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65 Cards in this Set
- Front
- Back
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Arterial disease: terms 1) arteriosclerosis 2) Atherosclerosis
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1) is a generic term for several diseases that produce changes in artery walls. 2)plaque that is patchy thickening that is not uniform which produces limitation of flow
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what are the changes of arteriosclerosis?
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thickening, ↓ elasticity which results in limitation of flow weakening of wall that can produce aneurysms (aka bulge) which may ruptures if the pressure gets high enough.
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Development of atherosclerosis –
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accum. of excess smooth muscle cells in intima → this accum lipids which produces irreg yellow streaks in wall (fatty streaks) → fibroblasts will manufacture scar tissue which produces white raised lesions. → cells and products will degen. leaving behind debris/ free fat which accums in tissue and occludes the lumen.
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Advanced lesions of atheromas can calcify can become necrotic and will eventually lose endotheliam which means no circulation. As endo degenerates it roughens which causes turbulence which means ↓ flow which means what will form ? And then that can mean?
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clots which means aneurysm.
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S&S of atherosclerosis-
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NONE until about 60% occluded.
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Atheroma causes ↑ resistance. flow=pressure/resistance so....
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↑ resistance causes ↑ pressure which some degree of hypertension (is 2nd to atherosclerosis.
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High Blood Pressure:
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consistent ↑ in arterial BP, on average for 2 or more readings on 2 consecutive visits.
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Isolated systolic hypertension-
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is just ↑ systolic (top #)
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combined hypertension
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-both systolic and diastolic are ↑ .
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Primary vs 2ndary hypertension.
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Primary (aka essential or idiopathic) means no known cause. It accounts for 80-90% of the cases. 2nd means due to some other cause like atherosclerosis, kidney disease, obesity.
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Results of chronic hypertension 1) smooth muscle hypertrophy and hyperplasia (more cells & bigger) 2) ↑ fibrous tissue in arterial walls. These 2 things cause what 2 things to happen?
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1) narrowing of arteries 2) damage to tissue which cause inflammation response → swelling and further narrowing.
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Aneurysms are what? Causes?
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isolated bulging of a vessel or chamber of the heart. Causes 1) weakening in the wall due to atherosclerosis 2) less common, congenital malformations. 3) hypertension 4)marfin syndrome, syphilis and other infections that affect arterial walls
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what are false aneurysms
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an extravascular hematoma that communicates w/ the intravascular space.
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Aneurysm types are based on shape. . 1) fusiform which is ? 2) Saccular, which occur frequently in 2% of population-cause congenital abnormalities. Subtypes of saccular: a-round w/ narrow stalk connecting to artery b-broad w/o stalk c–cylindrical d-dissecting. Saccular are rare in adults or children?
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uniform in all directions, berry, childhood, age risk is 20-50 y/o's
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S&S of aneurisms -1) often asymptomatic 2)) pressure related symptoms- dysphagia which is what? or dyspnea-which is what? Due to aneurysms pressure on surround organs. Symp depend on where the aneurysm is located. 3) pain-only if dissection type 3) signs of ischemia (inad. Blood flow) if in the extremity (abnormal pulse)
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difficulty swallowing difficulty breathing
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dx of aneurysm confirmed by what?
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ultrasonography, mri or angiography.
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Tx of aneurysm
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is to maintain a low blood volume and low BP. or surgery
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varicose veins-distended, palpable veins containing what? Caused ↑ venous failure which eventually means the vein will become fibrotic due to tissue damage/scar tissue. What causes valve failure?
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pooled blood. Initially: 1) congenital (most common) 2) trauma-inflammation (standing/crossing legs)
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chronic venous insufficiency Results: 1) hyperpigmentation of feet, ankles; leakage of RBC thru capillary due to ↑ capillary hydrostatic pressure (looks like bruising) 2) stasis ulcers-poor flow produce poor tissue nutrition which leads to necrosis. Susceptible to infection why? 3) deep venous thrombosis in up to 15%.
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because it can't deliver the defense mechanisms to the site.
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wound healing, leg elevations, compression stockings and exercise. Invasing: sclerotherapy or surgical ligation and vein stripping.are tx for what?
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Tx of varicose veins and CVI:
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Coronary artery disease -the arteries that supply the heart. Narrowing of coronary arteries is usually due towhat? Which leads to what? And that can lead to?
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atherosclerosis → leads to Myocardial ischemia → which leads to myocardial Infarction.
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Infarction vs ischemia
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what disease causes 1/3 of all deaths in the 35-65 y/o range, responsible for 50% all all deaths in USA.
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Risks for CAD 1)unmodifiable
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2)modifiable -age -gender – race -genetic predisposition. males more susceptible until age 60 then =. race- blacks, Asians. Modifiable-1) hyperlipidema 2) hypertension 3) nicotine 4) Diabetes 5) obesity.
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Hyperlipidema is what?
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↑ concentrations of lipo-proteins, ↑ VLDP and LDP means they have ↑ risk for CAD
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Hypertension ↑ formations of atheromas which meanswhat?
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↑ resistance which means ↑ pressure
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Nicotine ↑ produces and release of epinephrine which does what?
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↑ arterial pressure. Risk ↓ by 50% 1yr after quit smoking
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Diabetes- have ↑ risk of what?
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atherosclerosis and hypertension.
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Obesity have higher rates of what?
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atherosclerosis and hypertension which means ↑ workload on the heart.
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Myocardial Ischemia non-myo tissue oxygen delivery is about 25% and blood going back to the heart still has 75%, so if the tissue needs more it just takes more and delivers less back to the heart (we tend to deliver more than we'll need). Called what?
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utilization coefficient
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But with myocardial tissue the utilization coefficient is 100%. so if we need more O2 how do we get it?
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We dilate the coronary arteries. So if there is CA disease you can't dilate them! - then there's not enough O2 to heart → ischemia
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lol you never hear of a biceps attack! Because why?
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Because we can get more O2 to the tissue
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S&S of what disease? substernal discomfort, varies per person: described as heaviness, all the way to sever pain. Very commonly it radiates to left arm, neck, jaw, back and even rt. Arm. Describes as indigestion/heartburn.
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Inadequate flow to the heart-Angina
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Causes of angina
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1) buildup of lactic acid 2) myocardial stretching in an ischemic area (the part w/ not enough O2 doesn’t contract but the rest does- the the part that doesn’t will bulge
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Timing of angina 3-5 minutes.
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Usually because they stop the activity causing it-so the flow for is restored so no damage.
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Angina initiates the what? so the person is cold, clammy, pale, dialed pupils, scared, fight/flight, short of breath.
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sympathetic response
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Name that angina. 1) stable 2) unstable 3) princemetal due to narrowing of RC w/ exercise Artery can't dilate which produces the symptoms. Same effect w/ same level of exertion every time. Relieved by rest, and nitro tabs.
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1) stable
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Name that angina. 1) stable 2) unstable 3) princemetal Caused by CAD + vaso-spasm (constriction). Worse each time, unpredictable. Sometimes occurs during rest.
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2) unstable
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Name that angina. 1) stable 2) unstable 3) princemetal Due strictly to vaso-spasm no CAD. Occurs @ rest/often during REM sleep. Cause malfunction of CA smooth muscle control.
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3) princemetal
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S&S of angina 1) ventricular gallop -which is what? 2) EKG changes seen only w/ acute attack -what are the changes?
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1)extra heart sound b4 the 1st heart sound (occurs when atria contract because the ischemic ventricle isn't relaxing fully it’s stiff and when the atria contracts it rumbles 2) ST segment depression (lower than usual) -T-wave inversion
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progression of cario illness
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CAD → Angina → myocardial infarction
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Myocardial Infarction (MI) aka heart attack.
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Causes: 1) atheroma in CA 2) hemorrhage into plaque -break in endothelium → flow inflates wall out like a balloon. 3) embolism-circulating mass usual blood,could be fat, air. 4) CA spasm.
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Specific events of MI 1-8 seconds
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1) will use up O2 reserves in the tissue, when that's gone muscle tissue goes from red to cyanotic (blue) 2) glycolytic/anaerobic metabolism will try to produce energy and ti will be inadequate → lactic acid. 3) ion imbalances develop due to malfunctioning pumps
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MI continued 30-60 seconds.
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EKG changes due to ion imbalances. 20 minutes. Cellular death. Eventually cells will degenerate and will release their contents-intracellular enzymes → will be in the ECF and blood. Those enzymes are diagnostic. Meaning they show up in blood tests so you can tell that at least some cells have died which r/i MI.
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Functional changes w/ MI 1) abnormal wall motion -area that doesn't contract, which means more what? ↑ 2a)- ↓ stroke volume output which means what? 2b) - ↓ ejection fraction which means? blood will then accumulate in the heart, stretching it out. 3) ↑ end diastolic volume which means? 4) arrhythmia –
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1)clots 2a) ventricle isn't squeezing out blood correctly 2b)the portion of ventricle contents pumped by beat usually 70% 3)heart that stretch out and _______ 4) abnormal patterns of depolarization if MI kills bundle cells it effects the the electrical current.
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Repair process for MI 1)necrosis- cells fall apart →2) inflammation leads to what? → depolarization has to go around that so the heart will always what? 3) fever, ↑ WBC all that goes along w/ inflammation. Healing takes a few weeks.
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scar tissue, function differently from here on out
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thromboembulous is what?
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a detached thrombus
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what 3 factors promotes venous thrombosis:
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1) venous stasis, venous endothelial damage and hypercoagulable states.
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Orthopedic trauma/surgery, spinal disorders, malignancy, pregnancy, oral contraceptives, hormone replacement increase likelihood of what? Aneurysm, embolism, deep venous thrombosis?
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Deep venous thrombosis.
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Superior vena cava syndroms is a progressive occlusion of the superior vena cava that leads to venous distention in what? Trunk and lower extremities or the upper extremities and head.
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upper/head
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bronchogenic cancer, lymphomas and metastasis or other cancers cause SVCS. T/F
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true
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edema and venous distention in upper extremities and face. “fullness in head, tightness of shirt collars, rings. Skin purple and taut. SVCS can lead to hydrocephalus. S&S of what?
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S&S of SVCS
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BP ranges normal, prehypertension, stage 1 hypertension, stage 2 hypertension
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120/80, 139/89, 159/99, 160+/100+ 20 thru 30's pre 40 thru50's stage 1 60+ stage 2
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primary hypertension risks:
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include family hx, aging, gender, black race, high Na intake, diabtetes, ciarette smoking, obesity, heavy alco consumption, low intake of K, Ca, Mg
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pressure- natriuresis relationship
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indiv. W/ hypertension tend to secrete less salt in their urine.
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Diastolic HF, Systolic HF, Left sided or right sided HF? Cardiac output decreases, hydrostatic pressure causes intracellular fluid to accup in pulmonary capillary bed → pulmonary congestion.
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Left sided.
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Congestive heart failure is AKA....
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left sided HF
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Diastolic HF, Systolic HF, Left sided or right sided HF? Hydrostatic pressures forces blood into systemic venous circulation.
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Right sided.
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Which side heart failure follows the other?
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Right follows left
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Left sided or right sided HF? Most common type of HF, ↓ cardiac output, ↓ ejection fraction, ↑ ventricular filling pressure (preload) ↑ systemic vascular resistance (afterload)
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left
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Diastolic HF, Systolic HF, Left sided or right sided HF? Ventricles can't fill properly (from ventricular hypertrophy & systemic hypertension), ventricles stiff and non compliant, unable to relax. Norm ejection fraction, norm cardiac output but w/ symptoms of HF.
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Diastolic HF.
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Right sided or left sided HF? Dizziness, syncope, Hepatomegaly, Ascites, Jaundice, Dependent pitting, edema, Weight gain, Nausea, vomiting, anorexia, abdominal distention, JVD
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right-sided
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Right sided or left sided HF? Elevated blood pressure,Dyspnea on exertion; Paroxysmal nocturnal dyspnea, Wheezing, crackles, Cyanosis or pallor, Palpitations, 3rd or 4th heart sounds
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left-sided
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What is a complicated plaque?
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Plaques that have ruptured
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Complicated hypertension
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Cardiac: LVH, ischemia & infarction, LHF Renal: microalbuminuria – early sign of renal dysfunction and failure Vascular: aneurysms, CVA, intermittent claudication of lower extremities and gangrene Eye: retinal damage and blindness
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