ClinMed 2 Cards 6 New 2024 PDF

CLINMED 2 CARDS 6 Jennifer Rayburn, M.D. MTSU Physician Assistant Studies  Differentiat Differentiate atherosclerosis and non- e atheromatous arteriosclerosis Question the diseases of the aorta and OBJECTIVES...

CLINMED 2 CARDS 6 Jennifer Rayburn, M.D. MTSU Physician Assistant Studies  Differentiat Differentiate atherosclerosis and non- e atheromatous arteriosclerosis Question the diseases of the aorta and OBJECTIVES Question its branches Inventory the various peripheral arterial Inventory disorders  ATHEROSCLEROSI S DEFINITION “Hardening of the Arteries” Responsible for almost all cases of CAD Pathologic process that causes disease of the coronary, cerebral, and peripheral arteries Arteriosclerosis: generic term for all lesions that lead to hardening of the arteries, stiffening, and consequent loss of elasticity of the arterial wall Three types of arteriosclerosis: 1. Atherosclerosis: hardening and narrowing of the large arteries 2. Moenckberg medial calcific sclerosis: Affects small to medium arteries. Non-obstructive calcification in the internal elastic lamina or tunica media of elastic arteries 3. Arteriolosclerosis: calcification of small arteries, arterioles, leading to systemic hypertension  RISK FACTORS FOR ATHEROSCLEROSIS Age (advancing age) Sex (male>female) Family History of premature CAD Hypertension Hyperlipidemia (elevated LDL/low HDL) Diabetes mellitus II Metabolic syndrome Smoking Lack of physical activity Poor Diet Added Healthy Sleep 7-9 Obesity hours per night  METABOLIC SYNDROME KNOW THE CRITERIA!!! Obesity, particularly abdominal obesity, is associated with resistance to the effects of insulin on peripheral glucose and fatty acid utilization, often leading to type2 diabetes mellitus. Insulin resistance, the associated hyperinsulinemia and hyperglycemia, and adipocyte cytokines may also lead to vascular endothelial dysfunction, an abnormal lipid profile, hypertension, and vascular inflammation, all of which promote development of atherosclerotic cardiovascular disease NCEP ATPIII criteria for metabolic syndrome (any 3 of 5 traits): 1. Abdominal obesity defined as a waist circumference of 40 inches in men or 35 inches in females 2. Serum triglycerides ≥150 mg/dL or drug treatment for elevated triglycerides 3. Serum HDL 0.5 cm/year), or symptoms resulting from the AAA (abdominal or back pain) Open versus endovascular repair (EVAR) is determined by the location of the AAA and involvement of the renal and mesenteric arteries Suprarenal or juxtarenal aneurysms often necessitate open repair EVAR is associated with greater need for repeat intervention, endoleak, device failure, and postimplantation syndrome (fever, leukocytosis, elevated CRP) B-Blockers to reduce shearing forces, decrease expansion, and rupture risl  AORTIC DISSECTION Life-threatening condition in which blood from the vessel lumen passes through a tear in the intima to the medial layer and spreads along the artery Any condition that interferes with the normal integrity of the elastic or muscular components of the medial layer can predispose to dissection (hypertension, aging, medial degeneration from genetic disorders), trauma Most common in sixth and seventh decades; more frequent in men. Two–thirds have history of hypertension. Ascending thoracic aorta (65%), descending thoracic aorta (20%), aortic arch (10%) and abdominal aorta (5%) Two categories (Stanford Class): 1. Type A dissection (proximal dissection): the ascending aorta and/or aortic arch is involved regardless of the site of primary tear 2. Type B dissection (distal dissection): does not involve the ascending aorta or arch. Confined to the descending thoracic aorta and abdominal aorta Two-thirds are Type A and one-third are Type B  AORTIC DISSECTION Tear through the innermost layer Symptoms: Chest or back pain are the most common symptoms (90%) – sudden of the aorta (intima) due to cystic onset of severe chest or upper back pain medial necrosis with a sharp, ripping, knife-like, or tearing quality that may radiate between Most common is Ascending the scapulae. (Type A dissection) and has high Type A dissection may have more anterior chest pain mortality Type B dissection may have more back, Risk Factors: Hypertension, abdomen or interscapular pain age>50 yrs, male, vasculitis, Pain may migrate with propagation trauma, FH of aortic dissection, Pain may be accompanied by other Turner’s syndrome, collagen symptoms such as abdominal pain, neurological findings (limb weakness or vascular disorders (Marfan, Ehlers- paresthesias due to spine ischemia), Danlos), pregnancy syncope, ACS, CHF, CVA  AORTIC DISSECTION Physical Exam: Blood Pressure: May be hypertensive (Type B more common) or hypotensive (ascending aorta) Pulse variation: Variation or discrepancy in BP – asymmetric BP > 20 mmHg difference in right and left arms. Asymmetric, decreased or absent pulses. Aortic regurgitation: of new onset if ascending (blowing diastolic decrescendo murmur) Neurological deficits: 20% of cases- stroke, altered mental status, acute paraplegia, Horner syndrome, hoarseness Muffled heart sounds if cardiac tamponade.  AORTIC DISSECTION: INITIAL EVALUATION ECG: Rule out MI, extension of Type A dissection can cause coronary ischemia CXR: Widening of the mediastinum or widened aortic silhouette are common. May be normal in 10%. CT angiogram, Transesophageal ECHO, and MR angiogram are all acceptable first line imaging modalities CTA in most EDs is the most commonly used first line imaging studies in hemodynamically stable patients TEE at bedside or in the OR if hemodynamically unstable, impaired renal function, contrast allergy, or strong suspicion of ascending dissection  AORTIC DISSECTION MANAGEMENT Surgical Management: used in acute proximal (Stanford Type A) OR acute distal with complications (Type B) with ischemia , progression, or impending rupture Preoperative BP control: BP and HR may rise during induction for emergency surgery, so lower readings prior to surgery are recommended (Beta Blockers) Medical Management: Acute descending dissection (Type B) without complications IV Beta blockers (esmolol, labetalol) – help lower systolic BP, HR, and prevent reflex tachycardia, and decrease LV contractility (all of which reduce aortic wall stress) The vasodilators Sodium nitroprusside or Nicardipine may be added AFTER Beta blockers to reach target BP if additional therapy is needed(can cause reflecx tachycardia if used alone or before BB). BP goal: systolic BP is rapidly lowered to a goal SBP 100-120 mmHg and maintain a HR 70 years); Northeastern Europeans and Caucasians; Smokers Clinical Manifestations: 1. Headache: new onset HA or change in baseline HA is the most common symptom (usually temporal); scalp tenderness while combing hair 2. Jaw claudication/exertional ischemia: mandibular pain, monocular vision loss, diplopia, & amaurosis fugax 3. Abnormal superficial temporal artery: Absent or decreased pulsation, local tenderness to palpation (including scalp tenderness), erythema, nodularity or thickening 4. Constitutional symptoms: fever, fatigue, weight loss, anorexia, malaise  GIANT CELL (TEMPORAL) ARTERITIS) Diagnosis: 1. Elevated ESR & CRP are the hallmark of GCA. Most will also have a normocytic, normochromic anemia. 2. Temporal Artery Biopsy: Criterion standard. Infiltrate predominantly of mononuclear cell infiltration or granulomatous inflammation, or multinucleated giant cells. Scheduling of the temporal artery biopsy should NOT delay treatment in patient with high likelihood of GCA since delay can increase complications such as vision loss!! Treatment: 1. High dose systemic glucocorticoids: initiated once GCA is suspected to prevent blindness and suppress disease activity. IV methylprednisolone pulses for 3-5 days prior to oral therapy. 2. Low dose Aspirin: helps reduce the risk of vision loss, TIA & strokes 3. IL-6 inhibitors (Tocilizumab)is an alternative to steroids if intolerant  ARTERIOVENOUS (AV) MALFORMATION Result from developmental defects of the arterial and venous vasculature, but without endothelial cell hyperplasia. Rare, affect