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Exam #2 Review
Endocrine System Endocrine System ● Secretion of hormones into the bloodstream ● The collection of glands that involve in the secretion of hormones, a complex messaging and control system that interacts with several body functions. ● Glands: a group of cells that secrete hormones ● Hormones: chemical substances that control and regulate the activity of certain target cells or organs ● Major endocrine glands? ● Thyroid, thymus(matures t cell), adrenal, pancreas, pituitary, pineal, testes, ovaries, parathyroid, and hypothalamus gland ○ Adrenal cortex secretes corticosteroids ○ Mineralocorticoids , Glucocorticoids, Gonadocorticoids = types ● Disorders of the endocrine system are common and related to either the excess or insufficient of a hormone Hormones ● Secrete in small amounts at variable but predictable rates ● Ability to bind to specific target cell receptors in a “lock-and-key” mechanism ○ Hormones only affect certain cells ● Tropic hormones: stimulates an endocrine gland to secrete its hormones ○ E.g., thyroid-stimulating hormone: stimulates secretion of thyroid hormones (T3, T4) ● Non-tropic hormones: directly stimulates cellular metabolism and other activities (do not target other glands) ○ E.g., Glucocorticoids, ADH, prolactin, oxytocin, growth hormone ● Release of hormones are regulated by Feedback mechanism (negative) ● Only 2 positive feedback is Blood Clotting/oxytocin ● Examples ○ Insulin reduces the serum glucose level ○ ↑ T3, T4 → ↓ TRH & ↓ TSH → ↓ T3, T Hypothalamus ● Regulates the pituitary gland ● Synthesizes and secretes neurohormones ○ Hormones ■ Gonadotropin-releasing hormone (GnRH) = activate FSH and LH ■ Thyrotropin-releasing hormone (TRH) = TSH activated ■ Corticotropin-releasing hormone (CRH) = ACTH activated ■ Growth hormone-releasing/inhibiting hormones = targets bones + muscles ● Released in the anterior pituitary gland ■ Prolactin and prolactin inhibiting = targets mammary glands ■ Oxytocin, ADH (vasopressin)
● Release in the posterior pituitary gland ● Releasing hormones stimulates release of pituitary hormones ● Inhibiting hormones suppresses the release of pituitary hormones ○ Hypothalamic-pituitary axis Pituitary Gland ● Also called hypophysis ● Melanocytes = secrete melanin ● Commonly referred to as the “master gland ” ● Located at the base of the brain underneath the hypothalamus , roughly a pea size ● Two lobes: anterior, posterior ● Anterior: accounts for 80% of the gland weight ○ Six (6) hormones are controlled by the hypothalamus by releasing factors: ■ FSH + LH: Stimulate gamete production and hormone production by the gonads = sex organs ■ Adrenocorticotropic hormone ACTH : Stimulates secretion of hormones by the adrenal cortex, especially glucocorticoids ■ Thyroid-stimulating hormone : Stimulates release of thyroxine(T4) and triiodothyronine (T3). ■ Prolactin : Stimulates milk production by the breast ■ Growth hormone : Stimulates cell growth and fat breakdown. Primary targets are muscle and bone, where GH stimulates amino acid uptake and protein synthesis ○ Out of the six, two (2) hormones are controlled by the hypothalamus by inhibiting factors: ■ Prolactin ■ GH ○ Hormones are released into the blood circulation and are transported to their targeted organs ● Posterior: ○ Composed of neuronal axons that store and secretes hormones into the blood circulation ○ Two (2) hormones ■ Oxytocin : Stimulates breast to release milk and uterine contractions during birth ■ Antidiuretic hormone ADH : Stimulates water reabsorption by nephrons of the kidney ○ Directly stimulates the targeted organ: nontropic Posterior Pituitary Gland: SIADH ● Syndrome of inappropriate antidiuretic hormone ● Overproduction of ADH : hyperpituitarism ● ADH (vasopressin): ↑ permeability of the renal distal tubule and collecting duct → ↑ reabsorption of H2O into the circulation ● Causes: CNS disorders, malignant tumors (e.g., small-cell lung cancer) ● Characteristics of the disorder:
Goiter ● Visible enlargement of the thyroid gland ● Painless but may affect the respiratory system ● Causes: iodine deficiency (worldwide), hypothyroidism ( T3/T4 is low), hyperthyroidism( T3/T4 high) ● determine the causes by blood test ● Increased hyperthyroidism/TSH can cause goiter Hypothyroidism ● Results from suboptimal(decreased) level of thyroid hormones ● Causes: Hashimoto’s disease (autoimmune thyroiditis), aging (atrophy), radiation (head, neck cancer), therapy for hyperthyroidism (e.g., thyroidectomy, radioactive iodine tx) ● Common, women 5 - 8x > men ; Most common in women ● Signs and symptoms: fatigue, dry skin , hair loss, brittle nails, loss of libido (sex drive) , cold intolerance, weight gain, constipation , hypotension, bradycardia , muscle weakness, lethargy ,depression, enlarged thyroid (goiter) ● Lab: free T4⬇, total T3 & T4⬇, TSH⬆ ● Most common cause: Hashimoto ● Management : ○ Oral: Levothyroxine ■ Synthetic version of T ■ Dose is increased at 4 to 6 weeks interval based on TSH levels ■ Interacts with many other medications → take it on an empty stomach in the morning/ night ■ Dosage is weight-based (1.6-1.7 mcg/kg) ■ Life long therapy is usually required ○ Myxedema ■ Administer IV T3 and T Hyperthyroidism ● Results from excessive secretion of thyroid hormones ● Much more common in females ● Most common cause: Graves Disease ● Causes: Graves’ disease; result from a form of type II hypersensitivity by antibodies that signal the thyroid on the THS receptor, excessive iodine or ingestion of thyroid hormone ● Signs and symptoms (increased) : nervousness, anxiety, irritability , heat intolerance , palpitations, ↑ RR, flushed skin, warm and moist skin , fine tremor, weight loss, increased appetite, hypertension, tachycardia , goiter, bruit over thyroid gland, exophthalmos, cardiac dysrhythmias , diarrhea ● Labs: free T4⬆, total T3 & T4⬆, TSH⬇ ● Exophthalmos: Protruding eyes with decreased blinking and movement. (EXPANDING) ● Management: ○ Radioactive iodine therapy ■ Destroys and shrinks the gland's cells (thyroid) ■ Goal: to eliminate the hyperthyroid state in a single dose of radiation (oral
capsule or liquid) ■ Can contaminate their household, avoid close contact with children and pregnant women ○ Antithyroid medications ■ Methimazole (MMI, Tapazol), propylthiouracil (PTU): inhibits synthesis of hormones ○ β - adrenergic antagonist ( propranolol= Beta ) to reduce cardiac symptoms (tachycardia, palpitations, ↑ BP) blocks beta receptors, lower BP + HR ■ Used with antithyroid drugs ○ Surgery (thyroidectomy) + hormone replacement ■ Reserved for patients that do not respond to or tolerate medications Myxedema ( skin change = edema) ● Advanced hypothyroidism ● Results from severe deficiency, symptoms are severe (advance hypothyroidism) ● Rare, but can be life-threatening ● Cause: long standing undiagnosed/untreated hypothyroidism ● Signs and symptoms: hypothermia, marked hypotension and bradycardia, respiratory depression, hypoxia, decreased cognitive status (lethargy, coma) Thyroid Storm ● Also called thyrotoxicosis ● Acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormone (infection, stress) ● Signs and symptoms: BT > 101.3 °F, tachycardia (>130bpm), altered mental status, exaggerated symptoms of hyperthyroidism (chest pain, dyspnea, diarrhea, abdominal pain) Parathyroid Glands ● Four glands located behind the thyroid gland ● Parathyroid hormone (PTH, parathormone) ○ Major role is to regulate calcium and phosphorus metabolism ○ Serum calcium level regulates the output of parathormone by negative feedback ● Hypoparathyroidism ○ Results from inadequate secretion of PTH ○ Cause: thyroidectomy, parathyroidectomy ○ Serum calcium ↓ phosphate ↑ ○ Signs and symptoms: manifest hypocalcemia , ○ Management : ( Eating food obtaning calcium) (vit D) ● Hyperparathyroidism ○ Results from an overproduction of PTH ○ Cause: noncancerous growth (adenoma) on the gland ○ Serum calcium ↑ phosphate ↓ ○ Signs and symptoms: manifest hypercalcemia & urinary calculi,
○ Reduce or taper corticosteroid medication to the minimum dosage to treat the underlying disease ○ Check lab values: Na, K, BSL Addison’s Disease ● Occurs when the adrenal glands cannot produce sufficient amounts of corticosteroid hormones ● Causes: autoimmune conditions (most common), adrenalectomy, pituitary dysfunction (↓ ACTH) ● Signs and symptoms: muscle weakness, fatigue, ↓ BP, ↓ BGL, ↓ serum Na, ↑ K, depression, amenorrhea, decreased libido ● Management: ○ Requires lifelong replacement of exogenous steroids ○ Check lab values: Na, K, BSL (Blood sugar levels) Pancreas ● Organ with both exocrine and endocrine functions ● Lies underneath the stomach between the two kidneys ● Endocrine functions are carried out by approximately 1 million Islet of Langerhans, situated among the many small acini (cell clusters that produce digestive enzymes) ● Each islet of Langerhans contains five types of cells: ○ Alpha cells (20%) secrete glucagon when serum glucose levels fall ○ Beta cells (70%) secrete insulin when serum glucose levels increase and amylin to enhance insulin activity (blocks glucagon secretion) ○ Delta cells (5%) secrete somatostatin, suppresses the release of both insulin and glucagon from alpha and beta cells ○ Pancreatic polypeptide cells ○ Epsilon cells: produce the hormone ghrelin that induces hunger. Diabetes Mellitus ● A group of conditions characterized by Hyperglycemia resulting from defects in Insulin production and action, or both ● Hyperglycemia: high serum glucose level ● Glucose: breakdown of carbohydrates, simple sugar that is the chief source of energy ● Three forms: type 1, type 2, gestational diabetes ● Clinical manifestations: three P’s (what are they= polyuria, polydipsia, polyasia ), hyperglycemia, glucosuria, weight loss, fatigue ● Treatment: depends on the type Diabetes Mellitus: Type 1 ● Also called insulin-dependent or juvenile-onset DM,onset is generally abrupt ● Diabetic Ketoacidosis ● Pancreatic beta cells are destroyed – little or no insulin production ● Usually occurs in children ● Causes: genetics, autoimmune reaction, viruses ● Treatment: Insulin Diabetes Mellitus: Type 2 ● Also called non insulin-dependent or adult-onset DM, onset is insidious
● Most common type ● Begins as insulin resistance (cells fail to respond normally to insulin) → pancreas gradually loses the capacity to produce enough insulin ● Causes: genetics, advanced age, environmental factors (obesity, physical inactivity) ● Treatment: lifestyle modification, oral medications that increase insulin production and action, insulin in severe cases Urinary System ● Structures of the Urinary System Include:
- Kidneys :
- Ureters: transport urine from the kidney to the bladder
- Urinary Bladder: storage of unit, muscular reservoir until excreted
- Urethra: two urethral sphincter ● Functions Include: Regulation ○ Fluid volume, blood pressure ○ Electrolytes ○ Acid-base balance ○ Metabolic waste and drug excretion ○ Vit D conversion to calcitriol ○ Hormone synthesis ■ Renin; when bp is low ■ Calcitriol; regulates calcium level ■ Vit d3 ; made by sunlight Size in urethra = 1.5 cm (female) 6 - 8 in (male) Creatine = break down of muscle ● Kidneys: bean-shaped organs l ocated in the retroperitoneal space , primary site of waste excretion ■ Other sites: ● Skin, liver, intestines ○ Renal Capsule : connective tissue that surround the kidney ○ Renal Cortex : mainly contains nephrons ○ Medulla : contains part of nephrons ○ Renal Hilum : opening where the blood vessels, nerves and ureter pass ○ Renal Sinus : cavity ○ Calyx : urine collection from the nephrons ○ Renal Pelvis : calyces convergence, funnel for urine flowing to the ureter ● Nephrons: functional unit of the kidney ○ One kidney contains about 1 - 2 million nephrons ○ Bowman’s capsule : cup-like double membranous sac ○ Glomerulus : bundle of capillaries ○ GFR (glomerular filtration rate) : the speed at which the blood moves through the glomerulus
○ Kidney releases Arterial potent in response to hypoxia and stimulates the BM to produce more RBCs ○ Renin Purine = if alot can have uric acid then can crystalize & become gout ● Renal Function Tests: Blood ○ EGFR (glomerular filtration rate) ○ BUN (blood urea nitrogen) : normally urea ( Break down of protein) is excreted by the kidneys, level varies with urine output (should not be high) ■ Best indicators of kidney functioning ■ Normal range: 10 - 20mg/dL ■ Decreased renal function, dehydration, increase protein intake are factors that increase BUN level ○ Creatinine (Cr): end product of muscle metabolism, excreted in the urine ○ Produced at a fairly constant rate by the body ○ As the kidneys become impaired, level in the blood will rise due to poor clearance of creatinine by the kidneys ○ Better indicator of renal function than BUN, the level does not vary with protein intake ■ Normal range: 0.7 - 1.4 mg/dL ● Question: Which of the following measurement is the best indicator of kidney functioning? Answer : EGFR ● Alterations in the Urinary System (Trouble peeing) ○ Urination requires: ■ A functioning bladder that can sense the stretch and filling of urine ■ An intact parasympathetic pelvic nerve to transmit signal (activation) ■ Working destructor muscle to initiate bladder contractions to expel urine ● Involuntary control: Sympathetic nerve, parasympathetic nerve ● Urinary Incontinence ○ Urination is controlled consciously in adults ○ The loss of bladder control ■ Overflow : the result of an inability to empty the bladder or retention ● Dribbling of urine, weak urine stream ● Causes: blockage (enlarged prostate, urethral stricture, stone), nerve damage ■ Stress : loss of urine from stress (pressure exerted on the bladder such as coughing , sneezing, laughing, exercising, lifting ● Causes: weakening of the detrusor muscle or sphincter (pregnancy, childbirth, aging) obesity, chronic coughing ■ Urge : sudden, intense urge to urinate, followed by an involuntary loss of urine ● Felt often and gives the individuals a short warning before voiding ● Causes: UTI, bladder irritants, nerve damage
● overactive bladder = if unknown cause ■ Mixed : occurs when symptoms of more than one type of urinary incontinence are experienced ■ Functional : occurs in many older adults ● Certain medication or health problems (physical/mental impairment) prevents toileting in time ○ Alcohol, opioids, immobility, severe arthritis, loss of normal dexterity, delirium, dementia ○ Cause/risk factors: depends on the type ■ Advantage age: detrusor muscle weaken, bladder capacity reduces ■ Being overweight: detrusor muscle weakens due to the increase pressure ■ Female: pregnancy, childbirth ■ Male: enlargement in prostate (urge and overflow) ■ Chronic cough (smoking) (Stress) ■ Acute: infection, stool impaction (Urge/Stress) ○ Management: depends on the type and cause ■ Treat cause ■ Urge: medication (anticholinergics - oxybutynin, tolterodine), Botox injection (Blocks Acetylcoline ; which causes muscle contratction) ■ Stress: pelvic floor muscle exercise (Kegel), artificial urinary sphincter, sling procedures ( Sphincter is usually in male ) ■ Fluid management (restriction) ○ Urinary Tract Infection (UTI) ■ Infection of the urinary tract ■ Most frequent sites are the bladder and urethra ■ Most often caused by direct invasion of bacteria ■ Most microorganisms are from ascending through the urethra ● More prevalent in females because: ○ Shorter urethras ○ Sitting position when using the restroom ○ Lace panties, sex, soap etc. ■ Urgency, frequency, dysuria, hematuria, cloudy and foul smelling urine, fever, chills, lower abnormal pain ○ Urinary Obstruction: causes altered urinary elimination by preventing the urine flow —> back up ■ Nephrolithiasis : presences of renal calculi (kidney stones) ■ Hydronephrosis : abnormal dilation of the pelvis and calyces of one or both kidneys ● result of urinary obstruction ■ Benign Prostatic Hyperplasia: benign prostatic hypertrophy ● Common, non malignant ● Enlargement of the prostate (affects men) ■ Tumors ● Wilms’ tumor : This tumor usually occurs in one kidney, but it can
of a walnut ■ Causes: exact cause is unknown, aging ■ As the prostate gland expands, it presses against the urethra and obstructs urine flow ■ Urine stream? ■ Incontinence: yes anything else? ■ BPH does not increase risk prostate cancer ■ Diagnosis: digital rectal exam, prostate-specific antigen (PSA) blood test, urine flow measures ■ Management: alpha- 1 blockers (-sin, first line), TURP (transurethral resection of the prostate) ○ Alterations in the Urinary System ■ 1. Conditions resulting in altered elimination ● Include structural barriers ○ Nephrolithiasis ○ Congenital disorder ○ Tumors ■ 2. Conditions resulting in impaired renal function ● Include disorders that prevent that kidneys from regulating fluid + excreting waste ● Requires dialysis to maintain homeostasis ○ Polycystic Kidney Disease (PKD) ❏ Genetic disorder (Mutation in chromosomes4&6) ○ Nephrotic Syndrome ■ A collection of symptoms due to kidney (glomerular) damage which includes: ● Massive proteinuria > 3.5 g/day ● Low serum albumin level ● High cholesterol/LDL level ● Significant swelling due to decreased oncotic pressure (periorbital, abdomen, dependent areas, anasarca) ■ Hallmark of disease = glomeruli ■ Causes: focal segmental glomerulosclerosis (FSGS), systemic diseases that damage the kidneys (e.g. SLE, DM), infections, medication reaction, idiopathic ■ Management: treat cause & symptom management ● Diuretic, strains (e.g. atorvastatin, simvastatin) ● Low-salt, low fat, low-cholesterol, protein diet, antibiotic therapy, BP management, temporary dialysis ○ Acute Kidney Injury (AKI) ■ Sudden/rapid loss of renal function ■ Generally reversible if cause is identified and treated promptly ■ Categories/causes:
● Prerenal conditions : hypoperfusion of kidney ○ Hemorrhage, GI loss, diuretics (low blood volume) ○ CO: MI, HF, cardiogenic shock ● Intrarenal conditions: actual damage to kidney ○ Glomerular diseases, pyelonephritis, nephrotoxic agents (NSAID, aminoglycoside abx) ● Postrenal conditions: obstruction to urine flow distal to the kidneys, interferences of urine excretion ○ BPH, nephrolithiasis, blood clots, strictures, tumors ■ 4 phases ● 1. Initiation : begins with the initial insult/injury and ends when the oliguria develops ○ Usually asymptomatic ● 2. Oliguria : < 400 - 500ml/day ○ Accompanied by decrease GFR, fluid volume and BUN (azotemia) ● Diuretic : gradual increase in UO, start of recovery ○ Lab values stable ● Recovery : improvement may take 3 to 12 months ○ Lab value returns to normal, symptoms start to resolve ○ Chronic Kidney Disease ■ Decrease in GFR lasting for 3 or more months ■ Los of renal function is irreversible ■ Cause/risk factors: aging, diabetes, HTN, chronic smoking, urinary obstruction, other renal diseases, sickle cell disease, etc. ■ Classified into 5 stages based on GFR ● 1. GFR > 90ml/min/1.73m ○ Kidney damage with normal or increased GFR ● 2. GFR - 60 - 89ml/min/1.73m ○ Mild decrease in GFR ● 3. GFR - 30 - 59ml/min/1.73m ○ Moderate decrease in GFR ● 4. GFR - 15 - 29ml/min/1.73m ○ Severe decrease in GFR ● 5. GFR <15ml/min/1.73m ○ End Stage Kidney Disease (ESRD) or chronic renal failure ■ Clinical manifestations develop gradually ● Hypertension ● Edema ● Respiratory distress ● Heart failure ● Weight gain ● Anemia
Conduction System ● Conduction: transmission of electrical impulse within the heart ● Coordinated contractions of the atria and ventricles occurs due to the conduction system ● Normally the conduction pathway originates in the Sinoatrial node (SA) ● Properties of the myocardial cells ○ Conductivity : the ability of the cells to conduct electrical impulse ○ Excitability : the ability of the cells to respond to electrical impulses ○ Automaticity : the ability to generate an impulse to contract without external nerve stimulus ○ Contractility : the ability to respond mechanically to an impulse ● Depolarization : electrical stimulation ○ Loss of polarization: loss of the difference in charge between the inside and outside of the plasma membrane of the myocardial cell generating a charge ○ A shift in electric charge distribution, resulting in less negative charge inside the cell ● Repolarization : electrical relaxation ○ Change in membrane potential that returns it to a negative value after the depolarization phase of an action potential ● Systole : mechanical contraction of ventricles ● Diastole : mechanical relaxation of ventricles, rest phase ● Myocardial cells require Na+, K+, Ca+ to conduct electrical signals that results in contraction and relationships Conduction Pathway ● Impulses originate in the SA node near the SVC in the right atrium at a rate of 60 - 100 bpm ○ Group of myocardial conducting cells ○ Conductor, generator, pacemaker of heart ○ Depolarizer by itself (automaticity) ● Impulses travel through the right and left atria, causing atrial contraction ● Impulses then travel to the atrioventricular node (AV), in the right atrium adjacent to the septum ○ Impulses are delayed or moves slowly (-0.1 sec) through the AV node to allow complete atria contraction and ventricle filling ● The AV Node can initiate impulses if the SA node fails at a rate of 40 - 60 bpm (intrinsic rate) ● When the SA and AV node both fail, ventricles will attempt to pace themselves, generating pulses at 20 - 40 bpm (not enough cardiac output). ● Impulses then move rapidly through the bundle of his right and left bundle branches and purkinje network of fibers, causing simultaneous ventricular contraction ○ The ventricles can initiate impulses if the SA and AV node fail (rate: 20 - 40 bpm) ○ Ventricles may beat before they fill with blood (not enough cardiac output) ● Electrocardiograph (ECG) ○ Graphic representation of the electrical impulse of the heart read by electrodes attached to the skin
○ The activity of the heart produces electrical potentials that can be measured on the surface of the skin Electrocardiogram (ECG): Components ● P wave: atrial depolarization (Contraction) ● QRS complex: ventricular depolarization (contraction) ● T wave: ventricular repolarization (relaxation) ● U wave: repolarization of the purkinje fibers, rarely observed ● Atrial repolarization does not appear on the ECG, it is hidden by other more prominent waveforms. Cardiovascular Center ● Also called cardiac control center ● Located in the medulla oblongata ● Responsible for altering the heart rate and BP if homeostasis is interrupted ● Short-term BP regulators: controls the cardiac function through the autonomic nervous system ■ Acts fast, temporary fix ○ Baroreceptors: response to changes in the circulating blood volume and relay the information to the cardiac control center, so that a proper blood pressure can be maintained. ■ BP ⬇: ⬆ sympathetic input and ⬇ parasympathetic input ➡ ⬆ stimulation to SA node, ⬆HR, ⬆contractility, and SV, vasoconstriction. ➡ ⬆BP ■ BP⬆: ⬇ sympathetic input and ⬆ parasympathetic input ➡ ⬇ stimulation of SA node, ⬇HR, ⬇ contractility, and SV, vasodilation ➡ ⬇BP ○ Chemoreceptors: detects changes in blood pH ■ increase in serum CO2 level (decrease in pH) ➡ ⬇ parasympathetic stimulation and ⬆ sympathetic stimulation ⬆HR, BP Cardiac Function ● Autonomic nervous system major functions on the heart ○ Chronotropic: rate of contraction (HR) ■ SA node ■ SNS: faster ■ PNS: slower ○ Dromotropic: conduction velocity, rate of electrical conduction (speed) ■ AV node ■ SNS: faster ■ PNS: slower ○ Inotropic: contractility (force), strength of contraction (ventricles) ■ Ventricles ■ SNS: stronger contraction ■ PNS: not major effect Circulation ● Two continuous circulatory loops: ○ Pulmonary circulation: movement of blood from the heart to the lungs for oxygenation, then back to the heart
● BP regulators (long term) ○ antidiuretic hormone (ADH): ■ Increase water absorption: ⬆blood volume ⬆BP ■ Secondary function: vasoconstrictor ➡ PVR ⬆ ○ Aldosterone: reabsorbs Na+ in the kidneys, water follows, excretes K+ ➡ BP ⬆ ○ renin-angiotensin-aldosterone (RAA) system becomes activated when renal blood flow decreases Pericardial Effusion ● Accumulation of the fluid in the pericardial sac ○ Normal: 50 mL ● Causes ○ pericarditis: inflammation of the pericardium ○ Autoimmune disorders ● Increase pressure within the pericardial sac ➡ heart compression ● effects as perdical fluid increases ○ ⬇ pressure in all cardiac chambers ➡⬇ cardiac output ○ ⬇ venous return due to atrial compression (accumulation) ● Large or uncontrolled pericardial effusion may progress to cardiac tamponade Cardiac Tamponade ● Clinical syndrome resulting from compression of the heart ○ E.g pericardial effusion ● Ventricles are unable to distend and fill adequately ➡ ⬇ cardiac output ● Clinical manifestation: ○ ⬇ BP, ⬆ HR (tachycardia), distant heart sounds (muffled) chest pan ○ ⬇ arterial pressure, ⬆ venous pressure ⬇pulse pressure ● may be life threatening ➡ HF, cardiogenic shock, death ● Management: ○ Treat the underlying causes (antibiotics) ○ Pericardiocentesis: punctuate of the pericardial sac to aspirate pericardial fluid Valvular Disorders ● Causes disruption of normal blood flow through the heart ● Stenosis: narrowing of the heart valves ○ Blood moving through the valve ⬇ ➡ backs up to the chambers just before the valve and ⬇ cardiac output ➡⬆chamber pressure, ⬆workload, ⬆O2 demand ➡ cell death, hypertrophy ➡ failure ○ Aortic valve stenosis: LV hypertrophy, ⬇ Cardiac output, ⬆afterload, pulmonary edema ● Regurgitation: occurs when the valves do not completely close ○ blood flows in both directions because of the incompetent valves ➡ ⬇ cardiac output ➡ ⬆ workload, ⬆O2 demand ➡cell death, hypertrophy ➡failure ● Causes: congenital defects, endocarditis, heart failure, rheumatic fever, hypertension ● Management: valve repair, valve ballooning (stenosis), prosthetic replacement Cardiomyopathy ● Heart muscle disease ➡ difficult to pump blood
● group of conditions that weaken and enlarge the myocardium ● classified into three groups: ○ dilated: occurs when the left ventricle becomes enlarged and weakened ■ most cases are idiopathic ■ can be inherited, hypertension, coronary artery disease (CAD), Myocardial infarction (MI) ■ Affects systolic function: ⬇ myocardial contractility ➡⬇ cardiac output, ⬆ pulmonary pressure ■ S/sx: fatigue, dyspnea, dizziness, activity intolerance, angina, week pulse ⬆ HR, thrombi ■ Management: mainly supportive (goal: ⬆ cardiac output) ○ hypertrophic: abnormal thickening of the heart muscle ■ Affects both systolic and diastolic function ■ Causes: hypertension, stenosis valvular disorders , HF ■ Hypertrophied ventricle walls become stiff, unable to relax during diastole and contract during systole ➡⬇ cardiac output, ⬆pulmonary pressure ■ s/sx: similar to dilated cardiomyopathy ■ management: maintain supportive (goal: ⬆ cardiac output) ■ affects young adults, especially athletes ○ restrictive: Heart Failure ● A condition in which the heart (ventricles) in unable to pump an adequate amount of blood to meet the body’s metabolic needs ● Causes: congenital heart defects, valvular disorders, MI, HTN, cardiomyopathy ● Usually considered a secondary disease ○ Caused by an underlying disease or infection ● Classification: by cardiac phase, anatomically ○ Systolic HF: due to weakened cardiomyocytes ■ ⬇ force of contraction, ⬇ pumping ability ( = ejection fraction): % of blood volume ejected during systole ■ muscle is thinner and chamber is dilated: cardiomyopathy , CAD, MI ○ Diastolic HF: not filling with enough blood ➡⬇ blood ejection (reserved EF) ○ hypertrophy, stiffness (⬇compliance): HTN, AVS, cardiomyopathy ○ Mixed: systolic + diastolic HF (combination of both) ○ EF (%) = blood ejected/blood filled = stroke volume/end diastolic ■ Normal = 55 - 70 ■ Less than 40 = systolic HF HF: Compensation and Decompensation ● Loss of cardiomyocyte function ➡ ⬇ cardiac output ● compensation ○ activate SNS: ⬆ HR, ⬆ contractility, vasoconstriction ○ ⬆Preload (RAA activation): ⬆contractility, Na ⬆ K⬇ ○ muscle hypertrophy: ⬆contractility ➡⬆ cardiac output temporarily⬇ ⬆ workload
