High-yield review for CVS system quiz #2

Published on May 21, 2018

Hypertension and vascular physiology

  • Velocity vs flow

  • Laminar vs turbulent flow

  • Pressures in the circulation
  • Resistance to blood flow

  • Poiseuille’s law

  • Peripheral resistance (all vesel types etc)

  • Series vs parallel circuits

  • Laplace law (tension in arterial walls)

  • Vascular compliance/distensibility

  • Arterial pressure pulsations

  • Pulse pressure

  • Damping of pressure pulses
  • Mean arterial pressure (MAP)

  • Vasodilation & O2 demand theory

  • Localized vasoconstriction
  • Metabolic theory (autoregulation of blood flow during changes in arterial pressure)
  • Myogenic theory (autoregulation of blood flow during changes in arterial pressure)

  • Kidney tubuloglomerular feedback (macula densa in early distal tube)

  • PROSTACYCLIN (inhibits platelet aggregation and promotes vasodilation) Vs THROMBOXANE A2 (promotes platelet aggregation and vasoconstriction) – They do opposite things

  • NITRIC OXIDE: formed in the endothelium and diffuses to smooth muscle cells, which in turn mediates the relaxation of vascular smooth muscle. NO is short-lived and is inactivated by hemoglobin

  • ENDOTHELINS: Endothelial cells also produce endothelin-1, one of the most potent vasoconstrictor agents

  • Vascular Growth Factors: • vascular endothelial growth factor (VEGF), • fibroblast growth factor, platelet-derived growth factor (PDGF), and • Angiogenin

  • Innervation of blood vessels

  • In Skeletal muscle vasculature, activation of β2-adrenoceptors on skeletal muscle blood vessels promotes vasodilation…In the veins, sympathetic stimulation produce venoconstriction
  • The vasodilator regulators include: ▪ Kinins ▪ VIP ▪ ANP • Circulating vasoconstrictor hormones include: ▪ Vasopressin (ADH) POTENT

  • VASOCONSTRICTOR▪ Norepinephrine and epinephrine ▪ Angiotensin II.

  • KININS: Two related vasodilator peptides, bradykinin and kallidin – They cause contraction of visceral smooth muscle, but they relax vascular smooth muscle via NO, lowering blood pressure. • They also significantly increase vascular permeability resulting in edema, attract leukocytes, and cause pain upon injection under the skin.
  • NATRIURETIC HORMONES: include ANP secreted by the heart, B-type natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). Antagonize the action of various vasoconstrictor agents and lower blood pressure. • ANP and BNP also serve to coordinate the control of vascular tone with fluid and electrolyte homeostasis via actions on the kidney.

  • Norepinephrine has a generalized vasoconstrictor action, whereas epinephrine dilates the vessels in skeletal muscle and the liver. • Angiotensin II has a generalized vasoconstrictor action.

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  • Regulation of arterial blood pressure • Hypertension • Pulmonary hypertension • Antihypertensive medications • Diuretics

  • When the sympathetic nerves are sectioned (sympathectomy), the blood vessels dilate. A change in the level of activity (increase or decrease) in sympathetic nerves is just one of the many factors that mediate vasoconstriction or vasodilation
  • The baroreceptors are stretch receptors in the walls of the heart and blood vessels. • The carotid sinus and aortic arch receptors monitor the arterial circulation. • The carotid sinus is a small dilation of the internal carotid artery just above the bifurcation of the common carotid into external and internal carotid branches. • The receptors are located in the adventitia of the vessels. • The afferent nerve fibers from the carotid sinus form a distinct branch of the glossopharyngeal nerve, the carotid sinus nerve. The fibers from the aortic arch form a branch of the vagus nerve, the aortic depressor nerve.

  • Cardiopulmonary receptors

  • an increase in arterial pressure in the human of only a few mm Hg can double renal output of water, a phenomenon called pressure diuresis, as well as double the output of salt, which is called pressure natriuresis.
  • Pressure Diuresis

  • Importance of Salt (NaCl) in Arterial Pressure Regulation • an increase in salt intake is far more likely to elevate the arterial pressure than is an increase in water intake
  • The Renin-Angiotensin System: Its Role in Arterial Pressure Control
  • Angiotensin II has two principal effects that can elevate arterial pressure. • vasoconstriction in many areas of the body occurs rapidly. • decrease excretion of both salt and water by the kidneys, occurs slowly.
  • Beta-blockers – cardioselective vs nonselective

  • calcium channel blockers

  • alpha 1 blockers, alpha 2 agonists (alpha 2 receptors in brainstem and periphery inhibit sympathetic activity and thus lower blood pressure. Alpha 2 agonists such as CLONODINE – reduce peripheral neurotransmitter release (anticholinergic side effects)

  • Reserpine – peripheral adrenergic antagonist (anti-HTN)

Hypertensive crisis

A 26-year-old primigravida presents for her routine 6-week postpartum evaluation.  Other than fatigue, which she attributes to doting on her newborn, she has no complaints.  The pregnancy was complicated by pregnancy-induced hypertension, which required induction at 34 + 2 weeks and culminated in an abdominal delivery due to a protracted latent phase.  The physical examination was significant for a BP of 210/130 mmHg.  Of note, the pre-pregnancy BP was 110/72 mmHg and the BP was 118/84 mmHg on methyldopa (500 mg bid) at the time of discharge from the postpartum ward.

  • Discuss the determinants of blood pressure regulation
  • Discuss the role of chemoreceptors in blood pressure regulation
  • Discuss the role of the renin-angiotensin-aldosterone system in blood pressure regulation
  • Discuss the relationship between extracellular fluid volume and blood pressure

  • Discuss pressure natriuresis
  • Discuss the pro- and anti-hypertensive properties of endothelin-1
  • Discuss the role of nitric oxide in hypertension
  • Discuss the role of ANP in blood pressure regulation
  • What is the differential diagnosis for a hypertensive crisis?
  • Discuss the drugs which are indicated for hypertensive emergencies
  • Discuss the long-term management of this patient

Vasovagal syncope

A 32-year-old chief boatswain mate, generally known among his shipmates to be fearless and intimidating, was noted to be pale and diaphoretic as the ship’s corpsman readied him for venipuncture during shipwide HIV screening.  Fortunately, 4 of his shipmates slowly lowered his 250-pound frame to the ground when he lost consciousness.

  • Discuss the different causes of syncope
  • Discuss the alterations in autonomic activation that characterize syncope
  • Discuss baroreceptor reflexes
  • Discuss the carotid sinus reflex
  • Discuss the symptoms which characterize syncope
  • What are the elements of the medical history for a patient with syncope?
  • What specialized testing is appropriate for patients with syncope?
  • What is the differential diagnosis for syncope?
  • Discuss the factors that affect cerebral perfusion
  • What treatment should be implemented in patients with vasovagal syncope

Peripheral vascular disease
A 58-year-old male diabetic smoker presents complaining of pain on walking of 6 months duration. He has a history of hypertension, for which he takes atenolol. He states that he has bilateral calf cramping with walking. The pain is worse in the right calf than the left and subsides when he stops walking. Recently, he has noticed that is able to walk less and less before the onset of symptoms. The impression is lower extremity peripheral arterial disease.

  • Review the key features of lower extremity atherosclerotic peripheral arterial disease, including narrowing of the lumen and possible aneurysm or thrombus formation
  • Describe the ankle-brachial index

  • Review risk factors for atherosclerosis, including cigarette smoking, hypertension, lipid abnormalities, and diabetes mellitus
  • Describe the pathobiology of acute limb ischemia

  • Describe the pathobiology of chronic limb ischemia
  • Describe the clinical manifestations of acute limb ischemia
  • Describe the clinical manifestations of chronic stable lower limb ischemia, especially claudication

  • Describe the clinical manifestations of chronic critical lower limb ischemia
  • Review the diagnosis of acute limb ischemia
  • Review the diagnosis of chronic limb ischemia
  • Describe the imaging procedures to diagnose vascular obstruction and estimate lesion severity
  • Describe the treatment options for acute limb ischemia
  • Describe the treatment options for chronic lower limb ischemia
  • Review risk factor modification
  • Describe exercise therapy
  • Describe anti-platelet and anti-thrombotic therapy
  • Describe the role of pentoxifylline and cilostazol in the treatment of intermittent claudication
  • Briefly review revascularization procedures
  • Discuss the prognosis of peripheral arterial disease

Atherosclerosis
A 38-year-old male was transported to the ED by ambulance for evaluation of chest pain x 1 h.  The history, physical examination, and EKG were consistent with a mild anterior wall MI.  He had no known medical problems and was on no medication.  He was overweight (BMI=32 kg/m2) and smoked 2 packs of cigarettes per day.  A CT scan was performed and the Agatson score was elevated.

  • Comment on how fissuring or erosion of atherosclerotic plaque triggers formation of a thrombus
  • Discuss atherosclerosis as a chronic inflammatory condition
  • Discuss the events leading to fatty streak formation

  • Review risk factors for atherosclerosis
  • Describe the processes that develop when LDL particles are trapped in the artery wall
  • Describe the uptake of oxidized LDL by macrophages through their scavenger receptors and their transformation into foam cells
  • Briefly describe the proposed role of T cells in atherogenesis

  • Describe triglyceride-rich remnant particles and their adverse effects on endothelial function, and how inflammation may inhibit clearance of these TG remnants
  • Describe the anti-atherogenic role of HDL particles
  • Describe the growth of early atherosclerotic lesions and formation of a sub-endothelial cap, in which collagen fibers are a major component
  • Discuss the importance of remodeling
  • Describe the contribution of rupture vs. erosion in causing myocardial infarction

Image result for rupture vs. erosion

Image result for rupture vs. erosion

  • Describe processes that are believed to contribute to plaque rupture and the impact of failure of removal of dead/dying cells by phagocytes (efferocytosis)
  • List the principles of anti-atherosclerotic therapy, including life-style modifications, statins, aspirin, and other inhibitors of platelet aggregation
  • Briefly describe new therapeutic approaches

 

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