Health differences 2 Metabloic Mechanisms

1. What is cholelithiasis?
2. What is a cholecystotomy

1. gallstones are usually made up of cholesterol, bile pigment, and calcium. They cause an obstruction preventing the gallbladder from contracting when fatty foods enter the duodenum. Inability to constrict cause pain.
2. A surgical incision into the gallbladder to remove gallstones.

1. what is cholecystitis?
2. What are the signs/sx?

1. acute or chronic inflammation of the gallbladder, most commonly associated with cholelithiasis.
2. episodic colicky pain in epigastric area, which radiates to back and shoulders, jaundice(causes pruritus), clay colored stools, dark amber urine, steatorrhea, flatulence. Indegestion or chest pain after eating fatty or fried foods, most often in fat, forty, females (3 f's), Causes: cholelithiasis, estrogen therapy, infection of the gallbladder and obesity.

Metablic disorders are responses to what?

obstruction, toxic substances, and inadequate production or utilization of secretions

What are the complications of pancreatitis?
1. hemorrhagic shock
2. hypokalemia
3. pancreatic abscess
4. pancreatic pseudocyst
5. peritonitis
6. pleural effusion
7. tetany

1. pallor, hypotension, and tachycardia
2. muscle weakness, arrhythmias
3.high fever and abdominal mass
4. increasing abdominal pain and a palpable epigastric mass
5. rigid abdomen, ascites, and increased abdominal pain
6. decrease SPO2 and absence of breath sounds
7. numbness and tingling around the lips and fingers

1. What is acute pancreatitis?
2. What are the causes?
3. What are the signs/sx?
4. What are the dx tests?
5. WHat are the tx?
6. What diet should be followed?
7. What activity level is recommended?

1. pancreatic enzymes are activated in the pancreas rather than the duodenum, causing tissue damage and autodigestion of the pancreas.
2. alcoholism, gallstones,hyperparathyroidism, blunt trauma to abdomen, drug induced(steroids, thiazide, diuretics, and oral contraceptives
3. abrupt onset of pain in right epigastric area that radiates to the shoulder substernal area, back and flank, N&V, ab tenderness & distention, tachycardia, jaundice, , (with puritus), steatorrhea
4. increased amylase, lipase & glucose, AST and lipid levels and a decrease in calcium and potassium levels
5. pain control, analgesic of choice is demerol (morphine is contraindicated, anticholinergic s to decrease gastric motility
6. bland, low fat, low-protein, restricted caffeine, alcohol & gas forming foods (may require TPN), May be npo with NG decompression to control N&V
7. bedrest, quiet restful environment, to lower metqbolic demands, iv fluids to replace electrolytes, bile salts and pancreatic enzymes, Pancrelipase with or bef

What is a positive cullen's sign?

bluish discoloration of the periumbilical skin caused intraperitoneal hemorrhage. May be caused by pancreatitis or ectopic pregnancy. Abdomen is hard like a board, sometimes accompanied by grey turners sign

what is chronic pancreatitis?

chronic inflammation results in fibrosis and calcification of the pancreas, obstruction of the ducts and destruction of the secreting acinar cells.

1. What is cirrhosis?
2. WHat diet should be followed?
3. What are the lab studies?
4. Which special precautions need to be taken?
5. WHat is the medical tx?

1. chronic hepatic disease characterized by diffuse destruction of hepatic cells which are replaced by fibrous cells impairing blood and lymph flow. Cirrhosis is irreversible. Decreased absorption and utilization of fat soluble vitamins (ADEK), Increased aldosterone, ineffective detox of proteinwastes, and alcoholism are the most common cause.
2. high calorie, high carbs, low fat, low Na+, & low protein. Restrict alcohol & fluid intake.
3. AST, Alt, LDH, PT, amylase, lipase, Hgb, HCT, Bilirubin, albumin, & WBC's
4. measure and record patients abdominal girth daily, use only small gauge needle for injection, provide prolonged pressure at venipuncture site, avoid IM injectables, avoid straining with defactation and vigorously blowing nose or coughing, use soft tooth brush, Pts at risk for bleeding, give vit K to increase prothrombin time
5. nutritional support (malnutrition), transfusion of platelets, packed RBC's & fresh frozen plasma, diuretics & stool softener, ammonia detoxicant:lactulose

1. What is NIDDM aka adult onset or type II diabetes?
2. What are the possible causes?
3. WHat are the risk factors?
4. What is the tx?
5. Is treated w/ what meds?

1. deficit in insulin release or an insulin-receptor defect in peripheral tissues. Usually develops after age 30.
2. low insulin secretion due to exhaustion of beta cells, decreased responsiveness of tissue to insulin or abnormal hepatic glucose regulation. Ex. genetics, hyperpituitarism, cushings, hyperthyroidism, infection, stress, pregnancy, etc.
3. female, over 40, overweight, high dose estrogen use, (ex. prostate cancer), american indian, high tryglicerides & cholesterol levels, family hx of NIDDM
4. diet, exercise (it increases insulin sensitivity & improves glucose tolerance& promotes weight loss)
5. oral antidiabetic drugs, to stimulate endogenous insulin production and increase insulin sensitivity at the cellular level. May need insulin if not controlled w/ diet, exercise, and oral antidiabetics, or during surgery, post op, and def during pregnancy.

What are the sx of hyperglycemia?

The Classic Symptoms

Polyphagia (frequently hungry)
Polyuria (frequently urinating)
Polydipsia (frequently thirsty)
Other Symptoms Might Include

Blurred vision
Fatigue
Weight loss
Poor wound healing (cuts, scrapes, etc.)
Dry mouth
Dry or itchy skin
Impotence (male)
Recurrent infections such as vaginal yeast infections, groin rash, or external ear infections (swimmers ear)

What are the sx of hypoglycemia?

tachycardia, moist skin, hunger, irritability, & tremors

1. WHat is hyperglycemic crisis? ex. diabetic ketoacidosis & Hyperosmolar Hyperglycemic Nonketotic Syndrome
2. What problems are both
associaed with?
3. What are precipitating factors in both?
4. For both, what is the classic clinical picture?

1. decreased effective action of circulation insulin, concomitant elevation of counterregulatory hormones (such as glucogen, catecholamines, cortisol, and growth hormone), this leads to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, this results in hyperglycemia & parallel changes in osmolality of the extracellular space
2. glycosuria, leading to osmotic diuresis, with loss of water, Na+, K+, and other electrolytes
3. infection, CVA, alcohol abuse, pancreatitis, MI, trauma, & drugs
4. hx of polyuria, polydipsia, polyphagia, weight loss, vomiting, ab pain(only in DKA), dehydration, weakness, clouding of sensoria, and coma
5. poor skin turgor, kussmaul resp. (in DKA), tachycardia, hypotension, alteration in mental status, shock, & ultimately coma (more frequent in HHS), up to 25% of DKA pts have emisis, which may be coffee-ground in appearance and guaiac positive.

1. WHat happens additionally in DKA?
2. What is the dx criteria in DKA?

1. it leads to the release of free fatty acids (Lipolysis) & to unrestrained hepatic fatty acid oxidation to ketone bodies (B-hydroxybutyrate[B-OHB] & acetoacetate), with resulting ketonemia & metabolic acidosis
2. blood glucose >250, arterial PH <7><15, and moderate ketonuria, or ketonemia

What is the dx criteria for HHNKS?

blood glucose >600, arterial PH >7.3, bicar >15, mild ketonuria or ketonemia, & effective serum osmolality >320mOsm/kg H2O

What is involved with a liver biopsy?

NPO after midnight, exhale & hold breath during needle insertion, observe for sx of shock & pneumothorax, position on Right lateral side for 2 hours for hemostasis. This stops leakage of bile, blood. Avoid intrathoracic or abdominal pressure

1. What is esophageal varices?
2. WHat are the sx?
3. What is the medical management?

1. a dilation of esophageal veins in the lower part of the esophagus due to portal hypertension
2. hematemesis, ascites, anorexia, n/v, fatigue, and weakness, peripheral edema, dysphagia
3. esophageal baloon tamponade w/ sengstaken-Blakemore or Minnesota tube. (keep scissors & suction at bedside), Paracentesis-pt positioned upright with feeton floor for procedure & positioned on right side afterward, Propanol, Inderal-to decrease BP, open veins, < portal hypertension, the goal is to prevent bleeeding, monitor pulse and pulse pressure. Withhold food and fluids with active bleeding. Check for signs of bleeding, avoid activities that increase intraabdominal pressure, assess LOC & impending encephalopathy

What is a hepatic coma?

its caused by > ammonia levels, give cephalic/lactulose to < ammonia level. Increase level of ammonia in the stool. Improved constipation.

What is IDDM aka Type I diabetes or juvenile onset?

chronic autoimmune metabolic disease. A result from the beta cells in the islets of langerhans of the pancreas not producing adequate endogenous insulin. (may not produce any), dysfunction of carbohydrate metabolism with subsequent protein & fat metabolism dysfunction

1. What are the sx of type I diabetes?
2. What are the complications?
3. What are the dx?

1. common sx=3 p's (polyuria, pludypsia, polyphagia), weight loss, > fatigue, irritability, blurred vision, poor wound healing
2. neuropathies, retinopathies, renalopathies, PVD, DKA, HHNK, CV disorders, (stroke, MI)
3. FBG level >or = 126mg/dl, glycosylated hemoglobin normal range 4-6%, high=poor control, GTT shows hyperglycemia (used more often during pregnancy) 2 hours post prandial blood glucose level shows hyperglycemia (greater than 200 mg/dl)

1. What is the medical management for type I diabetes?
2. What is the diabetes NSG interventions teachings?

1. diet, exercise, meds=insulin, & hypoglycemics: A. short acting(regular, semilente), B. intermediate acting (NPH, lente), C. long acting (PZI, ultralente)
2. it is usually divided into basic info needed for survival leading to more complex, stress to pt that meds treat the sx they dont cure the disease, therapy is long-term,, teach basic patho interrelationship b/t meds, exercise, and nutrition, teach nutritional guidelines food guide:bread 6-11 serv., fruit 2-4 serv., veggie 3-5, dairy/meat 2-3, fats and sweets use sapringle, exercise guidelines: not to exercise if >250 will increase the hyperglycemia-regular exercise same time every day is optimal, prevention of hypoglycemia with increased exercise, spontaneous exercise (eat snack, have glucose handy, check BG), tell pt to carry a source of sugar (candy, sugar packets), & ID describing their disease ant tx regimen at all times. teach type of insulin, equipment (syringe, cartridge pens, alcohol swabs), storage and place to discard syringes, importance o

What are the lab finding for hyperglycemic crisis ( DKA, HHNKS)?
2. What is the tx?

1. -leukocytosis proportional to blood ketone body concentration,
-Na+ usually (osmotic flux of H20 from the Intracellular to the extracellular less commonly concentration may be falsely lowered by severe hypertrygliceridemia. (less common),
-K+ may be (EC shift of K+ caused by insulin deficiency, hypertonicity, and acidemia. Low normal or low serum K+ have severe total body K+ deficiency- careful cardiac monitoring -more vigorous K + replacement needed. Tx.-k+ further and can provoke heart dysrythmia also monitor for rebound hyperkalemia.
2. correct dehydration, hyperglycemia, and electrolyte imbalance. Identification of comorbid precipitating events, increase patient monitoriing. Regular insulin by continous IV infusion , bicarb therapy (DKA), isotonic (.9% NaCl) or hypotonic saline (NS .9%) after pt is stabilized monitor for rebound effects ex. hypoglycemia,

What are the sx for ketoacidosis?

ab pain, acetone breath, altered consciousness, hot flushed skin, kussmaul respirations, N/V, decrease BP, oliguria, and tachycardia

What are the sx from an insulin reaction (hypoglycemia)?

hunger, weakness, hand tremors, pallor, tachycardia