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GI,GU, and Multisyst
PCU training
| Question | Answer |
|---|---|
| Hormones that affect gastric enzymes to stimulate and inhibit gastric motility in small intestine | *motilin, secretin, and cholecystokinin |
| Digestive enzymes of small intestine | *amylase, trypsin, lipase |
| peritoneum | the serouse membrane lining abdominal cavity and covering most of the intraabdominal organs*composed of layer of mesothelium supported by thin layer of connective tissue*serves as channel for blood vessels, lymph vessels, and nerves of abdominal organ |
| Peritoneum two functions | *supports abdominal organs*surface area 1.7m |
| semipermeable membrane (peritoneum) | *passive membrane *fluids solutes permitted;bacteria restricted to certain areas *clearing of bacterial from peritoneal cavity *fluid shifts caused by peritonitis and ileus |
| liver | largest organ in the body*located in RUA*blood supply through hepatic artery or portal vein*bacteria and other foreign substances filtered out of blood thru kupffer cells*glisson capsule:connective tissue capsule covering the liver |
| Liver function | *metabolize and store nutrients*synthesize clotting factors and breakdown of RBC's*detoxify bld *produce bile |
| Gallbladder* | *movement of bile *blood supply through hepatic and cystic arteries *venous drainage thru cystic vein |
| Function of gall bladder | *concentrate and store the bile being constantly produced by the liver*flow of bile important for keeping bilirubin concentration in plasma form becoming elevated |
| ct scan | *shows slices of patient *good for detecting lesions/tumors >2cm |
| MRI | *more detailed than CT shows lesions/tumors <2cm |
| Nuclear medicine scan | *useful for detecting source of bleeding in GI tract especially when rate of bld slow. |
| angiography | *used for evaluating bleeding in the lower GI*close monitoring after procedure required |
| Serum albumin | *key transport mechanism for meds, horomones, and enzymes |
| serum proteins | *levels in presence of injury,disease,autoimmune disease*maintains osmotic pressure within vascular bed |
| Clotting factors primarily produced by the liver | INR, PT, PTT |
| lactate levels | *high levels indicate liver not functioning well and/or pt is septic |
| Elevated serum amylase and lipase | *if pancrease inflammedSerum amylase: pancreatitis indicated if elevated at least 5-10 times norm*lipase:indocator of pancreatitis but less exact |
| liver biopsy patient considerations | *NPO 6 hrs before procedure *Inform MD of any med that might affect coagulation ex. ibuprofen,aspirin,herbal supplements |
| postprocedure patient considerations of liver biopsy | *observe for signs of bleeding and possible pneumothorax *pain leves |
| paracentesis | *procedure that removes fluid from abdomen due to infection, inflammation,cirrhosis, or cancer |
| Angiodysplasia | *stretched and fragile blood vessels*ex portal htn in cirrhosis increases pressure in collateral blood vessels surrounding rectum |
| Upper GI bleed symptoms | *vomiting bright red or coffee ground bld, bloody stool when bleeding is rapid. |
| lower GI bleed symptoms | Blood per stool. |
| Signs of bleeding | *Tachycardia,Hypotension,Cold clammy skin,decreased urine output,hypoxia |
| Patient management during bleeding | *Supplemental oxygen, NG tube,IV access,F/C |
| clinical presentation of liver failure | *jaundice(from bilirubin)*confusion*palmar erythema*bruising*met acidosis*ascites*spider agiomata*asterixis=abnormal muscle tremor and jerks in hands,tongue and feet |
| hepatic encephalopathy | alteration in mental status that develops as a direct result of hepatic failure. *caused by inability of the liver to process by products of nitrogen metabolism, primarily ammonia. *decreased albumin because can't produce*hypoglycemia (liver=glycogen) |
| Patient characterstics and monitoring in hepatic encephalopathy. | *cerebral edema in 80% of acute hepatic fail. monitor ICP*Cardiac dysrythmias resulting from the cerebral edema,hypoxemia,lactic acidosis and electrolyte imbalance*atelectasis,PNA,Pulmon Edema b/c compromised respiratory status |
| pt characterstics and monitoring in hepatic encephalopathy | *Acute respiratory failure and ARDS resulting from compromised respiratory status*Acute renal failure resulting form hypoperfusion, acute tubular necrosis*hepatorenal syndrome resulting from the altereed renal perfusion. |
| categories of liver damage | *cholestatic:related to bile transport within liver*hepatocellular:resulting from liver cell damage/destruction *mixed:combination of cholestatic and hepatocellular injury |
| clinical presentation of hepatitis | *flu-like symptoms*loss of appetite,nause,vomiting,abd pain, fever*jaundice*dark urine*joint pain |
| Acute pancreatitis | *two types pancreatitis and necrotizing pancreatitis(more severe and has systemtic effect such as SIRS)*pts with acute pancreattitis do not develop organ dysfunction or complications with other organs. *acute pancreatitis usually self-limiting |
| Chronic pancreatitis | causes:ETOH, blocked or narrow pancreatic duct, heredity, idiopathic |
| autodigestion (chronic pancreatitis) | Activation of pancreatic enzymes b4 they flow out of the pancreas (hallmark of pancreatitis) |
| acute pancreatitis symptoms | *fever c/o sudden onset of pain in epigastric area radiating to back.Presence of Cullen's (bleeding in flank) signs. |
| Cullens sign | bruise-like area under umbilicus (ascitic blood) |
| pancreatitis and bowl infarcts or acute mesenteric ischemia | *appears very late/advanced stages. *results from a reduction in either venous or arterial blood flow. |
| Mesenteric Arterial Emboli | *Pain may be the only presenting symptom: sudden in onset,severe,poorly localized,periumbilical,n/v and frequent BM's.Out of proportion to physical findings*abdomen may be soft with only mile tenderness*BS absent*Abd distention |
| Neuro nutritional needs | *Dysphagia and weakness of swallowing muscles common in those with neurologic disorders,creating and increased risk of aspiration. Brain injury, wound, and burn pts require a high-protein feeding. If needs not met increased secondary brain injury can be |
| Pancreas (endocrine system) | consists of islets of langerhans: alpha cells (secrete glucagon) beta cells (secrete insulin) delta cells (secrete gastrin, somatostaing or both) |
| Insulin promotes | *glucose uptake from bld into target cells of the liver,k adipose tissue, and skeletel muscle *glucose storage within cells as either glycogen (for short term) or triglycerides (longterm storage)*lipogenesis (buildup of lipids)and protein synthesis |
| Glucagon regulation | *catabolic hormone secreted by alpha cells*mobilizes glucose,fatty acid, and amino acids from stores into the blood |
| Release/secretion of glucagon | *triggered by:decreased level of blood glucose*amino acids*stimulation of sympathetic nervous system*ihibition triggered by fatty acids, somatostatin and insulin |
| Somostatin | helps regulate islet hormone secretion*inhibits both glucagon and insulin secretion*stimulated by hyperglycemia, glucagon, and amino acids*plays a role in carb,protein,and fat metabolism |
| Pituitary function (two glands) | Adenohypophysis(anterior lobe)Neurohypophysis (post lobe)*located on superior surface of the sphenoid bone |
| Pituitary hormones | TSH,ACTH(adrenal cortex)FSH and LH, GH, Prolactin,Endorphins |
| Posterior Pituitary Gland | *ADH and oxytocin-made in hypothalamus.stored in and secreted by the posterior pituitary*released when norepinephrine receptors in brain stem are stimulated |
| Thyroid gland | Thyroid hormones regulated through negative feedback loop.*keeps constant concentration of free T3 and free T4 in bld strm.*when T3 and 4 levels too high, pituitary inhibits TSH production.*when T3 and 4 too low pituitary produces more TSH |
| Thyroid hormone function | *stimulated metabolic activity and o2 consumption*produces heat or thermogenesis*stiumlates carbohydrate,fat,&protein metabolism*increases rate of glucose absorption |
| Thyroid hormone function | required for normal respiratory response to hypoxia and hypercapnia respir drive*increases Erythropoiesis |
| T4 thyroxine | *causes adrenergic receptors to be activated. then causing stronger/greater hrt contractions, hrt rate and cardiac output |
| parathyroid | *produces parathyroid hormone. *the major regulator of calcium.*inhibited by increase in serum calcium and vit D metabolites and Increas/decrease in mg levels |
| Adrenal medulla (inner organ) | Epinephrine and norepi release*triggered by flight/fight,trauma, surgery,hypoxia,hemorrhage,low bld sugar, fluid loss,hypotension, increased hrt rate and CO |
| Adrenal medulla (inner organ) causes? | *vasoconstriction of arterioles and release of renin from kidneys.*dilates bronchial smooth muscle *increase of breakdown of glycogen in liver-causes glycogen release form pancreas. |
| Vit D | necessary for absorption of calcium and phophorous from food in small intestine. *prolonged doses cause hypercalcemia with anorexia, nausea,vomiting, polyuria,polydipsia,weakness,pruritus, and altered renal function |
| pituitary assessment | *question HA's,confusion,or behavioral changes,recent trauma,head injury |
| thyroid assessment | *family hx*fatigued,nervous,weak,change in appetite,weight changes,heat or cold intolerance,changes in sweating, or palpitations,VS,LOC,exophthalmos,skin turgor and texture,deep tendon reflexes,tenderness,lumps in neck |
| parathyroid assessment | *question if pt been depressed,nervous,anxious,muscle cramps,abdominal pain,fatigue,polyuria,polydipsia |
| adrenal gland assessment | *tremors,orthostatic hypotension,temperature,pigment changes,fat deposits in neck or facial areas,note tachycardia,murmurs, or extra hrt sounds |
| Type 1 DM | *failure of body to produce insulin-beta cells in islets of langherhans destroyed.puts body into catabolic state*not treated fast=DKA |
| Type 2 DM | Failure of body to properly use insulin *pt complains of fatigue,visual changes, and recurrent infections |
| Symptoms of DM | *polyuria,polydipsia,and polyphagia |
| Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) | Creates some insulin but no ketone |
| DKA | *commonly occurs in pts with type I *presenting factor in newly dx pt*insulin deficiency |
| Symptoms DKA | *nausea,vomiting,"polys",HA,dehydration,blurred vision,Hypotension,tachycardia,kussmaul's respirations,pt confused,dry flushed skin,dry mucous membranes,poor skin turgor,"fruity breath" |
| DKA lab | *serum glucose >350*hyperkalemia*hyponatremia*elevated BUN and CR*pH <7.30*bicarb <15 |
| DKA management | *insulin *IV saline to help dhd and hyponatremia* |
| Hyperglycemia HHNS | *occurs in pts with Type 2 DM*Hyperosmolarity and osmotic diureses result causing severe dhd and hypovolemia.*occurs commonly in elderly, following acute illness.*onset slow and insidious |
| HHNS assessment | "Polys"*weight loss*weakness *muscle cramping. |
| HHNS s&s | *increased pulse and respiratory rate*hypotension*dry mucous membranes and poor skin turgor *fluid deficit 9-12Liters |
| HHNS Labs | *bld glucose <600 *serum osmolality >350 *normal or decreased K+,Mg,Ca,Phophate*elevated BUN CR*normal bicarb and pH *elevated Hmg and Hct |
| Pituitary Gland Disorders | *DI*SIADH |
| Diabetes Insipidus | *occurs when there is an ADH deficiency or an inability of the body to respond appropriately to ADH Result in massive Urine Out,excessive thirst,hyperosmolality*hypernatremia |
| Labs for DI | *urine specific gravity <1.005*eventually Na >145 *if DI suspect then vasopressin test to confirm |
| SIADH | *ADH is produced from sites other than the post pit and result in an ADH excess *causes-malignancies,CNS injury or disease,stressors,alteration in adrenal or thyroid gland |
| SIADH patho | *renal tubules inhibited from excreting H20 and H20 retention results inducing dilutional hyponatremia.*aldosterone suppressed and normal Na regulation interrupted *low UO |
| S&S SIADH | *lethargy,nausea,vomiting,lack of appetite,LOC,confusion |
| Labs SIADH | *Na <120 *serum osmolality <250 |
| Hyperthyroid | *Graves disease *if not treated then can be Thyrotoxic crisis or storm*more common in women |
| Thyrotoxic storm | *triggered by increase physical or emotional stress*extreme irritability,HTN,rapid hrt rate,vomiting, high fever,delirium,coma,death |
| Thyrotoxic storm patho | *sharp rise in metabolic rate*eventual hrt failure,pulmonary edema*met acidosis=severe dhd from diarrhea, nausea, vomiting |
| thyrotoxic storm labs | *no specific lab test *confirmed only through medical hx and clinical presentation |
| Hypothyroidism causes | *current/ongoing inflammaiton of thryoid gland*radiation |
| Myxedema coma | *Acute hypothyroidism (from MI,systemic infection,respiratory failure)not adequate hormone replacement *most common in women. |
| Patho of myxedema coma | *severely decreased metabolic rate*decreased erythropoiesis*decreased glomerular filtration rate*hypoventilation*insufficient throid hormone*acidosis*hypothermia*increased capillary permeability |
| Clinical pres Hypoparathyroid | *halmark sign=tetany Positive trousseau's(bld pressure cuff and then carpal twitch) and Chvostek signs(tap nerve on cheek-facial twitch) *ca <7 *phosphorous >7 |
| Primary adrenal insufficiency=Addison's crisis | *Inadequate function and cortisol secretion*disease progression-low corticol levels,low aldosterone secretion, hyponatremia,hyperkalemia,hypotension |
| S&S addison's disease | *anorexia,weakness,malaise,e's imbalance*hypotension,hyperkalemia,hypglycemia |
| Cushings syndrome | *condition resulting in excess cortisol levels |
| cushing disease s&S | *rounded face (moon facies) *insomnia *increased total body fat *easy bruising *hair thinning*muscle wasting/weakness *HTN Na and water retention |
Created by:
Natalyjm
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