Claire’s Deck Block 3 Flashcards
1
Q
If X is filtered AND secreted, what is kidney clearance (C) equal to?
A
C is equal to the renal plasma flow.
2
Q
How can GFR be estimated?
A
GFR can be estimated using a substance that is filtered but not reabsorbed or secreted.
Examples of such substances are inulin and creatinine.
3
Q
What percentage of total body weight does intracellular fluid make up?
A
40%
4
Q
What percentage of total body weight does interstitial fluid (ISF) make up?
A
15%
5
Q
What percentage of total body weight does plasma make up?
A
5%
6
Q
What does ISF contain in contrast to plasma?
A
ISF contains no protein.
7
Q
How much water does the average body contain?
A
Around 40 L.
8
Q
What regulates water loss from the body?
A
The kidney.
9
Q
What occurs when too much water and solute are taken in at the same time?
A
Hypervolemia.
10
Q
What occurs when too much water and solute are lost at the same time?
A
Hypovolemia.
11
Q
What occurs when too much water is taken in without solute?
A
Overhydration.
12
Q
What occurs when water is lost without solute?
A
Dehydration.
13
Q
What occurs if water is lost without solute?
A
Dehydration or hypovolemia occurs.
14
Q
What happens when solute follows the water?
A
Hypo or hypervolemia occurs.
15
Q
What happens when solute does not follow the water?
A
Overhydration or dehydration occurs.
16
Q
What happens if blood volume falls too low?
A
GFR will stop.
17
Q
What is water loss through the kidney called?
A
Diuresis.
18
Q
What type of urine is produced if water excretion increases?
A
Diluted urine.
19
Q
What type of urine is produced if water excretion decreases?
A
Concentrated urine.
20
Q
What is the ISF of the cortex in relation to plasma?
A
Isosmotic.
21
Q
What is the ISF of the medulla in relation to plasma?
A
Hyperosmotic.
22
Q
What is reabsorbed in the ascending loop of Henle?
A
Only solutes.
23
Q
What happens to filtrate entering the descending limb?
A
It loses water, becoming more concentrated.
24
Q
What maintains a hyperosmotic medulla and drives water reabsorption?
A
Countercurrent exchange.
25
Under normal conditions, what is the ADH concentration?
Low, and diuresis is high.
26
What does ADH do to water permeability in the tubule?
Increases it, meaning more water gets reabsorbed and urine becomes more concentrated.
27
What three things stimulate ADH secretion from the hypothalamus?
Increase in ECF osmolarity, decrease in blood volume, decrease in BP.
28
What happens when ECF osmolarity rises?
Water moves out of cells, causing them to shrink.
29
What does natriuresis refer to?
The excretion of sodium in the urine.
30
What does aldosterone do?
Causes more Na+ to be reabsorbed through the distal tubule and collecting duct.
31
What does ANP cause?
Increased sodium excretion in urine (increased natriuresis).
32
What effect does aldosterone have on Na+ excretion?
Decreases it, whereas ANP increases it.
33
What is ADH secretion dependent on?
Pressure receptors in the left atrium.
34
What does ADH do to blood pressure?
Raises it by increasing water reabsorption in the kidney.
35
What factors can affect ECF volume?
Salt loading, transfusion, heart failure, dehydration, bleeding, space flight, posture.
36
What must the pH of ECF be maintained at?
7.35 to 7.45.
37
How can pH of body fluids be maintained?
By chemical buffers, ventilation, and kidneys.
38
What does ventilation determine in the blood?
The PCO2.
39
What happens during hyperventilation?
PCO2 decreases.
40
What happens during hypoventilation?
PCO2 increases.
41
What compensates for metabolic acidosis/alkalosis?
Ventilation.
42
How can the kidney compensate for pH disturbances?
Directly: excretion or reabsorption of H+. Indirectly: excretion or reabsorption of HCO3-.
43
What do the proximal tubules secrete and reabsorb?
Secrete H+ and reabsorb HCO3-.
44
What controls acid excretion in the kidney?
The collecting duct through intercalated cells.
45
How can HCO3- be produced in the kidney?
Using ammonia.
46
In what state do type A intercalated cells function?
In an acidosis state.
47
In what state do type B intercalated cells function?
In an alkalosis state.
48
What is the arterial pH range compatible with life?
6.8 to 8.
49
What is the normal HCO3- to CO2 ratio?
20/1.
50
What arises from an increase in CO2?
Respiratory acidosis.
51
What arises from a decrease in CO2?
Respiratory alkalosis.
52
What arises from an increase in HCO3-?
Metabolic alkalosis.
53
What arises from a decrease in HCO3-?
Metabolic acidosis.
54
What is the most important compensatory organ in respiratory acidosis?
The kidney.
55
What is Lead I in ECG?
Right arm to Left arm (0 degrees).
56
What is Lead II in ECG?
Right arm to Left leg (-60 degrees).
57
What is Lead III in ECG?
Left arm to Left leg (+120 degrees).
58
What do vector directions point towards?
The positive pole.
59
What is Lead aVR in ECG?
Left arm/Left leg to Right arm (-150 degrees).
60
What is Lead aVL in ECG?
Right arm/Left leg to Left arm (-30 degrees).
61
What is Lead aVF in ECG?
Right arm/Left arm to Left Leg (+90 degrees).
62
What do precordial leads assess?
Spread of depolarization from a lateral angle.
63
How many precordial leads are there?
6.
64
What type of leads are created using Wilson's Central Terminal?
Unipolar leads.
65
What happens when current flows towards the arrowheads in ECG?
Upwards deflection occurs.
66
What happens when current flows away from the arrowheads in ECG?
Downwards deflection occurs.
67
What happens when current flows perpendicular to the arrowheads in ECG?
Biphasic aka equiphasic deflection
68
What happens when current flows obliquely towards the arrowheads in ECG?
A less strong upwards deflection occurs.
69
What happens when current flows obliquely away from the arrowheads in ECG?
A less strong downwards deflection occurs.
70
What are the phases of cardiac muscle action potential?
Phase 0: Na+ channels open, causing depolarization. Phase 1: Na+ channels close, K+ are open, repolarization begins. Phase 2: Ca2+ channels open, K+ channels start to close. Phase 3: Ca2+ channels close, K+ continues to exit the cell. Phase 4: Cells reach resting membrane potential.
71
What does one square on ECG graph paper represent?
0.04 seconds and 1mV in voltage.
72
What is the first negative component on the ECG graph?
The Q wave.
73
What is the first positive component on the ECG graph?
The R wave.
74
What is the negative component following the R wave?
The S wave.
75
How are large waves indicated on an ECG graph?
By capital letters.
76
How are small waves indicated on an ECG graph?
By lowercase letters.
77
Does ventricular rhythm have a P wave?
False. Only the atrial rhythm has a P wave.
78
What determines the heart axis?
The vector of depolarization from all limb leads.
79
What is the normal axis range?
-30 and 90+ degrees.
80
What is Lead I positive between?
-90 and +90 degrees.
81
What is Lead II positive between?
-30 and +150 degrees.
82
If both Lead I and II are positive, what is likely?
The axis is likely normal.
83
What does the PR interval represent?
Depolarization of the atrial and AV node.
84
How long does the PR interval normally last?
0.12 to 0.20 seconds.
85
How long does depolarization of the ventricles (QRS complex) normally last?
0.07 to 0.10 seconds.
86
What is the QT interval longer in?
Women than men and varies with changes in heart rate.
87
What should you be suspicious of regarding the Q-T interval?
When it is greater than half of the R-R interval.
88
What is the normal duration of the QRS complex?
0.07 to 0.10 seconds
89
How does the QT interval vary between women and men?
The QT interval is longer in women than men and varies with changes in heart rate.
90
What is the QT interval at 60 bpm?
0.44 seconds
91
What is the QT interval at 80 bpm?
0.37 seconds
92
What is the QT interval at 100 bpm?
0.30 seconds
93
When should you be suspicious regarding the QT interval?
When the Q-T interval is greater than half of the R-R interval.
94
What characterizes Atrial Fibrillation?
Numerous small depolarizations spread through the atria, electrically neutralizing each other, with no P wave and a normal QRS-T complex.
95
What are Premature Ventricular Contractions?
Contractions that occur before the normal time, caused by ectopic foci emitting abnormal impulses during cardiac rhythm, leading to a prolongation of the QRS complex.
96
What is Torsades de Pointes?
A condition characterized by delayed repolarization of ventricular muscles after action potential, with premature ventricular beats leading to pauses and excessively long Q-T intervals.
97
What is Atrial Flutter?
A rapid rate of atrial contraction, typically 2 to 3 beats of the atria for every 1 beat of the ventricle in ECG (2:1).
98
What is Supraventricular tachycardia?
An aberrant rhythm involving the AV node or the atrium, with an almost normal QRS-T complex and may or may not have a P wave.
99
What defines First degree block?
A delay of conduction from atria to ventricle without blockage, characterized by an increased P-R interval (<0.20 sec).
100
What is Second degree block?
Conduction through the A-V bundle may or may not pass to the ventricles, with an increased P-R interval (up to 0.45 sec) and possibly two P waves for every QRS complex in severe cases.
101
What is Complete A-V block (third degree block)?
A complete block of impulse from the atria to the ventricles, where the ventricles establish their own signal, leading to disassociation of the P wave from the QRS complex.
102
What is Electrical Alternans?
A blockage of impulse conduction in the peripheral ventricular Purkinje system causing alternating QRS amplitudes in ECG.
103
How do you find the QRS axis?
The vector will be away from the most negative QRS complex.
104
How do you find the QRS axis in relation to the equiphase complex?
The vector will be perpendicular to the most equiphase (big positive + big negative) QRS complex.
105
How do you find the QRS axis in relation to the positive QRS complexes?
The vector will be in the general direction of the most and second most positive QRS complex.
106
What is the symbol for capillary hydrostatic pressure?
Pc
107
What is the symbol for ISF hydrostatic pressure?
PISF
108
What is the symbol for plasma colloid osmotic pressure?
πP
109
What is the symbol for interstitial colloid osmotic pressure?
πISF
110
Describe capillary hydrostatic pressure (PC).
Capillary hydrostatic pressure (PC) pushes ISF from capillary into interstitium.
111
Describe ISF hydrostatic pressure (PISF).
ISF hydrostatic pressure (PISF) pushes ISF from interstitium into capillary.
112
Describe plasma colloid osmotic pressure (πP).
Plasma colloid osmotic pressure (πP) draws ISF from interstitium into capillary.
113
Describe interstitial colloid osmotic pressure (πISF).
Interstitial colloid osmotic pressure (πISF) draws fluid from capillary into interstitium.
114
What is a cardiomyocyte's resting membrane potential (Vm)?
-90mV
115
Why is the resting membrane potential electronegative?
There is a deficit of positive charges in the cytosol compared to the extracellular space.
116
What are the ion concentrations in extracellular space and in the SR (of cardiac cells) compared to the cytosol?
There is WAY more calcium outside the cytosol (20,000x) and in SR (10,000x), more sodium (15x) outside the cell, and more potassium inside the cell (40x). This creates a concentration gradient that allows the action potential to happen.
117
What maintains the concentration gradients in cell walls?
Active transporters.
118
What informs the resting membrane potential (Vo) aside from concentration gradients?
The permeability of the cell to K+ at rest.
119
What is the threshold potential of a cardiac cell action potential?
-70mV (Na+ TP)
120
What is a voltage-gated channel?
A voltage-sensitive protein that modulates membrane permeability to ions.
121
What happens to Vm and ion channels?
Changes in Vm lead to conformational changes in ion channels, causing pores to open and ions to enter.
122
What are the channel activation thresholds of sodium, calcium, and potassium?
Na+ = -70mV, Ca2+ = -40mV, K+ = it depends, but near/above 0mV. This means that Na+ channels open first, followed by Ca2+, followed by K+.
123
Explain the cycle/mechanism of action of a voltage-gated channel.
Vm reaches activation threshold (e.g., -70mV for Na+) → channel opens, Na+ enters cell → channel closes once the membrane potential becomes positive → ions are pumped out eventually → repeat.
124
What are the 5 steps of the cardiac action potential?
Phase 4 = resting state, membrane potential = -90mV; Phase 0 = depolarization above -70mV → Na+ channel opens; Phase 1 = Na+ inside cell eventually causes Na+ channel to close; Phase 2 = at -40mV, Ca2+ channel opens, Ca2+ enters cell; Phase 3 = gradients returned to normal (repolarizing).
125
What is the refractory period for a cardiomyocyte?
It lasts from depolarization to muscle relaxation and is long, allowing for full contraction/relaxation of the heart and preventing tetanus.
126
Characterize a fast action potential.
Stable resting potential (-90mV), threshold potential = -70mV (max = +30mV), needs a trigger, fast Na+ entry.
127
Characterize a slow action potential.
Unstable resting potential (-60mV), threshold potential = -40mV (max = 0-20mV), spontaneous (diastolic) depolarization.
128
Which neurotransmitter and receptor are associated with SNS modulation of pacemaker activity?
Norepinephrine and beta-1 receptors.
129
How does the SNS increase heart rate?
Vo increases (threshold is closer to 0/less electronegative) and IH is sped up.
130
Which neurotransmitter and receptor are associated with PNS modulation of pacemaker activity?
Acetylcholine and muscarinic receptors.
131
How does the PNS decrease heart rate?
Vo decreases (hyperpolarized/becomes more electronegative) and IH is slowed down.
132
What is vagal tone?
It refers to the way the PNS decreases heart rate.
133
What is the pacemaker current (IH)?
It's the reason the heart can beat on its own, activated by repolarization.
134
Why is the pacemaker current so slow?
It is driven by K+ efflux, a gradual process.
135
Where does the pacemaker current originate?
From the HCN channel superfamily, which conducts Na+ and K+.
136
What connects cardiomyocytes electrically?
Gap junctions.
137
What determines how fast action potentials will be propagated in cardiac tissue?
The type and density of gap junctions.
138
Which parts of the conduction system have slow conduction/APs?
SA node and AV node.
139
Which parts of the conduction system have fast conduction/APs?
Atria, ventricles, and His-Purkinje system.
140
What allows interatrial conduction of action potentials?
Bachmann's bundle.
141
What is the significance of the AV node being the only conduction pathway between the atria and ventricles?
It allows for full atrial contraction and diastolic filling of ventricles before ventricular contraction.
142
What are subsidiary pacemakers?
Any part of the conduction system that can develop auto-rhythmic activity, such as the AV node and Purkinje fibers.
143
What is Image Occlusion?
Image Occlusion is a technique used to hide parts of an image to test knowledge on the occluded areas.
144
What 5 things can you find in the upper right quadrant of the abdomen?
Liver, Gallbladder, Hepatic flexure (of colon), Head of pancreas, Right kidney
145
What 5 things can you find in the upper left quadrant of the abdomen?
Stomach, Spleen, Splenic flexure of colon, Tail of pancreas, Left kidney
146
What 2 things are in the lower right quadrant of the abdomen?
Cecum, Appendix
147
What's in the lower left quadrant of the abdomen?
Sigmoid colon
148
Describe diastole for me real quick.
The passive phase of the cardiac cycle. Associated with ventricular relaxation and filling, and low ventricular pressure.
149
Describe systole for me?
The active phase of the cardiac cycle. Associated with excitation (depolarization), contraction, development of pressure, and ejection of blood.
150
Tell me about how the heart valves keep blood flowing in one direction only.
It's all about pressure gradients! When there's high pressure coming from behind the valve, it opens. When there's high pressure against the front of the valve, it closes.
151
In the Wigger's diagram, what does the P wave indicate?
Atrial depolarization (should result in contraction)
152
In the Wigger's diagram, what does the QRS complex indicate?
Ventricular depolarization (should result in contraction)
153
In the Wigger's diagram, what does the T wave indicate?
Ventricular repolarization (should result in relaxation)
154
What's stroke volume? How do you calculate it?
The volume of blood pumped by the ventricle in one beat. SV = end diastolic volume (EDV) - end systolic volume (ESV)
155
What determines stroke volume?
Contractility, or how forcefully your LV contracts; Afterload, or the load that your LV has to work against.
156
What's the ejection fraction? How do you calculate it?
The proportion of blood that the LV actually ejects when it contracts. EF = Stroke volume (SV)/End-diastolic volume (EDV)
157
What's a normal LV ejection fraction? When should you start worrying?
>=55% is normal; <40% is a red flag for LV dysfunction.
158
What's cardiac output (CO)? How do you calculate it?
How much blood your LV can pump in 1 minute. CO = Stroke volume (SV) x heart rate.
159
What's a typical cardiac output?
~5L/min
160
What's preload? In cardiac ventricles, what determines preload?
Preload = the load imposed at rest. In cardiac ventricles, preload is determined by end diastolic volume.
161
What are 5 factors affecting preload?
Filling time (HR), Atrial contraction, Filling pressure, Venous return, LV compliance.
162
What does the 'intrinsic' heart rate refer to?
Just the fact that if you just turned your SNS and PNS off for a minute, the heart would beat around 100 BPM.
163
What are the two main influences on heart rate?
SNS and PNS inputs.
164
What are three other things that affect HR?
Body temp, Cardiac pressures (e.g., exercise), Function/dysfunction of conducting system.
165
What might cause an increase in EDV?
Decreased HR, Lying down, Fluid loading.
166
What might cause a decrease in EDV?
Increased HR, Standing up (too fast), Fluid loss/dehydration, Reduced LV compliance (increased stiffness).
167
What's afterload?
How much resistance cardiomyocytes have to pump against when ejecting blood.
168
Which 3 factors determine afterload?
LV pressure during ejection, BP in aorta, Vascular tone.
169
How are afterload and stroke volume related?
Inverse relationship: Decreased afterload increases stroke volume; Increased afterload decreases stroke volume.
170
How are contractility and stroke volume related?
Direct relationship: Increased contractility = increased stroke volume and vice versa.
171
How do SNS and adrenergic stimulation impact contractility?
Contractility is increased by SNS and adrenergic stimulation (e.g., norepinephrine).
172
What's the Frank-Starling law?
Stroke volume rises in proportion to ventricular filling (preload).
173
How will an increase in afterload change the Frank-Starling curve?
Increased afterload = downward shift.
174
How will an increase in contractility change the Frank-Starling curve?
Increase = curve shifted up.
175
What's the formula for hydrostatic pressure?
P = height of fluid column (fluid density).
176
What's the relevance of hydrostatic pressure to taking blood pressure?
If you don't take it at the right height (at level of heart), the value will be wrong unless you adjust for the height difference.
177
What are venous pressures like at the heart level?
At heart level, typically below 10mmHg; can vary widely above and below the heart (~74mmHg per meter of fluid column).
178
What's the difference between a static and a flowing system with respect to pressure?
In a static system, pressure is consistent everywhere; in a flowing system, pressure decreases due to energy loss (friction → heat).
179
Tell me about the issues associated with inadequate and excessive BP.
Inadequate = reduced tissue blood flow and shock; Excessive BP = high microvascular pressures and flows, strains LV function and increases O2 consumption.
180
Tell me about how BP changes as you move from LV back to the right atrium.
LV = massive fluctuations; Arteries = rapid fluctuation; Arterioles = pressure falling off; Capillaries, Venules, veins = steady fall in pressure; Right atrium = very low pressure.
181
What's diastolic BP? When does it occur?
Minimum arterial BP; occurs just at the beginning of LV ejection.
182
What's systolic BP? When does it occur?
Peak arterial BP; produced by LV ejection.
183
What's arterial pulse pressure?
The difference between systolic and diastolic BPs.
184
What's the mean arterial pressure? How do you calculate it?
The average of your diastolic and systolic BPs; MAP = diastolic + ⅓ pulse pressure.
185
How do you calculate arterial BP?
BParterial - Pvenous ≈ CO(TPR); Pvenous is usually negligible.
186
What's total peripheral resistance? How do you calculate it?
The resistance of the entire systemic vasculature; TPR = BP/CO.
187
What determines TPR?
Blood vessel properties (length, radius, tone); TPR tends to remain pretty consistent in the short term.
188
How do you calculate resistance?
R = 8Lη/πr^4; L = length, η = viscosity, r = radius.
189
Which factor has the most impact on resistance?
Radius; the fastest way to change resistance is to vasodilate/vasoconstrict.
190
How are CO and TPR related to mean BP?
Directly related; an increase in CO or TPR will increase BP.
191
What are 3 factors influencing pulse pressure?
Intermittency of LV ejection, Size of LV stroke volume, Compliance of central arteries.
192
What might cause long-term BP elevation?
Increased CO, Increased TPR (or both); typically linked to increased TPR but normal CO.
193
What are 2 effects of stiffened central arteries?
Increased systolic pressure, Increased pulse pressure.
194
What are baroreceptors, and how do they modulate BP?
Located in aorta and carotid arteries; sense and respond to BP-induced distension.
195
How do your kidneys regulate BP? (2 processes)
Increase salt and water retention = increased fluid volume; Renal renin release = vasoconstriction and sympathetic activation.
196
Is renal regulation of BP short or long term?
Long term.
197
Which two things determine blood flow to a tissue?
Pressure gradient (drives flow through vasculature); Ease with which blood can actually flow through vessels (resistance or conductance).
198
What do hemodynamics describe?
Physical factors that govern blood flow (pressure and resistance) through a vascular system.
199
How do you calculate blood flow (F)?
F = ΔP/R or F = ΔP(C).
200
What's a pressure gradient? How do you calculate it?
Refers to the pressure gradient driving flow through a tissue; Pressure gradient = arterial pressure - venous pressure.
201
If the pressure gradient is held constant, what's the relationship between blood flow and vascular resistance?
The two are inversely proportional.
202
What's conductance?
The ease with which blood flows through a vessel; opposite of vascular resistance.
203
If the pressure gradient is held constant, what's the relationship between blood flow and vascular conductance?
Direct relationship.
204
What's the relationship between conductance and resistance?
They're inverses of one another.
205
What are 5 factors that might induce vasoconstriction?
Increased myogenic activity, Increased O2, Decreased CO2, Increased endothelin, SNS activation.
206
What are 5 factors that might induce vasodilation?
Decreased myogenic activity, Decreased O2, Increased CO2, Increased nitric oxide, PNS activation.
207
What's the most effective way to adjust vascular resistance and blood flow?
Vasoconstriction/dilation (smooth muscle, especially in arterioles).
208
Assuming pressure gradients are held constant, what determines the distribution of flow across vascular beds?
Vascular conductance.
209
What's the difference between an extrinsic and an intrinsic mechanism of blood flow regulation?
Extrinsic = mechanism is external to the tissue; Intrinsic = mechanism is contained within the tissue.
210
What are three extrinsic mechanisms that regulate blood flow?
SNS, PNS, Circulating factors.
211
Tell me about how the SNS regulates blood flow.
Vasoconstriction in most tissues.
212
What's the difference between an extrinsic and an intrinsic mechanism of blood flow regulation?
Extrinsic = mechanism is external to the tissue or vascular bed. Intrinsic = mechanism is contained within the tissue or vascular bed.
213
Tell me about how the SNS regulates blood flow.
Vasoconstriction in most tissues. Epinephrine or norepinephrine and alpha adrenergic receptors. Very fast.
214
Tell me about how the PNS regulates blood flow.
Doesn't do a lot actually. Vasodilation in some tissues (e.g., skin, penis). Mediated by nerves releasing acetylcholine, peptides, and nitric oxide.
215
Tell me about how circulating factors regulate blood flow.
Substances circulating in your blood. Vasoconstrictors = noradrenaline, angiotensin II, ADH (antidiuretic hormone/vasopressin), endothelin. Vasodilators = histamine, adenosine, nitric oxide.
216
Which vascular beds are capable of autoregulating blood flow?
All of them except the pulmonary vascular bed.
217
What type of regulation is metabolic autoregulation? What does it refer to?
Intrinsic regulation. Flow is adjusted to match metabolism (O2 consumption).
218
Tell me about how metabolic autoregulation functions in active tissues.
Active tissues produce metabolites that are vasodilators (e.g., adenosine, ATP, K+, CO2, H+, etc.) which can trigger metabolic autoregulation, reactive hyperemia, and pressure autoregulation. Relevant in all tissues.
219
What type of regulation is pressure autoregulation? What does it refer to?
Intrinsic regulation. Local mechanisms that act to maintain consistent blood flow despite fluctuations in BP. Don't work well at extremes of pressure.
220
What does the myogenic response/myogenic tone refer to?
Pressure/stretch-induced vasoconstriction. May contribute to pressure autoregulation.
221
What does reactive hyperaemia refer to?
When circulation is occluded, it's followed by a period of increased blood flow.
222
Where is autonomic (extrinsic - SNS/PNS) control most prevalent?
In skin (autoregulation present but weak).
223
Where is autoregulation (intrinsic) most prevalent?
In CNS (local metabolic needs are defended).
224
Why does the CNS exhibit little/no response to autonomic stimulation?
Because it'd be really bad if your brain got shut off every time your SNS started firing.
225
Which system (sympathetic/autoregulatory) dominates in skeletal and cardiac muscle?
Trick question, they compete to control blood flow.
226
How do intrinsic and extrinsic systems relate to one another?
Intrinsic = adjust blood flow to suit local needs. Extrinsic = Can override autoregulatory dilation to ensure BP meets needs of CNS and other vulnerable tissues. Note: Extrinsic overrides don't apply to CNS.
227
How do you calculate resistance of compartments (vessels) connected in series?
Literally just add 'em all together. Rtotal = R1 + R2 + R3 etc.
228
How do you calculate resistance of compartments (vessels) connected in parallel?
Add the inverse of the sum of the inverses. Rtotal = 1/(1/R1 + 1/R2 + 1/R3 etc).
229
How does the total resistance of a network of parallel vessels compare to the resistance of its constituent vessels?
Total resistance parallel arrangement of vessels greatly reduces blood flow.
230
What are standard limb leads?
Lead I = RA → LA 0° Lead II = RA → LL 60° Lead III = LA → LL 120°
231
What are augmented limb leads?
Lead aVR = LA + LL → RA -150° Lead aVL = RA + LL → LA -30° Lead aVF = RA + LA → LL 90°
232
What are precordial leads and what do they assess?
6 standard leads attached to the chest Used to assess depolarization from a lateral angle
233
How is precordial lead placement done?
V6 on lateral left at 0°, V1 is sorta on the right side of the sternal border (at 120°? Unclear)
234
What is the relationship between the direction of flow of current (depolarization) and the magnitude of deflection on the EKG?
Current flow aligns with axis lead (flows from negative to positive) = strong positive deflection Current flow runs against axis lead = strong negative deflection Current flow runs obliquely to axis lead (at a diagonal) = weak deflection in direction of flow with respect to axis of lead If perpendicular to EKG lead, biphasic/equiphasic deflection seen
235
Describe contraction activity of the heart at each part of a QRS complex.
Q wave = depolarization down the interventricular septum/bundle branches R wave = Depolarization has reached the apex, starting to split (second half is when it reaches apex and sorta reverses direction) S wave = Depolarization is pretty much finished, the top part (nearest the atria) of ventricles has contracted
236
What is the grid size of ECG paper and ECG paper speed?
1mm^2 grid used Normal speed = 25mm/s 25 blocks/s (each block = 4ms)
237
What are 3 ways to estimate heart rate using an ECG?
Determine time between RR intervals 60 000/RR interval (in milliseconds) QRS complexes in 10s timeframe x 6
238
What is the ECG voltage standard?
It should be about 20mm/20 blocks high
239
How are the components of the QRS complex named?
First negative component = Q wave First positive component = R wave Negative component following R wave = S wave
240
What is the convention used to indicate magnitude when naming a QRS complex?
Capital letter = large wave Small letter = small wave
241
What is the J point?
Marks where the QRS complex ends and the ST segment begins In heart, marks end of depolarization/start of repolarization
242
How do you determine ST segment elevation or depression?
ST segment elevation/depression is relative to the preceding PR segment
243
When the heart has an atrial rhythm, what will you always see?
P wave preceding a narrow QRS complex Constant PR interval
244
What does no P wave indicate?
Ventricular rhythm (SA node broke)
245
How might you determine the QRS axis?
Find the most equiphasic QRS (vector is perpendicular to this direction) Find the most positive QRS complex (vector will be pointing in that general direction)
246
How do you estimate heart axis using the quadrant method?
You're gonna have two leads, determine which half of the circle is significant (and where you divide), then read off the part that overlaps
247
Why is three lead analysis better than the quadrant method?
More specific - you're looking for overlap from 3 things instead of 2.
248
If you can't remember your ECG lead angles, what's a useful trick to see if the axis is in normal range?
If lead I and II are both positive, there's a pretty good chance that it's in normal range.
249
What's happening in the heart during the PR interval, and what's a normal range?
Depolarization of atria and AV node 120-200ms is normal
250
What's happening in the heart during the QRS duration, and what's a normal range?
Ventricular depolarization 70-100ms is normal
251
How do you determine whether the QT interval is within normal range?
Bazzet's formula (yuck) Or if QT interval is greater than ½ of RR interval, that's a red flag
252
What are the two flavours of cardiac arrhythmia?
Disorders of impulse formation Disorders of impulse conduction
253
What might cause a disorder of impulse formation?
Abnormal rhythmicity of pacemaker Shift of pacemaker from SA node to somewhere else
254
What might cause a disorder of impulse conduction?
Blocks at different points through the conduction system Abnormal pathways of conduction False impulses from parts of the heart that have no business generating impulses
255
What is atrial fibrillation and how does it look on an ECG?
Numerous small depolarizations across atrial that electrically neutralize each other No P waves Normal QRS-T complex
256
What are premature ventricular contractions, what causes them, and how do they look on an ECG?
When contraction occurs before you'd expect it to (incomplete ventricular filling) Caused by [ectopic foci] emitting irregular impulses On ECG QRS complex is longer than it should be
257
What are Torsades de Pointes and how do they look on an ECG?
Delayed repolarization after AP Premature ventricular contraction → pauses and prolonged post-pause QT intervals Excessively long QT intervals on ECG
258
What are premature ventricular contractions? What causes them? What do they look like on an ECG?
When contraction occurs before you'd expect it to (incomplete ventricular filling). Caused by ectopic foci emitting irregular impulses. On ECG, QRS complex is longer than it should be.
259
What are Torsades de Pointes? What do they look like on an ECG?
Delayed repolarization after AP. Premature ventricular contraction → pauses and prolonged post-pause QT intervals. Excessively long QT intervals on ECG.
260
What's atrial flutter? What do you look for on an ECG?
Electrical signals travel as a single wave around the atria → rapid rates of atrial contraction. 2-3 atrial contractions for each ventricular contraction. 2:1 atrial:ventricular rhythm on ECG.
261
What's supraventricular tachycardia? What does it look like on an ECG?
Abnormal rhythm of AV node or atrium. QRS-T complex looks almost normal. P wave might be there, might not be. If present, characteristics might be changed.
262
What's a first-degree block? What does it look like on an ECG?
Delayed conduction from atria → ventricles (no true blockage). PR interval is increased (>20ms).
263
What's a second-degree block? What does it look like on an ECG?
Potential block from AV bundle → ventricles. PR interval increased up to 45ms. If severe, see 2:1 P wave:QRS complex.
264
What's a third-degree block? What does it look like on an ECG?
No conduction between atria and ventricles. Ventricles will establish own signal. P wave and QRS complex are dissociated from one another.
265
What's electrical alternans? What does it look like on an ECG?
Impulses not reaching Purkinje system. Inconsistent QRS complex amplitude.
266
What mediates the response to hypoglycemia? What 3 effects does it have?
Epinephrine. Increases hepatic glucose production. Decreases insulin secretion. Increases glucagon secretion.
267
Tell me about fuel sources used by the body during starvation.
Brain prefers glucose but will use ketone bodies if no glucose available. Tissues without mitochondria require glucose. Other tissues can use fatty acids.
268
How does the body maintain normal tissue function during periods of fasting/starvation?
Conserve protein.
269
How does adipose tissue respond to the drop in insulin associated with fasting/starvation?
Decreased glucose uptake (via GLUT-4). Decreased pentose phosphate pathway. Increased glucagon (decreased fatty acid and TAG synthesis, decreased glycolysis, increased fatty acid oxidation). Increased NADPH.
270
Which hormone starts the process of breaking down triglycerides from fat stores? How do these components get used?
Hormone-sensitive lipase (HSL). Triglycerides → any tissue with mitochondria for ATP synthesis. Glycerol → liver for gluconeogenesis.
271
How does the liver respond to decreased blood glucose?
Glycogenolysis (glycogen → glucose). Can maintain blood glucose levels for <12h.
272
What effect does increased glucagon have on the liver?
Decreased glycolysis (decreased glucokinase, PFK-1 and pyruvate kinase). Decreased pentose phosphate pathway. Increased NADPH (not consumed by anabolic processes). Increased gluconeogenesis.
273
Which 2 things inhibit glycolysis but activate gluconeogenesis?
Citrate. Glucagon.
274
What's one thing that inhibits glycolysis but doesn't activate gluconeogenesis?
ATP inhibits glycolysis but doesn't activate gluconeogenesis.
275
Which 2 things activate glycolysis but inhibit gluconeogenesis?
AMP. Fructose 2, 6-bisphosphate.
276
What prevents glycolysis and gluconeogenesis from operating at the same time?
Glucagon inhibits production of fructose 2, 6-bisphosphate.
277
What is the effect of glucagon on fat metabolism in the liver?
Decreased fatty acid synthesis (TAG and VLDL). Increased fatty acid → mitochondria. Increased beta-oxidation.
278
What happens to acetyl CoA in the liver that isn't needed for the Krebs cycle?
Converted into ketone bodies. Acetoacetate and beta-hydroxybutyrate.
279
Where do ketone bodies come from? How are they used?
Come from liver. Used by any extrahepatic tissue with mitochondria. Ketone bodies → acetyl CoA → ATP.
280
When do levels of ketone bodies in the blood peak?
2-3 weeks into starvation.
281
How is amino acid metabolism sustained during fasting?
Amino acids come from muscle (mostly alanine, glutamine, and glycine). Carbon skeletons → pyruvate or Krebs cycle intermediates → gluconeogenesis substrates (except leucine and lysine). Excess nitrogen → urea → urea cycle.
282
What are the substrates for gluconeogenesis?
Amino acid carbon skeletons (except leucine and lysine). Lactate. Glycerol.
283
Where does the brain get its fuel from in early starvation?
Glucose from hepatic glycogenolysis and hepatic gluconeogenesis (mostly from muscle protein).
284
Where does the brain get its fuel from in late starvation?
Ketogenesis.
285
Why can't the brain use fatty acids for fuel?
Fatty acids can't pass through the blood-brain barrier (because they're bound to albumin).
286
What effects do decreased insulin and increased glucagon have on carbohydrate metabolism in muscle?
Decreased glucose uptake via GLUT-4. Decreased glucose-6-phosphate. Decreased glycolysis. Decreased glycogenesis.
287
What receptors does adipose tissue have that muscles lack?
Glucagon receptors.
288
What stimulates glycogen release in muscle?
Physical activity (Ca2+ release, AMP increase).
289
How does muscle use fat for fuel during fasting/starvation?
Increased LPL in muscle vasculature → fatty acid uptake from VLDL.
290
What is the main source of fuel for muscle during a prolonged fast?
Fatty acids (for beta-oxidation) are the main fuel. Ketones also used.
291
How does protein metabolism compare in early vs late fasting?
Early = rapid proteolysis for gluconeogenesis to supply glucose to brain and tissues without mitochondria. Late = Decreased proteolysis because ketone bodies are being produced.
292
What effect does exercise have on metabolism in muscle?
Similar effect to insulin in that it stimulates GLUT-4 receptors (i.e., glucose can enter myocytes).
293
What does the kidney do during periods of fasting/starvation?
Keeps ripping ammonia off of glutamine and glutamate (glutaminase and glutamate dehydrogenase) to make α-ketoglutarate for ATP production and renal gluconeogenesis.
294
What proportion of glucose does the kidney produce during a prolonged fast?
Up to 50% of it.
295
How does the urea/NH4+ balance in the kidney change during prolonged fasting?
Urea decreases, NH4+ increases. NH4+ used to facilitate H+ (acid) removal from body to spare Na+ and K+.
296
What is the diameter of a capillary? A red blood cell?
Both about 6 microns.
297
How does the velocity of blood in capillaries compare to velocity in veins and arteries?
Lower in capillaries.
298
How does total cross-sectional area in capillaries compare to that of veins/arteries?
Higher cross-sectional area in capillaries.
299
How does nitric oxide (NO) impact microcirculation?
Causes vasodilation (in microcirculation).
300
How thick are capillary walls?
Around 1 micron thick.
301
How does most diffusion through capillaries occur?
Through gaps between adjacent endothelial cells.
302
What is interstitial space?
The space between cells.
303
Through what does solute diffusion between blood and tissue occur?
Through the ISF fluid.
304
What is diffusion?
The main mode of exchange of solutes between blood, ISF, and cells.
305
What determines bulk flow of ISF?
Starling's forces.
306
What does capillary hydrostatic pressure (PC) do?
Pushes ISF from capillary into interstitium.
307
What does interstitial colloid osmotic pressure (IIISF) do?
Draws fluid from capillary into interstitium.
308
When is PISF increased?
When tissue is swollen with excess ISF (edema).
309
Tell me about Starling's forces in a healthy patient.
Outward = 11 mmHG. Inward = 9 mmHG. This results in a net exchange pressure of 2 mmHg and accounts for the net outward flow of ISF (reabsorbed by lymphatics).
310
Tell me about how lymph is drained back into circulation.
Most lymph = thoracic duct. A much smaller area = right lymphatic duct.
311
What is edema?
Swelling of tissues that occur when too much ISF accumulates.
312
Describe capillary hydrostatic pressure (PC).
Pushes ISF from capillary into interstitium.
313
Describe ISF hydrostatic pressure (PISF).
Pushes ISF from interstitium into capillary.
314
Describe plasma colloid osmotic pressure (πP).
Draws ISF from interstitium into capillary.
315
Describe interstitial colloid osmotic pressure (πISF).
Draws fluid from capillary into interstitium.
316
What are the 4 components of the urinary system?
Kidneys, Ureters, Bladder, Urethra
317
Are kidneys intraperitoneal or retroperitoneal?
Retroperitoneal
318
The kidneys are (approximately) at the level of which vertebra? Are they at the same level?
T12-T13. Not on the same level - right kidney sits lower because of your liver.
319
What is the capsule of the kidney?
Outer protective layer
320
Trace the path of vessels from renal artery → nephron.
Renal artery → Segmental artery → Interlobar artery → Arcuate artery → Interlobular/cortical radiate artery → Afferent arteriole → nephron
321
Approximately how many nephrons per kidney?
1 million
322
Where are the nephrons located/what do they span?
Medulla and cortex
323
What are the two components of a renal corpuscle?
Bowman's capsule, Glomerulus
324
What are glomerulus (singular? Plural? idk man)?
Vessels in Bowman's capsule
325
What are the 4 components of a renal tubule?
Bowman's capsule, Proximal (convoluted) tubule, Loop of Henle, Distal (also convoluted) tubule
326
Tell me about how the renal tubule is situated in situ.
It's folded in on itself such that the renal corpuscle is in contact with the distal tubule.
327
Where are the renal corpuscles located within the kidney?
All in the cortex
328
What's the difference between a cortical and a juxtamedullary nephron?
Cortical = short loops, Juxtamedullary = long loops, extend deep into the medulla
329
The majority of nephrons are which type? What proportion of filtrate do they produce?
90% are cortical (short loops). Produce 90% of filtrate.
330
What are the two arterioles associated with the renal tubule?
Afferent and efferent arterioles
331
What are the two sets of capillaries associated with the renal tubule?
Glomerular (glomerulus) and peritubular
332
Trace the path of blood through the cortical nephron (from the afferent arteriole).
Afferent arteriole → glomerular capillaries → efferent arteriole → peritubular capillary
333
What type of circulation is renal microcirculation?
Portal circulation
334
How is juxtamedullary nephron circulation different from cortical nephron circulation?
Peritubular capillaries include vasa recta (long, narrow capillaries with thin walls)
335
What are vasa recta?
Long, narrow capillaries with thin walls. Associate with long loop of Henle that extends into the medulla.
336
Trace the path from renal artery to renal vein for me.
Renal artery → segmental artery → interlobar artery → arcuate artery → cortical radiate artery → afferent arterioles → glomerulus → capillaries → cortical radiate vein → arcuate vein → interlobar vein → segmental vein → renal vein
337
What is filtration? Where does it happen?
Blood → tubular filtrate in the renal corpuscle only
338
What is reabsorption? Where does it happen?
Filtrate → blood in peritubular capillaries
339
What is secretion?
Blood (in peritubular capillaries) → filtrate
340
What's the difference between secretion and excretion?
Secretion = blood (in peritubular capillaries) → filtrate; Excretion = filtrate → bladder and external environment
341
How much plasma entering the glomerulus actually gets filtered? Where does the rest go?
20% gets filtered. The rest leaves through the efferent arteriole.
342
What's the normal filtration fraction?
~ 0.2
343
How does the renal corpuscle develop?
The (developing) glomerulus sorta wiggles itself into the head of the primitive renal tubule.
344
What are podocytes? What do they make up?
Cells in Bowman's capsule that wrap around capillaries of the glomerulus. Make up the epithelial lining of Bowman's capsule.
345
What are the two structures associated with the two layers of the glomerular filtration barrier (GFB) that actually allow filtration?
In endothelium of glomerular capillary = fenestrations; In podocytes = gaps between the foot processes form filtration slits.
346
What gets filtered into Bowman's capsule?
Water, Small solutes (ions, glucose, amino acids, etc)
347
What doesn't get filtered into Bowman's capsule?
Large particles (albumin, antibodies, hormones, enzymes, etc), Blood cells
348
What's the glomerular filtration rate (GFR)?
Rate at which ultrafiltrate of plasma moves from glomerular capillaries → Bowman's capsule
349
What's a normal GFR (per minute? Per day?)
125ml/minute, 180L/day
350
What determines filtration strength and direction?
Starling forces (capillary BP, pressure inside Bowman's capsule, osmotic pressures of plasma and filtrate)
351
What are the two types of starling force?
Hydrostatic force (push forces) in capillaries and in Bowman's capsule; Osmotic/oncotic force (pull forces)
352
What's the predominant component of Starling forces in the kidney?
Blood pressure (pushes substances into renal space)
353
GFR is directly determined by what?
Blood pressure
354
Is GFR directly determined by arterial BP?
Between 40-80mmHg yes, but between 80-180mmHg (normal BP), no. So functionally, no.
355
Tell me how the myogenic response regulates GFR.
Afferent arteriole constricts in response to BP-related stretch of vascular wall to limit excessive BP in glomerulus.
356
Tell me how tubulo-glomerular feedback regulates GFR.
Macula densa sense [Na+] increases in filtrate (caused by increase GFR) → secretes paracrine to cause vasoconstriction in afferent arteriole.
357
If GFR decreases, what 2 things happen?
Macula densa decreases paracrine production (reduces vasoconstriction of afferent arteriole); Granular cells release renin.
358
What's the point of reabsorption? What gets reabsorbed?
The point: so your body can hang onto stuff it needs. All glucose, most water and sodium (99% and 99.5%) get reabsorbed from filtrate → peritubular blood circulation.
359
What are some other bits and bobs that your body probably doesn't want to excrete?
Other sugars, amino acids, medications, etc.
360
What are two features of the structure of the epithelial cells of the proximal tubule facilitate solute exchange?
Large surface areas (microvilli on apical membrane + infoldings of basal membrane); Polarized epithelium.
361
What are the four steps that facilitate reabsorption of solutes and fluid (tubule → ISF)?
Na+ reabsorbed via active transport; Anions follow Na+ out; Fluid follows particles (osmosis) from tubule → ISF; Permeable solutes diffuse out.
362
Tell me how BP facilitates reabsorption.
BP in glomerular capillaries higher than BP in peritubular capillaries.
363
How are most substances reabsorbed?
Specific transport systems (carriers)
364
What's maximum transport (Tm)? What happens if Tm is exceeded?
Tm = rate of transport when all carriers are occupied. When Tm is exceeded, you start seeing filtrate in the urine.
365
What's the renal threshold?
The plasma concentration after which a substance starts appearing in the urine.
366
What's the purpose of secretion in the kidney?
Clears substances from the 80% of blood that's not filtered by the glomerulus.
367
What's the main way that substances are cleared from the blood via secretion?
Active transports (specific to substances - K+, H+, NH4+, medications and metabolic waste products...)
368
What does renal clearance evaluate? What can it give an estimate of?
Evaluates overall renal function. Also gives estimates of GFR and renal blood flow.
369
What are the two principles to keep in mind when looking at renal clearance?
Only consider routes in (renal artery) and out (renal vein, ureter); Everything in the urine comes from blood plasma.
370
How does clearance (C) relate to GFR when: X is filtered, but not reabsorbed or excreted?
If filtered but not reabsorbed or excreted C = GFR.
371
How does clearance (C) relate to GFR when: X is filtered and excreted?
If filtered and excreted C > GFR.
372
How does clearance (C) relate to GFR when: X is filtered and partially reabsorbed?
If filtered and partially reabsorbed C < GFR.
373
How does clearance (C) relate to GFR when: X is completely reabsorbed?
If completely reabsorbed C = 0.
374
How do you calculate clearance (C)?
C = (U*V)/P where: U = [substance] in urine in mg/ml, V = rate of urine production in ml/min, P = [substance] in plasma in mg/ml.
375
How can you use renal clearance to estimate renal plasma flow?
If X is filtered and secreted, C > GFR but also C = RPF.
376
If a substance is both filtered and secreted by the kidney, how can you estimate renal blood flow?
Recall that C = RPF in this situation; RBF = RPF/Htc (hematocrit). Therefore, just divide C/hematocrit to get renal blood flow.
377
How do you use renal clearance to estimate GFR?
If X is filtered but not reabsorbed or secreted, C = GFR.
378
In which tissues is glycolysis found? What are its main functions?
Found in all tissues. Main functions: ATP production (aerobic or anaerobic), Produces intermediates for other pathways.
379
In which tissues is the Krebs cycle found? What are its main functions?
Any tissue with mitochondria. Main functions: ATP production (aerobic), NADH and FADH2 for electron transport chain and gluconeogenesis.
380
In which tissues is the electron transport chain found? What are its main functions?
All tissues with mitochondria. ATP production (requires O2).
381
In which tissues is gluconeogenesis found? What are its main functions?
Liver and Kidney. Intermediates of other pathways → glucose (for release during fasting).
382
In which tissues is the Cori cycle found? What are its main functions?
Lactate producing tissues (muscle + red blood cells) → Liver. Lactate from anaerobic glycolysis → gluconeogenesis in liver.
383
In which tissues is glycogenolysis found? What are its main functions?
Most tissues. Main functions: Substrate for gluconeogenesis (liver and kidney only), Substrate for glycolysis (most tissues).
384
In which tissues is glycogen synthesis found? What are its main functions?
Most tissues (important in liver and muscles). For carbohydrate storage.
385
In which tissues is the pentose phosphate pathway found? What are its main functions?
Partially active in most tissues. Provides ribose for nucleotide synthesis, Provides NADPH for metabolic reactions.
386
In which tissues is glycogen synthesis found? What are its main functions?
Most tissues (important in liver and muscles)
## Footnote
For carbohydrate storage
387
In which tissues is the pentose phosphate pathway found? What are its main functions?
Partially active in most tissues
## Footnote
Provides ribose for nucleotide synthesis and NADPH for metabolic reactions (synthesis of fatty acids, steroids and sterols, control of oxidative stress)
388
In which tissues is lipogenesis found? What are its main functions?
Liver and adipose tissue
## Footnote
Main functions: Carbs → triglyceride synthesis (mostly liver), Fatty acids → triglycerides
389
In which tissues is lipolysis (via hormone sensitive lipase) found? What are its main functions?
Adipose tissues
## Footnote
Mobilize triglyceride stores
390
In which tissues is lipolysis (via lipoprotein lipase and hepatic lipase) found? What are its main functions?
Capillaries of many tissues (muscle, adipose, not brain)
## Footnote
Release free fatty acids from circulating VLDL and chylomicrons
391
In which tissues is fatty acid b-oxidation found? What are its main functions?
Most tissues with mitochondria
## Footnote
Main functions: ATP production (aerobic)
392
In which tissues is ketogenesis found? What are its main functions?
Liver
## Footnote
Fatty acids → ketone bodies for fuel during prolonged fast
393
Which tissues can use ketone bodies? What are ketone bodies used to produce?
Most extrahepatic tissues with mitochondria
## Footnote
Used to produce substrates for krebs cycle and electron transport chain for ATP production
394
In which tissues does transamination occur? What are its main functions?
Most of 'em
## Footnote
Main functions: Amino acid synthesis and metabolism, Synthesis of nitrogen-containing compounds
