Cardiovascular Flashcards

Question

For each blood group, name: -Red blood cell type -Antibodies in plasma -Antigens on red blood cells

Answer 1

Over 45 different Rh antigens

Answer 2

Chromosome 1

Answer 3

-Co-dominant -2 genes -RHD for RhD -RHCE for RhC and RhE

Answer 4

-Highly immunogenic -High proportion of D neg people will form anti-D if exposed to D pos blood

Answer 5

-Haemolytic transfusion reactions -Haemolytic disease of the fetus and newborn (HDFN)

Answer 6

-Haemolytic disease of foetus/newborn -Rh D sensitisation most common cause -Development of antibodies from sensitising event

Answer 7

Hydrops fetalis

Answer 8

-Detect mothers at risk -Maternal-fetal free DNA -Anti D prophylaxis

Answer 9

-Patient's RBC -Separate testing with anti-A and anti-B regent -Testing with anti-D reagent

Answer 10

-Patient's plasma -Test with A or B RBC -Indirect Coomb's test

Answer 11

Testing donor RBC with recipient plasma to see if there will be a transfusion reaction

Answer 12

Detecting autoantibodies on the surface of RBC

Answer 13

-Exact blood type -Compatible blood type

Answer 14

-Patient with possible autoimmune haemolysis -Transfusion reactions -Detecting haemolysis due to fetal/maternal group incompatibility -Can be positive for many other reasons - many not clinically significant

Answer 15

17-65 year olds

Answer 16

Donation centers

Answer 17

-Highlight those at risk of infectious or transmissible disease -Health, lifestyle, travel, medical history, medications

Answer 18

Minimum 50kg

Answer 19

Test for anaemia in selected patients

Answer 20

-Temporary: -Travel -Tattoos -Lifestyle -Permanent: -Certain infectious diseases -Received a blood transfusion or organ-tissue transplant since 1980 -notified risk of vCJD

Answer 21

-Whole blood -Apheresis - Blood is removed and separated externally and then the components not needed are returned

Answer 22

-Hep B -HIV -Hep C -Syphylis -Human T cell lymphotropic virus -Groups and antibodies

Answer 23

-CMV -Malaria -West nile virus -Trypanosoma

Answer 24

-Whole blood donated into closed-system bags -Blood spun to separate down to packed red cells/ buffy coat and plasma

Answer 25

Male donors

Answer 26

-FFP (fresh frozen plasma) -Further processed to make cryoprecipitate

Answer 27

-Red cells kept at ambient temperature for a short time -Passed through a leucodepletion filter and resuspended in additive

Answer 28

Buffy coats pooled with donations of matching ABO and D type and then leucodepleted to make platelets

Answer 29

-Stored at 4^oC -35 day shelf life -Some units are irradiated to eliminate risk of transfusion-associated graft (lymphocyte in bone marrow) vs host disease)

Answer 30

Severe anaemia (not purely iron deficiency)

Answer 31

-Haemoglobin <70g/dL or <80g/dL if symptomatic -Transfuse 1 unit and re-check FBC (unless massive transfusion required)

Answer 32

Emergency stocks of OD^-

Answer 33

4 donations

Answer 34

-Stored at 22^oC -Continuous agitation -7 day shelf life if they are monitored for bacterial contamination

Answer 35

-Thrombocytopenia and bleeding -Severe thrombocytopenia <10 due to marrow failure (normal plt 150-450)

Answer 36

-<10 x 10⁹ if not bleeding and asymptomatic -<30 x 10⁹ if minor bleeding -<50 x 10⁹ if significant bleeding -<100 x 10⁹ if critical site bleeding (brain/eye) -Part of a massive transfusion protocol -ABO type still important as antibodies present in plasma still able to cause recipient red cell haemolysis

Answer 37

-Whole blood donations or apheresis -From male donors only

Answer 38

-Only patients born >1996 -Can only receive plasma from low vCJD risk (not UK plasma)

Answer 39

-Single donor have a variable amount of clotting factor -Pooled versions can be more standardised

Answer 40

-Multiple clotting factor deficiencies and bleeding (DIC) -Some single clotting factor iron deficiencies where a concentrate isn't available

Answer 41

-Thawing FFP to 4^oC and skimming off fibrinogen rich layer

Answer 42

-Therapeutic dose is 2 packs each pooled from 5 donations of plasma -Used in DIC with bleeding and massive transfusion

Answer 43

Immunoglobulin (IVIg)

Answer 44

-Contains Ab to viruses common in the population -Used predominantly in immune conditions such as ITP

Answer 45

-Chosen for selected patients -Contains known high Ab levels to particular infections/conditions -Anti-D immunoglobulins used in pregnancy -VZV immunoglobulin in severe infection

Answer 46

-Very rarely as effectiveness is controversial -Severely neutropenic patients with life-threatening bacterial infections -Must be irradiated

Answer 47

-Recombinant versions from the lab concentrated -Reduces risk of viral or prion transmission

Answer 48

-Factor VIII for severe haemophilia A -Factor I (fibrinogen) -Prothrombin complex concentrate -Multiple factors -Rapid reversal of warfarin

Answer 49

-Patient identification checked -2 sample rule (2 people take 2 samples at 2 different times) -Hand-written patient details -Blood selected and serologically cross-matched

Answer 50

-Most common is patient identification errors -Wrong blood in wrong tube -Less commonly - lob errors -Blood transfusions delayed -Too much blood transfused

Answer 51

-Optimise patients with planned surgical procedures pre-op -Use of erythropoietin-stimulating drugs -Renal failure and cancers -Intra-operatively -Cell salvage -IV iron for severe iron deficiency -Some patients may tolerate lower Hbs and if well not require transfusions at all

Answer 52

-Very safe -Heavily regulated and monitored (SHOT,MHRA)

Answer 53

-Hep B <1 in 1.2 million -Hep C <1 in 7 million -HIV <1 in 28 million

Answer 54

Risk reduced by leucodepletion and then even further by irradiation

Answer 55

After the blood leaves the lab - patient misidentification, over/under transfusion

Answer 56

-ABO incompatibility -Rapid intravascular haemolysis -Cytokine release -Acute renal failure and shock -Disseminated intravascular coagulation -Can be rapidly fatal -Can be acute or delayed (=>24 hours after transfusion)

Answer 57

-Stop transfusion immediately -Fluid resuscitate - A,B,C

Answer 58

Bacterial contamination

Answer 59

-Occurs very soon after starting transfusion -Fevers and rigors -Hypotension -Shock -Inspection of the unit may show abnormal colouration/ cloudiness

Answer 60

-Transfusion-related acute lung injury

Answer 61

-Ab in donor blood reacting with recipient pulmonary endothelium/neutrophils -Inflammatory cells cause plasma to leak into alveolar spaces

Answer 62

-SOB -Cough productive of frothy sputum -Hypotension -Fevers

Answer 63

Supportive treatment

Answer 64

Transfusion-associated circulatory overload -Acute or worsening pulmonary oedema within 6 hours of transfusion -One of most common adverse events related to transfusion

Answer 65

Older patients

Answer 66

-Respiratory distress -Evidence of positive fluid balance -Raised blood pressure

Answer 67

-Careful assessment of transfusion need -Limiting amount can help to avoid

Answer 68

-Chromosome 7 -EPOR - chromosome 19

Answer 69

Anaemia causing hypoxia

Answer 70

-Hypo-regenerative - Bone marrow can't produce enough RBC -Hyper-regenerative - Increased destruction of RBC

Answer 71

-Corpuscular - Inside RBC -Extra-corpuscular - Outside RBC

Answer 72

-Too many RBC -Thrombosis -Primary and secondary (caused by other things)

Answer 73

-Membrane (spherocytosis, PNH) -Haemoglobin (haemoglobinopathy) -Enzymes (G6PD, PK)

Answer 74

-Reduced production -B12 -Folate deficiency -Increased destruction/loss -Bleeding -Haemolysis -Auto or alloimmune -Redistribution (hypersplenism)

Answer 75

Hb destruction product in urine

Answer 76

-Rigid RBC -Vaso-occlusion event -Ischaemia -Haemolysis -Decreased NO

Answer 77

Dactylitis

Answer 78

-Acute chest disease -Clinical or radiological evidence of consolidation

Answer 79

-Chest pain -Fever -Dyspnoea -Cough

Answer 80

-Binds to P-selectin -Blocks its interaction with PSGL-1 on neutrophils and monocytes -Prevents platelet aggregation, maintaining blood flow -Minimize sickle-cell related pain crisis

Answer 81

Hours/days/years

Answer 82

-Thymus -Bone marrow -Blood -Lymphatic organs

Answer 83

-Neutrophil -Eosinophil -Basophil -Macrophage -Mast cell

Answer 84

-CD4 T-helper cells -CD8 T-cells -B-cells -DCa

Answer 85

-Neutrophil leukocytosis/ neutropenia -Eosinophilia/ eosinopenia -Basophilia -Monocytosis/ monocytopenia -Lymphocytosis/ lymphopenia -Myeloid malignancies -Lymphoid/plasma cell malignancies

Answer 86

When a patient would not respond to chemotherapy (failed 2 lines)

Answer 87

-Take out patient's T cells -Genetically engineered molecule added to T-cells -Genetically modified T-cells put back into patient which attack cancer

Answer 88

-Chemotherapy destroys recipient's bone marrow -Graft from donor replaces stem cells -Recipient immune system supressed

Answer 89

-Gut -Skin -Liver -Lung -(Acute or chronic) -Can attack remaining malignant cells (+ve)

Answer 90

-Lymphocyte infusion from donor -Kill donor haemopoiesis

Answer 91

-Modify immune cells -Link patient immune system to cancer

Answer 92

-Haematocrit -Normal is 0.45

Answer 93

-Cellular 45% -fluid 55%

Answer 94

Haemopoiesis

Answer 95

Bone marrow

Answer 96

Bone marrow -Adults - Axial skeleton -Children - All bones

Answer 97

-12.5-15.5 g/dl -Lower = anaemia (reduction in haemoglobin in blood)

Answer 98

-Megakaryocytes -Exocytosis

Answer 99

-Bone marrow -Blood

Answer 100

Thrombopoietin

Answer 101

-Plasma membrane -Cytoskeleton -Dense tubular system -Secretory granules: -Alpha (VWF, PF4, plasminogen) -Dense (serotonine) -Lysosome -Prexisome

Answer 102

-Platelet type (thrombocytopenia/thrombocytopathy) -Haemophilia type

Answer 103

-Hx of skin & mucosal bleeding (GI,GU) -Early post-procedural bleeding -Petechial rash -VW disease, ITP, congenital thrombocytopathy -Medication, liver disease, renal failure

Answer 104

-Hx of muscle/ joint bleeding, late post-procedural bleeding -Large suffusions, haemotomas -Haemophilia A,B,C -Non-functioning coagulation cascade, platelet unaffected

Answer 105

-Non-blanching petechial rash -Watch signs of malignancy, liver disease, splenomegaly

Answer 106

-Large suffusions -Haematoma -Likely haemophilia

Answer 107

-Reduced production (reduced megakaryocytes) -Congenital -Acquired -Increased destruction -Immune (auto/allo) -Increased megakaryocytes -Altered redistribution -Pseudothrombocytopenia

Answer 108

Low platelet count in the blood

Answer 109

Congenital: -Adhesion - Bernard-Soulier (GPIb-IX-V), PLT type vWF(GPIb) -Aggregation - Glanzman (GPIIb-IIIa) -Secretion - Gray platelet (alpha granule), storage pool disease (dense granule) -procoagulant activity Acquired: -Medication related -Underlying disease

Answer 110

Platelet counts prior to procedure to see risk of internal bleeding

Answer 111

-Liver cirrhosis patients are anticoagulating themselves - prone to bleed -Procedures and anticoagulation are not safe in liver cirrhosis patients

Answer 112

-Primary haemostasis -Normal PLT count & function -Coagulation cascade -Normal procoagulants (PT, APTT) and anticoagulants -(PC, PS, AT), normal FBG level and structure -Termination -Fibrinolysis -Normal pro and antifibrinolytics

Answer 113

-Primary haemostasis -Low PLT count but vWF high -ADAMTS13 very low, increased PLT activation to rebalance the low activation of platelets -Coagulation cascade -Low procoagulants (prolonged PT, APTT - except FVIII) and anticoagulants -Low fibrinogen but prothrombotic FBG -Termination -Fibrinolysis -Low pro and antifibrinolytics to rebalance the low procoagulants

Answer 114

-No -They develop different systems to balance -Most patients even with acute liver failure has normal haemostasis

Answer 115

-Thromboprophylaxis and anti-thrombotic treatment is underused which increases the risk of thrombosis

Answer 116

High platelet count

Answer 117

-Clonal -Reactive

Answer 118

-Bleeding/iron deficiency -Infection/inflammation -Hyposplenism -Trauma surgery/haemolysis -TREAT UNDERLYING CONDITION

Answer 119

-MPN -MDS (JAK-2, CALR, MPL, BCR-ABL, 5q-) -Increased risk of arterial or venous thrombosis -TREATMENT: ANTIPLATELET, ANTICOAGULANTS, CYTOREDUCTION, VENESECTION, APHERESIS

Answer 120

-Liquid component of blood that holds the cellular components of blood -55% of blood volume

Answer 121

-95% water -6-8% proteins (fibrinogen, albumin, globulin) -Glucose -Coagulation factors -Electrolytes (Na, Ca, Mg,HCO, CL) -Hormones -Carbon dioxide and oxygen

Answer 122

Blood plasma with clotting factors taken out

Answer 123

-FFP -Human albumin -Cryoprecipitate -Fibrinogen -Coagulation factor -IVIG

Answer 124

-Volume -Massive transfusion packs -Bleeding disorders -Passive immunisation -PEX -Albumin replacement

Answer 125

-Coagulation cascade -PLT -Vascular -Inherited/acquired

Answer 126

-Prothrombin time (PT) -Activated partial thromboplastin time (APTT) (POOR TESTS)

Answer 127

-0.04s -0.2s -0.2s -1s

Answer 128

-25mm/sec (speed) -10mm/mV (voltage)

Answer 129

A copy of one of the leads for better examination

Answer 130

-300/no. large squares in between each cycle -Number of cycles every 10s x 6

Answer 131

-60-100bpm - <60 = bradycardia - >100 tachycardia

Answer 132

The summation of all of the action potentials across the heart

Answer 133

-Positive = current flowing towards the lead -Negative= current flowing away from the lead -0 = isoelectric point (no current)

Answer 134

-SAN -Sets the pace of the heart

Answer 135

-AVN -Has an in-built delay to allow the atria to fully empty their blood into the ventricles during their contraction

Answer 136

-3 bundles of His -1 right -2 left

Answer 137

Spread the electrical activity throughout the ventricles

Answer 138

-1st step -SAN depolarises and spreads across atria -Atrial depolarisation followed by atrial contraction

Answer 139

Atrial repolarisation

Answer 140

-Delay -Current flows through the AVN

Answer 141

Ventricular depolarisation

Answer 142

Ventricular repolarisation

Answer 143

Sinus rhythm

Answer 144

-Atrial fibrillation -Random atrial activity -Random ventricular capture -Irregularly irregular rhythm

Answer 145

-Atrial fluttering -Organised atrial activity (300/min) -Ventricular capture at ratio to atrial rate (2:1) -Usually regular -Can be irregular is ratios vary

Answer 146

-120-200ms -(3 to 5 small squares) -Small delay between atrial and ventricular contractions)

Answer 147

-Degeneration of conduction system -1st heart block -Delayed AV conduction -Can lead to total heart block (stop)

Answer 148

-Less than 120ms -(3 small squares)

Answer 149

-Bundle branch block -One of bundle of His working slowly -Widening of the QRS due to different times of depolarisation of right and left ventricle

Answer 150

-Men - 350-440ms -Women - 250-460ms -Measure of time of ventricular repolarisation -Time from onset of QRS to end of T

Answer 151

-Congenital -Drugs -Predisposed to arrhythmia

Answer 152

-12 lead -Rhythm strip

Answer 153

I, II, III

Answer 154

-Electrode: -Physical connection to patients in order to measure potential at that point -10 electrodes to record a 12 lead ECG -Lead: -Graphical representation of electrical activity at a particular vector -Calculated by machine -12 leads -I-III, aVL, aVF, aVR, V1-6

Answer 155

Arms and legs

Answer 156

-Bipolar lead: -Measures pd between two electrodes -One electrode designated +ve and other -ve -Unipolar lead: -Measures pd between an electrode (+ve) and a combined reference electrode (-ve) -Known as augmented leads

Answer 157

-Right leg -Not directly involved in ECG measurement

Answer 158

-RA = NEG -LA = POS -RA -> LA = POS deflection

Answer 159

-RA = NEG -LL = POS -RA -> LL = POS deflection

Answer 160

-LA = NEG -LL = POS -LA -> LL = POS deflection

Answer 161

-I = 0 -II = +60 -III = +120

Answer 162

-60 degrees -Heart is offset at roughly this angle

Answer 163

--30 - +90 in reference to lead I -Away from this is axis deviation

Answer 164

-aVR -aVL -aVF

Answer 165

-aVR = -150 -aVL = -30 -aVF = +90

Answer 166

Lead I and II are both +ve

Answer 167

Left axis deviation

Answer 168

Right axis deviation

Answer 169

Coronal (frontal) plane

Answer 170

Transverse (horizontal) plane

Answer 171

-Left ventricle -V1+2 = Septal -V3+4 = Anterior -V5+6 = Lateral

Answer 172

Which vessels of the heart are likely to be blocked that supply the corresponding part of the heart to that chest lead

Answer 173

Acute myocardial ischaemia

Answer 174

-Lateral - Circumflex artery -Anterior - Left anterior descending artery -Inferior - Right coronary artery

Answer 175

-I = lateral -II = Inferior -III = Inferior

Answer 176

-aVR = None -aVL = lateral -aVF = Inferior

Answer 177

Ions that can cross the membrane

Answer 178

-K⁺ ions diffuse outwards (high to low concentration) -Anions cannot follow -Excess of anions inside the cell -Generates negative potential inside the cell

Answer 179

-K⁺ pumped IN cells -Na⁺ and Ca²⁺ pumped OUT of cells -Pumped against their concentration gradients -This requires ATP for energy for active transport

Answer 180

-Sodium and calcium have to be actively transported out of the myocyte -Potassium would passively diffuse out of the myocyte

Answer 181

-4 = polarised (resting potential) -0 = action potential/depolarisation -1 = initial repolarisation -2 = gradual repolarisation (plateau) -3 = quick repolarisation -4 repeats again (maintenance of resting potential)

Answer 182

Stage 4 - resting potential

Answer 183

-Stage 4 -Resting potential

Answer 184

-Stage 4 (resting potential)

Answer 185

-Stage 0 (depolarisation)

Answer 186

-Stage 1 (initial repolarisation)

Answer 187

-Stage 2 (plateau)

Answer 188

-Stage 2 (plateau)

Answer 189

-Stage 3 (repolarisation)

Answer 190

QRS complex lines up with depolarisation

Answer 191

-Local depolarisation activates nearby Na⁺ channels (voltage gated) -This causes a further influx of sodium ions -This causes adjacent voltage gated sodium ions to open, causing further sodium influx

Answer 192

The action potential to spread across the membrane

Answer 193

Gap junctions

Answer 194

Contraction of the heart muscle requires appropriately timed delivery of Ca²⁺ into the cytoplasm

Answer 195

-Depolarisation of membrane -Calcium influx through surface ion channels -2

Answer 196

-Amplification of calcium ions with NaCa transporter

Answer 197

-Calcium ions induce the sarcoplasmic reticulum to release more calcium ions -Concentration of calcium ions in the sarcoplasm is now high

Answer 198

-Calcium ions bind to troponin -Conformational change of tropomyosin reveals myosin binding sites -Myosin head cross-links with actin -Myosin head pivots causing muscle contraction

Answer 199

-Cardiac muscle contraction lasts longer than skeletal muscle -Up to 15 times longer -Due to slow calcium channels -Decreased permeability of membrane to potassium after action potential

Answer 200

-SAN -AVN -His/Purkinje system

Answer 201

-Upsloping phase 4 -Less rapid phase 0 -No discernable phase 1/2

Answer 202

-Gradual depolarisation -Until a threshold of roughly 35mV -Then rapid depolarisation via calcium ion influx

Answer 203

-Funny current -Transient calcium current -Long lasting calcium current

Answer 204

-Autonomic tone -Drugs -Hypoxia -Electrolytes -Age

Answer 205

-Drifts towards the threshold -Steeper the drift, the faster the pacemaker

Answer 206

-Higher sympathetic innervation = Higher gradient -Higher vagal = lower gradient

Answer 207

-Increase heart rate (+ve chronotropic) (up to 180-250bpm) -Increase force of contraction (+ve inotropic) -Increase cardiac output (large, by up to 200%)

Answer 208

-Decrease heart rate (-ve chronotropic) -Decrease force of contraction (-ve inotropic) -Decrease cardiac output

Answer 209

-Andrenaline and noradrenaline -Type 1 beta adrenoreceptors -Increases adenyl cyclase -> increases cAMP

Answer 210

-Decreased heart rate -Decreased force of contraction -Decreased cardiac output (by up to 30%)

Answer 211

-Acetylcholine -M2 receptors -Inhibit adenyl cyclase -> reduced cAMP

Answer 212

-Decreased heart rate (temporary pause or as low as 30-40bpm) -Decreased force of contraction -Decreased cardiac output (up to 50%)

Answer 213

increased heart rate

Answer 214

-Transmits cardia impulse between atria and ventricles -Delays impulse -Limits dangerous tachycardias

Answer 215

-Fewer gap junctions -AV fibres are smaller than atrial fibres -Allows atria to empty blood into ventricles -Limits dangerous tachycardias

Answer 216

-Faster in specialised fibres -Purkinje fibres - 4m/s

Answer 217

-Atrial and ventricular muscle - 0.3 to 0.5m/s -Purkinje fibres - 4m/s

Answer 218

-Transmit impulse from AVN to ventricles -Rapid conduction

Answer 219

-Allow coordinated ventricular contraction -Very large fibres -High permeability at gap junctions

Answer 220

-Spontaneous discharge rate of heart muscle cells decrease down the heart -SAN usually the fastest -Ventricular myocardium the slowest -This relates to the speed of repolarisation (3)

Answer 221

-Forms the refractory period in between channel proteins being open and being closed but activatable -Channel proteins are closed and in activatable

Answer 222

-Approx 0.25s -Less for atria than ventricles

Answer 223

-Prevents excessively frequent contraction -Allows adequate time for heart to fill

Answer 224

-Absolute refractory period - No depolarisation can take place -Relative refractory period - Some strong stimuli can cause action potentials -Some sodium channels still inactivated -Potassium channels still open -Affected by heart rate

Answer 225

-Tachyarrhythmia -Myocytes are less polarised -Less polarised myocytes are more easily activated

Answer 226

-How they might interact with cardiac ion channels -Will they affect QT interval?

Answer 227

Prolong the refractory period of cardiac tissues

Answer 228

-Calcium channel blockers -Potassium channel blockers -Beta-blockers -Sodium channel blockers

Answer 229

-Abnormality of K⁺ channel causes loss of function -Slower outward K⁺ current delays repolarisation -This increases risk of Early Afterdepolarisations (EAD) -Risk of syncope/ sudden cardiac arrest

Answer 230

-Contractile tissue -Connective tissue -Fibrous frame -Specialised conductive system

Answer 231

Interactions between contractile proteins in its muscular wall

Answer 232

-Transform chemical energy derived from ATP into mechanical work -This moves blood under pressure from the great veins into the pulmonary artery, and from the pulmonary veins into the aorta

Answer 233

Signalling process called excitation-contraction coupling

Answer 234

-Begins when action potential depolarises the cell -Ends when Ca²⁺ in the cytosol binds to the Ca²⁺ receptor of the contractile apparatus

Answer 235

-Passive movement -Mediated by Ca²⁺ channels

Answer 236

Ion exchangers and pumps transport Ca^{2+^{out of the cytosol against a concentration gradient}}

Answer 237

-Regulates excitation-contraction coupling and relaxation -Separates the cytosol from extra-cellular space and sarcoplasmic reticulum

Answer 238

Cross-striated myofibrils

Answer 239

-Free fatty acids during aerobic respiration -Efficient energy production

Answer 240

-No FFA metabolism -Anaerobic metabolism of glucose ensues -Produced energy sufficient to maintain survival of affected muscle without contraction

Answer 241

Contractile proteins arranged in a regular array of thick and thin filaments (organelle)

Answer 242

Region of the sarcomere occupied by the thick filament

Answer 243

-Area occupied only by thin filaments that extend towards the centre of the sarcomere from the Z lines -Contains tropomyosin and troponins

Answer 244

Bisects each I band

Answer 245

Functional unit of the contractile apparatus

Answer 246

The region between a pair of Z lines

Answer 247

-Two half I bands -One A band

Answer 248

-Membrane network that surrounds the contractile proteins -Sarcotubular networks at the centre of the sarcomere -Subsarcolemmal cisternae - abut the T-tubules and the sarcolemma

Answer 249

-Transverse tubular system -Lined by a membrane continuous with the sarcolemma -Lumen of the T-tubules carries extracellular space towards the centre of the myocardial cell

Answer 250

-Sliding of actin over myosin by ATP hydrolysis through the action of ATPase in the head of the myosin molecule -Heads form cross-bridges that interact with actin

Answer 251

-After linkage between calcium and TnC -Deactivation of tropomyosin and TnI

Answer 252

-2 heavy chains - also responsible for the dual heads -4 light chains -Heads perpendicular on thick filament at rest, bend towards centre of sarcomere during contraction -Alpha and Beta myosin

Answer 253

-Globular protein -Double stranded macromolecular helix (G) -Both form the F actin

Answer 254

-Elongated molecule made of two helical peptide chains -Occupies each longitudinal groove between the two actin strands -regulates the interaction between the other three

Answer 255

-I - With tropomyosin, inhibits actin and myosin interaction -T - binds troponin complex to tropomyosin -C - High affinity calcium binding sites, signalling contraction

Answer 256

Drives TnI away from actin, allowing its interaction with myosin

Answer 257

Bends towards the M line (centre of sarcomere)

Answer 258

-Calcium ions -Troponin phosphorylation -Myosin ATPase

Answer 259

-Maintain blood flow -Maintain arterial pressure -Distribute blood flow -Auto-regulate/homeostasis -Function normally

Answer 260

-Anatomy -Blood -Pressure -Volume -Flow

Answer 261

-Liver - 27% -Kidneys - 22% -Muscle = 155 -Brain - 14%

Answer 262

-Skin - 6% -Bone - 5% -Heart - 4%

Answer 263

-Low resistance conduits -Elastic -Cushion systole -Maintain blood flow to organs during diastole

Answer 264

-Principal site of resistance to vascular flow -TPR = total arteriolar resistance -MAJOR role in determining arterial pressure -Major role in distribution flow to organs/tissues

Answer 265

-Local -Neural -Hormonal

Answer 266

-Vascular smooth muscle (VSM) -VSM contract = lower radius = higher resistance = lower flow -VSM relaxes = increase radius = lower resistance = higher flow -(Vasoconstriction/vasodilation)

Answer 267

The vascular smooth muscle is never completely relaxed

Answer 268

-40,000km length -Large area

Answer 269

Allows time for nutrient/waste exchange

Answer 270

-Plasma or interstitial fluid flow determines the distribution of ECF between compartments -Arteriolar resistance -No. of open pre-capillary sphincters

Answer 271

-Compliant -Low resistance conduits -Capacitance vessels -Valves aid venous return (VR) against gravity

Answer 272

-70% of blood volume -10mmHg

Answer 273

-Valves -Skeletal muscle/ respiratory pump -SNS mediated vasoconstriction maintains VR/VP

Answer 274

-Fluid/protein excess filtered from capillaries -Return of this interstitial fluid to CV system -Thoracic duct, left SC vein

Answer 275

-Uni-directional flow -Aided by: -Smooth muscle in lymphatic vessels -Skeletal muscle pump -Respiratory pump

Answer 276

Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)

Answer 277

Blood Pressure (BP) = CO x Total Peripheral Resistance (TPR)

Answer 278

Pulse Pressure (PP) = Systolic pressure - Diastolic pressure

Answer 279

Mean Arterial Pressure (MAP) = Diastolic pressure + 1/3PP

Answer 280

-Ohm's Law -Poiseuille's equation

Answer 281

-P = pressure -u = viscosity -L = length -Q = flow rate -R = radius

Answer 282

-SV increases as EDV increases -Due to length-tension relationship of muscle -Higher EDV = more stretch = higher force of contraction -Cardiac muscle at rest is NOT at optimum length

Answer 283

-Frank-Starling relationship -Higher venous return = higher EDV = higher SV = higher CO -(Even if HR constant)

Answer 284

-Important beat to beat (FS mechanism) -Blood volume is an important long term moderator

Answer 285

-Na⁺, H₂O -Renin-Angiotensin-Aldosterone system -ADH -Adrenals and kidneys

Answer 286

MAP = CO x TPR

Answer 287

-Maintain blood flow -Needs pressure to push blood through peripheral resistance -MAP = CO x TPR

Answer 288

Pressure of blood within and against arteries

Answer 289

-Systolic - Highest, when ventricles contract (100-150mmHg) -Diastolic - Lowest, when ventricles relax (NOT 0 due to aortic valves and aortic elasticity, 60-90mmHg)

Answer 290

-Sphygmomanometer -Brachial artery -Convenient. to compress -Level of heart

Answer 291

-Autoregulation -Local mediators -Humural factors -Baroreceptors -Central (neural control)

Answer 292

-Stretch of vascular smooth muscle -Contraction until diameter is normalised or slightly reduced

Answer 293

-Intrinsic ability of an organ -Constant flow despite perfusion pressure changes

Answer 294

-Renal/cerebral/coronary = Excellent -Skeletal muscle/splanchnic = Moderate -Cutaneous = Poor

Answer 295

-Intrinsic control -Maintain BF to vital organs

Answer 296

-Extrinsic -BF is important in general vasocontrictor response and also responses ti temperature via extrinsic via hypothalamus

Answer 297

-BOTH -At rest, vasoconstrictor is dominant (extrinsic) -Upon exercise, intrinsic mechanisms predominate

Answer 298

-Endothelin-1 -internal blood pressure (myogenic autoregulation)

Answer 299

-Hypoxia -Adenosine -Bradykinin -Small molecules (NO, K⁺, CO₂, H⁺) -Tissue breakdown products

Answer 300

-Control functions

Answer 301

-Nitric Oxide (NO) = potent vasodilator -Prostacyclin = potent vasodilator -Endothelin = potent vasoconstrictor

Answer 302

-Two vessels, one without endothelium -Expose to Acetyl choline -One with endothelium dilates, other constricts -Endothelium produces NO

Answer 303

-Epinephrine (skin) -Angiotensin II -Vasopressin (ADH)

Answer 304

-Epinephrine (muscle) -Atrial natriuretic peptide

Answer 305

Pressure sensing receptors

Answer 306

-Primary (Arterial) = carotid sinus & aortic arch -Secondary = veins, myocardium, pulmonary vessels

Answer 307

-Afferent = Glossopharyngeal (IX) -Efferents = Sympathetic and vagus (X)

Answer 308

-MAP -PP -integrated in the medulla

Answer 309

Increased BP = increased firing = Increased PNS / Decreased SNS = decreased CO/TPR = Decreased BP

Answer 310

-Short-term regulation of BP -minute to minute control -response to exercise -haemorrhage

Answer 311

-They adapt/reset to new baseline pressure -e.g. in hypertension -Major factor in long-term BP control is blood volume (H₂O, Na⁺

Answer 312

-Atria -Ventricles -PA stretch

Answer 313

Atrial natriuretic hormone (ANP)

Answer 314

-Lower activity of vasoconstrictor centre in medulla -Lower BP -Lower release of angiotensin, aldosterone and vasopressin (ADH), fluid loss -Blood volume regulation

Answer 315

-Baroreceptors -Chemoreceptors -Hypothalamus -Cerebral cortex -Skin -Changes in blood O₂ and CO₂

Answer 316

Hypothalamus and pons

Answer 317

-Decreased Bp and HR -Reverse happens with posterolateral hypothalamus

Answer 318

Regulation of skin blood flow in response to temperature

Answer 319

-Blood flow and pressure -Stimulation usually = increased vasoconstriction -Emotion can increase vasodilation and depressor responses e.g. blushing, fainting -Effects mediated by medulla but some directly

Answer 320

Chemosensitive regions in the medulla

Answer 321

-High and low PaCO₂ -High and low pH

Answer 322

-Increase = Vasoconstriction = Increase in peripheral resistance = Increase in BP -Decrease = Decrease medullary tonic activity = Decrease in BP -pH reverse (more peripheral)

Answer 323

-Peripheral chemoreceptors -In central chemoreceptors: -Moderate decrease = vasoconstriction -Severe decrease - general depression

Answer 324

-Baroreceptors -Increase BP = Increase firing = Increased PNS/Decreased SNS = Lower CO/TPR = Lower BP

Answer 325

-Volume of blood -Na⁺, H₂O, RAAS and ADH

Answer 326

-Peripheral -Blood vessels (vasoconstriction & vasodilation - affects TPR) -Heart (rate & contractility: CO = HR x SV) -Kidney (fluid balance - longer term control)

Answer 327

-LV contraction -LV relaxation -LV filling

Answer 328

-Isovolumetric contraction (b) -Maximal ejection (c)

Answer 329

-Start of relaxation and reduced ejection (d) -Isovolumetric relaxation (e) -Rapid LV filling and LV suction (f) -Slow LV filling (diastasis) (g) -Atrial booster (a)

Answer 330

-Wave of depolarisation arrives -opens the L-calcium tubule (R peak on ECG) -Ca²⁺ arrive at contractile proteins -LVp rises > LAp -MV closes - M₁ of 1st HS -LVp rises (isovolumetric contraction) >Aop -AoV opens and ejection starts

Answer 331

-LVp peaks then decreases -Influence of phosphorylated phospholambdan, cytosolic calcium is taken up into the SR -"phase of reduced ejection" -Ao flow is maintained by aortic distensibility -LVp < Aop, Ao valve shuts, A₂ of the 2nd HS -"isovolumetric relaxation", then MV opens

Answer 332

-A measure of elasticity -How well something (vessel) can stretch under pressure

Answer 333

-LVp < LAp, MV opens, Rapid filling starts (E) -Ventricular suction (active diastolic relaxation), may also contribute to E filling -Diastasis (seperation): LVp = LAp, filling temporarily stops -Filling is renewed when A contraction (booster) raises LAp creating a pressure gradient

Answer 334

-Physiological: -Isovolumetric contraction -Maximal ejection -Cardiological: -From M₁ to A₂ -Only part of isovolumteric contraction (includes maximal and reduced ejection phases)

Answer 335

-Physiological: -Reduced ejection -Isovolumetric relaxation -Filling phase -Cardiological: -A₂ to M₁ interval (filling phases included)

Answer 336

The load present before LV contraction has started

Answer 337

The resistance the left ventricle must overcome to circulate blood

Answer 338

Within physiological limits, the larger the volume of the heart, the greater the energy of its contraction and the amount of chemical change at each contraction

Answer 339

-Difference between the LAp and LV diastolic pressure -The relationship reaches a plateau

Answer 340

-Force produced by the skeletal muscle declines when the sarcomere is less than the optimal length (Actin's projection from Z disc "1um" X 2) -In the cardiac sarcomere, at 80% of the optimal length, only 10% of maximal force is produced

Answer 341

-Must function near the upper limit of their maximal length -L_max = 2.2um

Answer 342

When the sarcomere lengthens from 85% of L_max to L_max

Answer 343

Steep relationship

Answer 344

Isovolumetric contraction

Answer 345

-Increased velocity and force of contraction -Isovolumetric contraction + Frank-Starling -Large force -+ve inotropic effect

Answer 346

-Inotropic state -State of the heart which enables it to increase its contraction velocity -Higher contractility = higher pressure achieved (independent of load)

Answer 347

Myocardial ability to recover its normal shape after removal of systolic stress

Answer 348

The relationship between the change in stress and the resultant strain - dP/dV

Answer 349

Pressure required to fill the ventricles to the same diastolic volume

Answer 350

Pressure-volume loop in the end-systolic pressure volume relationship

Answer 351

End diastolic pressure volume relationship

Answer 352

Isovolumetric contraction

Answer 353

-NEVER -Isotonic contraction is totally impossible in the heart

Answer 354

Mass movement and invagination of the blastula to form three layers: ectoderm, mesoderm (middle) and endoderm

Answer 355

-Skin -Nervous system -Neural crest (contributes to cardiac outflow, coronary arteries)

Answer 356

-All types of muscle -Most system -Kidneys -Blood -Bone

Answer 357

-GI tract (inc liver, pancreas, but not smooth muscle) -Endocrine organs

Answer 358

-Cells which were situated in the mesoderm -Blood, heart, smooth muscle, endothelium

Answer 359

Cardiac neural crest cells from the ectoderm

Answer 360

-Basic tube -Single loop -Double loop septated heart

Answer 361

-Heart and blood vessels sometimes try to turn into bone -Both derived from the mesoderm

Answer 362

-First heart field = Red -Second heart field = Yellow -Day 15

Answer 363

Generates a scaffold which is added to by the second heart field and cardiac neural crest

Answer 364

-FHF = Future left ventricle -SHF = Outflow tract, future right ventricle, atria

Answer 365

-Single ventricle -Inflow tract into 2 structures that will become right and left atria -Conus trunk (truncus arteriosus)

Answer 366

-More looped structure -R atrium + Left atrium -R ventricle + L ventricle -Conus trunk (truncus arteriosus)

Answer 367

-Fully developed heart

Answer 368

DNA which when expressed is transcribed into RNA which is translated into protein with a function

Answer 369

A type of protein which when expressed "turns on/off" many other gene(s) expression: master regulators of complex processes

Answer 370

-NKx2.5 -GATA -Hand -Tbx MEF2 -Pitx2 Fog-1

Answer 371

They are expressed in a tissue-specific manner

Answer 372

-As organisms evolve, gene duplication occurs sporadically (from single gene to entire genome) -Each copy of each gene can evolve separately into different (but related) genes

Answer 373

-Formation of the primitive heart tube -Cardiac looping -Cardiac septation

Answer 374

-Formed from cells that form a horseshoe shape called the cardiogenc region

Answer 375

-Day 19 -Two endocardial tubes form -Two tubes will fuse to form a single, primitive heart tube

Answer 376

-Day 21 -Embryo undergoes lateral folding -Two endocardial tubes have fused to form. a single heart tube

Answer 377

-Most of the right ventricle -Parts of. the outflow tract for aorta and pulmonary trunk

Answer 378

Most of the left ventricle

Answer 379

Anterior parts of the right and left atria

Answer 380

-Superior vena cava -Part of the right atrium -Splits between right and left horn

Answer 381

Increases heart size (Fish heart)

Answer 382

-Induces cardia bifida -Failure of the endocardial tubes to fuse (Chick heart)

Answer 383

-Tubus cordis moves inferiorly, anteriorly and to the embryos right

Answer 384

The primitive ventricle moves to the embryo's left side simultaneous to the movement of the bulbis cordis

Answer 385

Primitive atrium and sinus venosus move superiorly and posteriorly -Sinus venosus is posterior ti the primitive atrium

Answer 386

Leftward ventricle

Answer 387

-Improper left-right positioning -Kartagener's syndrome

Answer 388

-The node secretes nodal, which circulates to the left due to ciliary movement -A cascade of transcription factors transduce looping

Answer 389

-One common atrium -One common ventricle -Joined by the atrioventricular canal -Future superior vena cava

Answer 390

-Masses of tissue called endocardial cushions grow from the sides of the atrioventricular canal -Position the canal into two separate openings as they fuse -Push the atrioventricular canal to the right -Now the right and left atrioventricular canals

Answer 391

Right and left atrioventricular openings of the heart

Answer 392

-Through primative atrium -Through both atrioventricular canals -Through primitive ventricle -Through trunucs arteriosus

Answer 393

-Thrombosis -Formation of a clot (thrombus) inside a blood vessel -Platelets have central role in arterial thombosis -Heart attack -Stroke -Sudden death

Answer 394

Antiplatelet medication

Answer 395

-Build up of fatty plaque -Eventual damage to endothelial wall and occlusive thrombus forming

Answer 396

Atherogenesis and atherothrombosis

Answer 397

-Shape change -Smooth discoid to spiculated + pseudopodia -Increased surface area -increased possibility of cell-to-cell interactions

Answer 398

-Surface of platelet -50,000-100,000 on resting platelet -Platelet activation: -Increases number of receptors -Increases receptor affinity for fibrinogen

Answer 399

Fibrinogen links glycoprotein IIb/IIIa receptors, binding platelets together

Answer 400

Platelets adhere to damaged vessel wall

Answer 401

-Collagen receptors on platelets bind to subendothelial collagen which is exposed -GPIIb/IIIa also binds von Willebrand factor (VWF) which is attached to collagen -Soluble agonists are also released and activate platelets

Answer 402

Endothelial damage

Answer 403

Initial adhesion vis GPIB/VWF

Answer 404

-Rolling GPIb/VWF -alpha2beta1/collagen adhesion -Platelets are activated

Answer 405

-Stable adhesion -Activation/aggregation -GPVI GPIIb/IIIa

Answer 406

GPVI to collagen

Answer 407

Due to all receptors adhering to collagen

Answer 408

-ADP -> P2Y₁ -Collagen -> GPVI -Thromboxane A₂ -> TPalpha -Thrombin -> PAR1 + PAR 4

Answer 409

-Shape change -Cross-linking of GPIIb/IIIa -Platelet aggregation

Answer 410

-Aspirin -Prevents production and release of Thromboxane A₂ when collagen binds to GPVI

Answer 411

-Left 5th intercostal space -Mid-clavicular line

Answer 412

-SVC -Right atrium

Answer 413

-Aortic knuckle -Left pulmonary artery -Left atrial appendage -Left ventricle

Answer 414

Mainly right ventricle

Answer 415

Mainly left atrium and pulmonary veins

Answer 416

The area in between the right and left pleura

Answer 417

-Plane between sternal angle and T4/5 divides superior and inferior mediastinum -Pericardium divides anterior, middle and posterior mediastinum

Answer 418

-Fibrous (parietal) layer -Visceral layer

Answer 419

-Pericardial space -Potential space

Answer 420

-Cardiac tamponade -Restricts and impairs filling

Answer 421

-Pleural reflection -From the left of the xiphisternum

Answer 422

-Atrioventricular valves -Tricuspid and mitral

Answer 423

Disorders of the ventricle often affect function of the relevant atrioventricular valve

Answer 424

-Papillary muscles -Connect via chordae tendinae

Answer 425

-Semilunar valves -Aortic and pulmonary

Answer 426

Function of their respective valve

Answer 427

-Arterial blood -Not always fully oxygenated

Answer 428

-Venous blood -Not always deoxygenated

Answer 429

Pulmonary artery

Answer 430

Pulmonary veins

Answer 431

Cyclooxygenase 1 and 2

Answer 432

-Arachidonic Acid -> Prostaglandin H₂ -In both platelets (COX-1) and endothelial cells (COX-1 and COX-2)

Answer 433

-In platelets: -Prostaglandin H₂ -> Thromboxane A₂ -In endothelial cells: -Prostaglandin H₂ -> Prostacylcin

Answer 434

-Thromboxane A₂ amplifies: -Platelet aggregation -Vasoconstriction -Prostacyclin inhibits above two processes

Answer 435

Thromboxane A₂ amplification pathway

Answer 436

-Low dose - inhibits COX-1 -High dose - inhibits COX-1 & COX-2 -Preferential effect on platelets as not much reaches endothelial cells -Inhibits platelets activation

Answer 437

-P2Y₁ - Gq protein -P2Y₁₂ - Gi protein

Answer 438

Signalling molecule

Answer 439

-Binds to P2Y₁ -Activates it -Amplifies Phospholipase C pathway -Triggers release of Ca₂₊ from intracellular stores -Activates protein kinase C

Answer 440

-Initiation of aggregation -Shape change (spiculated)

Answer 441

ADP amplification pathway P2Y₁

Answer 442

-P2Y₁₂ protein -Activates it -Inhibits Adenylate cyclase -Inhibits formation of Cyclic AMP (cAMP) from adenylate cyclase -Activates PI3 kinase

Answer 443

-Amplification of: -Platelet activation -Aggregation -Granule release

Answer 444

ADP amplification pathway P2Y₁₂

Answer 445

-ADP binds to P2Y₁ and activates it -This induces platelet activation -This activates GPIIb/IIIa -Fibrinogen can bind to GPIIb/IIIa and cause cross-linking platelet aggregation

Answer 446

-ADP binds to P2Y₁₂ -This amplifies the activation of platelets through P2Y₁ -Sustains platelet activation and aggregation

Answer 447

-Dense granules -Released from the cell surface to bind to P2Y receptors

Answer 448

Amplifies the platelet activation response

Answer 449

-Thrombin is generated through the coagulation cascade -Binds to PAR-1 receptor -Can bind to PAR-4

Answer 450

-Release of ADP through dense granules -ADP binding to P2Y₁ activating platelets -ADP binding to P2Y₁₂ further amplifying activation

Answer 451

Platelets provide a surface for proteins involved in coagulation to assimilate on

Answer 452

-Aminophospholipids only on inner surface of bi-layer -Maintained by protein called translocase

Answer 453

-Thrombin activates PAR-1 -Amplification of Ca²⁺ release from intracellular stores

Answer 454

-Negative inhibition of translocase -Positive amplification of scramblase -Scramblase causes aminophospholipids to move to the extra-cellular side of membrane

Answer 455

-Allows assembly of proteins of the coagulation cascade -Va and Xa can bind together to form prothrombinase -This complex can then convert prothrombin into thrombin

Answer 456

Amplifies its own production

Answer 457

-Platelet-fibrin clots -Fibrin at the centre of this relationship

Answer 458

-tPA - tissue plasminogen activator -Converts plasminogen into plasmin

Answer 459

Converts fibrin into fibrin degradation products

Answer 460

Antiplasmin (plasmin, antiplasmin complex)

Answer 461

-Coagulation factors -Inflammatory mediators

Answer 462

-Pro-inflammatory and prothrombotic interactions with leukocytes -Release inflammatory mediators from alpha granules -Through P-selectin

Answer 463

-Contained in alpha granules -When released, expressed on platelet surface -Leukocytes have counter-receptor called PSGL-1 -Binding of two receptors -Increases inflammatory response

Answer 464

-Left ventricle -Systemic ventricle -Right ventricle has a thin muscular wall -Atria are thin walled

Answer 465

-Four pulmonary veins (usually) -Drain into the left atrium

Answer 466

-Coronary sinus -Right atrium

Answer 467

-Smooth (from sinus venosus) -Trabeculated (from original atrium)

Answer 468

Crista terminalis

Answer 469

Remains of the foramen ovale which was present in foetal life

Answer 470

-Cross-link -Join at intercalated discs

Answer 471

-Arise from the aortic root sinuses -Supply the heart itself

Answer 472

-Yes (bypass surgery) -They are epicardial

Answer 473

Left and right main coronary arteries

Answer 474

-Functional end arteries -Only one area of tissue is supplied by the artery (do not connect) -Unless collateral supply has developed

Answer 475

-Left anterior descending (LAD) -Circumflex (Cx)

Answer 476

Runs in the anterior interventricular groove

Answer 477

-Septal branches - Septum -Diagonal branches - Left ventricular myocardium

Answer 478

Runs in the left atrioventricular groove

Answer 479

Obtuse marginal branches to the posterolateral LV wall

Answer 480

Right atrioventricular groove

Answer 481

-SAN -AV node -Branches to the anterior RV wall

Answer 482

-Posterolateral arteries -Posterior descending artery (70%)

Answer 483

-Posterior interventricular groove -Supplies inferior septum and LV

Answer 484

-Refers to the artery which supplies the posterior descending artery -RCA or Cx

Answer 485

-10% left dominant - Cx -20% co-dominant - Cx + RCA -70% right dominant - RCA

Answer 486

-Every cell in body need bathed in fluid and 2mm from oxygenation -Reproduces extracellular primitive uni and multi-cellular organisms in primeval ocean

Answer 487

-Conduits of blood -Physical properties: -Elastic arteries - increase efficiency -Muscular arteries - regulatory control of distribution

Answer 488

-Major distribution vessels -Aorta, brachiocephalic, carotids, subclavian, pulmonary -Biggest

Answer 489

-Mains distributing arteries -Smaller than elastic, bigger than arterioles

Answer 490

-Terminal branches -Smaller than muscular and elastic arteries - <300 um diameter

Answer 491

-Functional part of circulation -Blood flow regulated by precapillarry sphincters -Between 3-40 microns in diameter -Three types: -Continuous (most common) -Fenestrated -Discontinuous (liver sinusoids)

Answer 492

-Return blood to heart -System of valves allows "muscular pumping" -Some peristaltic movement

Answer 493

-Abberrant embryology accounts for many congenital abnormalities in fetal death -Many processes which pattern blood vessels in embryo are also used in post-natal physiological and pathalogical processes

Answer 494

Axial vessel formation

Answer 495

Other mesodermal cells are recruited

Answer 496

-Angiogenic growth factors (vascular endothelial growth factor, angiopentin 1 and 2) -Repulsive signals -Attractive signals (VEGF)

Answer 497

-Structure -Flow conditions -Specific features -Specific embryonic proteins in arteries and veins (gene activation)

Answer 498

-Aortic arches -7 weeks

Cardiovascular Flashcards

(598 cards)