Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Cardio Exam
CV Exam Cards
| Question | Answer |
|---|---|
| C Wave of Atrial Pressure | Pressure increase in the atrium when the ventricles contract. Pressure pushes the AV valve up into atrium, increasing atrial and venous pressure. |
| A Wave of Atrial Pressure | A pressure increase during atrial contraction. It can be seen in the jugular and pulmonary veins since there is no valve (atrium and previous veins). |
| V wave of Atrial Pressure | The pressure increase that occurs as new blood flows into the atrium. (This occurs along with ventricular contraction & ejection). Stiffness in atrial wall = higher V wave pressure. |
| When does peak systolic pressure occur? | Between aortic valve opening and closing. |
| When is the blood flow through the coronary arteries the lowest? | During Isovolumetric contraction. |
| What causes autoregulation of Cerebral blood flow to shift? | Hypertension |
| Inhibition of cutaneous sympathetics during exercise leads to what? | dilation of arterioles |
| What effect do hypertrophy and infarction have on vector? | Vector moves away from infarction and towards an area of hypertrophy. |
| Tunica Intima | Innermost layer of arteries. Contains endothelium, Tightly anchored to a basal lamina. -Contains an internal elastic lamina |
| Tunica Media | contains a variable amount of reticular fibers, elastic fibers, and/or smooth muscle cells. Also contains an external elastic lamina. |
| Tunica Adventitia | Outer lining of Vessels. Contains the connective tissue that anchors the vessels in place. This layer may contain vessels and nerves. (vaso vasorum, nervi vasorum) |
| Elastic Arteries | The big arteries. Contain a large amount of layers of elastic fibers in tunica media. Also, an incomplete internal elastic lamina. |
| Muscular Arteries | identifiable by the well-defined internal elastic lamina and several layers of smooth muscle in the tunica media. May also have a well-defined external elastic lamina. |
| Arterioles | Usually do not have a well defined internal or external elastic lamina. They contain a few layers of muscle in tunica media. |
| Capillaries | Have a single layer of endothelium. Also some connective tissue in adventia. |
| Continuous Capillary | Have a connected endothelium and basal lamina. These are the most common capillaries. Have tight junctions between endothelial cells in the CNS. |
| Fenestrated Capillary | Small holes in the endothelium but an intact basil lamina. Found in: endocrine organs, GI, urinary filtration apparatus. |
| Sinusoidal Capillary | large fenestrae in endothelium, holes in basal lamina, large gaps between adjacent endothelial cells. Liver, spleen & bone marrow. |
| Arteriosclerosis | degeneration of the tunica intima by cholesterol deposition, inflammation occurs as macrophages engulf cholesterol and cause inflammation. Clotting of the blood can occur in the inflamed and endothelium-deficient area. |
| Restenosis | proliferation of smooth muscle in the tunica media that can block the lumen. |
| Aneurysm | weakening and expansion of the vessel due to weakness in the tunica media. |
| Vericose Veins | tortuous, dilated veins caused by decrease in muscle tone and failure of venous valves. Blood pools and may thrombose within the vessel. |
| Venous Valves | Prevent backflow in veins. Usually found in medium sized veins. |
| Deep Vein Thrombosis (DVT) | Clots that have formed inside Veins. Occur due to blood stasis or trauma to veins. Can cause a pulmonary embolism. |
| Lymphatics around vessels | Drauin the fluid, proteins, enzymes, lipids, antibodies, hormones, and other macromolecules in the interstitial space and return to subclavian veins. |
| Exceptions to Blood Volume Distribution | The heart has a high resting O2 consumption, but receives a lower % of resting CO. The Kidneys have low O2 consumption and a higher % of resting CO. |
| Mean Arterial Pressure (MAP) equation | diastolic + (1/3 (s-d)) |
| where is the majority of the systemic blood held? | In the veins because they are so compliant. |
| Windkessel Effect | The arterial stretch during systole which contributes to production of diastolic pressure. |
| How does resistance change with increase in diameter | Inversely proportional to radius increase. 1/x^4 |
| How do you calculate resistance in parallel and series | Parallel= 1/Rtotal (1/2+1/2+1/2 = 2/3) series= R total (add them all up) |
| What are the 3 patterns of blood flow? | Laminar, Turbulent, and single-file |
| Turbulence | Promoted by high blood flow In Ventricles and stenosed arteries. Depends on Velocity, vessel diameter, and blood viscosity. Makes a whooshing sound (Bruits). |
| Sinus arrhythmia | disturbance of regular rhythm that is NOT abnormal. Instead it is caused by respiration. Inspiration accelerates, expiration decelerates. |
| Normal automaticity | arrhythmias associated with normal automatic pacemakers |
| Abnormal automaticity | arrhythmias associated with non-pacemaker cells that develop automaticity. Cannot be overdrive suppressed. |
| Triggered activity and Examples | Oscillations in membrane potential that trigger an action potential. -EAD & DAD |
| Afterdepolarization | an oscillation in membrane potential following the upstroke of an action peotential. DAD and EAD |
| 1st degree block | consistent prolongation of the PR interval but every impulse gets through. |
| 2nd degree block | not all impulses get through the AV node. Some beats are dropped -Wenckeback -Mobitz (Mobitz Type II) |
| Wenckeback (Mobitz Type I) | Progressive prolongation through the AV node with an eventual dropped beat. Then cycle repeats. Occurs in AV node soley. |
| Mobitz (Mobitz Type II) | Dropped beats without the prolongation of the PR interval. This is a serious problem. Occurs in bundle fibers. |
| 3rd Degree AV block | complete block through the AV node. The normal P wave doesn't conduct through the node; therefore, on e of the latent pacemakers below the region of block may instead excite the ventricles. |
| Re-entry | an arrhythmogenic mechanism in which the impulse does not die out; it instead continues to circulate and re-excite tissue. |
| Conditions necessary for Re-entry to occur? | Unidirectional block Slowed conduction Re-excitation of tissue proximal to block |
| Examples of Re-entry on EKG | atrial and ventricular fibrillation. |
| Wolf-Parkinson-White Syndrome | when the patient has an accessory pathway from atrium to ventricles. This pathway is fast and can allow conduction quicker than through the AV node. Produces a delta wave on an EKG. |
| Supraventicular tachycardia (Reentrant Tachycardia) | usually caused by WPW syndrome where the conduction of impulse goes through the AV node and back up the accessory pathway creating a circus rhythm. Produces retrograde P waves. |
| Antidromic atrioventricular reentrant tachycardia | Impulses are conducted anterogradely down the accessory tract and retrogradely up the AV node. The QRS complex is very widened because the ventricles are stimulated by abnormal conduction thru accessory pathway. |
| Cardiac Output | volume of blood pumped by each ventricle per minute |
| Stroke Volume | Volume of blood ejected per beat |
| Heart Rate | Number of beats per minute |
| Cardiac Output equation | CO=HR * SV |
| Stroke Volume Equation | SV = EDV-ESV |
| Ejection Fraction | =SV/EDV This should be higher than 55% in a healthy person. |
| Afterload | The resistance the heart must overcome to get blood into the periphery. 1.Pressure (hypertension) 2. vent. Radius (dilation) 3. vent. Wall thickness (hypertrophy) |
| Preload | Amount of myocardial stretch @ end diastole. -Compliance -Diastolic Filling Time -increased inflow resistance (tricuspid stenosis) |
| Frank Starling Law of the Heart | increased length (volume)of myocyte, increase force of contraction. This allows the heart to have enough force to propel the amount of blood it takes in. |
| What does Increasing Preload do? | inc EDV inc EDP inc SV and CO |
| Effect of Increasing Afterload? | increases ESV inc pre ejection pressure dec SV and CO |
| Effect of Increasing Contractility (inotropy)? | Decreases ESV Increases SV and CO |
| Positive Inotropic Effects | Open Ca Channels Inhibit Na/Ca Exchanger Inhibit plasma membrane Ca pump 1.Intrinsic Contractility 2.HR effect |
| What do cardiac Glycosides do? | They inhibit the Na/K exchanger, making high Na inside cell. This therefore inhibits the Na/Ca exchanger leading to an inc Ca level inside. Therefore inc contraction. |
| Examples of Negative Inotropes | Ca Channel blockers Low Ca (extracellular) High Na (extracellular) |
| Increased parasympathetic effects on heart rate | dec Ifunny channels (Na) Opens GIRK (K) channels dec I calcium channel. |
| GIRK Channels | These are the inward rectifier K channels. Therefore opening these causes more hyperpolerization across the membrane. More depolarization will be needed to cause a contraction, and thus contractibility decreases. |
| Sympathetic effect on Heart Rate | inc Ifunny slope inc ICa channels. |
| Equation for Mean Arterial Pressure. | MAP = CO * TPR (SVR) |
| Sympathetic stimulation on Blood Vessels | A-1 & B-2 receptors. A is vasoconstriction, B is Vasodilation. A constricts most blood vessels. B dilates blood vessels to coronary, cerebral, liver, sk muscle. |
| Parasympathetic stimulation on Blood Vessels | Blood vessels to salivary, some GI, and erectile tissue. ACH acts on M3(endothelial) receptors. This releases NO to act on the smooth muscle cells to cause vasodilation. |
| ways to alter the Central Blood Volume | change total BV redistribute the BV you have. |
| Ways to increase total Blood Volume | infuse fluid retain salt and H2O Shift fluid from interstitial to Plasma |
| Ways to decrease total Blood Volume | Hemorrhage Sweat Shift plasma fluid to interstitial |
| Mean Circulatory Filling Pressure (Pmc) | The pressure in the system when the heart is stopped. It is a measure of the "fullness of the system". |
| When does your right atrial pressure (Pra) equal your mean circulatory filling pressure (Pmc)? | When the heart is stopped. Also when CO ( and VR) are zero. |
| What three things effect the vascular function(Venous Return) curve? | Blood Volume (how full system is) Capacitance Slope of curve (Total peripheral res) |
| When does Pmc (mean circulatory pressure) not change? | It does not change with an increase or decrease in vascular resistance. |
| What can change Pmc (mean circulatory filling pressure) | SNS tone Blood Volume compression of veins |
| What three things effect the Cardiac function curve? | Afterload Inotropy Heart Rate |
| What are the inhibitors of Oxidative Phosphorylation? | I - Rotenone II - Malonate III - Antimycin A IV - Cyanide V - Oligomycin |
| Describe the order of proteins in the Oxidative Phosphorylation mechanism. | I, Coenzyme Q, III Cytochrome C, IV, V(atp synthase). |
| Effect of DNPH on Oxidative Phosphorylation | It destroys the proton gradient by bringing H+ back onto the other side of the mitochondrial membrane. Uncoupling, releases heat. |
| Brown Fat Cells and oxidative phosphorylation | These produce heat when uncoupling agents react on the oxidative phosphorylation cycle. |
| What is the major source of Free radicals in ox Phos | coenzyme Q |
| Problems resulting from Reactive Oxidative Species Production? | -Protein damage -membrane damage -DNA damage -Lipid peroxidation -Ca influx (massive) -increased permeability -Cell swelling -Mitochondrial damage |
| Sources of Free Radicals in Ox Phos | Coenzyme Q Peroxisome NADPH oxidase Myeloperoxidase Ionizing Radiation |
| Superoxide Dismutase | responsible for converting superoxide to hydrogen peroxide. This enzyme is presence both in the cytosol and mitochondria. |
| Catalase | converts hydrogen peroxide to water |
| Glutathione peroxidase | converts hydrogen peroxide to water. |
| Ischemia | Reduced blood flow to provide adequate oxygen |
| hypoxia | reduced oxygen |
| Transmural MI | Infarction that affects the full thickness of the ventricular wall |
| subendocardial MI | An infarction that effects about 1/3-1/2 of the total ventricular wall. |
| What is the Number one lab test for acute myocardial infarct? | Troponin I or Troponin T |
| Microscopic changes after an MI | 1 hr - intracellular edema and cells at edge of mi may become wavy and buckled. 1 day - neutrophilic invasion, coagulative necrosis, 3-7 days - dead myocytes desintegrate and absorbed by macrophages. 7-10 days - granulation tissue replaces necrot tiss |
| Head and Neck symp/ parasymp | t1-t4, Vagus |
| Cardiovascular symp/para | T1-T5, Vagus |
| Respiratory symp/para | T2-T7, Vagus |
| Liver, Stomach, Gall bladder symp/para | T5-T9, Vagus |
| Pancreas symp/para | T5-T11, Vagus |
| Small intestines symp/para | T9-T11, Vagus |
| Ovary, testicle symp/para | T9-T10, S2-4 |
| Kidney, ureter, bladder symp/para | t10-L1, S2-4 |
| Large intestine symp/para | T8-L2, Vagus S2-S4 |
| Uterus symp/para | T10-L1, S2-4 |
| Prostate symp/para | L1-2, S2-4 |
| Angiotensin, Renin, and ACE effects on Blood Pressure | These enzymes/proteins cause an increase in arterial constriction to the kidneys. This reduces Na+ secretion and H20 secretion. Thus, increasing blood pressure |
| Antidiuretic Hormone (ADH) | released when low pressure in atrium (non activated stretch receptors). |
| Effect of activated Low pressure receptors | These are activated when pressure is high in the atrium. This signals an increase in venous return. Thus, Heart rate is INCREASED, and VASODILATE. Also ADH is decreased, and Atrial natriuretic peptide (ANP) |
| What is the orientation of the superior intervertebral facets? | Backward, Upward and Lateral (BUL) |
| Pectus Excavatum | Indented Chest |
| Pectus Carinatum | points out (like a bird beak) |
| Rule of Threes | Way to find transverse process of thoracic vertebrae. 1-3: lateral to sp process, 4-6: midway between upper and same vertebrate, 7-9: lateral to sp process of segment above. T10-12: same as 1-3. |
| Which somatic dysfunction is associated with visceral problems? | Type II somatic dysfunction. |
| Right lymphatic duct Junctions | Right subclavian v, right jugular v. |
| Left Lymphatic Duct Junctions | Left Subclavian v., Left Brachiocephalic V. |
| Which somatic dysfunction should be treated first? I or II? | type II first. Also, treat thoracic spine before ribs. |
| What is the major enzyme that digests dietary triacylglycerols? | lipase |
| Which enzymes break down short and medium chain fatty acids (12-C or less)? | lingual and gastric lipases |
| Action of Secretin | Signals the liver, pancreas, and intestinal cells to serete bicarb which raises ph to 6. This is optimal for action of digestive enzymes. |
| Action of colipase | binds to dietary fat and to the lipase, relieving the bile salt inhibition and allowing the triglyceride to enter the active site of the lipase. |
| Pacreatic Lipase breaks down TG to? | 2 fatty acids and a 2-monoglyceride |
| What is the critical micelle concentration (CMC) | 5-15mM concentration of bile salts that must be intestines for micelles to form. These then proceed to the microvilli and allow FA and 2-monoglycerol to be absorbed. |
| What happens to absorption of short and medium chain Fatty Acids in the intestines? | Absorbed without producing micelles. They enter the portal blood rather than the lymph and transported to liver. |
| Difference between TAG synthesis in intestinal cells and adipose? | intestinal cell: FA to 2-mono (intermediate)= diglyceride + FAcyl CoA to form triglyceride Adipose: phosphatidic acid |
| Components of chylomicrons | cholesterol and fat-soluble vitamins, proteins, phosphlipids, TG from diet. |
| Major apo protein of chylomicrons from intestines? | Apo-B 48. |
| Hypertriglyceridemia leads to what | pancreatitis |
| Primary hyperlipoproteinemias | rare, caused by a monogenic defect. can elevate LDL-C or can elevate VLDL and triglyceride levels. |
| Secondary hyperlipoproteinemias | commonly caused by presence of alcoholism, diabetes mellitus, or uremia or by the use of drugs such as B-adrenoceptor antagonists, isotretinoin, etc. |
| Niacin (B3) | used to treat hypertriglyceridemia and to increase HDL-C by inhibiting formation of hepatic VLDL. Acts through inhibiting lipolysis in adipose. Needs to be large doses (several grams) each day. |
| Fibric Acid | reduces LDL-C and triglyceride levels while raising HDL-C by activating (PPAR-a) which increases expression of lipoprotein lipase. |
| Fenofibrate | A fibric acid drug that is used to lower LDL-C levels. |
| Where is DHAP used for triglyceride synthesis? | It is used in ADIPOSE and the liver. |
| Where does the liver get its glycerol from for making TG? | DHAP as well as glycerol kinase (phosphorylates glycerol) |
| What is the intermediate used to make TG in intestinal cells? | 2-monoacylglyceride |
| What is the intermediate used to make TG in adipose and Liver? | Phosphatidic Acid |
| Cholesterol ester | Similar to Cholesterol molecules except with long chain FA attached. More hydrophobic. Found primarily in lipoproteins and are the storage form of cholesterol. |
| Cholesterol Acyl Transferase (CAT) | Esterifies cholesterol to cholesterol ester. |
| Cholesterol Esterase | Removes the F.A. from 'cholesterol ester' to make 'Cholesterol' |
| Acyl CoA cholesterol transferases (ACAT) | esterifies cholesterol within cells |
| Lecithin cholesterol acyl transferase (LCAT) | esterifies cholesterol, found on lipoproteins. |
| HMG-CoA reductase | The rate limiting enzyme in cholesterol synthesis. Highly regulated by the amount of free cholesterol in the body. High levels produce a conformational change, making it more susceptible to proteolysis. |
| What are some factors that regulate HMG CoA reductase? | Cholesterol, AMP, and Insulin/Glucagon. |
| AMPK's effect on HMG-CoA reductase | High levels of this will reduce the function of HMG-CoA. Thus producing less cholesterol. |
| Conjugation of Bile Salts (Primary Conjugated Bile Salts) | The addition of glycine or taurine to bile salts. This decreases the salt's pkA value and therefore makes them a better detergent. After this process, they are stored in gall bladder. |
| Secondary Bile Salts | Conjugated Bile salts are deconjugated and dehydroxylated by bacteria to produce these. These are less soluble and more likely to be secreted in the feces. |
| How is bile acid/salt regulated? | By the amount of bile salt reabsorbed or excreted. The more reabsorbed, the less salts needed to be produced. Acts on the enzyme 7-A-hydroxylase |
| ApoCII | Found on HDL, chylomicrons, VLDL, IDL, activates lipoprotein lipase |
| What are the two forms of cholesterol found in the body? | Cholesterol and Cholesterol ester |
| Which apo protein is used to make VLDL? chylomicrons? | VLDL uses apoB-100 (liver) while apoB-48 is added to chylomicrons, produced in the intestinal cells. |
| Cholesterol Ester Transfer Protein (CETP) | transfers TG from VLDL, LDL, and IDL to HDL in exchange for CE. (CE to VLDL x TG to HDL) |
| How to IDL and LDL get into peripheral cells? | LDL receptor related Protein (LRP) and the scavenger family (SR family). The LDL receptor recognizes ApoB-100 and Apo E. |
| Free cholesterol's effects on uptake receptors | It will cause a decline in LDL receptor while not having an effect on LRP or SR receptors. |
| precontemplation | not ready. people are not intending to take action in the foreseable future, and can be unaware that their behavior is problematic |
| Contemplation | (getting ready). People are beginning to recognize that their behavior is problematic and start to look at the pros and cons of their continued actions |
| Preparation | Ready. People are intending to take action in the immediate future, and may begin taking small steps toward behavior change. |
| Action | People have made specific overt modifications in modifying their problem behavior or in acquiring new healthy behaviors |
| Maintenance | People have been able to sustain action for awhile and are working to prevent relapse. |
| Know the Keller/White Model of Change | Convinced/Ambient = Conviction. Helpless/Powerful = Confidence |
| Therapeutic Triangle | You, the patient and the EHR |
| How do Statins work? | They inhibit the rate limiting enzyme of cholesterol synthesis in the liver (HMG-CoA Reductase). This causes an upregulation of LDL receptors which removes more LDL from the circulation. |
| How will statins reduce TG in the blood? | By decreasing the production of cholesterol needed for VLDL production. and By increasing the LDL receptors which remove LDL from the circulation. |
| Statin dose and its relation to lowering LDL | The greatest decrease in LDL occurs from the original dose of a statin. Doubling this dose only decreases it by 6%. |
| Statins to take at Night | Lovastatin, Simvastatin, Fluvastatin,Pravastatin. Short half life of less than 4 hours. |
| Statins to take any time of the day | Atorvastatin, Rosuvastatin, Pitavastatin. Long half life, 12-30 hours. |
| Why would you take a statin at night? | Because hepatic cholesterol synthesis is maximal between 12 and 2. |
| HMG CoA reductase inhibitor (statins) adverse effects? | G.I. problems and increase in hepatic transaminases. Myalgia (muscle pain), Myositis (inc x10 of creatine kinase), and Rhabdomyolysis (extensive msk damage). |
| HMG-CoA reductase inhibitors drug interactions | Fibrates (gemfibrozil), niacin, and CYP3A4 inhibitors |
| Contraindications for taking statins? | Pregnancy/ lactating and active hepatic disease. |
| Name the Bile Acid Binding Resins | Cholestyramine, Colestipol, Colesevelam. |
| How do Bile Acid Binding Resins reduce LDL in blood? | These reduce the recirculation of binding acids by binding to the bile acids. This increases the need for more BA so more cholesterol is needed in liver, this inc LDL receptors which removes more LDL from blood. |
| Can resins be used for the reduction in Triglycerides? | No |
| If you are taking other drugs with a Resin, when should you take them? | 1 hour before or 4 hours after. |
| Which transmembrane protein is essential for the transport of free cholesterol from the gut lumen into the enterocyte? | NPC1L1 |
| Ezetimibe does what? | It inhibits NPC1L1 from brining dietary cholesterol into the intestinal cells, lowering total cholesterol. |
| What enzyme does Niacin act on? | DGAT 2 |
| What is significant about the size of LDL's? | smaller, more dense LDL's are more atherogenic and not as easily cleared by the LDL receptor. |
| Nutrient | a substance that must be consumed for growth, maintenance, and repair of body tissue. |
| Monosaccharides | Glucose, galactose, fructose |
| Soluble Fiber | Dissolves or swells in water and can be broken down by intestinal bacteria |
| Insoluble Fiber | Does not dissolve in water and resists digestion. |
| Reduced/Less | 25% less than comparable standards |
| Trans Fatty Acids | Artificially heating liquid vegetable oils with metal catalysts and hydrogen to make the fat solid. |
| Which Fats are worse for you sat, trans, or cholesterol | Trans are worst, sat are better, chol is best |
| Complete/Whole protein foods | Contain all the 9 essential amino acids, in proportions and amounts needed by the body. |
| Aerobic Exercise Criteria | F-frequency (3 days a week) I- Intensity (@ or above target HR) T- Type (continuous, rhythmic, uses large muscles T- Time (20 continuous minutes or more) |
| Children and Adolescent Exercise Reccommendations | 60 minutes a day, vigorous 3 times a week, muscle/bone strengthening 3 times a week |
| Adult Exercise Reccommendations | 150 minutes of moderate exercise a week, 75 minutes of vigorous activity a week, Strength training 2 times a week. |
| Most Common Exercise Risks | Heart Attack, Muscle/joint injuries, Heat disorders. |
Created by:
622988909
Popular Medical sets