NURS 208 Exam 2 Review | Download To Score An A

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 co ntrol 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) ● 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: ● Fluid retention ● Serum osmolality ↓, serum sodium level ↓ ● Urine concentration Increased, urine osmolality ↑ ● Manifestations: weight gain (blotted), ↑ BP, ↓ urine output, cerebral edema, lethargy(loss of energy), confusion, seizures → due to too much water in the brain (hyponatremia) ● Management: treat cause ● If symptoms are mild: fluid restriction or diuretic ● For severe hyponatremia (< 120 mEq/L): IV solution(hypertonic), fluid restriction of 500 ml/day Posterior Pituitary Gland: DI ● Diabetes insipidus (DI) ● Underproduction of ADH: hypopituitarism ● Most common disorder of the posterior pituitary gland ● Cause: hypophysectomy or radiation due to tumor (pituitary tumor: 95% benign) ● Characteristics of the disorder: ○ Urine output ↑ (more than 3 L a day) ○ Serum osmolality ↑, serum sodium level ↑ ○ Urine concentration decrease urine osmolality ↓ ○ Manifestations: excessive thirst (polydipsia), weight loss, dry mucous membrane, ↓ BP, ↓ HR ● Management ○ Administer Desmopressin (DDAVP): SC, IV, intranasal (spray), oral ○ Fluid replacement: oral, IV (Hypertonic) → monitor for s/sx of hyponatremia ○ Low sodium diet Thyroid Gland ● Located at the base of the neck below the larynx ● Produces 3 hormones: thyroxine (T4), triiodothyronine (T3), calcitonin ○ T4: accounts for 90% of produced thyroid hormone ○ T3 is much more potent (short life) ○ T3 and T4 affects metabolic rate, O2 consumption, growth and development, brain function, protein, fat, and carbohydrate metabolism ○ Function of calcitonin= Decrease calcium level into blood ● Iodine is essential to the thyroid gland for synthesis of its hormones ● TSH from the anterior pituitary gland controls the secretion of T3, T4 ● Blood studies ○ TSH: considered the most sensitive diagnostic test for evaluating thyroid dysfunction, used to monitor treatment (0.4-4.2 mU/L) ○ Free T4 (0.8-2.7 ng/dL) (Bounded by protein) ○ Total T3 (70-204 ng/dL) and T4 (4.6-11.0 mcg/dL) ○ Thyroid antibodies: measures levels of thyroid antibodies in the blood (not normal) ■ Assist in the diagnosis of autoimmune thyroid disease ■ Immune system makes antibodies that mistakenly attack normal tissue 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 T4 ■ 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 T4 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, ○ management ■ Hydration - isotonic fluids ■ Calcitonin Adrenal Glands ● Small, paired, highly vascular glands located on the upper portion of each kidney ● Adrenal medulla (center): secretes catacolenes ○ Catacolenes ○ Release of epinephrine (90%), norepinephrine, dopamine ● Adrenal cortex (outer portion): Mineralocorticoids ○ Necessary to adapt to stress of all kinds ○ Secretion of hormones are regulated by the hypothalamic (CRH) - pituitary (ACTH) - adrenal axis (negative feedback) Corticosteroid Hormones ● Glucocorticoids ○ Secretes mainly Cortisol (stress hormone) Glucose ○ Promotes gluconeogenesis in the liver (↑ cortisol → ↑ BGL), suppress inflammation and autoimmune response, control allergic reactions, released in stress response, promotes sodium absorption, stimulates hydrochloric acid secretion, etc. ○ S/E: diabetes, osteoporosis, peptic ulcer, poor wound healing, ↑ risk of infection ● Mineralocorticoids ○ Secretes mainly Aldosterone secreted in response to decrease fluid volume. ○ Regulates Sodium (Na) & Water (H2O) balance ○ Act principally on the renal tubule- Angiotensin II produces vasoconstriction ● Gonadocorticoids or sex hormones ○ Controls sexual development ○ Secretes small amounts of male; Androgen -Testosterone and female; Estrogen hormones Cushing’s Syndrome ● Occurs when exposed to excess amount of corticosteroid hormones ● Cause: use of glucocorticoid medications (most common) ex. prednisone, tumor of pituitary gland (overproduction of ACTH), adrenal hypertrophy ● Manifestations: ○ Glucocorticoid excess: weight gain, thin and fragile skin, bruises, purplish red striae, “moon-faced” appearance, heavy trunk (central-type obesity), relatively thin extremities, fatty “buffalo hump” in the neck and supraclavicular area, insomnia, hyperglycemia, osteoporosis, etc. ○ Mineralocorticoid excess: sodium and water retention, hypokalemia, edema, hypertension, hypervolemia ○ Gonadocorticoid excess: acne, virilization (hirsutism(female), breast atrophy, voice deepens(female)), loss of libido, muscle wasting ● Management: depends on the cause ○ Surgical removal of tumor ○ 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: 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 located 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 ■ Best measurement of renal functioning ■ Calculated by using a formula incorporating serum creatinine levels, age, gender, and ethnicity ■ Normal range: > 125mL/min/1.73m^2 ○ Filtration: a type of passive transport that results from hydrostatic pressure, mass movement of water and solutes from plasma to the renal tubule ○ Components of the nephrons ■ Proximal convoluted tubule: reabsorbs 75% of the filtered water and Na ■ Loop of Henle: Participate in countercurrent exchange, which maintains the concentration gradient ; loop diuretic - blocks reabsorption of water/ sodium ■ Distal convoluted tubule: Site of tubular secretion of H+, potassium, and certain drugs ■ Collecting Duct ○ Processes of urine formation ■ Filtration: capillaries —> tubules ■ Reabsorption: tubules —> capillaries ■ Secretion: opposite process of reabsorption (mainly waste) ■ Excretion: end result, what goes into the urine ● detrusor: a voluntary act to force urine out through the urethra ○ Urge is felt when bladder is filled with - 300 ml of urine ● Fluid and electrolyte balance ○ 4 processes ○ Most accurate indicator of fluid loss or gain is weight ○ RAA system: activated in response to renal flow decrease ■ Aldosterone reabsorbs sodium and water mainly in the distal tubule/collecting duct, excretes potassium ○ ADH: alters tubular reabsorption (pituitary gland) ■ Increase ADH: Increase reabsorption of water, increase fluid volume ○ Urine Test: urine specific gravity (USG): (higher)measures the concentration of particles in urine and the density of urine compared with the density of water ○ Acid Base Balance: reabsorption and excretion of sodium and potassium ● Excrete waste products ○ Ammonia: toxic product (Break down) of amino acid catabolism, converted to a less toxic urea ○ Urea: converted in the liver and released in the bloodstream ○ Uric acid: product of the metabolic breakdown of purine nucleotides (e.g. increase gout, kidney stones) ○ Creatinine (Normal muscle metabolism) ● Vit D (inactive form) conversion to calcitriol (active form) ○ Promotes absorption of dietary calcium from the GI tract —> increase serum Ca level ■ Increase renal tubular reabsorption of calcium —> serum Ca level decrease ○ 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 affect both ● rare kidney cancer ○ Affects children 3-4yrs ● Renal cell carcinoma: is a primary tumor arising from the renal tubule ○ Nephrolithiasis: refers to renal calculi (renal stones) hard masses of crystals composed of minerals ■ Most common type is calcium containing calculi (+ oxalate) ● Other types include struvite (mag-ammonium-phos), uric acid, cystine ■ Common cause of urinary obstruction in the renal pelvis, ureter, and bladder neck ■ Risk factors: dehydration, excess dietary increases (calcium, salt, caffeine), urinary stasis, family shorty, frequent UTI (struvite) ■ Calculi causes symptoms only when urine flow is obstruction —-> hydronephrosis ● Pain (flank, lower abdomen, groin), bloody/cloudy urine, dysuria, fever, chills, nauseas, vomiting, straining to void (bladder calculi) ● Diagnosis: CT(W/o contrast), KUB (Kidney Ureter Bladder) x- ray, US (Ultrasound) ● Medication = Alpha 1 blocker ■ Management: depends on the type ● Increase fluid intake (small calculi , 6mm (No surgery) likely will pass through the urinary system) ● Stone laser lithotripsy and extraction surgery ○ Hydronephrosis: an abnormal dilation (swelling) of the renal pelvis and calyces of one or both kidneys ■ Causes: obstruction to the urine flow (e.g. nephrolithiasis, urethral stricture, BPH, tumors) ■ Clinical manifestation: flank pain or pressure on the affected side, decreased urine output ■ Lab EGFR =Low / BUN/Cr=High ■ Management: focuses on resolving the underlying cause of preventing UTI Renal calculi = 3 cm ○ Question : The nurse monitors for which complication in the patient with large renal calculi Answer: Hydronephrosis ○ Question: Examination of a patient’s kidney stones reveal that they are primarily composed of uric acid. The nurse would expect to provide the patient with which type of diet ? Answer : Low Purine ○ Benign Prostatic Hyperplasia (BPH) ■ Common in men , nonmalignant enlargement of the prostate gland; size 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/1.73m2 ○ Kidney damage with normal or increased GFR ● 2. GFR - 60-89ml/min/1.73m2 ○ Mild decrease in GFR ● 3. GFR - 30-59ml/min/1.73m2 ○ Moderate decrease in GFR ● 4. GFR - 15-29ml/min/1.73m2 ○ Severe decrease in GFR ● 5. GFR <15ml/min/1.73m2 ○ End Stage Kidney Disease (ESRD) or chronic renal failure ■ Clinical manifestations develop gradually ● Hypertension ● Edema ● Respiratory distress ● Heart failure ● Weight gain ● Anemia ● Fatigue and weakness ● Itching, nausea, vomiting: metabolic toxins ● Electrolyte imbalance: K, Pho, Ca, Mag, Na ? ● Azotemia, uremia ● Acid-base imbalance: Cannot produce enough ammonia or buffer hydrogen ions Arterial pH ■ Management ● Treatment of the underlying cause/risk factor ● Early referral for initiation of renal replacement therapies ● Dialysis Cardiovascular System Cardiovascular System ● Heart + circulatory system (blood vessels, blood, lymphatic system) ● Functions: ○ Delivers vital oxygen and nutrients to cells (Blood) ○ Removes metabolic waste products (CO2, urea, uric acid) ■ E.g ammonia, filters through kidneys ○ Transports hormones ○ Disease protection ■ E.g WBC, lymphocytes ○ Regulates body temperature ■ Blood vessels dilate (hot) ■ Blood vessels contract (cold) Heart ● Located between the lungs and behind the sternum ● Base: top of heart ● apex: bottom of heart ● Heart walls ○ Pericardium ○ Myocardium ○ Endocardium ● 4 Chambers ○ Right atrium ○ Left atrium ○ Left ventricle ○ Right ventricle ■ Ventricles have thicker walls ● 4 valves: prevent backflow of blood ○ Tricuspid valve : guides blood from right atria to right ventricle (AV valve) ○ Pulmonic valve: guides blood from right ventricle to pulmonary artery ○ Mitral valve (bicuspid): guides blood from L atria to left ventricle (AV valve) ○ Aortic valve: guides blood from the left ventricle to aorta 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 ■ O2 depleted blood from body to SVC and IVC right atrium right ventricle pulmonary artery lungs (gas exchange)pulmonary veins left atrium ○ Systemic circulation: movement of blood from the heart through the body to provide oxygen and nutrients, then back to the body ■ O2 saturated blood from lungs leaves pulmonary circulation left atrium left ventricle aorta body SVC and IVC Blood Vessels ● A tubular structure that carries blood ● Three layers of the blood vessel wall: ○ Tunica Intima: smooth, thin, inner layer ○ Tunica media: smooth muscle, middle layer ○ Tunica adventitia: elastic connective tissue, outer layer ● Heart arteries arterioles capillaries venules veins heart ● Artery: carry blood away from the heart, thicker wall, higher pressure (oxygen saturated) ○ Exception: Pulmonary artery ● Capillary: small, thin walled vessels, site of exchange ○ O2, nutrients shift out of the capillaries and into the cells/tissue ○ CO2, waste products shift from the cells to the capillary ■ Occur through Diffusion ○ H2O exchange ● Vein: carry blood back to the heart, thinner wall, lower pressure, valves (oxygen depleted) ○ Exception: Pulmonary vein Blood Pressure ● Measurement of the force of the blood pushing against the arterial wall ○ Normal BP: 120/80 ● Pulse pressure = 40 ○ Represents the force the heart generates each time it contracts ○ Normal: 40 to 60 mmHg ○ Low (narrow): ⬇ left ventricular stroke volume ○ High (widen): HTN, atherosclerosis ● Determinants of BP ○ Cardiac output: amount of blood the heart pumps in 1 min ○ Peripheral vascular resistance increases as the diameter of blood vessel ⬇ ○ volume of circulating blood ○ viscosity: thickness of blood ○ elasticity of arterial walls ○ arteriosclerosis: thickening of the arterial walls ○ atherosclerosis: plaque in arteries ○ Afterload: the pressure that the left ventricle must exert to get the blood out of the heart during systole (⬆ PVR ⬆afterload ⬆BP, ⬇SV) ○ Preload: the volume of blood in the ventricles at the end of diastole (⬆preload ⬆SV, ⬆BP) ● 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 and ⬆O2 demand ● Decompensation: heart weakens left sided HF, ⬇CO, ⬇contractility blood backs up to pulmonary circulation ⬆ resistance for right ventricle right sided HF HF: Anatomical Classification ● Left sided HF: decreased CO and pulmonary congestion ○ Forwards effects: fatigue, weakness, ⬇ urine output, ⬆HR ○ backup effects: pulmonary congestion/edema ● Right sided HF: decreased CO and systemic congestion ○ Forward effects: fatigue, weakness (⬇ O2) ⬇HR ○ Backup effects: systemic congestion/edema (JVD, LE edema, weight gain, nocturia) Hyperlipidemia ● Elevated levels of lipids in the blood ○ Two main fats: 6 ■ Cholesterol = liver ■ Triacylglycerol ● ⬆ levels are associated with atherosclerosis, peripheral vascular disease (PVD), coronary artery disease (CAD), HTN, Stroke accumulation of fat ● lipids: cholesterol, triglycerides ● lipoprotein = cholesterol + triglyceride + protein ○ Lipoprotein transport all hydrophobic fat molecules ○ LDL: low protein to lipid ratio, ⬇ (good) ■ <100 Optimal ○ HDL: high protein to lipid ratio ⬆ (bad) ■ >60 High ○ Triglycerides ■ < 150 normal ● Often asymptomatic until develops other diseases ● Excessive calories convert to triglycerides ● Goal: normalize lipid levels and prevent complications ● Treatment: lifestyle modifications, (diet), lipid lowering drugs (statins) Atherosclerosis ● An abnormal accumulation of lipids and fibrous tissue in the lining of arterial blood vessel walls ● Developments is initiated by endothelial injury to the vessel wall inflammatory response is triggered ⬆ vessel walls permeability plaque accumulation what happens to the artery ⬇ blood flow (ischemia) ● causes of endothelial injury: hyperlipidemia, HTN, Stress, DM, tobacco ● most common cause of cardiovascular disease in the US ● Possible complications ○ Clear artery heart coronary arteries partial occlusion total occlusion MI ○ Partial Obstruction brain carotid or cerebral arteries partial occlusionstotal occlusion cerebrovascular accident (CVA) ○ Total Obstruction Aortic rupture and hemorrhage ○ Coronary Artery Disease (CAD) Legs gangrene and amputation ● Also known as ischemic heart disease ● Most common cause = atherosclerosis ● Develops when atherosclerosis develops in the arteries supply the myocardium blood flow ⬇ in the coronary arteries lactic acid accumulation sympathetic cardiac afferent neuron activation produces angina ● clinical manifestations: Agina (most common), indigestion-like sensation, N/V, diaphoresis, cool and clammy extremities, fatigue ● commonly leads to stable angina, unstable angina, and myocardial infarction (MI) ● Risk factors ○ Nonmodifiable risk: middle-aged, white, male ○ Modifiable risk: tobacco use, physical inactivity, hyperlipidemia, hypertension ○ Negative risk factors (good): high HDL cholesterol ⬇ changes of CAD Angina Pectoris ● A clinical syndrome characterized by episodes of pain or pressure in the anterior chest (= chest pain) due to ischemia ( ⬇ O2 supply to the myocardium) ● types of angina ○ Stable angina: predictable and consistent pain that occurs on exertion/activity (⬆ O2 demand) and is relieved by reduction of that demand (e.g. rest) and or nitroglycerin ○ unstable angina: pain increase in frequency and severity; unpredictable; not relieved with rest or nitroglycerin Unstable Angina ● Myocardial ischemia without detectable myocardial necrosis/infarction ● Preinfarction state change in chest pain that is unpredictable, increases in frequency or intensity. ● Most common cause is an atherosclerotic plaque ulceration prone to rupture injury to coronary blood vessel inflammatory response, platelet aggregation, blood clotting (thrombi), arterial spasm further ⬇blood supply ○ Due to thromboxane A2 ● However, artery is not completely occluded ● Signs and symptoms ○ Pain increase in frequency and severity; unpredictable; may not be relieved with rest or nitroglycerin ● SOB, indigestion, nausea, vomiting, anxiety, restlessness, cool pale, and moist skin, diaphoresis, fatigue, lightheadedness ● No elevation in cardiac biomarkers ○ Blood test (measurable indicators for cardiac disease) ● ECG changes: may or may not be changes Myocardial Infarction ● Also called a heart attack or acute coronary syndrome (ACS) ● Death of myocardium by blockage of the coronary artery blood flow ● Atherosclerotic plaque rupture injury to coronary blood vessel platelet aggregates thrombi, vasospasm complete occlusion infarction ● early recognition and treatment is key to improve outcomes/prognosis ● signs and symptoms: similar to unstable angina + obvious ECG changes, elevation of cardiac biomarkers ○ 12 lead ECG identifies the type and location ● Cardiac enzymes (biomarkers): blood test ○ used to diagnose an acute MI ○ Lab values are based on the release of cellular contents into the circulation when the myocardial cells die ○ Troponin: a protein found in myocardial cells, three subunits (C, I, T), ■ troponin I or T, C is not for cardiac ■ troponin I and T: sensitive and specific indicators of damaged heart muscle ■ detected (elevated) within a few hours during an acute MI ■ Onset: 2 to 6 hours ● Goals: to minimize myocardial damage, preserve myocardial function, and prevent complications ● Old MONA ○ Morphine: drug of choice to reduce pain and anxiety ○ Oxygen: start with NC 2-4L/min ○ Nitroglycerin ○ Aspirin: antiplatelet, thin the blood, prevent blood clots ■ Cox (cyclooxygenase) 1 + 2 ■ Cox 1: found in platelets ● Aspirin - cox 1, irreversible ● Ibuprofen - cox 1, reversible ● New MONA: THROMBINS2 ○ Thienopyridines: inhibits platelet activation ○ Heparin: anticoagulation ○ RAA system blockade: ACEI ○ Oxygen ○ Morphine ○ Beta-blockers: reduce heart rate and myocardial oxygen consumption ○ Invasive cardiac interventions ○ Nitroglycerin ○ Statin/salicylate (aspirin) Thrombi and Emboli ● Thrombus: blood clot ● Embolus: when a portion or all of the thrombus travel through the circulatory system ● Virchow’s triad: conditions that promote blood clot formation ○ Vessel wall injury (epithelial damage) ■ Hemostasis: a process which causes bleeding to stop (attracts platelets and inflammatory mediators to the site) ■ Platelet plugging + fibrin = clot ○ Circulatory stasis: allow platelets, RBCs, clotting factors to aggregate and adhere to the vessel wall ■ Standing, long time ○ Hypercoagulopathy: too many blood clots, certain cancers, or pregnancies ● Leads to blood vessel occlusion and infarction ● Can affect both arteries and veins ○ Arterial thrombus, venous thrombus (DVT) ● Clinical manifestation depends on the location and blood vessel involved ○ DVT: cal swelling, pain travel to the right side of the heart pulmonary circulation ○ Pulmonary embolism (PE, a blood clot blocking the pulmonary artery): dyspnea, tachypnea, sudden chest pain, anxiety, cough ○ Ischemic stroke: weakness, paralysis, memory loss, difficulties in comprehension, forgetfulness, confusion ○ Management ○ Thrombolytic therapy: dissolves the blood clot (e.g., tissue plasminogen activator, t-PA) ○ Anticoagulation therapy Varicose Veins ● Also called varicosities ● Dilated, tortuous, engorged veins ● Cause: increased venous pressure and blood pooling → vein enlargement → stretching of the valves → improper venous valve function → ↑ capillary pressure → edema & skin discoloration ● Risk factors: pregnancy, obesity, prolonged sitting or standing (RNs!) ● Risk of thrombus formation ⬆ Hypertension ● Persistent elevation of blood pressure in the arteries ● One of the most prevalent chronic health conditions in the US ● Leading risk factor for cardiovascular diseases ● Silent killer because many people do not have s/sx ● risk factors: age, race (African American) sodium intake , obesity ● Classification: ● Primary (essential): idiopathic, may be multifactorial, develops gradually over time ○ Most common type ● Secondary: result of a specific underlying condition with a well-known mechanism ● Malignant: intense form of hypertension that does not respond well to treatment ● Pregnancy-induced ● Sympathetic overdrive is commonly thought to contribute to the development of hypertension → ↑ HR, ↑ CO, systemic vasoconstriction ● → ↓ or ↑ PVR → further ↑ BP ● → renal blood flow ↓ or ↑ , activating the RAA system → sodium and water retention → ↑ BP ● Prolonged excessive pressure on arterial walls → damages vessels and organs ● Kidney damage, HF, aneurysms, vision loss, stroke, etc. ● Early detection and treatment is crucial to prevent and minimize complications ● Classification: JNC 8 vs. ACC/AHA ● Shock ● Definition: a clinical syndrome that results from inadequate tissue and organ perfusion due to decreased blood volume ● Cells do not get the oxygen they need (delivery < required) ● Cellular changes: ● Cells need O2 to create energy to perform necessary functions ● Energy can also be synthesized in the absence of O2 ● The cells lack inadequate blood supply (deprived in O2) and produce energy through anaerobic ● By-product of anaerobic is lactic acid and can accumulate to toxic levels ● Types: ○ Hypovolemic: decrease volume in the ? ○ Cardiogenic: inability of the heart to contract ○ Distributive (septic, anaphylactic) ● Stages: ○ Compensatory: responses that become active when tissue perfusion and BP decrease, and responses that represent an effort to maintain CO ○ Progressive: begins when the compensatory mechanisms fail to maintain CO ■ Tissue becomes hypoxic ■ acid-base imbalance occurs (metabolic acidosis) ○ Irreversible: organ damage occurs Hypovolemic Shock ● Most common type of shock ● Decreased intravascular space volume due to blood/fluid loss (e.g., DI, hemorrhage, severe dehydration/edema, ascites, etc.) ● Signs and symptoms: ● ↓ or ↑ preload, ↓ or ↑ SV → ↓ or ↑ CO, ↓ or ↑ BP, ↓ or ↑ HR, skin? ● Medical management: ● Goal is to restore intravascular volume (e.g., isotonic solution , blood transfusion) ● Treatment of underlying cause Cardiogenic Shock ● Occurs when the LV contractility is impaired and cannot maintain adequate CO ● Causes: acute MI, cardiac tamponade, dysrhythmias ● Compensatory mechanisms of HF are triggered: ● → ↓ or ↑ workload & O2 consumption/demand → decompensation→ ● ↓ contractility → ↓ tissue and organ perfusion → multisystem organ failure ● Signs and symptoms: ↓ CO, ↓ BP, ↑ HR, force of pulse?, cool skin, fatigue, cerebral hypoxia ● Medical management: ○ Goal: increase oxygenation ○ Treatment of underlying cause ○ Fluids, inotropic Gastrointestinal Function Gastrointestinal System ● Also called digestive system ● Consists of structures responsible for consumption, digestion, and elimination of food ● These processes provide absorption of the essential nutrients, water, and electrolytes required for the body’s physiologic activities ● Alimentary Canal: food passes through ● Oral cavity, pharynx, esophagus, stomach, small and large intestines, anus ● Accessory organs: aid in digestion ● Tongue, salivary glands, hepatobiliary system (liver, gallbladder, and pancreas) Layers of the GI Tract ● Mucosa: innermost layer, produces mucus ○ Mucus: Functions: ■ Protect GI lining from extreme PH ■ Movement of food ■ Lubrication ● Secreted by surface mucous cell (foveolar) of stomach and goblet cells of the intestine ○ Parietal cells in the stomach secrete Hydrochloric acid and intrinsic factors ○ Chief cells: ■ Amylase: saliva ■ Lysosome: stomach (pepsin) trypsin chymotrypsin ■ Lipase: gastric ○ Submucosa: includes blood vessels, nerves, lymphatics ○ Muscularis: circular (inner) and longitudinal (outer) smooth muscle layers → causes involuntary peristalsis ○ Serosa: the outer layer Peritoneum ● Function: lines the abdominal cavity ● Parietal layer: outer ○ Covers the abdominal wall ● Visceral layer: inner ○ Encases the abdominal organs ● Peritoneal cavity: space between the two layers, contains peritoneal fluid ● Mesentery: double-layer of the visceral layer, contain blood vessels and nerves ● Retroperitoneum: anatomical space behind the peritoneum ● An increase volume of peritoneal fluid is called Atcis Upper GI Tract ● Oral cavity: chemical and mechanical digestion begins ● Saliva: moistens food and contains enzymes that start the digestion ● Chewing (mastication): pulverizes the food into small pieces ● The tongue pushes the food to the back of the throat where it is swallowed ● Swallowing: tongue + smooth muscles of the pharynx and soft palate + esophagus + shutting the epiglottis ● What are the major CNs involved in swallowing= CN V. ○ CN V: chewing ○ CN VII: facial expression ○ CV IX: swallowing ○ CV X: vagus ○ CV XII: Hypoglossal/under the tongue ● Esophagus: moves food towards the Stomach ● Upper esophageal sphincter (UES) ● Lower esophageal sphincter (LES) relaxes to allow food mass (bolus) to enter the stomach, closes to prevent stomach contents from refluxing ● Smooth muscles create a peristaltic wave pushing food down (one-way) ● Stomach: Expandable, food and liquid reservoir ● Epithelial Cells: protects from damage of the inner lining ● HCl: sterilizes ingested food and activates pepsinogen into pepsin ● Epithelial cells that secrete HCl and intrinsic factors? ● Enzymes (pepsin, gastric lipase) digest food → chyme → leaves the stomach into the duodenum through the pyloric sphincter Liver ● Functions: ● Produce bile (600-1200ml/day): ○ Stored in the gallbladder and drains into the small intestine( duodenum) via the common bile duct ○ Green/yellowish liquid that aids the digestion of lipids in the small intestine ○ Neutralize the acidic gastric contents ● Metabolize medications ● Serve as a blood reservoir (~450ml) ● Synthesize plasma protein (albumin, lipoprotein), clotting factors, cholesterol ● Store glycogen and lipid (fatty acids) → used as energy when needed ● Convert excess carbohydrates and protein into triglyceride ● Breakdown fatty acids to ketones ● Breakdown of amino acids, ammonia → urea ● Detoxify the blood of potentially harmful chemicals (e.g., alcohol) ● Glisson's capsule: a layer of connective tissue surrounding the liver ● Blood supply ○ Hepatic artery ○ Portal vein: a blood vessel that transports blood from the stomach, intestines, gallbladder, pancreas, and spleen to the liver which contains nutrients and toxins extracted from digested contents ○ Portal vein branches into smaller vessels and travels through the liver Pancreas ● Located behind the stomach ● About 95 % of the pancreas is exocrine tissue ● Exocrine function: ○ Secretes enzymes (proteases- trypsin and chymotrypsin, lipase, amylase) for digestion ■ All 3 enzymes ○ Secretes pancreatic juice containing enzymes and bicarbonate ○ Bicarbonate neutralizes acidity of chyme moving in from the stomach into the duodenum ● Pancreatic duct ○ A duct joining the pancreas to the common bile duct to supply pancreatic juice provided from the exocrine pancreas ○ Drains into the duodenum Lower GI tract ● Small intestine and large intestine (cecum, colon, rectum, anus) ● Small intestine: longest ● Digestion of food and absorption of nutrients from food ● Protein → amino acids, carbohydrates → simple sugar, lipids → fatty acids and glycerol ● Small intestines: circular folds of mucous membrane covered with villi and microvilli ● Food mixture is moved by a series of muscle contractions, peristaltic wave ● Large intestine: ● Absorbs 90% of water and electrolytes ● Small intestine → mixture of water, undigested/unabsorbed food molecules, indigestible food residue, electrolytes enters ● Escherichia coli organisms are normally found in the lower GI tract and feed off the undigested food ● The chyme moves through the colon → feces (dense) ● Feces contain undigested food + dead bacteria + mucus ● Why are feces dark/brown? Due to the presence of bile ● Rectum serves as a reservoir to store feces → rectal wall expands → stretch receptors activated → defecation through anus ● Defecation: similar to urination ● Internal and external anal sphincters Vomiting (Emesis) ● Forceful ejection of chyme ● Common event that results from many different causes (e.g., bacteria, food poisoning) → vomiting center gets activated ● May be preceded by nausea or retching ● Voluntary vs involuntary ○ A deep breath is taken ○ The glottis closes and the soft palate rises ○ The gastroesophageal sphincter (LES) relaxes ○ The abdominal muscles contract, squeezing the stomach against the diaphragm → forces chyme upwards ○ Reverse peristaltic waves eject chyme out of the mouth ● Recurrent vomiting may lead to fluid, electrolyte, and acid-base imbalances ● Aspiration of chyme into the lungs, when: ○ Vomiting or cough reflex depressed ○ Supine or unconscious when vomiting ● Vomitus: content vomited ○ Hematemesis: blood present in vomitus ○ Coffee ground: characteristic of blood in the vomitus ○ Yellow or green color: indicates the presence of bile ○ Deep brown color: indicated content from the lower intestine possibly fecal ● Projectile vomiting: ○ Sudden ejection of vomitus with great force which propels a significant distance (e.g., pyloric stenosis – infants, overeating, increased ICP, intestinal obstruction), ○ Not preceded with nausea Hiatal Hernia ● A section of the stomach protrudes upward through an opening (hiatus) in the diaphragm ● Causes: ○ Weakening of the diaphragm muscle (e.g., coughing, straining) ○ Increased intra-abdominal pressure (e.g., pregnancy, obesity) ● Clinical manifestations: rare if small, usually in large Hiatal hernias ○ Indigestion, heartburn, chest pain, dysphagia, nausea, frequent belching ○ May worsen in recumbent (flat) positioning, bending over, after large meals Gastroesophageal Reflux Disease (GERD) ● A condition where chyme periodically backs up from the stomach into the esophagus Cause: opening of Lower esophagus sphincter ○ ↓ pressure (e.g., certain medications and foods, smoking) ○ ↑ stomach pressure (e.g., hiatal hernia, obesity, pregnancy) ● Varies in severity depending on the degree of LES weakness ● Clinical manifestations: heartburn, chest/epigastric pain, nausea, dry cough, regurgitation of food, laryngitis, pharyngitis, ulceration ● Management (p. 274); Anti-acid, avoid alcohol, medication, nicotine NSAIDs, tight clothing around the waist, eating small and frequent, reducing stress and surgery Gastritis ● Inflammation of the mucosal lining of the stomach ● Acute vs chronic ● most common cause H. Pylori ● Causes: Helicobacter pylori, long-term use of NSAIDs, stress, excessive alcohol consumption ● Clinical manifestations: heartburn, chest/epigastric pain, nausea/vomiting, anorexia, fever, ulceration, bleeding ● Chronic gastritis increases the risk for peptic ulcer and gastric cancer Peptic Ulcers ● An ulcer or open sore in the inner lining of the esophagus, stomach, and duodenum ● Duodenum ulcers are the most common ● Causes/risk factors: H. pylori infection, NSAIDs, smoking, alcohol use ● Gastric ulcer: ○ Pain worsens with eating food, shortly after a meal ● Duodenal ulcer: ○ The most common cause is H. pylori and excessive acid. ○ Pain improves with eating food, pain occurs 2-3 hrs after meal ○ Commonly wakes up patient at night with upper abdominal pain ● S/Sx: heartburn, epigastric/abdominal pain, indigestion, nausea, vomiting, hematemesis (gastric), melena; black color stool, weight loss Cholelithiasis ● Gall stones or calculi ● Risk factors: family history, diet high in fat and cholesterol, obesity, diabetes, liver diseases, sickle cell anemia (hemolysis) ● Types: cholesterol, pigmented, mixed ○ Cholesterol: most common, develops when the bile contains high concentration, yellow ○ Pigmented: develops when the bile contains high concentration of bilirubin(yellow) and biliverdin(green), dark color ○ Mixed: bile contents are mixed within the stone (cholesterol, bilirubin, calcium) ● Small stones (calculi) can be excreted with the bile ● Presence and blockage of the stones can cause inflammation known as cholecystitis ● Clinical manifestations: Inflammation or infection + Obstructed bile flow ● Biliary colic (RUQ or mid epigastric sudden cramping and pain that worsens after a fatty meal) ● Pain may radiate to the back or right shoulder (right upper quadrant area) ● Jaundice ● Pruritus- intense itching ● Dark tea-colored urine ● Clay-colored stool- lack of bilirubin ● Fever ● Nausea and vomiting- chemoreceptor trigger as a signal to the medulla oblongata Hepatitis ● Inflammation of the liver ● Causes: pathogens (usually viral), alcohol or substance use, medications, autoimmune diseases ● Viral hepatitis is contagious and accounts for 50% of all acute cases in the US ● An estimated 3.5–5.3 million people in the United States live with chronic viral hepatitis (2010) ○ 5 types: A, B, C, D, E ○ Each has its own characteristics: route of transmission(e.g., blood, body fluids, fecal-oral), s/sx ● Clinical manifestations (acute): RUQ pain, hepatomegaly, jaundice, dark tea-colored urine, clear colored stool, fever, nausea, vomiting, fatigue ● Type B and C can progress to cirrhosis and Liver cancer Cirrhosis ● Chronic, progressive, irreversible, diffuse damage → scarring and nodule formation → impaired blood flow → liver failure ● Most frequent causes: hepatitis C and chronic alcohol abuse( alcoholic liver disease) ● Hepatic artery and portal vein become constricted: ○ ↑ BP, portal hypertension ○ Back up of blood → enlargement of organs e.g., spleen, pancreas, stomach & veins (varices) ○ Ascites- fluids accumulation in the peritoneum cavity ● Altered protein metabolism: ↓ clotting factors → decrease levels of protein muscle wasting ● Altered fat metabolism: hyperlipidemia ● Altered carbohydrate metabolism: hyper or hypoglycemia ● Bile flow obstruction and accumulation s/sx: Jaundice ● Ammonia accumulation: neurological impairment (e.g., disorientation, hand tremors, hepatic encephalopathy) ● Best outcome management: Liver transplant Diarrhea ● Characteristics: increase frequency and amount and water content of the stool ● Causes: ○ Increase secretion of fluid into the intestine ○ Decrease absorption of fluid from the intestine ○ Alteration in GI peristalsis: the rapid passage of stool ● Acute vs Chronic ○ Acute: usually self-limiting, cause is usually viral, bacterial, or certain medications( antibiotics and laxatives) ○ Chronic: more serious causes (e.g., Irritable bowel disease, IBS, malabsorption, chemotherapy, radiation) ● Clinical manifestations vary depending on the underlying etiology ○ Abdominal cramping; frequent and loose stool; blood, pus, or mucus present; hyperactive bowel sounds Constipation ● Characteristics: Infrequent and hard to pass stool. ● Diagnosis depends on individual patient’s perception ● Stool remains longer in the large intestine than usual→ more water remo