDV - ESV
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Name 4 things that increase myocardial 02 demand
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An INCREASE in Afterload, contractility, heart rate, and heart size
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What is Wolff-Parkinson-White syndrome
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accessory conduction pathway from atria to ventricle (bundle of kent), bypassing AV node. As a result ventricles partially depolarize earlier giving rise to the characteristic
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What is the characteristic wave in WPW syndrome
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delta wave
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What can WPW lead to
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reentry current and supraventricular tachycardia
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Forces that move fluid out of capillary?
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Capillary pressure (Pc) and Interstitial fluid colloid osmostic pressure
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Forces that move fluid into capillary?
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Interstitial fluid pressure (Pi) and Plasma colloid osmotic pressure
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Equation for net filtration pressure?
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P net = [(Pc - Pi)] - (colloidc - collidi)]
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Conditions that cause edema by increased capillary pressure?
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heart failure
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Conditions that cause edema by increased capillary permeability?
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toxins, infections, burns
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Conditions that cause edema by decreased plasma proteins?
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nephrotic syndrome, liver failure
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Conditions that cause edema by increased fluid colloid osmotic pressure?
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lymphatic blockage
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What are the physiological responses to high altitude: 1-, 2-, 3-, 4-, 5-, 6-, 7-
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1- acute increase in ventilation, 2- chronic increase in ventilation, 3- increase in EPO leading to an increase in hematocrit and hemaglobin (chronic hypoxia), 4- increase in 2,3-DPG, 5- Cellular changes (increase in mitochondria), 6- increase in excretion of bicarbonates to compensate for respiratory alkalosis, 7- chronic hypoxic pulmonary vasoconstriction results in RVH
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What is the action of 2,3-DPG?
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binds to hemaglobin so that hemoglobin releases more O2
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What does acetazolamide doe?
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it increases the renal excretion of bicarbonates.
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What are 5 important lung products?
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Surfactant, prostaglandins, histamine, ACE, Kallikrein
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What does surfactant do? What is Surfactant? What makes Surfactant?
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It decreases alveolar surface tension which increases complaince, it is made of dipalmitoyl phosphatidylcholine (lecithin), it is produced by type II pneumocytes
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What pathologic process has a deficiency of Surfactant?
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Neonatal RDS
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What are the funcitons of ACE
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converst angiotensin I to Angiotensin II, inactivates bradyykinin (ACE inhibitors yield increase bradykinin and cause cough, angioedema)
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What is the colapsing pressure
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2(tension)/Radius
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What does Kallikrein do?
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It activates bradykinin
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What is the Residual volume (RV)?
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air left in lung after max expiration
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What is the expiratory reserve volume (ERV)?
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air that can still be breathed out after nml expiration
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What is the tidal volume (TV)?
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air that moves into lung with each quiet inspiration (nml = 500ml)
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What is the inspiratory reserve volume (IRV)?
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Air in excess of tidal volume that moves into lung on max inspiration
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What is the vital capacity (VC)?
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TV + IRV + ERV
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What is the functional reserve capacity (FRC)?
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RV + ERV (volume in lungs after normal espiration)
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What is the inspiratory Capacity (IC)?
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IRV+ TV
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What is the total lung capacity (TLC)?
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IRV+TV+ERV+RV
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Decreased affinity of hemoglobin for O2 = shift ___
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Right
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A right shift is caused by an increase or decrase in each of the following factors: P50, metabolic needs, PCO2, temperature, H+, pH, altitude, and 2,3-DPG
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Increase in all but pH
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Fetal Hb curve is shifted ___
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Left (increased affinity for O2)
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T/F: Pulmonary circulation is normally a low-resistance, low-compliance system
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F - Low-resistance, high-compliance
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Cor pulmonale and subsequent RV failure are a consequence of pulmonary ______
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Hypertension
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Hypoxic vasoconstriction that shifts blood away from poorly ventilated regions is caused by ______
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Decrease in PaO2
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In normal health, O2 is perfusion or diffusion limited?
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Perfusion limited - gas equilibrates along the length of the capillary
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Which of the following is diffusion limited: CO2, N2O, or CO?
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CO - gas does not equilibrate by the time the blood reaches the end of the capillary
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When is O2 diffusion limited? What is the equation for Vd?
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Exercise, emphysema, fibrosis
Vd = (Vt) x (PaCO2 -PeCO2)/PaCO2 Pa = arterial & Pe = expired air |
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What is the ideal V/Q ratio?
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V/Q = 1 (permits adequate oxygenation)
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At the base of the lung, there is greater ventilation, perfusion, or both?
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Both are greater
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What is V/Q at the apex of the lung?
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V/Q = 3 (wasted ventilation)
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What is V/Q at the base of the lung?
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V/Q = 0.6 (wasted perfusion)
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V/Q = 0 implies _____
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Airway obstruction (shunt)
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V/Q = infinity implies ______
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Blood flow obstruction (physiological dead space)
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Organisms such as TB that thrive in high O2 flourish in the apex or base of the lung?
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Apex
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During exercise (increased cardiac output), the vessels in the apex of the lung ___-------_______
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Vasodilate such that V/Q approaches 1 (versus normal apex V/Q of 3)
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CO2 is transported from tissue to lungs in these 3 forms: ______
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(1) Bicarbonate (2) Bound to hemoglobin (3) Dissolved CO2
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What percentage of CO2 is transported in the form of bicarbonate?
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90%
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What is the intracellular enzyme that converts CO2 into H2CO3?
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Carbonic anhydrase
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H2CO3 is broken down into H+ and HCO3. What happens to the H+?
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H+ combines with Hb to form HHb (deoxyhemoglobin)
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H2CO3 is broken down into H+ and HCO3. What happens to the HCO3?
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HCO3 is pumped out of the red blood cell in exchange for Cl-
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What is the Haldane effect?
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Oxygenation of hemoglobin promotes the dissociation of CO2 from hemoglobin
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What does kallikrein do
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Activates bradykinin
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What affect to ACE inhibitors have on bradykinin
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Increase bradykinin, which lead to cough and angioedema
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Equation for clearance?
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Cx = UxV/Px; Cx = clearance of X; Ux = urine concentration of X; Px = plasma concentration of X; V = urine flow rate
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Significance of Cx < GFR?
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net tubular reabsorption of X
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Significance of Cx > GFR?
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net tubular secretion of X
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Significance of Cx = GFR?
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no net secretion or absorption of X
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The two determinants of filtration across the glomerular filtration barrier are - and -.
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size and charge
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Components of filtration barrier?
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Fenestrated capillary endothelium, fused basement membrane with heparin sulfate, epithelial layer
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What comprises epithelial layer?
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podocyte foot processes
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The charge on the fused basement membrane is -.
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Negative
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The charge barrier is lost in - , characterized by what four findings?
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nephrotic syndrome, albuminuria, hypoproteinemia, generalized edema, hyperlipidemia
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What substance is freely filtered and is neither reabsorbed nor secreted?
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inulin
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Clinically, - clearance is a good measure of GFR.
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creatinine
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Equation for GFR
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GFR = U(in) X V/P(in) = C(in)
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Where in nephron is PAH secreted?
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proximal tubule
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By what mechanism is it secreted?
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2˚ active transport. Mediated by a carrier system for organic acids
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What drug competively inhibits PAH's secretion?
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probenecid.
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What substance entering the nephron is filtered AND secreted?
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PAH
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Equation for effective renal plasma flow?
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ERPF = U(pah) X V/P(pah) = C(pah)
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Equation for renal blood flow?
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RBF = RPF/1-Hct
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Equation for filtration fraction?
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FF = GFR/RPF
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Class of substances responsible for dilating afferent arteriole?
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Prostaglandins
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Class of drug that inhibits production of above substances?
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NSAIDS
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Substance responsible for constricting efferent arteriole?
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angiotensin II
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Class of drugs that inhibits production of angiotensin II?
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ACE inhibitors
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What factors do you need to know to calculate free water clearance?
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urine flow rate, urine osmolarity, plasma osmolarity
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Equation for free water clearance?
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C(H2O) = v - C (osm)
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Where is glucose absorbed in the nephron?
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proximal tubule
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At what plasma glucose level does glucosuria begin?
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200 mg/dL
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At what plasma glucose level is the glucose threshold mechanism (Tm) saturated?
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350 mg/dL
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How many carrier systems involved in amino acid reabsorption?
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3
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Where does 2˚ active transport occur?
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proximal tubule
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Substances reabsorbed in the early proximal tubule?
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all glucose and amino acids; most bicarbonate, sodium, and water
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- is secreted in the early proximal tubule, which acts as a buffer for -.
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ammonia, H+
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Section of the nephron that is impermeable to sodium?
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thin descending loop of Henle
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Substances actively reabsorbed in the thick ascending loop of Henle?
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Na+, K+, Cl-
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- and - are indirectly reabsorbed in the thick ascending loop of Henle.
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Ca+2 and Mg+2
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Substances actively reabsorbed in the early distal convoluted tubule?
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Na+ and Cl-
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|
|
Reabsorption of - is under the control of - (hormone) in the early distal convoluted tubule,
|
Ca+2, PTH
|
|
|
Substances regulated by aldosterone in collecting tubules?
|
Na+, K+
|
|
|
Reabsorption of water is regulated by - in the collecting tubules?
|
ADH
|
|
|
Osmolarity of the medulla can reach a concentration of -.
|
1200 mOsm
|
|
|
Relative concentration equation for comparing concentrations of substances in renal tubule to plasma?
|
[tubular fluid]/[plasma]; TF/P
|
|
|
Substance with highest TF/P?
|
PAH
|
|
|
Why does this substance have the highest TF/P?
|
Its both filtered and secreted
|
|
|
Substances with lowest TF/P?
|
glucose and amino acids
|
|
|
Why do these substances have the lowest TF/P's?
|
They are reabsorbed almost completely in the early proximal tubule
|
|
|
What substance has a TF/P = 1?
|
inulin
|
|
|
Where does renin come from in the kidney?
|
Cells in the juxta-glomerular apparatus
|
|
|
Mechanism stimulating renin release?
|
Decrease in blood pressure in kidneys
|
|
|
What does renin do?
|
Cleaves angiotensinogen to angiotensin I
|
|
|
Angiotensin I is then cleaved by -, primarily in the -, to make -?
|
angiotensin converting enzyme, lung capillaries, angiotensin II
|
|
|
4 actions of angiotensin II?
|
1) Potent vasoconstriction, 2) Release of aldosterone from adrenal cortex, 3) release of ADH from the posterior pituitary, 4) Stimulates hypothalmus to increase thirst.
|
|
|
Overall actions of angiotensin II?
|
Increase intravascular volume and blood pressure
|
|
|
- (hormone) released from the - may act as a "check" on the renin-angiotensin system in such cases as heart failure.
|
ANP, atria
|
|
|
Endothelial cells of peritubular capillaries secrete - in response to hypoxia.
|
erythropoietin
|
|
|
What is the enzyme responsible for converting 25-OH vitamin D to I,25-(OH)2?
|
1-alpha-hydroxylase
|
|
|
What hormone activates this enzyme?
|
PTH
|
|
|
What is the function of secreted prostaglandins in the kidney?
|
Vasodilation of the afferent arterioles to increase GFR
|
|
|
Class of drugs that can cause renal failure in high vasoconstrictive states due to inhibition of prostaglandin production?
|
NSAIDS. Prostaglandins are keeping the afferent arterioles vasodilated to maintain GFR. Inhibition of prostaglandin production leads to acute renal failure.
|
|
|
Name two stimuli for ADH secretion?
|
Increased plasma osmolarity; decreased blood volume
|
|
|
Two actions of ADH other than increasing water permeability in the collecting duct
|
Increase urea absorption in the collecting duct; Increase Na/K/2Cl activity in thick ascending limb
|
|
|
Hormones stimulated to be released by a decrease in blood volume?
|
ADH, aldosterone, angiotensin II (via renin)
|
|
|
Hormones that increase Na+ reabsorption?
|
Aldosterone (distal tubule); angiotensin II (proximal tubule
|
|
|
Three effects of PTH on the kidney?
|
1) Increase Ca+2 reabsorption, 2) Decrease phosphate reabsorption, 3) Increase vitamin D production
|
|
|
Hormone that decreases sodium reabsorption?
|
ANP
|
|
|
What is the primary disturbance in Metabolic acidosis?
|
a decrease in bicarbonate
|
|
|
What is the compensation?
|
A drop in CO2 by hyperventilation
|
|
|
What are common causes?
|
diabetic ketoacidosis (production of ketone acids), diarrhea (loss of GI bicarb), salisylate overdose, acetazoleamide (diuretic) OD, lactic acidosis, renal failure (can't excrete organic acids), ethylene glycol ingestion
|
|
|
What is the primary disturbance in respiratory acidosis?
|
A build-up in CO2
|
|
|
What is the compensation?
|
Increased bicarb reabosrobtion from the kidney
|
|
|
What are some common causes?
|
COPD, airway obstruction, opiates and sedatives, guillan-barr or ALS,
|
|
|
What is the primary disturbance in metabolic alkalosis?
|
increased bicarbonate
|
|
|
What is the compensation?
|
Increased CO2 by decreased respiration
|
|
|
What are some common causes?
|
hyperventilation, high altitude, pneumonia and pulmonary embolus (hypoxemia causes hyperventilation_
|
|
|
What is the Henderson Haselbach equation?
|
pH = pKa + Log (HCO3-)/(.03*pCO2)
|
|
|
Acid Base Nomogram Low pH, low pCO2 (low HCO3-)
|
metabolic acidosis
|
|
|
Low pH, high pCO2 (high HCO3-)
|
chronic respiratory acidosis
|
|
|
High pH, low pC02 (low HC03-)
|
acute respiratory alkalosis
|
|
|
High pH, high pCO2 (high HCO3-)
|
metabolic alkalosis
|
|
|
Anion gap acidosis How do you calculate it
|
Na - Cl - HCO3
|
|
|
What is normal?
|
8-12 mEq/L
|
|
|
What is the mnemonic
|
MUD PILES
|
|
|
M
|
Methanol
|
|
|
U
|
Uremia
|
|
|
D
|
DKA
|
|
|
P
|
Paraldehyde or Phenformin
|
|
|
I
|
Iron tablets or INH
|
|
|
L
|
Lactic Acidosis
|
|
|
E
|
Ethanol, Ethylene Glycol
|
|
|
S
|
Salicylates
|
|
|
Acid Base Compensations Metabolic acidosis
|
pCO2 = 1.5(HCO3) + 8 +/- 2
|
|
|
Metabolic alkalosis
|
pCO2 increases 0.7 mm Hg per 1 mEq/L HCO3 increase
|
|
|
Respiratory acidosis (acute)
|
HCO3 increases by 1 mEq/L for every 10 mmHg increase of pCO2
|
|
|
Respiratory acidosis (chronic)
|
HCO3 increases by 3.5 mEq/L for every 10 mmHg increase of pCO2
|
|
|
Respiratory alkalosis (acute)
|
HCO3 decreases by 2 mEq/L for every 10 mmHg decrease of pCO2
|
|
|
Respiratory alkalosis (chronic)
|
HCO3 decreases by 5 mEq/L for every 10 mmHg decrease of pCO2
|
|
|
Factor initiating intrinsic pathway?
|
XII
|
|
|
Factor(s) initiating extrinsic pathway?
|
VII and tissue factor
|
|
|
Function of factor XIII?
|
Forms cross-linked fibrin
|
|
|
Factors examined with prothrombin time (PT)?
|
VII, X, V, prothrombin, fibrinogen (Hoffbrand. Haematology. 247)
|
|
|
Factors examined with partial thromboplastin time (PTT)?
|
VIII, IX, XI, XII, X, V, prothrombin, fibrinogen (Hoffbrand. Haematology. 247)
|
|
|
Vitamin K dependent factors?
|
II, VII, IX, X, protein C, protein S (243)
|
|
|
Factors requiring phospholipid surface for activation?
|
IX and X
|
|
|
Factor I also known as?
|
Fibrinogen
|
|
|
Factor II also know as?
|
Prothrombin
|
|
|
Two substrates of Factor XIIa?
|
Factor XI and Prekallikrein
|
|
|
Components involved in the activation of factor XII?
|
Collagen, basement membrane, activated platelets, HMWK (cofactor [high molecular weight kallikrein])
|
|
|
Two substrates of kallikrein?
|
HMWK and Plasminogen
|
|
|
Complement protein on which plasminogen acts?
|
C3
|
|
|
Three functions of bradykinin?
|
Increase vasodilation, increase permeability, increase pain
|
|
|
What converts HMWK to bradykinin?
|
kallikrein
|
|
|
What does plasmin's action on fibrin produce?
|
fibrin split products
|
|
|
Hormones released from the posterior pituitary?
|
ADH and oxytocin
|
|
|
Where are they made?
|
hypothalamus
|
|
|
Hormones released from the anterior pituitary?
|
FLAT PiG: FSH, LH, ACTH, TSH, prolactin, GH
|
|
|
Embryological origin of anterior and posterior pituitary, respectively.
|
oral ectoderm (anterior), neuroectoderm (posterior)
|
|
|
Hormones derived from proopiomelanocortin?
|
ACTH, MSH
|
|
|
hormones with common alpha subunit?
|
TSH, LH, FSH, hCG
|
|
|
Subunit determining hormone specificity?
|
beta subunit
|
|
|
Cells in the parathyroid that secrete PTH.
|
Chief cells
|
|
|
Organs/tissue on which PTH acts.
|
Bone, small intestine (via 1, 25 dihydroxy vitamin D), kidney
|
|
|
Cells stimulated in bone by PTH.
|
osteoblasts (directly) AND osteoclasts (indirectly)
|
|
|
How does PTH affect phosphate levels?
|
Decreases them; it’s the Phosphate Trashing Hormone
|
|
|
What is the function of PTH on bone?
|
Increase bone resorption of calcium and phosphate
|
|
|
What stimulates PTH release?
|
Low free serum Ca+2
|
|
|
Three action of PTH on the kidney.
|
1) Increase vitamin D production, 2) Phosphate secretion, 3) Calcium reabsorption (distal convoluted tubule)
|
|
|
What are two sources of Vitamin D?
|
Plants, and sun exposire on skin
|
|
|
What are they converted to in the kidney?
|
1,25-OH-vitamin D (biologically active form)
|
|
|
What are three fucntions of Vitamin D?
|
Increases calcium and phosphate absorbtion from the gut, increases bone resobtion of Calcium and phosphate.
|
|
|
If calcium or potasium in the blood drop, what effect does that have on vitamin D procudtion?
|
They both act to increase it. Makes sens, if you think about its actions.
|
|
|
What effect does PTH have on vitamin D?
|
increases its formation - again, PTH wants to increase blood calcium levels, so an increase in vitamin D would help that.
|
|
|
What effect do vitamin D levels have on vitamin D production?
|
negative feedback loop
|
|
|
If you lack vitamin D as a child you get:
|
Rickets
|
|
|
If you lack vitamin D as a adult you get :
|
osteomalacia
|
|
|
What are som common cuases of Hypercalcemia?
|
Malignancy, Intoxication with Vit. D, Sacroidosis, Hyperparathyroidism, Alkalie syndrome, and Pagets (bone). Remember: MISHAP
|
|
|
What is alkaline phsphtase a measurement of?
|
It is an enzyme found in bone and liver. The bone specific enzyme indicates attemtped growth in the bone.
|
|
|
In Hyperparathyroidism, what are the Ca levels?
|
Increased, remember, PTH acts to increase CA in the serum.
|
|
|
In Hyperparathyroidism, what are the Phosphate levels?
|
Decreased. TPH increases its secretion in the kidney to keep serum Ca high
|
|
|
In Hyperparathyroidism, what are the Alk Phos levels?
|
Elevated, because PTH actiavrse osetoblasts as well as osteoclasts
|
|
|
In Paget's (bone) what are the Ca levels?
|
Normal or elevated
|
|
|
In Paget's (bone) what are the Phosphate levels?
|
Normal
|
|
|
In Paget's (bone) what are the Alk Phos levels?
|
Elevated a lot, becxuase of all the bone formation going on.
|
|
|
In Vit. D intoxication what are the Ca levels?
|
High. Vit. D increase absorbtion in the gut.
|
|
|
In Vit. D intoxication what are the Phosphate levels?
|
High.
|
|
|
In Vit. D intoxication what are the Alk Phos levels?
|
Normal or high, as the calcium is incorperated
|
|
|
In Osteoperosis what are the Ca levels?
|
Normal
|
|
|
In Osteoperosis what are the Phosphate levels?
|
Normal
|
|
|
In Osteoperosis what are the Alk Phos levels?
|
Normal
|
|
|
In renal insufficiency what are the Ca levels?
|
Low - no vit. D means less abosorbtion
|
|
|
In renal insufficiency what are the Phosphate levels?
|
High - kideny can't excrete well
|
|
|
In renal insufficiency what are the Alk Phos levels?
|
Normal
|
|
|
Where is calcitonin made?
|
Thyroid gland
|
|
|
What cells?
|
Parafolliclular cells (C cells)
|
|
|
What is it's function?
|
supresses osteoclasts
|
|
|
What triggers its release?
|
Increases serum calcium and calcium secretion
|
|
|
Is this important in humans?
|
No. It oppses PTH, but in humans it is not vital to ca+ homeostasis.
|
|
|
What do T3 and T4 do, basically?
|
Control the body's metabolic rate
|
|
|
What are the four Bs that describe T3's function?
|
Brain maturation, bone growth, beta adrenergic effects, basal metabolic rate increased
|
|
|
What is the mechanism by which metabolic rate is increased?
|
Increased Na+/K+ ATPase activity: increased O2 consumption, increased body temperature
|
|
|
What happens to glucose and lipid balance under T3's effect?
|
Increased glycogenolysis, gluconeogenesis, lipolysis
|
|
|
What tells the thyroid to release T3?
|
Hypothalamus releases TRH which stimulates TSH from the pituitary which stiumlates follicle cells
|
|
|
What prevents there from being too much thyroid hormone?
|
Negative feedback of T3 to the anterior pituitary: decreases sensitivity to TRH from hypothalamus
|
|
|
What also stimulates follicle cells (pathological)?
|
TSI - Grave's disease
|
|
|
Describe how T3 andd T4 are made?
|
Iodine enters follicle cells and is oxidized; goes into lumen as I2. Thyroglobulin (made from tyrosine) enters lumen and combines with I2 to form monoiodotyrosine and di-iodotyroside (2 of di makes T4 and one di and one mono makes T3). The T3 and T4 re-enter the follicular cell and are degraded by proteolysis, releasing the T3 and T4 into the bloodstream
|
|
|
How doees a steroid hormone effect its function?
|
Binds to a receptor in the nucleus or cytoplasm and moves to the nucleus; the receptor transforms to expose the DNA binding domain and the hormone/receptor complex binds to an enhancer-like element in DNA. Bottom line: steroids and thyroid hormone cause gene transcription and protein formation
|
|
|
Why are the actions of steroid and thyroid hormones delayed?
|
You have to wait for the gene transcription and protein synthesis to happen.
|
|
|
What are the steroid hormones?
|
I had a PET CAT who was buff because she took steroids. Progesterone, Estrogen, Testosterone, Cortisol, Aldosterone, Thyroxine
|
|
|
How do steroids circulate if they are lipophilic?
|
Bound to binding globulins: increases their solubility and allows for increased delivery to the target organ
|
|
|
What enzyme does ACTH work on?
|
Desmolase: convesion of cholesterol to pregnenolone
|
|
|
What does ketoconazole do?
|
Inhibits desmolase, see above
|
|
|
What happens if you have a 17 alpha hydroxylase deficiency?
|
You can't make sex hormones, cortisol but you can make mineralcorticoids. You get hypertension and hypokalemia because you are wasting all the K in your kidneys while retaining Na. You are phenotypically femal but have no maturation.
|
|
|
What happens in 21 beta hydroxylase deficiency?
|
This is the most common. You have decreased cortisol, increased ACTH, decreased mineralcorticoids, and increased sex hormones. You are masculinized and have female pseudohermaphroditism.
|
|
|
What is blood pressure and electrolytes in 21 beta hydroxylase deficiency?
|
Hypotension, hyponatremic, hyperkalemic, volume depleted and increased renin activity to compensate
|
|
|
What condition do you suspect if a newborn has hypovolemic shock?
|
21 beta hydroxylase deficiency
|
|
|
What happens if you don't have 11 beta hydroxylase?
|
Decreased cortisol, decreased aldosterone and corticosterone, increased sex hormones
|
|
|
What does angiotensin II work on?
|
Aldosterone synthase: creates more aldosterone from corticosterone
|
|
|
What does DHT come from and how?
|
Testosterone via 5 alpha reductase
|
|
|
What does estradiol come from?
|
Testosterone via aromatase
|
|
|
What does estrone come from?
|
Androstenedione via aromatase
|
|
|
What does DHEA lead to eventually?
|
Testosteron (and its byproducts)
|
|
|
What can progesterone be enzymatically transformed to?
|
Glucocorticoids, Androgens and estrogens eventually
|
|
|
What cells can take in glucose regardless of insulin levels? Via what receptoir?
|
Bran and RBC: GLUT-1 receptor
|
|
|
What does the brain use in starvation when there is no glucose?
|
Ketone bodies
|
|
|
What does prolactin have to do with dopamine?
|
Prolactin increases dopamine synthesis and secretion from the hypothalamus, which then inhbits prolactin secretion
|
|
|
What do dopamine agonists do to prolactin secretion? Eg bromocriptine
|
Inhibit it
|
|
|
What does prolactin do to GnRH and what does this mean clinically?
|
Inhbitis synthesis and release: inhibits ovulation
|
|
|
What is a common sign of prolactinoma?
|
Amenorrhea
|
|
|
What causes prolactin releas?
|
TRH from hypothalamus works on anterior pituitary to cause prolactin release
|
|
|
What is the order of potency for estrone, striol, estradiol?
|
Most to least: estradiol >estrone>estriol
|
|
|
Where does estradiol come from?
|
Ovary
|
|
|
Do the testes make estrogen?
|
Yes
|
|
|
Where does estriol come from?
|
Placenta
|
|
|
What are the benefits of hormone replacement therapy with estrogen post-menopause?
|
Less hot flashes, less bone loss
|
|
|
What are the negative effects of unopposed estrogen?
|
Increased risk of endometrial cancer.
|
|
|
What can decrease the risks of giving estrogen?
|
Giving progesterone with it.
|
|
|
What does estrogen do to the follicle?
|
Makes it grow
|
|
|
What does estrogen do to the endometrium and the myometrium?
|
Growth and excitability
|
|
|
What does estrogen do to the genitalia?
|
Development
|
|
|
What does estrogen do to breasts?
|
Stromal development
|
|
|
What does estrogen do to fat distribution?
|
Female pattern
|
|
|
What does estrogen do to transport proteins?
|
Increases hepatic synthesis
|
|
|
What does estrogen do to FSH?
|
Feedback inhibition
|
|
|
What does estrogen do to LH?
|
Causes surge: feedback switches from negative to posititve just before LH surge.
|
|
|
What does increased progesterone indicate?
|
Ovulation
|
|
|
What does progesterone come from?
|
Corpus luteum, placenta, adrenal cortex, testes.
|
|
|
What does progesterone do to the endometrial glands and spinal artery development?
|
Increase secretions, increase artery growth
|
|
|
What does progesterone do for a pregnancy?
|
Maintains it
|
|
|
What doe progesterone do to myometrial excitability?
|
Decreases it
|
|
|
What does progesterone do to sperm travel?
|
Creates thick cervical mucus that inhibits sperm entry into uterus
|
|
|
What does progesterone do to body temperature?
|
Increases
|
|
|
What does progesterone do to gonadotropins?
|
Inhibits (LH, FSH)
|
|
|
What does progesterone do to uterine smooth muscle?
|
Relaxes
|
|
|
Follicular grwoth is fastest when?
|
during the 2nd week of the proliferative phase
|
|
|
The grafian follicle matures when?
|
The proliferative phase day 0-14
|
|
|
What is the sequence of Hormone surges prior to Ovulation?
|
Estrogen surge, then LH surge along with FSH surge.
|
|
|
When does Progesterone surge
|
During the Secreoty phase days 14-21
|
|
|
What hormone is associated with the Maintance of the Endometrium
|
Progesterone
|
|
|
What is the sorce of hCG
|
The syncytiotrophoblasts
|
|
|
What is Function of hCG: 1- physiologic, 2-diagnostic, 3-diagnostic
|
1- maintains the corpus luteum throughout the 1st trimester (acts like LH) 2- is useful for pregancy detection. Appears in urine 8 days post fertilization, 3- hCG is elevated in wone with hydatidiform moles
|
|
|
What is the average age of Menopause
|
51 (earlier in smokers)
|
|
|
Wge linked decline in number of ovarian follicles is associeated with decline in what hormone
|
Estrogen
|
|
|
What are th hormoneal changes during menopause
|
decreased estrogen, increased FSH, increased LH (but no surge), increased GnRH
|
|
|
What are the si/sx of menopause
|
HAVOC: hot flashes, Atrophy of vagina, osteoprosis, coronary artery disease
|
|
|
What are the androgens? Where are there sources?
|
Testosterone , dyhydrotestosterone (DHT), androstenedione: testis, testis/adrenal, adrenal
|
|
|
What are the potencies of the Andrognes?
|
DHT > testosterone > androstenedione
|
|
|
What are the targets of androgens
|
skin prostate, seminal vescles, epididymis, liver, muscle, brain
|
|
|
What active molecule is testosterone converted to? What converts it? What Drug inhibits it's conversion?
|
Testosterone is converted to DHT bu 5 alpha reductase which is inhibited by finasteride
|
|
|
What are the functions of androgens: 1-, 2-, 3-, 4-, 5-
|
1- differentiation of wolffian duct system into internal gonadal structures, 2- secondary sex characteristics and growth spurt, 2- required for normal spermatogenesis, 4- anabolic effects (increase in muscle size, increase in RBC production, 5- libido
|
|
|
What is the fate of Testosterone and androstenedione in adipose tissue?
|
testosterone and androstene dione are converted to estrogen in andipose tissue by enzyme aromatase.
|
|
|
Male sperpatogeneis What is the function of FSH?
|
Stimulates sertoli cells to produce ABP and inhibin, stimulates sperm production.
|
|
|
What is the function of LH?
|
stimulates testosterone release from Leydig cells.
|
|
|
What is the function of ABP (androgen-binding protien)?
|
ensures that testosterone in seminiferous tubule is high
|
|
|
What is the function of Inhibin?
|
It inhibits FSH release from the anterior pituitary
|
|
|
What is the function of testosterone?
|
differentiates male genitalia, has anabolic effects on protein metabolisim, maintains gametogenesis, maintains libido, inhibits Gn RH, fuses epiphyseal plates in bone.
|
|
|
What are the 3 glands involved in salivary secretion?
|
Parotid, submandibular, sublingual
|
|
|
What compound begins starch digestion?
|
Alpha-amylase
|
|
|
What does bicarbonate in the salivary solution do?
|
Neutralizes bacterial acids and maintains dental health
|
|
|
These compounds in saliva lubricate food
|
Mucins (glycoproteins)
|
|
|
T/F: Parasympathetic activity stimulates salivary secretion while sympathetic activity does not
|
F - Both parasympathetic and sympathetic activity stimulate salivary secretion
|
|
|
Mucus functions to:
|
1) Protect the stomach surface from H+, 2) Lubricant
|
|
|
Intrinsic factor is needed to absorb which vitamin?
|
B12
|
|
|
Which cells secrete intrinsic factor?
|
Parietal cells
|
|
|
What are 3 functions of H+ in stomach secretions?
|
Kills bacteria, breaks down food, activates pepsinogen
|
|
|
Chief cells secrete _____
|
Pepsinogen
|
|
|
G cells secrete _____
|
Gastrin
|
|
|
Gastrin stimulates parietal cells to secrete _____
|
Acid
|
|
|
Autoimmune destruction of _____ leads to chronic gastritis and/or pernicious anemia
|
Parietal cells
|
|
|
Name 3 compounds that stimulate gastric acid secretion
|
Histamine, Ach, gastrin
|
|
|
Name 2 compounds that inhibit gastric acid secretion
|
Somatostatin, GIP, prostaglandin
|
|
|
Absence of this product is not essential for digestion but increases the risk of Salmonella infections
|
Gastric acid
|
|
|
Optimal pH for protein degredation by pepsin is ___
|
pH 1.0 - 3.0
|
|
|
G cells are located in which 2 places?
|
Antrum and duodenum
|
|
|
T/F: Gastrin stimulates gastric motility
|
TRUE
|
|
|
Name 4 things that stimulate gastrin secretion
|
Stomach distention, amino acids, peptides, vagus (via GRP)
|
|
|
What 2 things inhibit gastrin secretion?
|
Secretin and stomach acid pH < 1.5
|
|
|
What is hypersecreted in Zollinger-Ellison syndrome?
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Gastrin
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Secretin stimulates secretion of ____ from surface mucosal cells of stomach and duodenum
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Bicarbonate
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I cells are located where?
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Duodenum and jejunum
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What stimulates the release of CCK from I cells?
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Fatty acids, amino acids
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Name 3 things CCK does
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Stimulates gallbladder contraction, stimulates pancreatic enzyme secretion, inhibits gastric emptying
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Why does pain worsen after eating in cholelithiasis?
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CCK release
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S cells secrete _____
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Secretin
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Where are S cells located?
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Duodenum
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What 2 things does secretin do?
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Stimulates pancreatic HCO3 secretion, inhibits gastric acid secretion (nature's antacid)
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What stimulates the release of secretin?
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Fatty acids and acid in the duodenum
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Somatostatin is secreted by __ cells located in ________
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D cells; pancreatic islets & GI mucosa
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Somatostatin inhibits (name at least 4 things):
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Gastric acid and pepsinogen secretion, pancreatic and small intestine fluid secretion, gallbladder contraction, and release of insulin and glucagon
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What stimulates somatostatin release?
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Acid
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What inhibits somatostatin release?
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Vagus
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This GI secretory product has anti-GH effects
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Somatostatin
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Name 4 types of secretory cells that are located in the duodenum
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G cells, mucosal cells, I cells, S cells
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function of nitrous oxide in GI
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causes smooth muscle relaxation (i.e. LES relaxation)
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3 things gastrin is secreted in response to
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(1) gastric distention, (2) vagal stimulation and (3) amino acid entering stomach
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action of gastrin
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causes gastric H+ secretion
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secretin is secreted in response to
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H+ and fatty acids entering duodenum
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action of secretin
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pancreatic secretion of HCO3- and inhibits gastric H+ secretion
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VIP (vasoactive intestinal peptide) is secreted by ---- and ----- of the -----
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secreted by smooth muscle and nerves of the intestines
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action of VIP
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relaxes smooth muscle, causes pancreatic HCO3- secretion and inhibits gastric H+ secretion
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Sympathetic (NE) action on GI (4 actions)
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(1) increases production of saliva, (2) decreases splanchnic blood flow in fight or flight response (3) decreases motility (4) constricts sphincters
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Parasympathetic (Ach) action on GI (5)
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(1) increases production of saliva, (2) increases gastric H+ secretion (3) increases pancreatic enzyme and HCO3- secretion (4) stimulates enteric nervous system to create intestinal peristalsis (5) relaxes sphincters
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Cholecystokinin is secreted in response to --- and --- entering the ----
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amino acids and fatty acids entering the duodenum
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CCK action of GI
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causes contraction of gallbladder, relaxation of sphincter of Oddi, and pancreatic seccretion of enzymes and HCO3-
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These are four receptors on the parietal cell that are involved in the regulation of gastric acid secretion
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(1) histamine receptor (H2); (2) Acetylcholine receptor (M3); (3) Gastrin receptor; (4) Prostaglandin receptor
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Regulation of gastric acid secretion: H2 receptor antagonists
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ranitidine, cimetidine, famotidine
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Gastrin is increased in this syndrome
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Zollinger-Ellison Syndrome
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Regulation of gastric acid secretion: Inhibitor of prostaglandin receptor
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Misoprostol
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Regulation of gastric acid secretion: agonists of prostaglandin receptors on pariental cell
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PGI2 and PGE2
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glucose absorption occurs at these two places
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duodenum and proximal jejunum
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glucose absorption occurs across the membrane through this mechanism
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sodium-glucose cotransporter
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Secretory acini of the pancreas secrete zymogens when stimulated by ---- and ---
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acetylcholine and CCK
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Pancreatic ducts secrete ---- and ---- when stimulated by ------
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secrete mucus and allkaline fluid when stimulated by secretin
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What is the enzyme for starch digestion that is secreted in active form from the pancreas?
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alpha-amylase
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What are the pancreatic enzymes for fat digestion?
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lipase, phospholipase A, colipase
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What aer the pancreatic enzymes for protein digestion?
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trypsin, chymotrypsin, elastase, and carboxypeptidases (secreted as proenzymes)
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What is the Proenzyme of trypsin?
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trypsinogen
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What enzyme that cleaves trypsinogen?
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enterokinase
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What is the enzyme that activates the other proenzymes and can also activate its own proenzyme through positive-feedback?
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trypsin
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What is the clinical presentation of pancreatic insufficiency?
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malabsorption and steatorrhea
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What are the clinical recommendations for pancreatic insufficiency?
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limit fat intake, monitor for signs of fat-soluble vitamin deficiency
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What stimulates ductal cells to secrete bicarbonate-rich fluid?
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secretin
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What is the major stimulus for secretion of enzyme rich fluid by pancreatic acinar cells
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cholecystokinin
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What is the major stimulus for zymogen release, poor stimulus for bicarbonate secretion
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acetylcholine
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What inhibits the release of gastrin and secretin
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somatostatin
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Carbohydrate digestion: this enzyme starts digestion, hydrolyzes alpha-1,4 linkages to give lmaltose, maltotriose, and alpha-limit dextrans
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salivary amylase
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Carbohydrate digestion: this enzyme has the highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides, maltose and maltotriose
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pancreatic amylase
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Carbohydrate digestion: these enzymes are at brush border of intestine, the rate-limiteing step in carbohydrate difestion, produces monosaccarides
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oligosaccharide hydrolases
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Bilirubin : this product of heme metabolism is taken up by hepatocytes
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bilirubin
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Bilirubin : conjugated or unconjugated version of bilirubin is water soluble
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conjugated version
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Bilirubin : condition that results from elevated bilirubin levels
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jaundice
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Bilirubin : condition with yellow skin and sclerae
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jaundice
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Bilirubin : normal life span of red blood cells
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120 days
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Bilirubin : where red blood cells are made
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bone marrow
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Bilirubin : where do the substrates of heme catabolism in the reticuloendothelial system come from
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80%RBCs and immature erythroid cells; 20% from bilirubin produced from nonerythroid enzymes in liver
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Bilirubin : free bilirubin is complexed with ---- in circulation
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albumin
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Bilirubin : bilirubin is conjugated in this organ
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liver
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Bilirubin : renal excretion of this form of bilirubin
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urobilirubin (4mg/day)
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Bilirubin : conjugated bilirubin is also called ---
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direct bilirubin
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Bilirubin : form of bilirubin excreted in feces
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stercobilin
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Bilirubin : bacterial conversion to this form of bilirubin in the colon
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urobilinogen
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Bilirubin : form of bilirubin in enterohepatic circulation from colon to liver
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urobilinogen
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Bile: T/F: Blood and bile flow in the same direction
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False - blood flows toward the central vein while bile flows in the oposite direction
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Bile: Sinusoids drain to the _____ vein
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Central vein
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Bile: What makes up the portal triad?
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Bile ductule, branch of portal vein, branch of hepatic artery
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Bile: What are the macrophage-like cells in the liver called?
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Kupffer cells
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Bile: Does the apical or basolateral surface of hepatocytes face the bile canaliculi?
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Apical
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Bile: The basolateral surface of hepatocytes faces ____
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Sinusoids
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Bile: What drains into the Space of Disse?
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Lymph
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