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Endocrine and Cardiovascular Disorders, Exams of Nursing

A comprehensive overview of various endocrine and cardiovascular disorders, including hyponatremia, diabetes insipidus, thyroid gland disorders (goiter, hypothyroidism, hyperthyroidism), pericardial effusion, cardiac tamponade, valvular disorders, and cardiomyopathy. It covers the causes, characteristics, management, and laboratory findings for each condition. The document also discusses the role of the posterior pituitary gland, the thyroid gland, and the renin-angiotensin-aldosterone system in regulating blood pressure. Additionally, it touches on the pathophysiology and clinical manifestations of heart failure, including systolic and diastolic dysfunction. This information would be valuable for students studying endocrinology, cardiology, or related medical fields, as it provides a solid foundation for understanding these complex disorders and their management.

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2024/2025

Available from 10/08/2024

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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, T4
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)
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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 corticosteroidsMineralocorticoids , 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 testIncreased 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 SystemStructures of the Urinary System Include:

  1. Kidneys :
  2. Ureters: transport urine from the kidney to the bladder
  3. Urinary Bladder: storage of unit, muscular reservoir until excreted
  4. 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