NURS-611 Patho Exam 3 Review
NURS-611 Patho Exam 3 Review- Kyle R. Marshall
? Hematologic Alterations:
❖ Blood:
➢ Erythrocytes (RBCs):
■ 1.
... [Show More] Have a biconcave shape, optimal for gas diffusion in and out of the cell
■ 2. Have the micro capacity to be reversibly deformed
● Can squeeze through the microcirculation, and then return to normal
➢ Hemoglobin Synthesis:
■ Dependent upon nutritional state
■ Most important nutrients:
● 1. Vitamin B6 (pyridoxine)
● 2. Iron
◆ Normal female: 14g/dL
◆ Normal male: 16g/dL
❖ Iron Cycle:
➢ Made possible by plasma carrier transferrin
➢ Tissue macrophages (primarily in the spleen) break down ingested erythrocytes and return iron to the bloodstream directly or after storing it
❖ Leukocytes (WBC’s):
➢ Defend the body against microorganisms that cause infection
➢ *Remove debris, including dead or injured cells of all kinds
➢ Act primarily in the tissues, but are transported in circulation
➢ Average: 5,000-10,000 per cubic centimeter of blood
❖ Neutrophils:
➢ Immature neutrophils are bands or stabs
➢ Mature neutrophils are called segmented d/t appearance of the nucleus
➢ Premature release of bands is responsible for shift-to-the-left/leukemoid reaction phenomena
➢ Normal: neutrophils in circulation are in a segmented form
➢ Left Shift:
■ Increasing number of non-segmented neutrophils (bands/stabs), typically indicates bacterial infection
➢ Right Shift:
■ Increasing number of hypersegmented neutrophils (monocytes/eosinophils), typically indicated viral infection
❖ Anemia:
➢ Reduction in the total number of RBCs in the circulating blood/decrease in the quality or quantity of hemoglobin itself
➢ Common Causes:
■ 1. Impaired erythrocyte production
■ 2. Acute or chronic blood loss
■ 3. Increased erythrocyte destruction
■ 4. Combination of the causes listed above
❖ Megaloblastic Anemia:
➢ Cells struggle to make DNA, however RNA production proceeds as normal
➢ Cells have slow-maturing nuclei, but normal maturing cytoplasm
➢ Megaloblastic erythroid precursors grow large before the larger nuclei becomes mature enough to signal division, thus causing the cell to be larger than normal
❖ Pernicious Anemia:
➢ This is a type of megaloblastic anemia
➢ Principal problem is lack of intrinsic factor (IF)
➢ IF is secreted by gastric parietal cells and creates a complex with dietary B12 in the small intestine
➢ Deficiency can lead to a wide spectrum of hematologic and neuropsychiatric disorders that can often be reversed with early diagnosis and treatment
➢ Increase in age and use of gastric-blocking agents increase prevalence
➢ Develops slowly (over 20-30 years)
➢ Average age of diagnosis is 60
➢ Due to slow onset, PA is usually severe by the time treatment is sought
➢ When hgb level is significantly decreased (7~8), individual experiences classic symptoms of anemia:
■ Weakness
■ Fatigue
■ Paresthesias of feet and fingers
■ Difficulty walking
■ Loss of appetite
■ Abdominal pain
■ Weight loss
■ Sore tongue- smooth and beefy red secondary to atrophic glossitis
❖ Microcytic-Hypochromic Anemia:
➢ Abnormally small erythrocytes that contain unusually reduced amounts of hemoglobin
➢ Associated with iron overload
❖ Iron Deficiency Anemia:
➢ Type of Microcytic-Hypochromic anemia
➢ Can arise due to inadequate dietary intake of iron or due to excessive blood loss
➢ Most common cause in developed country is due to pregnancy and chronic blood loss
➢ May occur due to occult blood loss secondary to gastrointestinal cancer or other lesions
➢ Symptoms begin gradually, individuals typically do not seek treatment until hemoglobin levels have decreased to 7~8
➢ Menorrhagia:
■ Excessive menstrual bleeding
■ Causes primary iron-deficiency anemia in females
➢ Males may experience excessive bleeding due to:
■ Ulcers
■ Hiatal hernia
■ Esophageal varices
■ Cirrhosis
➢ Early symptoms (iron deficiency anemia):
■ Fatigue
■ Weakness
■ Dyspnea
■ Paleness of earlobes, palms, and conjunctiva
■ Hemorrhoids
■ Ulcerative colitis
■ Cancer
❖ Aplastic Anemia:
➢ Critical Condition
➢ Typically a critical condition caused by an autoimmune disease against hematopoiesis by activated cytotoxic T cells
➢ Characterized by pancytopenia, a reduction or absence of all three blood cells types, resulting from failure or suppression of bone marrow to produce adequate amounts of erythrocytes, leukocytes, and thrombocytes
❖ Anemia of Chronic Disease:
➢ Common type of anemia in hospitalized individuals
➢ Results from a combination of
■ 1. Decreased erythrocyte life span
■ 2. Suppressed production of erythropoietin
■ 3. Ineffective bone marrow erythroid progenitor response to erythropoietin
■ 4. Altered iron metabolism and iron sequestration in macrophages
❖ Post-Hemorrhagic Anemia:
➢ Reduction in tissue oxygenation stimulates production of erythropoietin and increasing production of erythrocytes (reticulocytes) in the bone marrow
➢ As bone marrow begins to produce more erythrocytes, and increase in the number of reticulocytes is seen, typically 10%-15% after 7 days
❖ Hodgkin Lymphoma:
➢ A malignant lymphoma characterized by its progression from one group of lymph nodes to another, the development of systemic symptoms, and the presence of Reed-Sternberg (RS) cells
➢ *Reed-Sternberg cells are the hallmark of Hodgkin Lymphoma
➢ *Most indicative and usually the sign is enlarged, painless lymph nodes in the neck
❖ Heparin-Induced Thrombocytopenia:
➢ Heparin is a common cause of drug-induced thrombocytopenia
➢ Approximately 4% of individuals treated with unfractionated heparin develop HIT
➢ HIT is an immune-mediated adverse drug reaction caused by IgG antibodies against the heparin, which is platelet factor 4 complex
➢ *Hallmark sign is thrombocytopenia
➢ Decrease in approximately 50% of the platelet count is seen in >95% of individuals with HIT
➢ HIT predisposes patients to thrombosis because platelets release microparticles that activate thrombin, thereby leading to thrombosis
➢ Venous thrombosis is common and results in DVT and PE
➢ Arterial thrombosis affect the large arteries and lower extremities, causing acute limb ischemia
➢ Arterial thrombosis may lead to CVA and MI
❖ Disseminated Intravascular Coagulation:
➢ Acquired clinical syndrome characterized by widespread activation of coagulation, resulting in the formation of fibrin clots in medium and small vessels
➢ Sepsis is the most common condition associated with DIC
➢ Thrombosis is generalized and widespread
➢ *Individuals are also absurdly at risk for hemorrhage, this occurs secondary to the high consumption of platelets and clotting factors
➢ Platelet consumption exceeds production, resulting in thrombocytopenia
? Hormonal Regulation:
❖ Hormones have specified rates and rhythms of secretions
❖ Three basic secretion patterns:
➢ Circadian or diurnal patterns
➢ Pulsatile and cyclic patterns
➢ Patterns that depend on levels of circulating substances
■ E.g., calcium, sodium, potassium, or the hormones themselves
❖ Hormones operate within feedback systems, positive or negative, to maintain an optimal internal environment
❖ Hormones affect only cells with appropriate receptors, and then act on those cells to initiate specific cell functions or activities
❖ Diseases of the Anterior Pituitary Gland:
❖ Hyperpituitarism: Primary Adenoma:
➢ Disease of the Anterior Pituitary Gland
➢ Primary adenomas are usually benign and slow growing
➢ Arise from cells of the anterior pituitary gland
➢ Local expansion may cause both neurologic and secretory defects
➢ Adenomatous tissue secretes the hormone of the cell type from which it arose, without regard to physiologic need and without regulatory feedback mechanisms
➢ Paradoxically, the pressure produced by the adenoma, is also associated with decreased function of neighboring anterior pituitary cells, resulting in hyposecretion of other anterior pituitary hormones
❖ Prolactinoma: Hypersecretion of Prolactin:
➢ Disease of the Anterior Pituitary Gland
➢ Pituitary tumors that secrete prolactin
➢ Most common of the hormonally active pituitary adenomas
➢ Other conditions or medications can elevate prolactin levels in the absence of a pituitary condition:
■ E.g., renal failure, PCOS
■ E.g., antipsychotics, metoclopramide, tricyclic antidepressants, methyldopa
● * Dopamine typically inhibits prolactin secretion, these medications block the effects of dopamine, thus more prolactin is secreted
➢ Physiologic actions of prolactin:
■ Breast development during pregnancy
■ Postpartum milk production
■ Suppression of ovarian function in nursing women
➢ Pathologic elevation of prolactin causes:
■ Amenorrhea
■ Infertility
■ Galactorrhea
■ Hirsutism in women
➢ Hyperprolactinemia in men:
■ Erectile dysfunction
■ Infertility
■ Osteopenia
❖ Diseases of the Posterior Pituitary Gland:
❖ Diabetes Insipidus:
➢ Result of insufficient ADH
■ *ADH=antidiuretic hormone, insufficient amount causes profound water deficit
➢ Must be distinguished from other polyuric states, including diabetes mellitus
➢ Basic criteria for the diagnosis of DI:
■ Polyuria
■ Polydipsia (thirst)
■ Hypernatremia
■ High serum osmolality (>300)
❖ Syndrome of Inappropriate Antidiuretic Hormone (SIADH):
➢ Characterized by high levels of ADH without normal psychological stimuli to stimulate its release
➢ Associated with ectopic secretion of ADH by several types of tumor cells, pulmonary disorders, and central nervous system disorders
➢ Symptoms result from hypotonic hyponetremia, and are associated with hypervolemia, and weight gain
➢ Severity and rapidity of onset of the hyponatremia determine the extent of symptoms
❖ Alterations of the Thyroid Gland:
❖ Hypothyroidism:
➢ Decreased thyroid hormone (TH) results in:
■ Decreased energy metabolism
■ Constipation
■ Bradycardia
■ Lethargy
➢ In primary hypothyroidism the loss of functional thyroid tissue leads to a decreased production of TH
➢ Causes in adults:
■ Autoimmune thyroiditis (Hashimoto)
■ Iatrogenic loss of thyroid tissue after surgical/radioactive treatment for hyperthyroidism
■ Head and neck radiation therapy
■ Certain medication
■ Endemic iodine deficiency
➢ Clinical Manifestations:
❖ Confusion
❖ Syncope
❖ Slowed speech and thought
❖ Memory loss
❖ Lethargy
❖ Headaches
❖ Decreased libido
❖ Menorrhagia
❖ Erectile dysfunction
❖ Anemia
❖ Bradycardia w/ decreased CO
❖ Dyspnea
❖ Constipation
❖ Weight gain
❖ Fluid retention
❖ Decreased nutrient absorption
❖ Reduced renal blood flow
❖ Reduced erythropoietin production
❖ Dry/flaky skin
❖ Coarse hair
❖ Reduced nail/hair growth
❖ Slow wound healing
❖ Hyperthyroidism:
➢ Graves disease results from a form of type II hypersensitivity reaction in which there is stimulation of the thyroid by autoantibodies directed against the autoantibodies
➢ The autoantibodies, called thyroid-stimulating immunoglobulins, override normal regulatory mechanisms
➢ The TSI stimulation of TSH receptors in the gland results in hyperplasia of the gland, called a goiter, and increased synthesis of TH
➢ Clinical Manifestations:
● Goiter
● Bruit over thyroid
● Hypercalcemia
● Decreased PTH
● Oligomenorrhea
● Amenorrhea
● Erectile dysfunction
● Decreased libido
● Weight loss
● Increased peristalsis
● Less formed/more frequent stools
● Hyperhidrosis
● Flushing
● Erythema
● Heat intolerance
● Hair loss
● Elevated upper eyelid
● Decreased blinking/staring
● Fine tremor of upper eyelid
● Increased CO
● Decreased peripheral resistance
● Tachycardia
● SVT
● Restlessness
● Attention deficit
● Fatigue
● Tremor
● Insomnia
● Increased appetite
● Emotional lability
● Dyspnea
❖ Hypoparathyroidism:
➢ Calcium and phosphate balance are regulated by PTH
➢ Decreased calcium signals PTH to increase osteoclastic activity
➢ Increased calcium levels suppress PTH secretion
➢ Most commonly caused by damage to parathyroid glands during thyroid surgery
? Alterations of the Pancreas:
❖ Diabetes Mellitus:
➢ Diabetic Ketoacidosis:
■ Results from dehydration during a state of profound insulin deficiency
■ Precipitated by an infection, newly diagnosed, non adherence to type 1 DM
■ Clinical Manifestations:
● Postural dizziness
● CNS depression
● Ketonuria
● Anorexia
● Kussmaul Respirations:
◆ Done in an attempt to compensate for the acidosis
◆ ABG ex: Compensated Metabolic Acidosis
➢ p.H.: 7.36 (side of acidotic)
● Nausea
● Abdominal pain
● Thirst
➢ PaCO2: 25mmhg (blowing off CO2 to increase pH)
➢ HCO3: 9 acidic
● Poluria & Dehyrdration:
◆ Results from osmotic diuresis associated with hyperglycemia
◆ Plasma glucose is higher than renal threshold allowing significant glucose to be excreted in the urine
❖ Hyperosmolar Hyperglycemic NonKetotic Syndrome (HHNS):
➢ Life threatening emergency
➢ Most often precipitated by infections, medication, nonadherence to type 2 DM, or coexisting disease
➢ Differs from DKA by degree of insulin deficiency (more profound in DKA) and degree of fluid deficiency
➢ Characterized by a lack of ketosis/ketones
❖ Hypoglycemia:
➢ Plasma glucose <45-60
➢ Clinical Manifestations:
■ Tachycardia
■ Palpitations
■ Diaphoresis
■ Tremors
■ Pallor
■ Arousal anxiety
■ Headache
■ Dizziness
■ Irritability
■ Fatigue
■ Poor judgment
■ Confusion
■ Visual changes
■ Hunger
■ Seizures
■ Coma
❖ Somogyi Effect:
➢ Morning hyperglycemia in patients with DM
➢ Occurence of hypoglycemia at round 0300 due to too much intermediate-acting insulin (NPH insulin) at dinner time, followed by rebound hyperglycemia in the early morning
➢ Rebound hyperglycemia occurs due to secretion of counter regulatory hormones that are released due to hypoglycemia
➢ Excessive carbohydrate intake can contribute to rebound hyperglycemia
➢ Treatment is to decrease evening insulin level
➢ Becoming less common due to increase using of long-acting insulin
❖ Dawn Phenomena:
➢ Morning hyperglycemia in patients with DM
➢ Caused by nocturnal elevation of growth hormone, this decreases glucose metabolism by muscle and fat
➢ Increasing the dose of evening insulin manages the problem
❖ Microvascular Disease (In Diabetics):
➢ Lesions in small arteries
➢ *Leading cause of blindness, end-stage renal failure, and neuropathies
➢ Thickening at the capillary basement membrane, endothelial cell hyperplasia, and thrombosis
➢ Thickening eventually results in decreased tissue perfusion
➢ Hypoxia and ischemia accompany, especially in the eyes, kidneys, and nerves
➢ Frequency and severity are proportional to the duration of diabetes
➢ Underscores the need for diabetic screen, as well as monitoring the patients HgbA1C, which determines glucose control over 3-4 months
❖ Macrovascular Disease (In Diabetics):
➢ Lesions in large and medium sized arteries
➢ Increases morbidity and mortality
➢ Higher mortality during the acute phase than non-diabetics because they often asymptomatic as a result of sensory and autonomic neuropathy
➢ Increases risk for:
■ Accelerated atherosclerosis
■ Myocardial infarction
■ Stroke
■ Peripheral vascular disease
? Alterations in Adrenal Function:
❖ Addison’s Disease:
➢ Characterized by inadequate corticosteroid and mineralocorticoid synthesis and elevated ACTH
➢ Symptoms are a result of hypocortisolism and hypoaldosteronism
➢ *Addisonian crisis- severe hypotension and cardiovascular collapse
➢ Clinical Manifestations:
■ Hypovolemia
■ Postural hypotension
■ Dizziness
■ Dehydration
■ Hyperkalemia
■ Craving of salt
■ Vililigo
■ Bronze-Colored skin
❖ Cushing’s Syndrome:
➢ Refers to the clinical manifestations from chronic exposure to excess endogenous cortisol, excess endogenous secretion of ACTH
➢ More common in women
➢ May develop as a long-term side effect of administration of glucocorticoids
➢ Clinical Manifestations:
■ Polyuria
● Result of hyperglycemia/glucosuria
■ Transient weight gain
● Result of sodium and water retention due to side effects of cortisol
● Truncal obesity
● Moon face
● Buffalo hump
■ Glucose intolerance
● Due to cortisol-induced insulin resistance, increased gluconeogenesis, glycogen storage
■ Overt Diabetes Mellitus
● In approximately 20% of individuals
■ Protein wasting and muscle weakness
■ Loss of collagen
● Leads to thin/weakened integumentary tissues
● Purple striae and easy bruising
? Cardiac Alterations:
❖ Electrical Activity of the Heart:
➢ Impulses begin in SA node, through the atria, through the AV node (responsible for impulse transit delay), and enters the ventricles
➢ Sympathetic nervous system increased heart rate and rate of electrical conduction
➢ Parasympathetic nervous system decreases heart rate and prolongs intranodal conduction time
❖ Atrial Fibrillation:
➢ Most common cardiac rhythm disorder
➢ Occurs when electrical impulses become disorganized
➢ 4-5x increase in the risk of stroke
➢ Electrical activity in the atria is rapid and irregular
➢ No coordinated end atrial contraction
➢ Depending on SA node filtering, response of the ventricles can become rapid and irregular
➢ Fundamentally involves atrial remodeling that generates ectopic foci (triggers) that serve as additional sources for electrical impulses
❖ Preload (Left Ventricular End-Diastolic Pressure):
➢ *Frank-Starling Law- cardiac muscle increases its strength of contraction when it is stretched
➢ Preload is the pressure generated at the end of diastole
➢ Determined by the left ventricular end-diastolic volume (LVEDV), which stretches the cardiac muscle fibers and, in turn, develops tension/force for contraction
➢ Increased preload means increased volume, thus the force of contraction is increased, thus cardiac output is also decreased
❖ Effects of Angiotensin II on the Heart:
➢ When presented in abnormal amounts, Angiotensin II contributes to hypertensive hypertrophy, this is due to an increase in peripheral vascular resistance that is caused by Angiotensin II
➢ Mediates arteriolar remodeling, which is a structural change in the vessel wall, this results in permanent increases in peripheral vascular resistance
➢ Associated with end-organ effects of hypertension:
■ Atherosclerosis
■ Renal disease
■ Cardiac hypertrophy
■ Fibrosis of cardiac muscle
➢ Drugs that block RAAS:
■ ACE inhibitors
■ Direct renin inhibitors
■ Angiotensin II receptor blockers (ARBs)
■ Aldosterone inhibitors
■ Decreased contractility
■ Increases susceptibility to arrhythmias
■ Heart failure
■ These meds are widely used to manage hypertension, myocardial infarction, heart failure, to improve cardiovascular and renal function
➢ Released during ischemia and contributes to myocardial infarction:
■ **Results in systemic effects of peripheral vasoconstriction and fluid retention
■ Homeostatic responses of Angiotensin II are counterproductive, they result in increased myocardial work on a heart that is already struggling, may exacerbate the effects of the loss of myocyte contractility after resolve of MI
❖ Coronary Artery Disease (CAD):
➢ Non-Modifiable Risk Factors:
■ Advanced age
■ Male/or post-menopausal female
■ Family History
➢ Modifiable Risk Factors:
■ Dyslipidemia
■ Hypertension
■ Cigarette smoking
■ Diabetes/insulin resistance
➢ Increased serum LDL is an indicator of risk
■ Obesity (BMI >30)
■ Sedentary lifestyle
■ Atherogenic diet (excess cholesterol and salt)
➢ Relative risk of LDL elevation depends on the presence of other risk factors such as age, diabetes, chronic kidney disease
➢ LDL is responsible for delivery of cholesterol to tissues
➢ Low HDLs are a strong indicator of coronary risk
➢ HDL is responsible for reverse cholesterol transport/return of excess cholesterol from tissues to the liver
❖ Acute Coronary Syndrome:
➢ Unstable Angina:
■ Plaque progression, disruption, and clot formation; same for MI as for unstable angina
■ Outcome is very different in that the myocardial ischemia in unstable angina is reversible
■ Usual interventions of angina do not relieve the pain- becomes an emergency
➢ Stable Angina:
■ Predictable, in that it occurs with exertion
■ Relieves with usual interventions such as nitroglycerin and rest
➢ NSTEMI:
■ Duration of ischemia determines the size and character of the infarction
■ If thrombus breaks up before complete distal tissue necrosis, the infarct will involve only the myocardium directly beneath the endocardium- this is called a subendocardial MI
■ Infarction presents with ST depression and T-wave inversion
➢ STEMI:
■ If the thrombus lodges permanently in the vessel, the infarction will extend through the myocardium all the way from the endocardium to the epicardium- called a transmural MI
■ This type of MI results in severe cardiac dysfunction
■ Transmural infarction causes marked elevations in the ST segment on an ECG
❖ Cardiac Markers:
➢ Cardiac troponin I (cTnI) is the most specific indicator of MI and should be obtained on admission to the emergency department
➢ cTnI is detectable 2-4 hours after onset of MI symptoms
➢ Additional biomarkers include CK-MB (creatine kinase muscle/brain) and LDH (lactate dehydrogenase)
❖ After an MI:
➢ Collagen matrix is deposited and is initially weak, mushy, and vulnerable to another injury
➢ This recovery period of 10-14 days after infarction, that individuals feel more capable of increasing activities, this causes excess stress on newly formed collagen matrix/scar tissue
❖ Acute Pericarditis:
➢ Acute inflammation of the pericardium
➢ Most often idiopathic, may be caused by a viral infection
➢ Causes:
■ MI
■ Trauma
■ Neoplasm
■ Surgery
■ Uremia
■ Bacterial infection (especially TB)
■ Connective tissue disease (especially Lupus & rheumatoid arthritis)
■ Radiation therapy
➢ Pericardium becomes inflamed and roughened, effusion may develop with serous, purulent, or fibrinous drainage
➢ Clinical Manifestations:
■ Follow several days of fever and begin with onset of severe, retrosternal chest pain that worsens with respiratory movements and when assuming a recumbent position
■ Dysphagia
■ Restlessness
■ Irritability
■ Anxiety
■ Weakness
■ Malaise
➢ Sequelae includes recurrent pericarditis, pericardial constriction, and cardiac tamponade (effusion)
❖ Heart Failure:
➢ The pathophysiologic condition in which the heart is unable to generate an adequate cardiac output
➢ Inadequate perfusion of tissues, and/or increased diastolic filling pressure of the left ventricle occurs
➢ Pulmonary capillary pressures are increased
➢ Left Sided:
■ Heart failure with reduced ejection fraction (HFrEF/systolic heart failure)
■ Ejection fraction of <40% and an inability of the heart to generate an adequate cardiac output in order to perfuse vital tissues/organs
■ Cardiac output is dependent on heart rate and stroke volume
■ Stroke volume is influenced by:
● Contractility
● Preload
● Afterload
■ Contractility:
● Reduced by disease that reduce myocyte activity such as MI, myocarditis, and cardiomyopathy: these diseases contribute to inflammatory, immune, and neurohumoral changes that mediate the process of ventricular remodeling
● When decreased, stroke volume decreases and left ventricular end-diastolic volume increases, thus dilation of the heart and preload increase occurs
■ Ventricular Remodeling:
● Results in disruption of the normal myocardial cellular structure with resultatant dilation of the myocardium and causes progressive myocyte contractile dysfunction
❖ (Heart Failure Continued)
■ Catecholamines:
● SNS activation initially compensates for a decrease in CO by increasing heart rate and peripheral vascular resistance
● Catecholamines cause numerous deleterious effects on the myocardium:
◆ Direct toxicity to myocytes
◆ Induction of myocyte apoptosis
◆ Myocardial remodeling
◆ Downregulation of adrenergic receptors
◆ Facilitation of dysrhythmias
◆ Potentiation of autoimmune effects on myocardium
■ RAAS:
● Angiotensin II
◆ Activation of RAAS causes not only increases in preload and afterload, but also direct toxicity to the myocardium
◆ Mediates remodeling of the ventricular wall, contributing to sarcomere death, oss of the normal collagen matrix, and intestinal fibrosis
◆ This leads to decreased contractility, changes in myocardial compliance, and ventricular dilation
● Aldosterone
◆ Causes salt and water retention by the kidney
◆ Contributes to myocardial fibrosis, autonomic dysfunction, and dysrhythmias
◆ Implicated in endothelial dysfunction and prothrombotic effects
● Arginine Vasopressin (ADH)
◆ Causes both peripheral vasoconstriction and fluid retention
◆ Actions of ADH exacerbate hyponatremia and edema in heart failure
● Natriuretic Peptides
◆ Atrial natriuretic peptides (ANP) and B-type natriuretic peptides (BNP) are increased and may have some protective effect by decreasing preload
◆ Compensatory mechanisms by peptides are inadequate in heart failure
◆ BNP:
➢ Produced and released in response to pressure and volume overload of the cardiac chambers
➢ Occurs in both systolic and diastolic heart failure
➢ Causes atrial and venous dilation, natriuresis, and suppression of the RAAS and SNS
➢ Inhibits myocardial fibrosis and hypertrophy
➢ Enhances diastolic function
■ Heart failure with preserved ejection fraction (HFpEF/diastolic heart failure):
● Occurs singly or alongside systolic heart failure
● When isolated- pulmonary congestion despite a normal stroke volume and cardiac output
● Associated with increased risk for diastolic dysfunction
● Major causes of HfpEF:
◆ Hypertension-induced myocardial hypertrophy
◆ Myocardial ischemia with resultant ventricular remodeling
➢ Right Sided:
■ Inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure
■ Most often results from severe left heart failure when increase left ventricular filling pressure is reflected back into the pulmonary circulation
■ As pressure in pulmonary circulation rises, the resistance to right ventricular emptying increases
■ The right ventricle hypertrophies in response to increased workload, and undergoes progressive diastolic and systolic deterioration and will dilate and fail
■ When right-sided heart failure occurs in the absence of left heart failure, most common cause is pulmonary hypertension; pulmonary HTN occurs secondary from diffuse hypoxic pulmonary disease such as chronic obstructive pulmonary disease (COPD) and cystic fibrosis, or from primary pulmonary arterial hypertension
❖ Cardiomyopathy:
➢ Dilated Cardiomyopathy:
■ Characterized by diminished myocardial contractility, this is reflected in diminished systolic performance of the heart
■ Impaired systolic heart function leads to increases in intracardiac volume, biventricular dilation, and systolic heart failure
➢ Hypertrophic Obstructive Cardiomyopathy:
■ Most common inherited heart defect through autosomal dominant inheritance
■ Thickening of the septum results in a hyperdynamic state, especially with exercise
■ Diastolic relaxation also is impaired and ventricular compliance is decreased
■ Significant risk for serious ventricular arrhythmia and sudden death
➢ Restrictive Cardiomyopathy:
■ Characterized by restrictive filling and reduced diastolic volume of either or both ventricles with normal or near-normal systolic function and wall thickness
■ May be idiopathic or as a manifestation of systemic disease such as scleroderma, amyloidosis, sarcoidosis, lymphoma, hemochromatosis, or a number of inherited storage diseases
■ Myocardium becomes rigid and noncompliant, impending ventricular filling and raising filling pressures during diastole
■ Most common clinical manifestation of restrictive cardiomyopathy is right heart failure with systemic venous congestion
❖ Hypertension: Target Organ Disease:
➢ Sodium retention leads to water retention and increased blood volume, which contributes to an increase in blood pressure
➢ Tissue ischemia causes inflammation of the kidney and contributes to dysfunction of the glomeruli and tubules and promoted additional sodium retention
➢ Vasoconstriction and the resultant decreased renal perfusion causes tubular ischemia
➢ *One sign/lab value to monitor to determine the effects of HTN on the kidneys is microalbuminuria
❖ Heart Valve Dysfunction:
➢ Normal blood flow through the heart is dependent on structurally sound and functioning heart valves
➢ The pumping action of the heart consists of contraction and relaxation of the myocardium
➢ Each ventricular contraction and the relaxation that follows constitute one cardiac cycle
➢ During relaxation/diastole, blood fills the ventricles
➢ During ventricular contraction/systole, blood propels out of the ventricles and into the pulmonary and systemic circulation
❖ Phases of the Cardiac Cycle:
➢ 1. Atrial Diastole:
■ Blood flows from veins into the relaxed atria (atrial diastole)
■ Once the atria are full, it is time for atrial systole/contraction
➢ 2. Atrial Systole:
■ The atria contract, propeling blood through the open AV (mitral and tricuspid) valves into the ventricles
■ During this time the semilunar (pulmonic and aortic) valves are closed
■ When the ventricles are full, it is time for ventricular systole/contraction
➢ 3. Ventricular Systole:
■ Ventricles contract
■ During this time the AV (mitral and tricuspid) valves are closed
■ During this time the semilunar (pulmonic and aortic) valves are open
■ Blood is propelled into the aorta and into the pulmonary and systemic circulation
➢ 4. Ventricular Diastole:
■ Semilunar (pulmonic and aortic) valves close and the cycle repeats
❖ Valvular Disease:
➢ Diagnosed via echocardiography, which is used to assess the severity of valvular obstruction or regurgitation before the onset of symptoms
➢ Management:
■ Careful fluid management
■ Valvular repair
■ Valve replacement w/ prosthetic valve followed by a long-term anticoagulation therapy
■ Valve replacement w/ mechanical valve requires lifelong antibiotic prophylaxis prior to invasive procedures is required
❖ Mitral Stenosis:
➢ Blood flow is impaired from the left atrium to the left ventricle
➢ Most commonly caused by acute rheumatic fever
➢ Results in incomplete emptying of the left atrium and elevated atrial pressure as the chamber works overtime to force blood through the stenosed valve
➢ If left untreated, pulmonary hypertension, edema, and right ventricular failure result
❖ Mitral Regurgitation:
➢ Backflow of blood from the left ventricle to the right atrium during ventricular systole
➢ Progression of regurgitation leads to impaired ventricular function and eventual left ventricular failure
➢ Increased atrial pressure leads to pulmonary hypertension and right ventricular failure
❖ Aneurysms:
➢ Atherosclerosis and hypertension are found in more than half of individuals with aneurysms
➢ Chronic hypertension contributes to vascular remodeling and weakening
➢ Atherosclerosis is a common cause of aneurysm because plaque formation erodes the vessel wall
➢ True Aneurysm:
■ Involves all three layers of the arterial wall
■ Best described as a weakening of the vessel wall
■ Most common are fusiform and circumferential
➢ False Aneurysm:
■ Extravascular hematoma that communicates within the intravascular space
■ Most common cause is a leak between a vascular graft and a natural artery
❖ Peripheral Artery Disease (PAD):
➢ Atherosclerotic disease of arteries that perfuse limbs
➢ Lower extremities are most affected
➢ Gradually increased obstruction of arterial blood flow to the legs is caused by atherosclerosis in the iliofemoral vessels
➢ Pain with ambulation results, but subsides with rest (intermittent claudication)
❖ Varicose Veins/Chronic Venous Insufficiency:
➢ Varicose veins are superficial veins in which blood has pooled
➢ May progress to chronic venous insufficiency, which sustained inadequate venous return
➢ Causes:
■ Trauma to the saphenous veins that damages one or more valves
■ Gradual venous distention caused by the action of gravity on blood in the legs
➢ Manifestations:
■ Edema of the lower extremities
■ Hyperpigmentation of the skin of the feet and ankles
? Obesity/Nutrition:
❖ BMI:
➢ Overweight: 25-30
➢ Obese: >30
❖ Obesity if the fifth leading cause of death in the United States
❖ Three leading causes of death in the US:
➢ Cardiovascular disease
➢ Type 2 DM
➢ Cancer
➢ All three of these are associated with obesity
❖ Obesity increases risk for:
➢ Hypertension
➢ Stroke
➢ Hyperlipidemia
➢ Gallstones
➢ Nonalcoholic steatohepatitis
➢ Gastroesophageal reflux
➢ Hiatal hernia osteoarthritis
➢ Infectious disease
➢ Asthma
➢ Obstructive Sleep Apnea
➢ Chronic Kidney Disease [Show Less]