Exam 1 Flashcards
1
Q
why are people with CVD given aspirin?
A
aspirin is COX inhibitor
PGH2 –> TXA2 (constrictor - produced by platelets) and PGI2 (dilator - produced by ECs)
PGI2 effects not taken out because ECs have nuclei
2
Q
caldesmon
A
binds to actin filaments at low Ca conc. to prevent actin and muosin from interacting (preventing contraction)
doesn’t do it’s job when phosphorylated (is phosphorylated by MAPK)
3
Q
what causes the water loss in the thin descending LOH?
A
the neighboring salt loss in the thick ascending LOH pulls water out of TDL into interstitum
(saltier the fluid means more Na is pumped out of the tubule)
4
Q
systolic right heart failure (HFrEF)
A
myocardium can’t generate enough force to eject blood. breathlessness, large diliated heart
heart sound 3
5
Q
2
A
interlobular artery
6
Q
which diuretic spares K loss?
A
amiloride (acts at collecting tubules)
channel is only Na so K not affected
7
Q
autoregulation
A
how we maintain constant blood flow despite changes in pressure
8
Q
what is the difference in generating activity induced flow in the brain vs everywhere else
A
neurotransmitters (espec. glutamate) rather than energy are the principal agents in generating activity induced flow
9
Q
what is excitation coupling? what are the two types?
A
the process where excitation triggers an increase in calcium
-
electromechanical coupling: contraction WITH a change in membrane potential
- AP dependent - Ca channels open slower in SM
- graded depolarization - no AP generated/is resting potential
- pharmacomechanical coupling: contraction WITHOUT a change in membrane depolarization - usually caused by local tissue factors that open Ca ion channel or GPCR and depolarize membrane without AP
10
Q
calsequestrin
A
Ca buffering molecule in the junctional SR
11
Q
what does countercurrent mean?
A
fluid flows in opposite directions - down descending limb, up ascending limb
12
Q
what are the steps of calcium excitation contraction?
A
- increase in calcium concentration (from AP)
- Ca binds to calmodulin (like troponin)
- Ca/calmodulin activates MLCK (myosin light chain kinase)
- MLCK phosphorylates and activates the myosin head ATPase activtiy
- ATP is cleaved and Pi is released resulting in confirmational changes
13
Q
eccentric hypertrophy/dilation
A
HF thinning of wall; increases wall stress
14
Q
heart sound 3
A
rapid blood flow from atria to ventricles (in kids). indicates CHF/Mitral regurg.
15
Q
3
A
Collecting Duct
16
Q
resitance compliance filter
A
what lets blood move through the CC even during diastole - guaruntees steady flow in capillaries
17
Q
where does most of the Ca influx come from?
A
25% influx thru plasma membrane
75% Sarcomplasmic reticulum
18
Q
pericyte
A
tight communication with ECs via gap junctions (in the brain). impacts phenotype to influence tightness of BBB - controls angiogenesis/vasculogenesis
19
Q
whats the BFD about convective transport?
A
its the movement of blood around the body so diffusion can occur over short distances
20
Q
1
A
PCT
21
Q
how is the Ca transient increased?
A
by increased TIME to bind to troponin
NOT BY SUMMATION!
22
Q
1
A
Macula Densa
23
Q
=GFR
A
creatinine (inulin)
all of it is eliminated in the urine
- freely filtered at the glomerulus
- not reabsorbed
- not secreted
24
Q
where is urea reabsorbed?
A
the collecting duct by vasopressin - puts VTA1 channels in the CT
25
#1
arcuate artery
26
type III CRS
acute RCS
abrupt kidney worsening (ischemia/glomerulonephritis--\> heart dysfunction)
27
what is GFR?
volume of filtrate kidneys produce each minute (avg 125 ml/min)
28
in the cardiac action potential, what is responsible for:
phase 4?
phase 0?
4: I k1 (resting potential)
29
what is the significance of the equilibrium point of a guyton curve?
this is where venous return equals the cardiac output
30
what does increasing TPR do to CO? to CVP?
reduces CO - heart has to overcome a higher pressure to eject
reduces CVP - have to translocate more blood from venous to arterial side
31
endothelin effects
causes vasoconstriction, induces hypertrophy of cardiac myocytes. stimulates and potentiates noradrenaline, AII and aldosterone
32
what is margination?
the process of leukocyte redistribution - WBC assume more peripheral position
33
pressure in the system when CO = 0
mean circulatory pressure (~7mmHg)
34
what happens at the thin descending LOH
constitutive water reabsorption - "concentrating segment"
35
cardiorenal syndrome
acute/chronic dysfunction in one may induce such dysfuntion in the other
36
what are the parasympathetic cholinergic nerves?
cranial nerves 3, 7, 9, 10
sacral 2-4
37
coronary steal syndrome
dipyrimidole: affects small (not large) vessels - blood flow to normal area increased, blood flow to ischemic area decreased
nitrate: collateral vessel dilated; bf to ischemic area increased
38
where would you find:
1. continuous capillary
2. fenestrated capillary
3. discontinuous
1. continious: BBB, muscle, lung
2. fenestrated: kidney, endocrine glands, GI, gall bladder
3. liver, bone marrow, spleen (RBC things)
39
what does the EDPVR determine?
compliance a decrease in EDPVR means an upward shift in the diastolic PVR. could be caused by scar tissue froman MI or calcified pericardium
40
unmyelinated mechanoreceptors
respond to distention of heart; ventricular ones during systole, atrial ones during inspiration
41
when insulin binds to receptor, what happens? (good and bad)
good: IRS --\> PI3K --\> increase glucose transport/NO production (GOOD for CV system to maintain bf, less thrombotic events)
bad: ras --\> raf --\> MEK --\> MAPK --\> VSMC growth and migration (atherosclerosis) and endothelian (thrombotic events)
42
ID #3
What is this space continuous with?
Urinary space
continuous with PCT
43
adenosine on vasoactivity of BV
released by heart, can dilate arteries. most important humoral agent in controlling BV vasoactivity!
increases bf in cerebral and coronary circulations
44
how long is the...
PR interval
QRS interval
PR = 120-200 ms
QRS = \<100 ms (AP fast)
45
ectopic atrial rhythm
different P waves (but present)
46
cardiac output
the volume of blood pumped by the heart per minute CO=SV\*HR
47
Blue arrow
Simple squamous epithelium of the parietal layer
48
what is a distinguishing feature histologically between elastic and muscular arteries?
muscular arteries have a very well defined IEL and EEL
49
exudation
the escape of fluids, proteins and blood cells from vascular system to interstitial tissue/body cavities
50
hypertensive heart disease on EKG
QRS amplitude is abnormally high and wide (high suggests heart enlarged with thickened walls, long because heart walls take longer for depolarization)
51
what happens to blood when temperature decreases
blood viscosity increases two fold
52
is water reabsorbed at the thick ascending LOH?
no!!!! impermeable to water
53
what is the breakdown of % of Na resorption along the nephron?
67% - PCT
20% - thick ascending LOH
6% DCT
2% Collecting tubules
54
major components of extracellular fluid
Na and Cl
55
Cushing Reaction
increased intracranial pressure, TPR, MBP (HTN, brady, resp. depression)
baroreceptor induced bradycardia
(due to hematoma/tumor/cerebral edema)
56
within each segment the vessels are arranged how?
in parallel decreases resitance because 1/R=...
57
tonus contraction
steady state contraction that smooth muscle can maintain
58
excretion
removal of organic wastes or drug metabolites from the blood into urine
59
phospholamban
protein - natural SERCA modulator (quickens SERCA pump when phosphorylated - disinhibition event)
increases calcium stored in SR for faster and greater uptake
60
AV fistula
extra flow back to the heart (preload pathology)
61
Frank starling mechanism
the intrinsic capability of the heart to change its SV in response to changes in preload
62
which is more concentrated, renal cortex or medulla?
medulla! (400-1200 mosm/L)
cortex is 300 mosm/L
63
valve disease
preload pathology
aortic/mitral regurgitation
64
atrial a wave atrial c wave atrial v wave
a: contraction of the atrium c: bulging of mitral valve leaflets into the LA during IVC v: filling of atria during ventricular systole
65
#3
Interlobular artery
66
#4
RBC
67
heart chemosensors
cause pain in repsonse to ischemia (K, lactic acid, bradykinin, PG's)
68
NADPH oxidase
CRS activates NADPH oxidase in end stage HF through angiotensin II resulting in ROS formation
69
neovascularization
necessary vascular repair mechanism to preserve tissue and organ viability in response to ischemia most common form: critical limb ischemia
70
mitral regurgitation
during systole when mitral valve is normally closed
71
type II CRS
chronic CRS
chronic HF --\> progressive CKD
72
transcellular pathway
(permeability maintenance in BVs) transports plasma proteins (size of albumin or greater) between cells
73
calcitriol
steroid hormone activated by kidneys in response to presence of PTH - stimulates Ca absorption along the digestive dract
74
list the steps of the CC in order
IVC ejection IVR relaxation atrial systole - small additional amount of blood into ventricles
75
preferred fuel of the heart
1. LCFA (80%)
2. lactate (18%)
3. glucose (2%)
76
the property of endothelial cells to change shape in the direction of flow is? what molecule mediates this?
mechanotransduction achieved by integrins: transmembrane linkers that connect ECM to actin filaments
77
how does aldosterone increase Na reabsorption and K secretion?
aldosterone binds to cytosolic receptor in tubular cell of CT and binds translocates to nucleus to activate increases in Na and K channels being made
78
countercurrent exchange system
maintains the gradient - involves vasa recta (surrounds juxtamedullary capillaries)
79
#3
CT
80
#2
afferent arteriole
81
type 1 CRS
acute CRS
abrupt worsening of heart --\> acute kidney injury
82
#1
PCT
83
what is the dicrotic notch?
the end of left ventricular systole - when the aortic valve closes and IVR begins. there is a transient change upon closure
84
is blood a newtonian fluid?
no! non-newtonian because it has anomolous viscosity
85
in doppler, you see an increase in velocity. what does this mean?
means decrease in area (because flow has to stay constant)
86
what are those blobs
vasa recta
87
what is voltage dependent (depolarization induced) Ca release?
it is in skeletal msucle where the extra transmembrane segment makes physical contact with RYR --\> during AP channel changes shape, pulling on RYR for it to open
results in most of the Ca comes from SR in skeletal muscle
88
5 abilities of pericytes
1. regulation of TJ and GJ and bulk flow fluid for **transcytosis**
2. regulation of **vascular stability** (pro/anti angiogenic)
3. regulation of **ECM** protein secretion/levels
4. regulation of **capillary diameter/blood flow**
5. **Phagocytosis**
89
in exercise, which receptors mediate local/systemic responses?
* local:
* B2: leads to dec. TPR and dilation of skeletal muscle arterioles
* systemic:
* A1: constriction of veins
* B1: inc. HR, contractility, CO
90
what is a retrospective (nonconcurrent) study
past exposure statys from prvious data. disease has long induction/latent period. save time and money through historical data
BUT CAN NEVER SAY COHORT STUDY DESIGN IS RETRO - ONLY EVEN PROSPECTIVE!
91
type V CRS
secondary CRS
systemic disorders (DM/sepsis) leads to heart and kidney disease
92
atrial natriuretic peptide
increases salt excretion by kidneys but reducing water reabsoprtion in collecting ducts; relaxes renal arterioles, inhibits Na reabsorption in DCT
93
diastolic heart failure (HFpEF)
EF at rest is normal. ventricle has to relax to permit filling of blood - lose compliance, becomes stiffer, cavity is reduced and can't fill with blood so reduced CO
heart sound 4
94
what is cold vasodilation?
with continued cold exposure, blood flow in the cold hand increases
95
heart sound 4
heard in hypertrophy - atria trying to fill stiffened ventricle
96
where do sympathetic vasodilator fibers come from/go to?
come from: motor cortex (cholinergic)
go to: vascular beds of skeletal muscle
97
function of the vasa recta
prevents dissipation of vertical osmotic gradient in medullary interstitum (prevents hyperosmolarity) - site of countercurrent exchange
98
what is a cell with stem cell/contracting capabilities but can also repair damage in blood vessels?
pericyte
99
stroke volume
the volume of blood ejected from the ventricle SV=EDV-ESV
100
what are two ways that Ca is lowered in the cell?
1. sequestration: Ca pumped from cytoplasm back to SR
2. Na:Ca exchange
101
lung stretch receptors
cause tachycardia during inspiration-
102
extravasation steps
1. rolling: P-selectin and E-selectin appear on EC surfaces from exposure to inflammatory cytokines 2. tight binding: interaction between LFA-1 and MAC-1 and ICAM-1 - stops rolling 3. diapedesis: leukocytes extravasates endotheliam well - involves PECAM 4. migration: of leukocytes guided by chemokine gradient
103
where do lasix diuretics act?
the thick ascending LOH
to quickly remove sodium
104
how do pericytes regulate capillary diameter/blood flow?
they act by Ca influx - contract to occlude capillary lumen - **no reflow phenomenon** - post stroke no flow through capillaries
105
how do Ca and Mg get into the blood? (thru resabsorption)
paracellular pathway - transports divalent cations
increase in positive charge from K into the lumen pushes through between the cells to the blood
106
why is injecting urself with EPO (like lance armstrong) a bad idea?
viscosity is proportional to hematocrit people have died from this from strokes
107
Green arrow
Glomerular capillary tuft
108
how does an adherens junction open?
phosphorylation of tyr residues on VE-cadherin
109
if RR=1
if RR\>1
if RR\<1
RR=1: risk in exposed equal to risk in unexposed
RR\>1: risk in exposed greater than risk in unexposed (pos. association) ex. 3 is 3x risk of... or 1.6 60% increase in...
RR\<1: risk less in exposed than risk in unexposed (neg. association) ex. 0.8 is 20% reduction of risk in...
110
what type of cells release renin?
juxtaglomerular cells
111
what is the most potent vasoconstrictor?
angiotensin II
112
two types of enzyme that makes NO
eNOS: constitutively active in ECs iNOS: inducible by cytokines and vascular injury
113
atrial fibrillation
lack of P waves, regular F waves instead
114
isotonic contraction
muscle develops force equivalent to load (afterload) that it wants to move - when it does, the muscle shortens
115
what is vasopressin's effects on vascular smooth muscle? (V1A receptors)
smooth muscle contraciton
vasoconstricton: increase TPR, increase BP
116
what is in the pars radiata?
LOH and collecting duct - aka the medullary ray
117
plasma clearance
volume of plasma that is completely cleared of a substance in 1 min
118
aortic stenosis
murmur between S1 and S2 during systole - greater pressure gradient due to stenosis makes turbulent flow/murmur
119
caveolae
lipid rafts - small invaginations of plasma membrane. acts as signaling hubs in ECs
120
left sided heart failure
fluid congestion in the lung (pulmonary edema), fluids leak out into interstitum
121
what is the afterload?
the pressure that ventricle must overcome in order to open the valve and eject blood during the entire ejection phase
122
junction rhythm
no P waves or atrial activity, regular QRS complexes at a slower rate
123
transcytosis
(permeability maintenance in BVs) transports smaller molecules in vesicle carriers thru the ell originating from caveolae
124
principal cells
nonmotile cilia and moderate infoldings and mito. respond to aldosterone - resorb Na and water and secrete K. cilium as mechanosensor of fluid flow/fluid content
125
Yellow arrow
PCT
126
BNP effects
inhibits RAAS, endothelin-1 and other vasoconstrictors
promotes diuresis, enhances Na excretion and GFR
127
where does most material in vessels get exchanged?
capillaries and post capillary venules
128
whats the BFD about astrocytes?
influence cerebral blood flow: change in flow with change in activtiy faster than in any other area - tight communincation between astrocytes and BVs
secrete vasodilators (NO, adenosine, EETs, PGs, K) or vasoconstrictors (AA) to incluence cerebral vascular resistance
129
cardiac contractility what is an index for it?
the intrinsic ability of the ventricle to develop pressure (independent of preload and afterload) closely related to intracellular Ca concentrations regulated by the sympathetic nervous system index for contractility is ESPVR/Emax
130
in clinical practice, what are indices of: left ventricular afterload right ventricular afterload contractility
LV: aortic pressure RV: pulmonary artery contractility: ejection fraction
131
filtration
transfer of water, ions and small soluble compounds from blood to urine
132
what is diastasis?
reduced ventricular filling (before the atrial kick)
133
eccentric CH
increase in both cardiomyocyte length and width
134
three ways that the body prevents too much stretch in the heart:
1. titin: goes from Z line to Z line (intracellular)
2. collagen/elastin: can't stretch past 2.2 (extracellular)
3. pericardium
135
136
#1
parietal layer of BC (SSE)
137
when does IVC begin? when does IVC end?
begins: when the mitral valve closes ends: when the aortic valve opens
138
processes involved with HCM
1. left ventricular outlfow obstruction
2. diastolic dysfunciton
3. myocardial ischemia
4. mitral regurgitation
139
juxtaglomerular cells
renin producing cells, stimulated to produce renin by NE and dopamine secretion. derived from SM cells, sit on afferent arteriole and secrete renin when BP falls.
140
what is the glomerular basement membrane made of?
type IV collagen, laminin, fibronectin, heparin sulfate containing proteoglycan
141
what are the final effects of RAAS
Na reabsorption
water reabsorption
K secretion
142
#5 (yellow box)
pedicles
143
what is shear stress?
the force of blood flowing on endothelial cells sigma=(4viscosityQ)/pi\*r^3
144
#2
vasa recta
145
a failing ventricle needs a higher _____ to achieve the same improvement of CO that a normal ventricle can achieve
EDV
146
what is Ca induced Ca release?
influx of Ca thru LTCC triggers Ca release from SR --\> Ca goes across junctional space and binds to RYR to open up.
in cardiac muscle
147
how does bicarbonate get reabsorbed, and where does it occur?
occurs at PCT
1. Na/H exchanger pumps H into lumen
2. H combines with HCO3 to make H2CO3
3. H2CO3 becomes water (excreted) and CO2 (diffuses into cell)
4. carbonic anhydrase combines CO2 and H2O in cell to make H2CO3
5. HCO3- pumped back into blood stream with Na
148
what is the osmolarity of isotonic ECF?
300 mosm/L
149
speed of conduction fibers in the heart (fastest to slowest)
purkinje fibers \> atria \> ventricles \> AV node \> SA node
150
in high CO2, how do coronary bv repsond?
they dilate
151
how are hypokalemia and exercise related?
exercise leads to water loss (inc. ADH) and sympathetic activation (RAAS activity from B1 and A2 receptors) (inc. aldosterone)
aldosterone leads to K secretion
152
how do parasympathetics slow the HR?
they activate K conductance; more K open means harder to depolarize the membrane
153
What is the arrow pointing to?
transitional epithelium
154
when is the AV shunt open/closed
open: heat
closed: cold
155
what is the calcium transient?
the increase and then decrease of cytosolic free Ca
156
#1
pars convoluta
157
what happens to SV during exercise?
it increases due to increase in contractility and venous return (diastolic filling)
158
osmotic pressure
force that must be applied to a solution to block the movemnt of water into that solution
159
how is a portal system unique from normal vascular arrangement?
blood drains from capillaries into artery/vein, and then into a second set of capillaries
160
major components of intracellular fluid
K and proteins
161
where do thiazide diruetics act?
DCT
162
what is cardiac hypertrophy
thickening of interventricular wall/septum characterized by increment in cardiomyocyte size with increase protein synthesis and changes in organization of sarcomeric structure
163
nested case control study
case control study within a cohort study
has efficiency of nonconcurrent study with strengths of concurrent study
164
how do endothelial cells have adaptable permeability? what molecule mediates this?
thru the opening/closure of adherens junctions composed of VE-cadherin
165
what channel is responsible for SA node phase 4 depolarization?
funny channel
unusual in that it opens with repolarization (phase 3) - a Na conducting channel; gets depolarization started
166
concentrations of Na, K and Ca in and out of the cell:
1. Na
1. in: 10
2. out: 140
2. K
1. in: 140
2. out: 4
3. Ca
1. in: 100 nM
2. out: 1 mM
167
latch state
low energy/high tension state to avoid burning thru ATP
unique to smooth muscle
168
albuminuria (proteinuria)
excess albumin (protein) in urine caused by disruption of the negative charges within the glomerular membrane. glomerular membrane becomes more permeable to negatively charged proteins despite capillary pore size remaining constant
169
#3
pars radiata (medullary ray)
170
what is bachmann's bundle?
takes electrical impulse from SA node to right atrium
171
arterial chemosensors
stimulated in response to hypoxaemia, hypercapnia (too much CO2), acidosis, hyperkalemia), regulate breathing
172
what does NO do thats so good for us?
1. inhibits leukocyte adhesion to endothelium 2. inhibits platelet aggregation 3. inhibits SM cell migration \*\*\*decreases blood pressure!
173
congestive heart failure
pathophysiologic state where heart is unable to pump blood at a rate that is equal to what the tissues need, or can only do so from an elevated filling pressure
(symptoms of increase venous pressure often prominent)
174
what is the BFD about glomerular shared basement membrane?
fused BM (from podocyte pedicles on one side, then endothelium on the other side)
175
adenosine hypothesis
whenever myocardial O2 consumption increases or O2 delivery decreases, ATP is metabolized to adenosine which diffuses across the cell membrane --\> dilation, reduced resistance, increased blood flow/O2 delivery
176
what is the difference between short and long term BP measurement?
short term: baroreceptors
long term: kidney RAAS, humoral mediators
177
epinephrine and cardiac contractility
binds to B adrengergic receptor and inc. Ca peak/shortens duration/stronger contraction as HR increased duration of CC is matched to increase in CO can occur
178
0
urea
half is eliminated in the urine, half is reabsorbed
1. freely filtered at glomerulus
2. partially reabsorbed
3. not secreted
179
180
concentric CH
increase in cardiomyocyte thickness more than length
181
\>GFR
H ions
non is reabsorbed and additional ions are secreted
1. freely filtered at glomerulus
2. not reabsorbed
3. secreted
182
P wave (PR interval) on ECG stands for
atrial systole (atrial depolarization)
183
how do catecholamines regulate contractility?
1. NE binds to B receptors (GPCR) activate cAMP/PKA
2. PKA phosphorylates LTCC which opens more Ca channels
3. PKA phosphorylates phospholamban to move off of SERCA (increases rate of decay of Ca transient)
184
assumptions in cohort study
1. exposed and non-exposed groups define the true population
2. absence of exposure maintained in non-exposed group
3. participants didn't have outcome of interest before beginning
185
how is NO produced in an EC?
arginine dependent eNOS produces NO which diffuses across thru paracrine signaling to the smooth muscle cell guanylate cyclase activated, converts GTP to cGMP which vasodilates
186
cardiac contraction is proprtional to the amount of Ca...
bound to troponin
187
veno-atrial mechanoreceptors
respond to changes in central blood volume
188
what is mechanotransduction?
the conversion of mechanical forces into biochemical signals
189
where is the major site of K secretion?
collecting tubules
190
2 ways that afterload can be assessed:
1. ventricular pressure during ejection (upper boundary of PV loop) 2. systolic ventricular wall stress: force within the myocardium during ejection that must be overcome for a sarcomere to shorten
191
site of different flavors of capillaries:
1. continuous - BBB 2. fenestrated - glomerulus and GI 3. discontinuous - lines sinusoids of liver and BM (deals with RBC
192
MLCP (myosin light chain phosphatase)
constitutively active phosphatase
removes phosphate from MLC preventing reattachment to actin --\> relaxation
193
aortic regurgitation
murmur in relaxation and filling. blood flows from aorta back into ventricle
194
what is the ultrafiltrate made of?
proteins and RBC
195
how does glucose get from the lumen into the tubular cell to be resorbed?
secondary active transport by Na
196
heart sound 2
end of systole occurs because of the vibrations from the closure of the aortic and pulmonic valves A precedes P can hear in inspiration
197
2 factors affecting MABP
blood volume
CO
198
where is aldosterone released from?
adrenal cortex
199
what is compliance?
the stretchiness of a vessel/structure C=dV/dP
200
autoregulatory escape
sympathetic stimulation produces decrease in BF which is not maintained - in response to vasoconstriction to override NE - once you remove the stimulus causing the change in BP
followed by reactive hyperemia
201
angiogenesis (steps too) vs. vasculogenesis
angiogenesis: sprouting from pre existing vessels caused in response to HIF-1 (hypoxia inducible factor), stops when VEGF is shut off 1. gf/hypoxia 2. ECs make proteases 3. ECs migrate to chemoattractant 4. ECs proliferate 5. ECs form tubes and differentiate 6. pericytes urround the new vessels vasculogenesis: using EPCs (endothelial precursor cells) from bone marrow and circulation to form new vessels
202
countercurrent multiplication system
involves juxtamedullary nephrons and surrounding medullary interstitum to establish the vertical osmotic gradient enabling concentration of dilute urine
203
#2
renal lobule
204
perfusion pressure
differnce in pressure between aorta and right atrium
205
type IV CRS
chronic RCS
CDK --\> heart dysfunction, risk of CV events
206
secretion
releasing or transferring an endogenous substance from one body compartment to another; unlike excretion, a secreted substance has a physiological or pharmalogical function
ex. NE needed by body
207
where do sympathetic vasoconstrictor (efferent) fibers come from and go to?
come from: T1-L3/sympathetic ganglia
go to: artery, arterioles, veins NOT CAPILLARIES
208
what is a lacteal?
a blind ending lymphatic capillary
209
mitral stenosis
during diastole
210
reactive hyperemia
transient increase in blood flow to an area following ischemia
ischemia - a decrease in blood flow / less removal of metabolic byproducts --\> dilation of resistance vessels
211
what are actin filaments in SM cells attached to?
dense bodies in the cytoplasm, attachment plaques on the inside surface of the cell membrane allows for contraction
212
what is the difference between a case control study and a cohort study?
case control: sapling with regard to disease/effect
case control: sampling with regard to exposure, characteristic or suspected cause
213
for a substance to be reabsorbed it has to pass through 5 layers. what are they?
1. luminal membrane of tubular cell
2. cytosol of tubular cell
3. basolateral membrane of tubular cell
4. ECF separating tubular cell and blood
5. capillary wall
214
what is filtration at the glomerulus based on?
size
215
macula densa
specialized cells of the DCT wall - sensitive to NaCl and affects renin release from JCGs. in response to high sodium, triggers contraction of afferent arteriole reducing blood flow to glomerulus/decreases GFR
216
what are 4 things that IRS-1 activation leads to?
1. anti-apoptosis
2. vasodilation
3. anti-inflammation
4. anti-oxidative stress
217
how does ADH work?
activates V2 receptor (on basolateral membrane of CT cell) and causes synthesis and insertion of pre-existing water channels into luminal membrane of collecting ducts.
increases cAMP leavels --\> PKA activation, phosphorylates cytoskeletal proteins that transport aquaporins from the cytosol to luminal membrane surface
218
what is a prospective (concurrent) study
exposure status collected in present, subject followed forward into the future. disease has short induction/latency with current/recent exposure
219
what is the diff between multiunit and single unit SM?
multi unit: composed of discrete, independently innervated fibers, controlled by nerve signals single unit: (in walls of gut and most arteries) gap junctions allow electrical activity to spread over a large area in unison - arranged in sheets so cell membranes touch
220
right sided heart failure
tissue congestion including jugular venous distention, peripheral edema, ascites, abdominal organ engorgement. impairment of ventricular systolic performance.
can be caused by severe left sided HF, severe lung disease, pulmonary HTN, RV MI, congenital abnormalities of the heart
221
pulmonary embolism EKG
inverted T wave due to increased myocardial O2 demand and strain on RV
222
what is the difference between diffusion and filtration? who's laws describe each?
diffusion: movement of material down concentration gradient (Fick's law)
J=-PA(Cin-Cout)
filiration: convective transport due to energy differences on each side of barrier (Starling Landis equation)
223
how are the various segments of the vasculature arranged in respect to one another?
in series means more resistance because additive!
224
concentric hypertrophy
HTN higher MAP - ventricle has to develop more pressure to overcome to eject the blood. can't optimize filling
225
what is the law of laplace?
wall tension: T=Pr wall stress: Pr/Th the force that makes structure open up
226
intercalated cells
microvilli and abundant mitochondria. secrete H or HCO3- and resorb K regulating acid base balance
227
sieve plates
fenestrae organized in large planar clusters
228
#2
DCT
229
three molecular hallmarks of pathological hypertrophy
1. GPCRs
1. neuroendocrine activation of ET-1 and AII
2. chronic elevated catecholamines/beta receptor activation
2. Ca homeostasis
1. increase Ca influx and activation of Ca signaling pathways
3. fetal gene program
1. fetal cardiac proteins and natriuretic receptors
230
when is coronary blood flow the lowest/highest?
lowest: IVC
highest: IVR
231
what are the steps of the cross bridge cycle?
1. myosin head is phosphorylated by MLCK and pivots to 45 degrees and reattaches - this is a cross bridge
2. myosin head is an ATPase - when Pi is released causes myosin head to pivot back to 90 degrees but stays attached - this is the power stroke (myosin head pivot)
3. myosin head is dephosphorylated by a phosphatase, releasing actin/set for another cycle
232
what type of exercise is accompanied by a dramatic increase in blood pressure?
isometric! (dynamic slow)
233
what is the organic acid/base secretory system and where is it?
transports organic acids/bases from the blood to the tubular fluid
occurs at the PCT
234
heart sound 1
start of systole (IVC) occurs because of the vibrations of the blood, myocardium, and mitral valve (closing) from cardiac contraction
235
elimination/detoxification
discharge of organic wastes from urine into exterior
236
mesangial cells
in the renal corpuscle; make matrix, cells in between the afferent/efferent arterioles filled with stroma in the VASCULAR POLE
237
what are the goals of local and systemic control in regulation of blood flow?
local: couple blood flow and tissue need of each organ (metabolic: ion changes, myogenic: pressure changes, endothelial: paracrine substance secretion)
systemic: maintain blood pressure (neuronal, hormonal)
238
hemodynamic changes in isometric exercise
huge increase in TPR because squeezing msucle fibers so tight + metaboreflex sense inc. in stiffness; activate SNS and release NE
bad for people with HTN! want dynamic to lower TPR over time
239
PTH regulates what type of Ca channel? How does it work?
TRPV5 - puts into the DCT, then once in cell Ca is coupled to Na gradient to go into the blood
240
do SM cells have tropinin?
NO! they have calmodulin instead
241
GFR=0
glucose
all of it is returned to plasma
1. freely filtered at glomerulus
2. reabsorbed
3. not secreted
242
What is the yellow arrow pointing to?
renal corpuscle
243
five functions of endothelial cells:
1. secretion: of factors like NO or VWF 2. surface expression: of binding proteins like adhesion molecules linked to thrombogenicity 3. contraction involved in hyperpermeability: maintenance of permeability barrier 4. mechanotransducers: mediate changes in flow 5. angiogenesis: generation of new BV
244
what is a renal lobule?
in between interlobular arteries; consists of collecting duct and surrounding nephrons that drain into it
(1/2 pars convoluta on each side)
245
does the portal vein autoregulate?
no!!!
hepatic artery does though
246
What is the blue arrow pointing to?
PCTs and DCTs
247
where is vasopressin made/released?
made in hypothalamus, released by posterior pituitary
248
#1
minor calyx
249
#2
podocyte cell body
250
glomerulonephritis
STREP INDUCED
inflammation of glomerulus disrupts filtration mechanisms develops after an infection. Ag-Ab complexes pass through capillary EC pores and clog the filtration slits so filtrate production declines
251
#2
DCT
252
does loop or thiazide diuretics have greater efficiency?
loop
has greater capacity to reabsorb Na ions (25% vs 6%) so blocking Na reabsorption there means more Na in tubule which creates osmotic gradient to pull water into tubular fluid at water permeable segments of the nephron
