NCM 118 Finals - Medical-Surgical Nursing PDF

NCM 118 MEDICAL-SURGICAL NURSING LEC / PROF. E. SALAVANTE...

NCM 118 MEDICAL-SURGICAL NURSING LEC / PROF. E. SALAVANTE FINALS TOPIC OUTLINE Nausea I. Critical Disorders and Complications of the GI Tract and Vomiting Accessory Glands a. Diarrhea Regurgitation b. GI Bleeding Dyspepsia c. Inflammatory Bowel Disease Heartburn d. Crohn’s Disease e. Ulcerative Colitis Pain II. Chronic Liver Disease Constipation a. Cirrhosis Diarrhea b. Jaundice Jaundice c. Portal Hypertension d. Ascites Stool changes e. Esophageal Varices f. Hepatic Encephalopathy Characteristics of Vomitus III. The Endocrine Complex a. Endocrine Function Presence of blood – hematemesis b. Disorders of the Adrenal Gland o Coffee ground vomitus – brown granular c. Addison’s Disease material indicates the action of HCl on d. Addisonian Crisis e. Cushing’s Syndrome hemoglobin. f. Pheochromocytoma o Hemorrhage – red blood may be in vomitus. g. Disorders of the Thyroid Gland Yellow or green-stained vomitus h. Hypothyroidism o Bile from the duodenum. i. Myxedema Coma j. Hyperthyroidism Deeper brown color k. Thyroid Storm o May indicate content from the lower intestine. IV. Complications from Parathyroid Gland Hormones Recurrent vomiting of undigested food a. Hypercalcemic Crisis b. Acute & Chronic Hypoparathyroidism o Problem with gastric emptying or infection. V. Diabetes Mellitus Ask the patient when did it start, what food did the a. Hypoglycemia patient ate prior to vomiting. b. Diabetic Ketoacidosis Look at the character – color is everything. Ano ang c. Hyperosmolar Hyperglycemic Nonketotic Syndrome VI. Chronic Complications of Diabetes amount – use a measuring cup. It is important to know a. Microangiopathy the amount. b. Macroangiopathy Ask the factors that led or caused vomiting – may c. Acute Renal Failure d. Chronic Renal Failure ginawa ba si patient, may kinain ba, may tinake ba na VII. Moodle Recorded Lectures gamot, did the patient underwent a certain procedure? a. Introduction to Complicated GIT Disorders Ask the patient what they did after vomiting – may b. Upper and Lower GIT Complications tinake ba na gamot? What did the patient do to relieve c. Accessory Organs d. Complications of Diabetes the pain from the vomiting? e. Macrovascular and Microvascular Effects of Diabetes f. Adrenal Gland Disorders Coffee Ground g. Thyroid Disorders h. Parathyroid Disorders i. Renal Failure j. Shock k. CVA l. Burns CRITICAL DISORDERS AND COMPLICATIONS OF THE GI TRACT If a patient vomits coffee grounds, you need to prevent AND ACCESSORY ORGANS aspiration. Hold any form of feeding – tube feeding, OF, GIT – mouth to anus and give the GIT some time to rest. Accessory organs – disorders of the liver, pancreas, and If may coffee ground vomit sa NGT, seek clarification sa gallbladder doctor if need magperform ng gastric lavage. Health History Bilious Vomiting Appetite Food intolerance Weight gain/loss Dysphagia 1  ▪ Presence interferes with the digestion of other nutrients. o Abdomen often distended. o Common with liver or gallbladder problems. You don’t just characterize the stool; you have to assess the patient for weight loss, skin turgor, and appetite if Bristol Stool Chart there are changes. Blood in Stool Blood may occur in normal stools with diarrhea, constipation, tumors, or an inflammatory condition. o Frank blood ▪ Red blood – usually from lesions in the rectum or anal canal. o Occult blood ▪ Small hidden amounts, detectable with a stool test. ▪ May be caused by small bleeding ulcers. We take note of the character, form, and odor of the o Melena stool – amoy dugo ba? ▪ Dark-colored, tarry stool ▪ May result from significant bleeding DIARRHEA in the upper digestive tract. Excessive frequency of stools. ▪ It may be upper or lower, but o Usually of loose or watery consistency. literature shows that it is more May be acute or chronic. common in lower. Frequently nausea and vomiting when infection or Is it bright red, streaks (occult), or dark, tarry stools? inflammation develops. What to do before performing a fecal occult blood test May be accompanied by cramping pain. (FOBT)? Prolonged diarrhea may lead to dehydration, o Meat-free diet for 48-72 hours prior to electrolyte imbalance, acidosis, and malnutrition. collection to prevent false-positive results. Don’t only note the amount of the stool, take note of o Avoid aspirin, anticoagulants, and iron the character as well. Is it watery mucoids or loose? Is it supplements to prevent false-positive results. coming from a secondary infection? May nakain ba si o Anything that can alter the color of the stool patient that triggered diarrhea? needs to be withheld. What to do with Melena? Common Types of Diarrhea o Seek immediate medical attention. Large-volume diarrhea (secretory or osmotic) o Avoid giving the patient food, water, or oral o Watery stool resulting from increased medications. secretions into the intestine from the plasma. What to do with hematochezia? o Often related to infection. o Anticipate for CBC o Limited reabsorption because of reversal of normal carriers for sodium and/or glucose. Melena o Blood, mucous, pus in diarrhea means it can be secondary to an inflammatory disorder happening within the small or large intestine. o It can also be clear enough which means electrolyte imbalance. Small-volume diarrhea o Often caused by inflammatory bowel disease. o Stool may contain blood, mucus, and pus. o May be accompanied by abdominal cramps Hematochezia and tenesmus Steatorrhea – “fatty diarrhea” o Frequent bulky, greasy, loose stools o Foul odor o Characteristic of malabsorption syndromes ▪ Celiac disease, cystic fibrosis o Fat is usually the first dietary component affected. 2  We smear the clot sa diaper to check if it is red, brown, or green, to know if what kind of blood ang na-excrete ni patient. Common Sites of Referred Abdominal Pain Kapag sumakit ang tiyan, tingnan mo ang referred pain. What is the pathogenesis of ulcer disease? How to assess abdominal pain? o Increase acid production kaya nagkakameron o COLDSPA (character, onset, location, ng lesions. The precursor of peptic ulcer duration, severity, pattern, associated factors) disease is gastritis, hindi agad nagkakameron o PQRST (provocation, quality, radiation/region, ng ulcer ang gastric lining. severity, timing) Ano ang stimulant ng hydrochloric acid? o Ipeprepare ng body mo ang stomach mo with Abdominal Pain Characteristic Possible Cause the presence of food. The stimulation is Burning Peptic ulcer, GERD hunger. Cramping Biliary colic, irritable bowel Hindi natigil ang peristalsis at hydrochloric acid. Dahil syndrome, diarrhea, constipation, flatulence walang laman ang tiyan, ‘yung rugae (stomach lining) Severe Cramping Appendicitis, Crohn’s disease, ay tuloy-tuloy nagc’churn with friction/hydrochloric diverticulitis acid. Stabbing Pancreatitis, cholecystitis Two reasons: (1) hindi ka nakain; (2) nag-intermittent Burning – sinisikmura fasting ka pero binigla mo ang sarili mo kumain, like Cramping – namumulupot; caused by structural sobra-sobra ang kinain mo. Pwede magkameron ng irritation and on severe cases, inflammatory response. ulceration, ‘yung protective coating ng stomach ay Stabbing – humihilab, tinutusok, hinihiwa numinipis hanggang maexpose na. Ulcer is a wound = ulcer comes in contact with hydrochloric acid. GI BLEEDING GERD: ‘yung cardiac sphincter ay hindi na competent A symptom of an upper or lower GI disorder. kaya nagkakameron ng reflux. So initially, nagkakameron ng erosion sa esophageal linings sa Etiology cardiac sphincter. Trauma Two things will happen, either mastimulate ng GERD Ulcerations ang reflux by eating the foods that should be avoided. Rupture of varices Chocolate and coffee. Complication = bleeding Inflammatory disorders Drug-induced Etiologies and Physical/Historical Signs of Upper GI Bleed (UGIB) Anal disorders 3  Problem of diverticulosis – nagkakameron ng small sacs or outpouching of the large intestine, specifically in the haustra. Once lower GI bleeding is present, magkakameron ng hematochezia kasi wala nang digestion na nangyayari. Always anticipate for the parameters and watch out for shock lalo na if ang blood na inilalabas ni patient ay in liters. Manifestations Characteristic of blood: Bright red – vomited from the esophagus Dark red – from the small intestine and higher portion of the colon Shades of black (coffee ground) – esophagus, stomach Melena – lower GI part mixed with stool One mechanism involved in liver failure is the development of esophageal varices. Kapag tumaas ang Signs and Symptoms of Bleeding in Various Degree intra-abdominal pressure, that is the time na pwede Massive bleeding magrupture ang varices. What caused this? Portal o Acute, bright red hematemesis or a large hypertension. amount of melena with clots in the stool. If the patient has right-sided heart failure, it can o Rapid pulse, drop in BP, hypovolemia, and contribute to venous engorgement, thus affecting the shock liver and leading to hepatomegaly. Subacute bleeding Any condition that can affect the production of o Intermittent melena or coffee ground emesis hydrochloric acid, such as infection, stress, can lead to o Hypotension, weakness, and dizziness peptic ulcer disease. Chronic bleeding Why behavioral? Eating disorders like bulimia and o Intermittent appearance of blood. anorexia nervosa can cause PUD because of excessive o Increased weakness, paleness, or SOB vomiting. o Occult Blood Once upper GI bleeding is present, you now have The more na extensive ang bleeding, the more na melena, coffee ground enema, and hematemesis. hanapin mo ang perfusion parameters if okay pa, Basta may nadugo, anticipate the perfusion signs na especially in massive bleeding. dapat hanapin, like hemoglobin, blood pressure, heart rate, O2 saturation. Management Note: management is always based on the primary disorder. Emergency Intervention Acute Lower GI Bleeds: Pathogenesis and Clinical Findings o NPO ▪ To promote gastric rest at para hindi lalo matrigger na magkameron ng irritation. o IV line and O2 therapy initiation ▪ Make sure to have an appropriate and functional IV line for boluses and blood transfusions. o Treat shock, administer blood replacement ▪ Kung ano ang nawawala, ‘yun dapat ang pinapalit. ▪ You also have to check if the platelets and plasma are low before doing blood replacement therapy to stop the bleeding kasi kahit anong salin ng dugo pero may bleeding, wala rin mangyayari. o Surgical intervention if needed ▪ Rubber band ligation o NGT intubation and possible gastric lavage ▪ Gastric decompression 4  ▪ Gastric lavage is introducing a absorb water and electrolytes, now prevents solution to clean the stomach. We the waste products from forming. introduce iced normal saline o Bleeding – coming from ulceration and solution, then we drain via gravity desquamation coming along the until clear. gastrointestinal lining of the large intestine. o Injection of sclerosant or epinephrine o Fever and malaise – infection Stricture – brought about by the ulceration or Complications desquamation of the GIT. Hemorrhage o Distention – decrease in movement of air and Shock mass inside. Death o Changes in bowel habits – konti, then strips, then loose na. Nursing Diagnoses Rectal Disease Fluid volume deficit o Urgency – tenesmus; the feeling of pressure Altered tissue perfusion or urge to defecate pero walang nalabas. Crohn’s and Ulcerative Colitis can be found in opposite Pharmacological Interventions ways in the large intestine, which is why it is important Roles of PPI in GI bleeding: to analyze them to know which is an ascending Reduces gastric acid secretion which promotes the infection and descending infection. healing of ulcers and erosions. Characteristic Crohn’s Disease Ulcerative Colitis To control hydrochloric acid Region affected Terminal ileum, Colon, rectum Prevents the effect of hydrochloric stimulation in sometimes colon bleeding of whatever structures are involved, such as Distribution of lesions Transmural, all layers Mucosa only Skip lesions Continuous, diffuse ulcers or varices. Characteristic stool Loose, semi-formed Frequent, watery, with blood and mucus Nursing Interventions Granuloma Common No Nursing assessment Fistula, fissure, abscess Common No Stricture, obstruction Common Rare Attain normal fluid volume Malabsorption, Yes Not common o NPO temporarily malnutrition o Administer IV fluids and blood products o Observe for shock Attain a balanced nutritional status o TPN nutrition if needed o After NPO status may begin with clear liquid then high caloric high protein on SFF pattern. INFLAMMATORY BOWEL DISEASE The large intestine is the focus. The large intestine absorbs water and electrolytes and propels feces towards the rectum for elimination. Colon – Crohn’s and Ulcerative Colitis Both would share the same mechanism = inflammation. Kapag nagkameron ng inflammation, magkakameron ng ulceration because the peristaltic movement will not stop. There will be friction. Toxic Disease o High fever – infection CROHN’S DISEASE o Distention – inflammation A disease involving inflammation in the GIT. o Pain – stretching of the lining of the large Commonly affected area is the ileum. intestine. Diffuse Disease Signs and Symptoms o Diarrhea – ulceration or desquamation of the lining of the large intestine, therefore Fever nawawala ng capacity ang large intestine to Abdominal pain Diarrhea 5  Bloody stools Liquid bowel movement Diagnosis Weight loss Abdominal tenderness Loss of energy Mass in the right lower abdomen Bloating Rectal exam may show blood Anal pain/bleeding Laboratory Findings Inflammatory Bowel Disease: Clinical Findings in Crohn’s Disease Anemia Vitamin B12 deficiency Elevated WBC Low albumin Elevated sedimentation rate Imaging Tests X-ray CT scan Barium enema Colonoscopy with biopsy Nuclear medicine scans MRI Treatment Diet – specific low or high-fiber diet depending on the location and current condition of the case. Habang na-eexpose ang lining ng GI, nagkakameron Antispasmodic medications – to control the effect of ng irritation leading to inflammation. inflammation. Inflammation leads to ulceration, which then leads to Surgery – colostomy or transplant bleeding. ULCERATIVE COLITIS Pathophysiology An inflammatory bowel disease that causes Crohn’s Disease inflammation and ulceration of the inner lining of the Edema and thickening of mucosa colon and rectum. The inflammation usually begins in o Leads to ulceration the rectum and sigmoid colon and spreads upward to Ulceration the entire colon characterized by remissions and o Pwede magkameron ng fibrotic changes exacerbations. overtime kaya nagkakameron ng narrowing ang large intestine. Inflammatory Bowel Disease: Clinical Findings in Ulcerative Intraluminal wall thickening with fibrotic changes Colitis Intraluminal wall narrowing Cobblestone in ascending colon o #1 triggering factor: stress o Kapag inflamed, sumisikip ang diameter. No medications. ‘Yung portion na nabubulok ay inaalis (surgical management). Ititira ang healthy portion tas Ulcerative colitis is the precursor of colon cancer. ipoprotrude para maging ostomy na. How to know that the intestinal flora is alive? Causes o ‘Yung ineexcrete mo will determine the Autoimmune factors intestinal flora. Food allergies 6  Collagen disorders Prevent skin breakdown Genetic factors Care of the patient with colostomy, ileostomy Infection – Clostridium difficile CHRONIC LIVER DISEASE Pathophysiology What Causes Chronic Liver Disease? Diffuse inflammation, multiple ulceration, and Alcohol desquamation of the superficial mucosal layer o Kapag hindi nailabas ang alcohol, The walls become edematous nagkakameron ng fatty liver, which then leads o Once edema is present, ulceration is worse. to fibrosis then necrosis. Abscess formation Hepatitis B Virus Narrowing of the lumen follows Hepatitis C Virus Manifestations CIRRHOSIS Severe diarrhea – 15-20x bowel movement Scar formation and liver structure change causing Vague abdominal to cramp-like pain/tenderness hardening and shrinkage of the hepatocytes. Weight loss, anorexia o Pwede magregenerate ang liver kapag Low-grade fever imbalanced na ang hepatocytes, mahihirapan Mucus bloody stool na magregenerate ang liver, which leads to Dehydration liver failure. Anemia Diffuse damage to hepatic cells with fibrosis. Propensity for malignancy May regenerate. Fibrosis of liver tissues surrounding the hepatic vessels Management causing portal obstruction. Prevent acute attack (stress and infection) Diagnostic Tests – hepatic scan, liver enzymes, UTZ No fiber during an acute attack o It can further increase inflammation and Types ulceration. Laennec’s Cirrhosis Increased CHON and calories, low roughage, and o Most common vitamin supplements o Alcoholic cirrhosis o Slow healing of wounds in the large intestine o Scar tissue surrounds the portal areas because of bacteria. o Chronic disease Avoid gas-forming foods (milk) Post-necrotic Cirrhosis All foods must be cooked o A sequelae of viral hepatitis TPN Biliary Cirrhosis Replace fluids 3-4L/day and add KCl o Due to chronic biliary obstruction and NPO in severe form infection. Pharmacological Interventions Stages of Liver Damage Sulfonamides (antibiotics) Immunosuppressive (steroids) Tranquilizer (to decrease peristalsis) Anticholinergics Surgery (hemicolectomy) o Ipasok ang colostomy care Nursing Management Maintain normal elimination patterns Relieve pain Pathophysiology o Anticholinergics 30 minutes before meals Liver insult, alcohol ingestion, viral hepatitis, exposure o Analgesics to toxins Maintain fluid intake o Na-expose pa lang kaya wala pang nakikita. o I&O Hepatocyte damage Maintain optimal nutrition Liver inflammation o TPN if indicated o Increased WBC o Low residue diet on SFF pattern o Fatigue, N/V, pain, fever, anorexia ▪ Dairy products Alterations in blood and lymph flow ▪ Eggs Liver necrosis Promote rest – intermittent rest periods Decreased ADH and aldosterone detoxification Reduce anxiety o Edema 7  Decreased androgen and estrogen Drug o Palmar erythema, testicular atrophy, spider Cholestyramine – it binds bile salts in the intestine and angiomas, gynecomastia, loss of body hair, is eliminated via feces. menstrual changes Look for the cause and manage it. Decreased metabolism of CHO, CHON, and fats o Ascites, edema, hypoglycemia and PORTAL HYPERTENSION malnutrition, steatorrhea Caused by portal vein obstruction. Decreased vitamin K absorption Increased collateral circulation. o Bleeding tendency Decreased bilirubin metabolism Clinical Manifestations o Hyperbilirubinemia = jaundice Esophageal varices, umbilical varices (caput medusae), o Decreased bile in GIT = clay-colored stool hemorrhoids o Increased urobilinogen = dark orange Fluid extravasation Liver necrosis Ascites and edema Liver fibrosis and scarring Spider angioma (dilated vessels w/d red center) Portal hypertension Palmar erythema (increased estrogen) o Edema, esophageal varices, hemorrhoids, Esophageal varices caput medusae, ascites o Splenomegaly = anemia, thrombocytopenia, ASCITES leukopenia Accumulation of free fluids in the peritoneum. ▪ Bleeding, delayed wound healing, o Bagsak ang albumin. infection Assessment: PE reveals fluid wave, shifting dullness. Liver failure Inability to metabolize ammonia to urea Pathogenesis and Clinical Findings o Increased serum ammonia, fetor hepaticus Hepatic encephalopathy o Asterixis, respiratory acidosis, sleep alteration, decreased LOC Hepatic coma o Death JAUNDICE Increased Bilirubin Direct > 0.1-0.3 mg/dL; Indirect > 0.2-0.7 mg/dL A symptom of a disease Yellow pigmentation of the skin Due to the accumulation of bilirubin pigment Usually observed first in the sclera (icteresia) Kernicterus (brain) fatal Yellowing is associated with the accumulation of bilirubin in the skin, most often caused by liver and gallbladder disorders. Complications Jaundice is a symptom where the skin and eyes become yellow. Clinical Manifestations Deep orange, foamy urine Dark tea-colored urine Clay-colored stool Severe itchiness-bile salts Steatorrhea Jaundice Management Control pruritus Calamine Baking soda NaHCO3 Antihistamine Soothing baths Medical Management 8 Supportive: Promote comfort Modify diet Monitor for further bleeding and signs of shock Bed rest Health teaching Albumin o Minimizing esophageal irritation )avoid ASA, Diuretic therapy and alcohol) Surgery o Avoid increased abdominal, and thoracic o Paracentesis – assessed for cell count, specific pressure. gravity, protein, and microorganisms. o Report signs of hemorrhage. Indicated for respiratory and abdominal distress. o Empty bladder before the procedure. Nursing Consideration ▪ Kasi baka mapuncture Monitor patient with Sengstaken Blakemore tube. o Monitor BP. o Facilitate placement of the tube. o Remove 1-1.5 L of fluid. o Prevent dislodgement by positioning (semi- fowlers) Nursing Considerations o Keep scissors at the bedside at all times. Monitor nutrition o Monitor respiratory status: if distress occurs, Modify diet cut the tube to deflate it and remove the tube. Restrict sodium (200-500 mg/day) o Care of nares to avoid cracking. Restrict fluids (1000-1500 mL/day) o Label each lumen, maintain the prescribed High-calorie diet amount of pressure of the esophageal Prevent increasing edema balloon, and deflate as ordered to avoid Administer diuretics as ordered necrosis. Monitor I&O Measure abdominal girth HEPATIC ENCEPHALOPATHY Administer salt-poor albumin to replace vascular The liver is unable to convert ammonia to urea causing volume (dextran10, Haemaccel) neurologic symptoms. Aggravated by GI bleeding. ESOPHAGEAL VARICES Dilatation of the veins of the esophagus. Assessment o Bantayan ang rupture gawa ng intra- Change of mental function abdominal rupture. o Irritability o Ang ginagawa ay rubber band ligation to o Insomnia prevent bleeding if nagrupture. o Slight tremor Resulting in distention, hypertrophy, and increased o Slurred speech fragility. o Babinski reflex o Hyperactive reflexes Assessment Progressive disease Anorexia o Asterixis N&V o Disorientation Hematemesis o Apraxia Fatigue, weakness o Tremors Splenomegaly o Fetor hepaticus Ascites Late manifestations of the disease Caput medusae o Coma Peripheral edema o Absent reflexes Medical Management Stages of Hepatic Encephalopathy and Possible Nursing Iced normal saline lavage Diagnoses Transfusion with FWB Stages Clinical Symptoms Clinical Signs and EEG Changes 1 Normal level of consciousness Asterixis; impaired writing and Vitamin K with periods of lethargy and ability to draw line figures. Sengstaken Blakemore tube (3 lumen) euphoria; reversal of day-night Normal ECG. o Emergency equipment: scissors to cut the sleep patterns tube at para madeflate. 2 Increased drowsiness; Asterixis; fetor hepaticus. disorientation; inappropriate Abnormal EEG with generalized Injection sclerotherapy behavior; mood swings; slowing. Surgery agitation o Ligation of esophageal varices 3 Stuporous; difficult to rouse; Asterixis; increased deep tendon o Surgery for portal HPN sleeps most of time; marked reflexes; rigidity of extremities. confusion; incoherent speech EEG markedly abnormal. 4 Hepatic comatose; may not Absence of asterixis; absence of Management respond to painful stimuli deep tendon reflexes; flaccidity 9  of extremities. EEG markedly Skin (MSH) abnormal. Bones (GH) Ovaries (GnRH) Diagnostic Test Testes (GnRH) Serum ammonia level Kidney tubules (ADH) Uterus (Oxytocin) Nursing Consideration Conduct neurologic assessment, report disorientation Classification of Hormones Restrict protein in the diet. High CHO, vitamin K. Hormones Site Administer enemas, cathartics, intestinal antibiotics, Steroid Hormones (hydrocortisone) Intracellular and lactulose. Peptide Hormones (Insulin) Cell surface Amine Hormones (Epinephrine) Cell surface Protect the patient from injury. Hormones will only act on specific receptor sites. Avoid hepatotoxic drugs The treatment for hormones is replacement. Whatever o Acetaminophen is missing, we will provide. Whatever is excess, we look o Phenothiazines into the gland and proceed with surgical management Bed rest para manormalize ang pagrelease. Drugs Health History and Assessment Neomycin – decreased bacterial flora responsible for Change in energy level NH4 production. o Is the patient lethargic? Conscious or Lactulose – promotes excretion of NH4 and causes unconscious? Weak or hyper? Anxious or osmosis decreasing stool transit time. agitated? Change in vital signs Surgical Intervention Change in body size and composition Transplant o Some would look obese, but they don’t eat o If liver transplant, pwedeng lobe or portion much. Some would look thin but eat a lot. lang kasi pwede magregenerate. Change in sexual function and secondary sex characteristics THE ENDOCRINE COMPLEX Change in mood, behavior, sleep pattern, appetite, ENDOCRINE FUNCTION memory and concentration Hypothalamus → Pituitary Gland or Hypophysis Anterior or Changes in physical appearance Adenohypophysis Posterior or Neurohypophysis → Blood → You have to quantify. Always look at the labs. For Target Glands → Specific tissue receptors example, masakit ang ulo ni patient at ihi nang ihi, The hypothalamus is stimulated to act based on the check the Hba1C or glucose ni patient, baka mamaya disturbance from the body/homeostasis. mataas ang values at yun ang nagcause ng manifestations ni px. Negative Feedback Mechanism Pathophysiology Dysfunction may result from defects o Glands ▪ It may be a defect in the gland itself. Okay ang hypothalamus and pituitary gland pero inflamed ang pancreas because of autodigestion. The hypothalamus will not stop. It may respond but not normally. o Release of hormones ▪ Obstruction or inflammation within the gland o Hormone transport The hormones are released because of stimulating ▪ Through circulation factors. These are released from the pituitary gland. The o Target tissue hypothalamus will keep on releasing the hormones ▪ Abscess formation, trauma responsible for waking up the pituitary gland. Endocrine disorders may be caused by: o Hypersecretion or hyposecretion Target Glands o Hyporesponsiveness of hormone receptor Thyroids (TSH) o Inflammation of glands Adrenal (ACTH) o Gland tumors Mammary (Prolactin) 10 Remember! Function in acute stress; increase heart rate & BP; dilate Disorders of the endocrine complex are similar to a UP bronchiole; convert glycogen to glucose when needed and DOWN phenomenon. by muscles for energy. DISORDERS OF THE ADRENAL GLAND ADDISON’S DISEASE Adrenal Cortex Hyposecretion of the adrenal cortex hormones. Addison’s disease o Lahat under ng adrenal cortex and medulla ay Cushing’s syndrome pababa. For example, instead na sodium Aldosteronism (Conn’s Syndrome) retention, sodium excretion na. o Some causes may include the patient is post- Adrenal Medulla adrenalectomy or an underlying cause that Pheochromocytoma can trigger the hyposecretion of hormones. Sepsis or infection. Cause Idiopathic atrophy TB Removal of both adrenal glands Neoplasms HIV Histoplasmosis Clinical Manifestations Muscle weakness, fatigue, lethargy, dizziness, fainting, Adrenal Cortex nausea, anorexia, abdominal pain/cramps Glucocorticoids (Cortisol, Cortisone, Corticosterone) V/S: decreased BP, orthostatic hypotension Increases blood glucose levels by increasing the rate of Pulse: increased, collapsing, irregular glyconeogenesis; increases CHON catabolism; Subnormal temperature increases the mobilization of fatty acids; promotes Vomiting, diarrhea, weight loss sodium & water retention; anti-inflammatory effect; Tremors aids the body in coping with stress. Skin: poor turgor, excessive pigmentation (bronze o This makes sure that the glyconeogenesis is tone) intact or the glucose is at the normal level. Hyponatremia, hypoglycemia, hyperkalemia o It helps the body produce enough glucose. Mineralocorticoids (Aldosterone, Deoxycortisone) Regulate F/E balance; stimulate reabsorption of sodium, chloride & water; stimulate potassium excretion. Adrenal Sex Hormones (Androgens) The adrenaline rush helps you, especially in times of crisis, stress, and acute biologic crises. If a patient is undergoing a respiratory failure, shock, or panic attack, the adrenal gland supplies byproducts of metabolism that are released during those episodes. The fight or flight response. The body is being prepared for glyconeogenesis while the body is on high alert. The vital signs will be elevated to boost perfusion para The patient may be thin because of fluid loss. makapagconcentrate ka. Once the body is in a state of shock, the organs will Medical Management conserve the fluids. The adrenal medulla will take place Prevent circulatory collapse by stimulating the epinephrine and norepinephrine Administer fluids para tumaas ang BP until homeostasis is achieved. o To prevent shock Administer hydrocortisone Adrenal Medulla Monitor vital signs closely Epinephrine and Norepinephrine Antibiotics if (+) for infection 11  Administer lifelong corticosteroids and Secondary: hyperfunctioning of the APG mineralocorticoids Tertiary: hypothalamic dysfunction o Lalo na if tanggal na ang glands niya. Clinical Manifestations Nursing Management Hypertension, weight gain, pitting edema Decrease stress Headache, backache, weakness, decreased work o Provide a quiet environment and a capacity nondemanding schedule. Characteristic fat deposits, truncal & cervical obesity Promote adequate nutrition (buffalo hump) o Diet: acute phase – high-sodium, low- Pendulous abdomen, purple striae, easy bruising potassium; non-acute phase – increase CHO Moon face, acne, hyperpigmentation, impotence and CHON Virilization in women: hirsutism, breast atrophy, o Fluids: force to balance fluid, monitor I&O amenorrhea ▪ Take note of fluid intake but with Pathologic fractures reduce height caution kasi baka masobrahan at Slow wound healing maglead sa edema. Hypernatremia, hyperglycemia, hypokalemia o Administer lifelong exogenous replacement Pataas lahat. Kabaliktaran ng Addison’s disease therapy as ordered ▪ Glucocorticoids – prednisone, hydrocortisone ▪ Mineralocorticoids – fludrocortisone (Florinef) Health teaching o Take medications with food and fluids ▪ Lalo na if lifelong na. o Avoid stress Monitor for S/Sx of Addisonian crisis ADDISONIAN CRISIS Life-threatening disorder caused by acute adrenal insufficiency precipitated by stress, infection, trauma, or surgery. Manifestations Surgical Management: Adrenalectomy Hyponatremia Surgical removal of one or more of the adrenal glands Hypoglycemia because of tumors or overactivity. Hyperkalemia For unilateral adrenalectomy, up to 2 years of Severe generalized muscle weakness glucocorticoid therapy is needed; for bilateral… lifelong Severe hypotension replacement. Hypovolemia Pre-op: reduce risk of post-op complications Shock (vascular collapse) #1 o Prescribed steroid therapy, given 1 week o Give glucocorticoids IV, e.g., hydrocortisone before surgery. Na succinate (Solu-Cortef), o Antihypertensive drugs were discontinued. mineralocorticoids, e.g., fludrocortisone o Sedation as ordered. (Florinef). During surgery: monitor for hypotension and o Check BP and electrolyte levels. hemorrhage. o Strict bed rest in a quiet environment and Post-op: promote hormonal balance protection from infection. o Administer hydrocortisone ▪ 1-hour bundle o Monitor for signs of Addisonian crisis Observe for hemorrhage and shock. CUSHING’S SYNDROME Prevent infection. Hypersecretion of corticoids. Administer cortisone or hydrocortisone as prescribed. o Nagkakameron ng unequal fat deposits na evident sa upper portion of the body. Nursing Management ▪ Buffalo hump and pendulous abdomen Promote comfort – protect from trauma. Prevent complications – monitor fluid balance, glucose Cause metabolism, hypertension, and infection. o Monitor blood pressure Primary: disease from the adrenal cortex Health teachings: 12  o Diet – increased protein, potassium, Hypothyroidism (Myxedema) decreased calories, sodium. Hyperthyroidism (Grave’s Disease) o Medications – cytotoxic agents – aminoglutethimide (Cytaden), trilostane Hormones (Modrastane), mitotane (Lysodren) – to Thyroxine & Triiodothyronine decrease cortisol production. o Control cellular metabolic activity o Replacement hormones as needed. o T3 more rapid than T4 o S/Sx of progression of disease. o Cell replication o Prepare client for adrenalectomy. o Major Organ System growth and development PHEOCHROMOCYTOMA Thyrocalcitonin Catecholamine-producing tumor usually found in the o Reduces high calcium levels through bone adrenal gland. deposition Originates from the chromaffin cells in the adrenal medulla. HYPOTHYROIDISM Causes hypersecretion of epinephrine and Primary hypothyroidism – thyroid norepinephrine by the adrenal medulla. Secondary hypothyroidism – pituitary D/O Complications include hypertensive crisis, CVA, & CHF. Tertiary hypothyroidism – hypothalamic D/O Central hypothyroidism – pituitary + hypothalamus (all) Diagnostic Tests Vanillymandelic acid test Metanephrine test Clonidine suppression test CT Scan, MRI, and I-metaiodobenzylguanide scintigraphy (MIBG) Assessment and Clinical Manifestations Hypertension, severe headache, palpitations, pain in the chest or abdomen Hyperglycemia and glycosuria Profuse sweating, nausea, and vomiting Dilated pupils, tachycardia, cold extremities 5 H: hypertension, headache, hyperhidrosis, Everything is SLOW and DRY. Mabagal ang hypermetabolism, hyperglycemia metabolism, mabagal din siya kumilos. Mabagal ang conversion ng glucose. Medical Management Common manifestations: intolerance to cold, dry skin, Hormonal replacement fatigue, and constipation ICU admission ECG monitoring MYXEDEMA COMA Alpha-adrenergic blocking agents (phentolamine), A rare but serious disorder resulting from persistently smooth muscle relaxants (sodium nitroprusside) low thyroid hormone precipitated by acute illness, Long-acting alpha-adrenergic blocking agents rapid withdrawal of thyroid medications, and use of (phenoxybenzamine) sedatives and narcotics. Beta-blockers The most extreme, severe stage of hypothyroidism. Definitive treatment: Surgical management o Adrenalectomy Predisposing & Precipitating Factors It can be an emergency depending on the blood Elevated cholesterol level pressure (hypertensive crisis) since it can lead to stroke Atherosclerosis or kidney failure. Coronary Artery Disease Poor Left Ventricular function Nursing Management Monitor for hypertensive crisis and avoid stimuli that Assessment & Clinical Manifestations trigger it such as increased abdominal pressure, Respiratory drive depression, Alveolar hypoventilation, vigorous abdominal palpation, and micturition. progressive CO2 retention Monitor blood glucose and urine for glucose and o Hirap huminga si patient hanggang sa acetone. magkameron ng respiratory depression na Instruct the patient to avoid stimulants. siya. Increasing lethargy DISORDERS OF THE THYROID GLAND Sleep apnea 13  Hypotension, bradycardia Knowledge and acceptance of the prescribed Hypothermia therapeutic regimen o Watch out for extreme hypothermia Improved respiratory status and maintenance of Hyponatremia, hypoglycemia normal breathing pattern Narcosis, coma = death Improved thought processes Absence of complications Medical Management Increased participation in activities and increased Objective: independence Restore normal metabolic state by replacing the missing hormone HYPERTHYROIDISM Prevention of Cardiac Dysfunction Prevention of Medication Interactions Supportive Management and Therapy o Maintain vital function ▪ If the patient is hypothermic, the immune response will become more fragile. Pwede rin maglead sa shock si patient. o ABG, pulse oximetry o Administer IVF with caution ▪ Baka magcause ng edema if nasobrahan o Treat hypoglycemia with a bolus of D5050 Everything is FAST and WET. Thyroid Hormones Common manifestations: intolerance to heat, increased Levothyroxine (Synthroid, Levothroid, Levoxyl); Thyroglobulin bowel movement, weight loss, tachycardia, increased (Proloid) appetite o Hindi biro ang magbigay ng medications sa patient, we have to educate them on when THYROID STORM and how to take them. Thyrotoxic crisis o How to know if levothyroxine is not effective Acute & life-threatening condition in uncontrolled anymore? Check their T3 and T4 levels. hyperthyroidism Controls the metabolic rate of tissues & accelerates Abrupt onset heat production & oxygen consumption Uncontrolled hyperthyroidism For hypothyroidism, myxedema & cretinism A/R: cramps, diarrhea, nervousness, tremors, Precipitating Factors hypertension, tachycardia, insomnia, seating & heat Stress (infection, injury, thyroid, and non-thyroid intolerance surgery, insulin reaction, acidosis, pregnancy, digitalis Taken same time every day preferably in the morning intoxication, emotional stress) o Thyroid hormone will be synthesized to Abrupt withdrawal of antithyroid medications produce energy or act on metabolism. Kaya it Vigorous palpation is given in the morning to prevent insomnia. Teach the client how to take HR Assessment & Clinical Manifestations Avoid foods that will inhibit thyroid secretions such as: High-grade fever (above 39 C) o Strawberries Extreme tachycardia (above 130 bpm) o Peaches Exaggerated symptoms of hyperthyroidism o Pears (hypotension, marked respiratory distress, pulmonary o Cabbage edema) o Turnips o Watch out for shock o Spinach Altered neurologic state (irritability, apprehension, o Brussel sprouts agitation, restlessness, confusion, seizures) o Cauliflower o Watch out for GCS o Peas o Radishes Management Wear Medic-Alert bracelet Immediate objectives are reduction of body temperature and Nursing Management heart rate and prevention of vascular collapse. Measures to accomplish these objectives include: Maintenance of normal body temperature A hypothermia mattress or blanket, ice packs, a cool Return of normal bowel function environment, hydrocortisone, and acetaminophen 14  (Tylenol), salicylates (aspirin) are not used because they o Monitor for respiratory distress and have a displace thyroid hormones from binding proteins and tracheostomy set, O2, and suction machine at worsen the hypermetabolism. the bedside. Humidified oxygen is administered to improve tissue o Maintain semi-fowler’s position to reduce oxygenation and meet the high metabolic demands. edema. Arterial blood gas levels or pulse oximetry may be used o Immobilize the head with pillows/sandbags; to monitor respiratory status. prevent flexion and hyperextension of the Intravenous fluids containing dextrose are neck. administered to replace liver glycogen stores that have o Check the surgical site for edema and been decreased in the hyperthyroid patient. bleeding PTU or methimazole is administered to impede the o Limit the client from talking and assess for formation of thyroid hormone and block the hoarseness. conversion of T3 and T4, the more active form of o Assess for laryngeal nerve damage – high- thyroid hormone. pitched voice, stridor, dysphagia, dysphonia, Hydrocortisone is prescribed to treat shock or adrenal and restlessness. insufficiency. o Monitor for signs of hypocalcemia and tetany, Iodine is administered to decrease the output of T4 and have calcium. from the thyroid gland. For cardiac problems such as How to assess bleeding in thyroidectomy? Look at the atrial fibrillation, dysrhythmias, and heart failure, nape and assess for bleeding. sympatholytic agents may be administered. How to assess for laryngeal nerve damage? Assess the Propranolol, combined with digitalis, has been effective voice quality of the patient. check if it is hoarse or in reducing severe cardiac symptoms. absent after 24 hours. Why do we need to have a standby tracheostomy set? Medications For emergency airway access. Propylthiouracil (PTU) Why tracheostomy and not endotracheal tube? o Blocks thyroid synthesis Because we need immediate access (below the o We want to block obstruction), and we can’t induce more trauma to the Methimazole (Tapazole) site. o To inhibit the synthesis of thyroid hormone Why are we monitoring for tetany? Since the o We want to stop parathyroid glands (regulate calcium levels) are located Iodine preparations (SSKI, Lugol’s Solution) close to the thyroid, pwede ito matamaan. o Decrease size & vascularity of the thyroid gland Nursing Management o Palatable if diluted with water, milk, or juice Maintain normal body temperature o Give through a straw to prevent staining of Monitor and manage complications teeth Improve nutritional status o Takes 2-4 weeks before results are evident ▪ In the first 2 weeks, magsstart pa COMPLICATIONS FROM PARATHYROID GLAND HORMONES lang ang effect. 3rd to 4th week, dito Parathormone pa lang masusustain ang effect. Regulates calcium and phosphorus metabolism Beta-blockers: propranolol (Inderal), atenolol o Calcium has an inverse proportion with (Tenormin), metoprolol (Lopressor) phosphorus. o Given to counteract the increased metabolic Vitamin D increases 2parathormone function effect of thyroid hormones o Relieve symptoms of tachycardia, tremors, HHYPERCALCEMIC CRISIS and anxiety Extreme elevation of calcium levels results in life- threatening cardiovascular, neurological, and renal Thyroidectomy disorders. Removal of the thyroid gland and performed for persistent hyperthyroidism Assessment and Clinical Manifestations Pre-operative care Increased bone decalcification o Assess V/S, weight, electrolyte & glucose o Fragile bones. Risk for fall levels Renal damage, formation of renal calculi o Teach DBE and coughing exercises as well as Fatigue, muscle weakness, nausea and vomiting, how to support the neck in the post-op period constipation, hypertension when coughing & moving. Incidence of gastrointestinal symptoms (peptic ulcer, o Administer antithyroid medications to pancreatitis) prevent thyroid storm. Incidence of psychological manifestations Post-operative care 15 Medical Management Mechanical ventilation Rehydration o Baka magrespiratory distress o Calcium is easily excreted through urination Tracheostomy set kaya important ang hydration but with caution kasi baka magpulmonary edema si Nursing Management patient. Diet: High calcium and low phosphorus Emergency dialysis Non-stimulating and non-stressful environment Watch out for signs of hypocalcemia and anticipate Pharmacological Management signs Phosphate therapy Watch out for respiratory distress Bisphosphonates What are the preparations for seizure precautions? Diuretics Non-stimulating environment (dimmer lights), low bed Corticosteroids position, padded side rails (cover with blankets), loose, Calcitonin, mithramycin nonrestrictive clothing, standby oxygen, a suction catheter (to prevent aspiration), position in the Nursing Management recovery position (para open ang airway). Diet: low-calcium diet Increase the oral fluid intake of more than 2000 DIABETES MELLITUS Advise intake of cranberry or prune juice Somogyi and Dawn Phenomenon Watch out for signs of Tetany Somogyi phenomenon Encourage mobility once stable o Hypoglycemia is usually at night followed by o Kapag immobile si patient, ‘yung calcium ay compensatory rebound hyperglycemia (lasts lumalabas sa buto. 12 to 72 hours). Usually caused by too much insulin or an increase in insulin sensitivity. Can ACUTE & CHRONIC HYPOPARATHYROIDISM be stabilized by a gradual lowering of insulin Extremely low levels of serum calcium. dose and an increase in the diet at the time of Related to surgical removal of the parathyroid gland the hypoglycemic reaction. through parathyroidectomy, thyroidectomy, or radical Dawn phenomenon neck dissection. o Blood sugar is normal until 3 a.m. and begins to rise in the early morning. Glucose is Assessment & Clinical Manifestations released from the liver early in the morning Neuromuscular irritability and must be controlled. Altering the time and Latent Tetany dose of insulin (NPH or ultralente) by two or o Numbness two units stabilizes the patient. o Tingling o Cramps o Stiffness of the hands and feet Overt Tetany o Bronchospasm o Laryngeal spasm Somogyi – ‘yung sugar at night ay bumabagsak until o Carpopedal spasm 3am, then magshoshoot up hanggang umaga. o Dysphagia o Ang problem dito ay ‘yung dose ng insulin ay o Photophobia seizure mataas at hindi kaya masuportahan ng diet. o Cardiac dysthymia Dawn – hindi maghyhypogly pero once nag-3 am na, Trousseaus sign, Chvostek’s sign biglang magshoshoot up until the morning. o Trousseau's sign involves muscle spasms in o Ang problem dito ay kulang ang insulin, either the hand and forearm triggered by inflating a noncompliant sa insulin or kulang na ang blood pressure cuff for 3 minutes. dose ng insulin. o Chvostek’s sign is the twitching of facial SOMOgyi – SO MOch insulin muscles in response to tapping over the facial Dawn – Down insulin nerve. Complications Medical Management Somogyi effect Administration of calcium gluconate o Hypoglycemia at night followed by rebound o Naka-piggy bag hyperglycemia in the morning. Parenteral parathormone o Hypoglycemia triggers the release of counter- Bronchodilators regulatory hormones: Aluminum carbonate and aluminum hydroxide gel ▪ Epinephrine, glucagon, GH, and Vitamin D (ergocalciferol, cholecalciferol) cortisol promote hepatic glucose 16  production and induce transient 4-6 ounces of fruit juice or regular soda insulin resistance. o Child: ½ cup or 120 mL of orange juice or o Treatment consists of decreasing insulin sugar-sweetened juice requirements or changing the time of 6-10 life savers or hard candy administration. o Child: 3-4 hard candies or 1 candy bar Dawn phenomenon o Why hard candy? Long-lasting effect para o Early morning rise in blood glucose with no masustain ang sugar. hypoglycemia during the night. 2-3 teaspoons of sugar or honey o This appears to be the effect of growth o Child: 1 small box of raisins hormones; Kung gaano karami ang binigay sa adult, half ang ▪ Increased liver glucose production. ibibigay sa bata. ▪ Decreased peripheral tissue use. If hindi makalunok nang maayos, bigyan ng D5050 ▪ Increased clearance of insulin from bolus. plasma may be a factor. Hypoglycemia DIABETIC KETOACIDOSIS Diabetic Ketoacidosis Acute complication of diabetes mellitus characterized Hyperosmolar Hyperglycemic Nonketotic Syndrome by hyperglycemia, ketonuria, acidosis, and If the patient is on NPO, what do you anticipate? Hook dehydration. to D10 IV (IV fluid with sugar). DKA – presence of ketone; HHNKS – no presence of If the patient has diabetes and is on tube feeding, what ketones do you anticipate? Check the components of the feeding to see if it is in line with the condition of the Pathophysiology & Etiology patient. also ensure the continuity of the feeding. If Insulin deficiency prevents glucose from being used for tube feeding, check the regulation if need islow down energy, forcing the body to metabolize fat for fuel. or irecalibrate. Free fatty acids released from the metabolism of fat are converted to ketone bodies in the liver. HYPOGLYCEMIA Ketone bodies result in metabolic acidosis. Occurs due to an imbalance in food, activity, and insulin/oral antidiabetic agent. Signs & Symptoms It is quantifiable. Early o Polydipsia, polyuria Signs and Symptoms o Fatigue, malaise, drowsiness Adrenergic Signs (Early) o Anorexia, N/V o Sweating o Abdominal pain, muscle cramps o Tremor Late o Pallor o Kussmaul respiration (deep respirations) o Tachycardia o Fruity, sweet breath o Palpitations o Hypotension, weak pulse o Nervousness from the release of adrenalin o Stupor, coma when blood glucose falls rapidly Neurologic (Late) Diagnostic Evaluation o Light-headedness Serum glucose level is elevated over 300