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Patho Arterial
| Question | Answer |
|---|---|
| 4 hormones secreted by the endothelium | Nitric oxide Prostacyclin VEGF Von Willebrand factor |
| Nitric Oxide | Vessel dilation |
| Prostacyclin | Inhibits clotting |
| VEGF | Angiogenesis |
| Von Willebrand factor (vWF) | essential for normal blood clotting and stopping blood loss after an injury |
| Endothelial Injury leads to | arteriosclerosis and atherosclerosis |
| Endothelial injury attracts | WBCs Initiates inflammation T lymphocytes: react against oxidized LDL B lymphocytes: produces antibodies against oxLDL |
| WF released increasing | platelet aggregation |
| Then what forms? (hint: squishy) | Foam cells (lipid-rich macrophages) |
| ______ release inhibited: vasoconstriction | NO |
| Finally.... | Plaque formation |
| Blood flow = Blood flow = | Blood pressure/resistance Cardiac Output (CO)/resistance |
| What does turbulent blood flow sound like | "Whooshing" sound known as bruit |
| RAAS key role | BP regulation |
| Renin | Released in response to low pressure or perfusion |
| Renin converts what into what | Angiotensinogen into Angiotensin I |
| Angiotensin I converted to Using what? | angiotensin II ACE (angiotensin-converting enzyme) in the lungs |
| Angiotension II | Potent vasoconstrictor • Activates aldosterone for adrenal cortex |
| Aldosterone | • Stimulates sodium and water retention |
| Result | • Increased BP |
| Types of lipids | Cholesterol Triglycerides |
| LDL: low-density lipoprotein | ‒ “Bad” cholesterol ‒ Involved in plaque formation in arteries |
| HDL: high-density lipoprotein | ‒ “Good” cholesterol ‒ Helps excrete cholesterol from body ‒ “Reverse cholesterol transport" |
| Effect of glucose on arteries | Injury of endothelial cells Inflammation and plaque formation may result • AGEs increase endothelin release • Vasoconstriction Diabetes mellitus and CAD |
| Injury of endothelial cells AGEs | advanced glycosylation end products |
| the liver’s role in blood cholesterol levels | The liver acts as the body's primary control center for blood cholesterol, producing the majority of your body's cholesterol and clearing it from the bloodstream HDLS and LDLs |
| Hyperlipidemia | Elevated levels of lipids • Cholesterol (hypercholesterolemia) • Triglycerides (hypertriglyceridemia) |
| Dyslipidemia | • Hypertriglyceridemia • Elevated LDL cholesterol levels • Decreased HDL levels ‒ Increases the risk for cardiovascular disease |
| Hyperlipidemia: Signs and Symptoms | Plaque formation Overt signs and symptoms • Xanthoma: cholesterol deposits under skin • Xanthelasma: cholesterol deposits around eyes All should prompt a review family history, risk factors for cardiovascular disease |
| Hypertension: Risk Factors | • Age • Male sex • African American ethnicity • Obesity • Family history • Diabetes mellitus • Tobacco use • Stress |
| Hypertension: What are the key assessments? | Often no symptoms • Target organ damage signs: ‒ Headaches ‒ Chest pain ‒ Vision disturbances ‒ Dizziness • Check for disorders and medications known to elevate BP |
| Hypertension: Pathology | Pathological effects • High shearing stress arterial walls • LV hypertrophy (LVH) |
| Hypertension: Assessment Findings 3 | Fundoscopic exam = Retinal vessels Chest = Alteration in PMI (point of maximal impact) Bruits = Turbulent flow |
| Hypertension: Assessment Findings 4 | Peripheral = arteries Temperature, sensation, pulses 12-Lead ECG = LVH Urinalysis = Proteins in urine (kidney damage) Blood laboratory tests = Factors associated with HTN |
| Hypertension: What are the complications LVH | Left ventricular hypertrophy Increased MI risk |
| Hypertension: What are the complications Aneurysm | Bulging artery May rupture |
| Hypertension: What are the complications Cerebral hemorrhage | Ruptured blood vessel in brain |
| Hypertension: What are the complications Hypertensive retinopathy | Damage to retinal vessels |
| Hypertension: What are the complications Renal disease | Damage glomeruli |
| Atherosclerosis | a chronic disease where fats, cholesterol, and other substances build up in and on your artery walls as sticky deposits called plaque |
| 5 Steps in Atherosclerosis Pathophysiology 1-3 | 1. Injury to endothelium 2. Attract WBCs • Vascular cell adhesion 3. WBCs differentiate • Macrophages • Fill with LDLs ‒ Become foam cells, release lipids into interior layers |
| 5 Steps in Atherosclerosis Pathophysiology 4-5 | 4. Fibroblasts attracted to the area by cytokines • Form fatty streaks that lead to plaques 5. Plaques • Calcify and cover with a fibrous platelet cap |
| Atherosclerosis Risk for | Rupture Plaque rupture • Causes bleeding • Breaks loose ‒ Travel to area and obstruct blood flow CRP is released!! |
| Atherosclerosis: Diagnosis | Lipid profile: Cholesterol, TGs, LDL, HDL - Endothelial function assessment - Homocysteine levels |
| Atherosclerosis: Diagnosis (continued) | Calcium computerized tomography scan • CT scan detects calcified plaques Cardiac angiography • Radiopaque dye study using cardiac catheterization to examine blocked vessel Intravascular ultrasonography |
| Peripheral Arterial Disease (PAD) | Peripheral artery disease (PAD) is a common circulatory condition where narrowed arteries reduce blood flow to your limbs, most often your legs |
| Peripheral Arterial Disease (PAD) Signs and Symptoms | Intermittent claudication: primary sign • Pain with exertion, relieved by rest Occlusion decreases oxygenation Reducing activity enables oxygen levels to meet metabolic demand, eliminating pain • Ischemic (activity)/reperfusion (rest) cycles |
| Peripheral Arterial Disease (PAD) Signs and Symptoms Lower extremity | pulse that is not palpable |
| Peripheral Arterial Disease: Assessment | Patient symptoms: Intermittent claudication Diminished or absent pulses Palpable coolness Paresthesia Pallor Sensation distal to proxima |
| Peripheral Arterial Disease: Diagnosis | Ankle-brachial index CBC, Lipid profile Inflammatory markers Impedance arterial plethysmography Ultrasonography, duplex ultrasonography MRA Conventional angiography CT |
| Aneurysm Presentation | Depends on size, location, and integrity • May be missed until rupture occurs Cerebral aneurysms are normally silent |
| If rupture: | subarachnoid hemorrhage |
| AAA: may present with | abdominal or back pain • Nausea and vomiting • In thin patient, may see pulsatile mass • Deep palpation should not be performed |
| Aneurysm Diagnosis | Diagnosis • Found incidentally • Ultrasonography |
| Aneurysm Treatment | Treatment • Smoking cessation, BP regulation • AAA: periodic follow up • Surgical treatment may be necessary |
| Aortic Dissection | Tear in lining • Between tunica intima and media of aorta • Blood flows between layers Potentially lethal |
| Aortic Dissection Symptoms | Symptom onset is sudden • Patient hears “ripping” or “tearing” sound • Pallor, tachycardia, BP presentation may be variable depending on dissection location |
| How does aortic dissection happen? | when a tear forms in the inner layer of the aorta—the body's main artery—allowing high-pressure blood to surge between and separate the wall's layers |
| Differences between bacteria and viruses | are single-celled living organisms, while viruses are smaller, non-living infectious particles that require a host cell to reproduce. |
| Thromboxane A2 | Activates Clotting |
| A patient has a blood pressure of 150/90 mm Hg. Which value represents the patient's pulse pressure? | 60mm |
Created by:
liladdoyle