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patho ch 17 nutritio
altered nutrition
| Question | Answer |
|---|---|
| GI track consists of what parts | mouth, pharynx/throat, esophagus, stomach, small intestine, large intestine, rectum and anus |
| functions of GI tract | production of enzymes and hormones storage/synthesis of vitamins dismantle/reassemble food entrance for nutrient/vitamin/mineral/electrolytes/water collection/elimination of waste |
| solid organs of GI tract | liver, pancreas, and GB |
| adequate nutrition requires? | optimal food intake, digestion, absorption, metabolism, nutrient transportation and waste excretion |
| metabolism | allows for chemical reactions from nutrients to produce heat, conduct impulses and contract muscles |
| types of nutrients | macronutrients and micronutrients |
| what are the types of macronutrients and what is it's main purpose | proteins, lipids, carbohydrates converted into useable sources of energy |
| what are the types of micronutrients | vitamins and minerals |
| proteins | linear chains of amino acids directed by DNA coding 20 different amino acids, 9 essential amino acids. |
| what are the major types of lipids | simple (fatty acid/glycerol) vs complex (phospholipid, lipoprotein, glycolipids), sterols (cholesterol, bile salts) |
| what is the role of lipids? | energy source facilitation of digestion and nutrient absorption |
| carbohydrates | digested and turned into glucose (oxidation) or stored as glycogen |
| vitamins role in the body | developing genetic material production of hormone, RBC, collagen, nervous tissues important vitamins include K, B1, B6, B12 |
| mineral role in body | bone, hemoglobin, enzyme, hormone, chemical mediators fluid + acid/base balance |
| macrominerals | Na, K, Ca, P, Mg, S |
| Micronutrients | Fe, Zn, F, Cu usually do not exist in blood/tissue/cellular fluids and are bound to proteins instead (called "trace metals") |
| water | largest body component essential for digestion, absorption, transportation, excretion dissolving, fluid balance, lubrication, temperature management |
| what is the critical level of water loss | 20% or more of total body water content |
| hypothalamus | secretes hormones that contribute to energy intake, expenditure, metabolism reduction/stimulation |
| adipocytes | store lipids |
| storage methods in the body | adipocytes liver = stores vitamins, Fe, Cu, Glycogen |
| effect of liver failure on nutrients | profound hypoglycemia, inability to convert amino acids/glycerol into glucose |
| nutritional intake requirement | based on RDA (kcal/kg) intake carbs: 45-65% protein: 10-35% fats: 20-35% |
| how does pregnancy affect kcal/day | 300 kcal/day increase breast feeding/lactation = 500 kcal/day |
| absorption | moving nutrients from GI tract to circulation for cellular use carbs broken down into monosaccharides proteins broken down into amino acids/smaller peptides lipids broken down into fatty acids/glycerol |
| absorption occurs in | mostly in small intestine, partially large intestine |
| duodenum role in absorption | fat and mineral absorption |
| jejunum role in absorption | glucose, galactose, fructose, water soluble vitamin and fat absorption |
| ileum role in absorption | amino acid, fat soluble vitamins, fats, sodium/potassium |
| colon role in absorption | water absorption |
| undernutrition definition | inadequate nutrient intake (caloric, vitamin/minerals) malabsorption/abnormal digestion or nutrient distribution |
| Marasmus malnutrition definition | starvation condition related to protein energy malnutrition from deprivation of ALL food |
| Kwashiorkor malnutrition definition | protein deprivation of individual who consumes adequate carbs |
| marasmus malnutrition involves | low insulin and high glucagon/cortisol state --> switch to fat burning and ketones visceral proteins preserved = no edema, but severe wasting of fat/muscle |
| Kwashiorkor malnutrition involves | hypoalbuminuria due to insufficient amino acid supply --> pitting edema (legs, face and ascites) low apolipoprotein --> fatty liver/hepatomegaly antioxidant/protein deficits --> skin/hair change + infection risk |
| sign of Kwashiorkor malnutrition | puffy look d/t edema, distended abdomen (hepatomegaly/ascites), flakey paint dermatitis, hair depigmentation (flag sign) EDEMA MASKS UNDERLYING MUSCLE MASS |
| sign of marasmus malnutrition | skin and bone look marked muscle/fat loss, low weight, no swelling, |
| malabsorption | lack of movement of one/more nutrient across GI mucosa |
| cause of malabsorption | short gut syndrome, bowel obstruction, pancreatic disease, inflammation (ie. crohn's/UC), celiac disease |
| exocrine pancreatic insufficiency | fat malabsorption leading to weight loss and fat soluble vitamin deficiencies |
| general manifestation of altered nutrition | weight loss/gain muscle wasting/weakness change in skin/mucus membrane (impaired healing, ulcerations, dry skin) dehydration/diarrhea/abdominal pain fatigue |
| GERD clinical manifestations | heartburn/epigastric pain (30-60 minutes after meal), pain radiating from epigastric to throat/shoulder/back dyspepsia nausea/regurgitation dysphagia hypersalivation |
| peptic ulcer | ulceration in mucosal wall of GI tract (stomach, duodenum, esophagus) gastric vs duodenal more common |
| causes of peptic ulcers | ASA/NSAIDs HP gastritis |
| GERD tx | EtOH/smoking cessation avoidance of lying down for 2-3 hr, anticholinergics (slow gastric emptying), NSAIDs head elevation while sleeping weight loss use of antacids/H2-blockers/PPI |
| gastric PUD clinical manifestations | sharp/gnawing pain in the epigastric area (30-60 mins post prandial) pain with food intake hematemesis (more common) and melena |
| duodenal PUD clinical manifestations | burning pain in the mid epigastric area 1.5-3 hr post prandial and nighttime pain melena (more common) vs hematemesis relief from food intake, but recurrent after meal |
| diagnostic criteria for PUD | endoscopy w/ or w/o bx CBC HP testing CT |
| peptic ulcer tx | HP eradication healing ulcer crater (acid neutralizing, acid inhibiting, mucosal protectives, antacids, PPI) |
| peptic ulcer complications | obstruction - d/t edema/spasm/scar tissue contraction perforation - erosion thru all the layers of stomach/duodenal wall GIB/hemorrhage - bleeding from granulation tissue/erosion in the ulcer (hematemesis vs melena vs hematochezia) |
| H. Pylori | colonization of mucus secreting epithelial wall of stomach enzyme/toxin production interferes with mucosal protection |
| HP diagnosis | C-urea breath test stool Ag test endoscopic bx serologic titer of HP Ab (bloodwork) |
| appendicitis | inflammation of appendix with risk of appendiceal rupture within hours leading to peritonitis/sepsis |
| what to avoid when treating appendicitis patient | avoid heat application, can cause ruptures |
| appendicitis tx | appendectomy |
| causes of appendicitis | GI tract infection, parasite, stool blockage, tumor (rare) |
| clinical manifestations of appendicitis | periumbilical pain radiating to RLQ or abdominal pain most intense @ McBurney's point rebound tenderness/abdominal rigidity low grade fever elevated WBC anorexia/nausea/vomiting constipation/diarrhea |
| McBurney's point | slightly to the right side of where the appendix is superior to the iliac |
| intestinal obstruction | intestinal content/gas/fluid accumulation above obstruction can result in rupture/perforation can result in ischemia d/t pressure from swelling |
| clinical manifestations of intestinal obstruction | abdominal distension lack of flatus nausea/vomiting possible no bowel sounds on auscultation |
| diagnostic criteria of intestinal obstruction | H/P abd XR CT Abd |
| treatment for intestinal obstruction | NPO bowel decompression with NG tube electrolyte/fluid monitoring acid-base balance |
| NPO | nil per os nothing by mouth |
| liver function | synthesis of glucose, plasma protein and clotting factors metabolism of toxins/drugs/steroid hormone metabolism of fats/proteins/carbs bile salt production bilirubin elimination blood filtration + removal of bacteria |
| endocrine pancreas | insulin/glucagon supply gluconeogenesis during starvation |
| gluconeogenesis | synthesis of glucose from lactate/amino acids |
| hepatitis causes | autoimmune hepatitis drug/toxin reaction infectious (malaria, mononucleosis, salmonellosis) hepatotropic viruses |
| hepatotropic viruses | hep A, B, C, D, E A/E = fecal oral route B/C/D = blood/body fluid route |
| stages of hepatitis clinical manifestations | asymptomatic prodrome (pre-icteric) icteric vs cholestatic pattern severe/fulminant red flags chronic |
| hepatitis prodrome phase clinical manifestations | fatigue, anorexia, nausea/vomiting, low grade fever, RUQ discomfort about 1-2 weeks prior to icteric phase hepatocyte injury = inflammatory cytokines = flu like systemic symptoms |
| icteric phase hepatitis clinical manifestations | jaundice, dark urine, pale stool, pruritis, tender heptatomegaly |
| cholestatic pattern hepatitis clinical manifestations | PROMINENT jaundice/pruritis, pale stool, dark urine, possible milder systemic symptoms labs show ALP/GGTP elevation vs AST/ALT elevation no hepatomegaly/tenderness c/w icteric hepatitis |
| dark urine means | conjugated bilirubin in the urine |
| pale stool means | reduced stercobilin in the gut |
| pruritis in hepatitis from | bile salts in skin cause itching |
| severe/fulminant hepatitis red flags | confusion/asterixis, easy bruising/coagulopathy, rapid jaundice, hypotension need immediate eval with INR/PT, bilirubin, glucose, ammonia, lactate |
| asterixis | loss of muscle tone, when occurring due to hepatitis means hepatic encephalopathy |
| encephalopathy | altered mental state with multitude of causes affecting brain function anoxic, CTEs, hepatic, metabolic, toxic |
| bilirubin conjugation | process of making unconjugated bilirubin (indirect bilirubin) water soluble (conjugation/direct bilirubin) |
| chronic hepatitis clinical manifestations | persistent fatigue, vague RUQ discomfort, intermittent pruritis over time = stigmata of chronic liver disease (spider angiomata, palmar erythema, gynecomastia), muscle wasting, splenomegaly, edema/ascites, portal HTN (variceal risk) |
| causes of jaundice | excessive hemolysis (pre-hepatic) impaired bilirubin uptake by hepatocytes, decreased bilirubin conjugation (intrahepatic) bile flow obstruction in canaliculi of hepatic lobule/intra or extrahepatic bile duct (post-hepatic) |
| clinical manifestations of jaundice | dark urine, pale/clay colored stool, yellow discoloration (icterus), skin xanthoma, pruritis, anorexia, malaise, fatigue |
| diagnostic test for liver | serum aminotransferase (AST/ALT) serum bilirubin/GGT/ALP INR, PT/PTT, lactate US, CT, MRI angiography (visualize hepatic/portal circulation) liver bx |
| INR | internationalized normal ratio |
| PT/PTT | prothrombin time and partial thromboplastin time |
| lactate significance in hepatitis | accumulates due to impaired hepatic clearance/poor perfusion |
| phenylketonuria | autosomal recessive disorder of PAH gene mutation inability to metabolize phenylalanine leading to accumulation in body fluids cannot convert phenylalanine to tyrosine |
| why does PKU cause neuropsychological issues | tyrosine deficit |
| clinical manifestations of PKU | intellectual disability/seizure disorder fair skin/hair eye hypopigmentation musty odor |
| pharmacologic treatment of PKU | palynziq (QD enzyme replacement) oral saproterin dihydrochloride (enzyme cofactor) |
| dx of PKU | metabolic screening at birth often undetected until severe developmental delay/intellectual disability |
Created by:
sleepingbear
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