Fluids and Electrolytes / GI Flashcards
Capillary hydrostatic pressure
facilitates the outward movement of water from the capillary to the interstitial space
-pushes
Capillary (plasma) oncotic pressure
osmotically attracts water from the interstitial space back into the capillary
-pulls
interstitial hydrostatic pressure
facilitates the inward movement of water from the interstitial space into the capillary
interstitial oncotic pressure
osmotically attracts water from the capillary into the interstitial space
Edema
excessive accumulation of fluid within the interstitial spaces
Increase in Capillary Hydrostatic Pressure
Edema
- hydrostatic pressure increases as a result of venous obstruction or salt and water retention
- venous obstruction causes hydrostatic pressure to increase behind the obstruction, pushing fluid from the capillaries into the interstitial spaces
Decrease in Capillary Oncotic Pressure
Edema
-the decreased oncotic attraction of fluid w/in the capillary causes filtered capillary fluid to remain in the interstitial space
Increase in Capillary Permeability
Either pores are enlarged or capillary wall is damaged and fluids and proteins leak out because normal barrier is not there
Lymphatic obstruction (lymphedema)
when lymphatic channels are blocked=proteins and fluid accumulate in interstitial space=lymphedema
Clinical Manifestations of Edema
Localized: site of cut/ trauma
Generalized: swelling of ankles
Pitting: scale of 0-5, 4= pitting
Water deficit: dehydration
water deficit, but also used to indicate both sodium and water loss (isotonic or iso osmolar dehydration)
Pure water deficit
(hyperosmolar or hypertonic dehydration) rare, because most ppl have access to water
Most common cause of water deficit
increased renal clearance of free water: result of impaired tubular function or inability to concentrate urine
Clinical Manifestations: Water deficit
- headache, thirst, dry skin and mucous membranes, elevated temp., weight loss, decreased or concentrated urine
- skin turgor may be normal or decreased
- hypovolemia: tachycardia, weak pulses, postural hypotension
Water Excess
-Water intoxication: compulsive water drinking
renal failure, severe congestive heart failure, cirrhosis
-Overall effect of dilution of the ECF, with water moving to the intercellular space by osmosis
Clinical Manifestations: Water excess
weakness, nausea, muscle twitching, headache and weight gain
Hyponatremia
serum sodium concentration falls below 135 mEq/L
-loss of sodium, inadequate intake of sodium or dilution of sodium by water excess
Dilutional hyponatremia
occurs when there is a replacement of fluid loss with intravenous 5% dextrose in water
Clinical Manifestations: hyponatremia
- decrease in sodium concentration changes the cell’s ability to depolarize and repolarize normally, altering the action potential in neurons and muscles
- neurological changes: lethargy, confusion, apprehension, depressed reflexes, seizures and coma
- muscle twitching and weakness are also common
- cerebral edema can be life-threatening complication of hypervolemic hyponatremia
Hypernatremia
serum sodium >145 mEq/L
-Related to sodium gain or water loss
Manifestations: Hypernatremia
Hyperactive reflexes
Neurological confusion
Coma
Convulsions
Hyperkalemia
evaluation of ECF [K] 5.5 mEq/L
Causes of Hyperkalemia
-Increased intake
-Supplements such as K salts, use of stored whole blood and intravenous boluses of K penicillin G, or replacement K
K going from ICF → ECF
-Cell trauma (such as burns, massive crush injuries, or extensive surgeries), changes in cell membrane permeability. acidosis, insulin deficiency, cell hypoxia
-Decreased Renal Excretion
renal failure that results in oliguria (
Clinical Manifestations for hyperkalemia
-Mild Attacks:increased neuromuscular irritability
-restlessness, intestinal cramping, and diarrhea
-Severe Attacks: muscle weakness, loss of muscle tone, paralysis
-May cause bradydysrhythmias and delayed conduction
ventricular fibrillation and cardiac arrest
-Causes decreased cardiac conduction and more rapid repolarization of heart muscle
Hypokalemia
when serum [K] fall below 3.5 mEq/L
Causes for hypokalemia
- reduced intake of K: dietary
- increased entry of K into cells: from ECF > ICF in exchange for H+ during respiratory or metabolic alkalosis; administration of insulin
- GI and renal disorders: diarrhea, intestinal drainage tubes or fistula, and laxative abuse
Clinical Manifestations for hypokalemia
- Mild: asymptomatic
- Severe: neuromuscular and cardiac manifestations: neuromuscular excitability causing skeletal muscle weakness, smooth muscle atony, cardiac dysrhythmias, glucose intolerance and impaired urine concentration ability
Hypercalcemia
serum concentration of > 10-12 mg/dl
Manifestations: hypercalcemia
fatigue, weakness, lethargy, anorexia, nausea, constipation, impaired renal function, kidney stones, dysrhythmias, bradycardia, cardiac arrest, bone pain, and osteoporosis
Hypocalcemia
serum [Ca]
Hypocalcemia causes
inadequate intestinal absorption, deposition of ionized Ca into bone or soft tissue, blood administration, decrease in PTH and vit D, inadequate dairy or green leafy veggie uptake
Manifestations of hypocalcemia
Manifests as increased neuromuscular excitability [tingling, muscle spasms (hands, feet, and face), intestinal cramping, hyperactive bowel sounds, convulsions and tetany, prolonged QT and cardiac arrest
Constipation
- normal transit= normal rate of stool passage with difficulty in stool evacuation
- slow transit= impaired colonic motor activity with infrequent BMs, straining to defecate, mild abdominal distention, palpable stool in sigmoid colon
- inability or difficulty expelling stool b/c of dysfunction of pelvic floor muscles or anal sphincter
Secondary Constipation
is difficult or infrequent BM due to neurogenic disorder caused by disease, lifestyle, diet, or drugs alter colonic movement.
Constipations Manifestations
2 of the following for at least 3 months
-Straining with defecation at least 25% of the time
-lumpy or hard stools at least 25% of the time
sensation of incomplete emptying at least 25% of the time
-manual maneuvers to facilitate stool evacuation at least 25% of the time
-less than 3 BMs per week
Diarrhea
increase in frequency of defecation fluid content and volume of feces
Large Volume
volume of feces is increased
small volume
volume is not increased, usually result of excessive intestinal motilit
osmotic diarrhea
nonabsorbable substance in intestine draws excess water > increases weight of stool and volume > large volume
secretory diarrhea
secretory diarrhea = excessive mucosal secretion of fluid and electrolytes > large volume
motility diarrhea
motility diarrhea = food is not mixed properly, digestion and absorption is impaired, motility is increased
aka when Austin eats at Pancho’s
Diarrhea manifestations
- dehydration, electrolyte imbalance (hyponatremia, hypokalemia), and weight loss
- with bacterial and viral infection = fever, w/ or w/o cramping
- inflammatory bowel disease or dysteria = fever, cramping, bloody stool
- malabsorption syndromes = steatorrhea, bloating
Abdominal Pain
- cause may be mechanical, inflammatory, or ischemic
- nerves respond to signals of stretching and distention (not so much cutting, tearing, or crushing) in both hollow and solid organs
- hindrance of blood flow from thrombosis, bowel obstruction
Parietal pain
- parietal peritoneum, more localized and intense than visceral pain, comes from organs themselves
- lateralizes because parietal peritoneum is innervated from only one side of the nervous system
- touch area, it hurts
Visceral pain
- from stimulus (distention, inflammatory, ischemia) acting on abdominal organ.
- poorly localized with radiating pattern and may be referred pain
- diffuse and vague due to sparse nerves
- hurts all over
Referred pain
- visceral pain felt at some distance from the diseased or affected organ
- well localized and felt in skin or deeper tissue because of shared central afferent pathway
- hurts somewhere the pain isn’t coming from (ex. left arm hurts = heart attack)
Upper GI bleeding
- bleeding of esophagus, stomach, or duodenum
- frank, bright red bleeding OR dark, grainy digested blood (coffee grounds)
- commonly caused by varices (varicose veins)
Lower GI bleeding
-bleeding from jejunum, ileum, colon, rectum
caused by polyps, diverticulitis, inflammatory disease, cancer, or hemorrhoids
-occult bleeding is caused by slow, chronic blood loss that is not obvious
-iron deficiency anemia and iron stores in bone marrow depleted
GI bleeding
-changes in blood pressure and heart rate
drop in blood pressure when moved from recumbent position to sitting or upright position
-light headedness and loss of vision
-tachycardia
-hypovolemic shock
-decreased renal output (tubular necrosis or renal failure)
-anoxia and death
Dysphagia
difficulty swallowing. Dysphagia can occur from mechanical obstruction or functional disorder.
Intrinsic (mechanical) obstruction
originate in the wall of the esophageal lumen.
EX: tumors, strictures, diverticular herniations
Extrinsic (mechanical) obstructions
originate outside the esophageal lumen and narrow the esophagus by pressings on the esophageal wall.
EX: tumors
Ex. Ryan choking himself while eating Jimmy Johns
Functional Dysphagia
caused by neural or muscular disorders that interfere with voluntary swallowing or peristalsis.
Oropharyngeal inhibition
Caused by dermatomyositis, neurologic impairment caused by cerebrovascular accidents, Parkinson, or achalasia.
Achalasia
rare form of dysphagia caused by loss of esophageal peristalsis and failure of the lower esophageal sphincter (LES) to relax.
Dysphagia Manifestations
Distention and spasms during drinking or eating.
Discomfort occurring 2-4 seconds after swallowing for upper esophageal obstructions; discomfort occurring 10-15 seconds after for a more common lower esophageal obstruction.
If caused by a tumor, dysphagia begins with solid foods, then progresses to semi-solid and eventually to liquids.
Aspiration of esophageal contents can lead to pneumonia.
GERD
reflux of chyme from stomach through LES to esophagus. The LES may spontaneously and transiently relax 1-2 hours after eating, allowing gastric contents to regurgitate.
NERD
non-erosive reflux disease
Symptoms, but no erosion/ damage
GERD causes
hyperemia (inflammatory response in esophageal wall), increased capillary permeability, edema, tissue fragility, erosion. Fibrosis and thickening may develop.
GERD Manifestations
heartburn acid regurgitation dysphagia chronic cough asthma attacks upper abdominal pain within 1 hour of eating laying horizontally can make it worse
Hiatal Hernia
type of diaphragmatic hernia with protrusion of the upper part of the stomach through the diaphragm and into the thorax
Sliding Hiatal Hernia
stomach slides up into the thoracic cavity through esophageal hiatus.
Paraesophageal Hiatal Hernia
greater curvature of the stomach herniates through secondary opening in diaphragm and lies alongside the esophagus.
Hiatial Manifestations
reflux peptic ulcer inflammation of gall bladder (cholecystitis) gallstones (cholelithiasis) chronic pancreatitis diverticulosis: having the pouches
Pyloric Obstruction
narrowing or blocking of opening between stomach and duodenum.
Ulcers come from obstructions caused by:
edema scarring spasm fibrosis inflammation
Pyloric obstruction manifestations
Early stages → vague feeling of fullness then become distressing
Accompanied by nausea, epigastric pain, seldomly weight loss
Severe obstruction → gastric distention → fullness → succussion splash → vomiting → dehydration → hypokalemia/hypochloremia
Prolonged obstruction causes:
malnutrition
dehydration
extreme debilitation
Intestinal Obstruction
caused by any condition that prevents normal flow of chyme through intestinal lumen.
Intestinal obstruction causes
Simple: mechanical blockage of the lumen by a lesion. (MOST COMMON)
Functional: failure of intestinal motility, often occurring after surgery.
FUNCTIONAL OBSTRUCTION A.K.A. PARALYTIC ILEUS
Intestinal obstruction manifestations
Crampy/colicky pain followed by vomiting and distention.
Colonic obstruction usually presents as hypogastric pain and abdominal distention.
gastritis
inflammatory disorder of the gastric mucosa. Gastritis is either acute or chronic and affects the fundus or antrum, or both (pangastritis).
acute gastritis
erodes the surface epithelium in a diffuse or localized pattern.
Erosions are superficial
the result from injury of prolonged use of NSAIDs (which inhibit secretions of mucous).
acute gastritis manifestations
vague abdominal discomfort
epigastric tenderness
epigastric bleeding
HEALS spontaneously within a couple days
chronic gastritis manifestations
tends to occur in elderly individuals and causes thinning and degeneration of gastric mucosa.
fundal gastritis
Mucosa degenerates extensively in body and fundus of stomach leading to gastric atrophy.
Pernicious anemia may develop
Antral Gastritis
involves the antrum only and is more common than fundal
Caused by H. pylori bacteria, alcohol, tobacco, non-steroidal anti-inflammatory drugs.
Greater risk for development of cancer.
–remember H. pylori
Duodenal ulcer
infection with H. pylori and chronic use of NSAIDS
duodenal ulcer manifestations
first manifestation may be hemorrhage or perforation
chronic intermittent pain in the epigastric area
pain begins 2-3 hours after eating, when stomach is empty
Gastric ulcer
ulcers of the stomach
25% as common as duodenal ulcers
Gastric ulcers develop in the antral region, adjacent to the acid-secreting mucosa of the body.
gastri ulcer manifestations
similar to duodenal ulcers
pain occurs immediately after eating
tend to be chronic
Stress-related ulcers
acute form of peptic ulcer that tends to accompany severe illness, systemic trauma, or neural injury.
Ischemic ulcer
develops within hours after hemorrhage, multisystem trauma, severe burns (called curling ulcers), heart failure or sepsis.
Cushing ulcer
stress ulcer associated with severe head trauma or brain surgery that results from decreased mucosal blood flow and hypersecretion of acid.
stress-related ulcer manifestations
bleeding
stress ulcers seldomly become chronic
Dumping Syndrome
Rapid emptying of hypertonic chyme from the surgical residual stomach (the stomach component remaining after surgical resection) into small intestine 10-20 minutes after eating.
Alkaline reflux gastritis
Stomach inflammation caused by reflux of bile and alkaline pancreatic secretions containing proteolytic enzymes that disrupt the mucosal barrier in the remnant stomach.
Afferent loop obstruction
Intermittent severe pain and epigastric fullness after eating as a result of volvulus, hernia, adhesion, or stenosis of the duodenal stump on the on the proximal side of the gastrojejunostomy. Vomiting relieves symptoms. Surgery required.
Diarrhea (in reference to gastric obstruction)
Either frequent, persistent elimination of liquid stool or intermittent, precipitous, and unpredictable elimination of large volume of stool; related to rapid gastric emptying and osmotic attraction of water into the gut especially after large intake of high carb liquids. Small, dry meals and anticholinergic drugs are effective treatments.
Weight loss
Commonly caused by inadequate caloric intake due to inability to tolerate carbs or normal-sized meals. Stomach is also less able to mechanically break down food.
Anemia
Iron malabsorption may result from decreased acid secretion or lack of duodenum after Billroth II procedure (gastrojejunostomy). Deficiencies of iron, vitamin B12, or folate may result.
Bone and mineral disorders
Related to altered calcium absorption and metabolism with increased risk for fractures and deformity and malabsorption of vitamins and nutrients (vitamin D).
Maldigestion
failure of chemical processes of digestion that take place in the intestinal lumen or at the brush border of the intestinal mucosa
Malabsorption
failure of the intestinal mucosa to absorb (transport) the digested nutrients
Pancreatic Exocrine Insufficiency
deficient production of pancreatic enzymes (lipase, amylase, trypsin, chymotrypsin)
Causes - chronic pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis
fat in stool
Lactase Deficiency (Lactose Intolerance)
inhibits the breakdown of lactose (milk sugar) into monosaccharides and therefore prevents lactose digestion and absorption across intestinal wall.
Caused by genetic defect in which a single enzyme (usually lactase) is lacking.
Bile Salt Deficiency
Formed in liver, and enter duodenum to aggregate with fatty acids to form micelles… making fats more soluble and able to pass through small intestinal villi-
-decreased production of bile salts resulting in decreased micelle formation and fat malabsorption.
Conditions include advanced liver disease, obstruction of common bile duct, intestinal stasis, and ileum diseases.
Bile salt deficiency manifestations
poor intestinal absorption of fat and fat-soluble vitamins (A,D,E,K). Increased fat in stool, diarrhea, and decreased plasma proteins
Diverticulitis
herniations or sac like outpouching of the mucosa and submucosa through the muscle layers, usually in the wall of the sigmoid colon.
Diverticulosis is asymptomatic diverticular disease. Diverticulitis represents inflammation.
–squirrels storing their nuts in sacs in your colon
Diverticulitis manifestations
Symptoms of diverticular disease may be vague or absent. Cramping pain of lower abdomen can accompany constriction of the thickened colonic muscles. Diarrhea, constipation, distension, or flatulence may occur.
Appendicitis
an inflammation of the vermiform appendix, which is a projection from the apex of the cecum. It is the most common surgical emergency of the abdomen.
IBS
a functional GI disorder with no specific structural or biochemical alterations as a cause of disease. Characterized by recurrent abdominal pain and discomfort w/ altered bowel habits that present as diarrhea or constipation.
IBS manifestations
IBS is characterized by lower abdominal pain or discomfort and can be diarrhea-predominant, constipation-predominant, or altering between the two. Symptoms include gas, bloating, and nausea.
obesity
defined as a body mass index that exceeds 30 (BMI = kg/m^2)
Anorexia nervosa
Psychologic and physiologic syndrome
bulemia nervosa
Bingering – the consumption of normal to large amounts of food followed by self-induced vomiting or purging of the intestines with laxatives
Short-term starvation
several days of total dietary abstinence.
long-term starvation
AFTER several days of dietary abstinence…causes DEATH
Portal hypertension
abnormally high blood pressure in the portal venous system. Normal pressure is 3mm Hg; portal hypertension is >10mm Hg.
common cause: cirrhosis of the liver
Long term portal hypertension can cause varices, splenomegaly, ascites, hepatic encephalopathy, and hepatopulmonary syndrome.
Portal hypertension manifestations
esophageal varices is the most common
anemia caused by slow chronic bleeding from varices
presence of digested blood in the stools
Ruptured esophageal varices
–causes hemorrhage and voluminous vomiting of dark-colored blood
Ascites
the accumulation of fluid in the peritoneal cavity
look pregnant
common cause: cirrhosis
Cause capillary hydrostatic pressure to exceed capillary osmotic pressure and pushes water into the peritoneal cavities.a
Hepatic Encephalopathy
A complex neurologic syndrome characterized by impaired cerebral function, flapping tremor (asterixis) (flapping of the wrist), and electroencephalogram (EEG) changes.
Develops slowly during the course of chronic liver disease and the development of portal hypertension.
Hepatic Encephalopathy manifestations
Initial manifestations – subtle changes in personality, memory loss, irritability, lethargy, and sleep disturbances
Progressed manifestations – confusion, flapping tremor of the hands (asterixis), stupor, convulsions, and coma*
*coma is sign of liver failure and results in death
Jaundice (icterus)
yellow or greenish pigmentation of the skin caused by excessive accumulation of bilirubin in plasma and tissue fluids – hyperbilirumbinemia (bilirubin concentration exceeds 2.0 mg/dl)
Obstructive jaundice: Extrahepatic obstruction
when common bile duct is occluded (by gallstone, tumor, or inflammation.)
o Bilirubin cannot flow into the duodenum, accumulates in the liver and enters the bloodstream causing hyperbilirubinemia and jaundice
Obstructive jaundice: intrahepatic obstruction
disturbances in hepatocyte function and obstruction of bile canaliculi. Bilirubin cannot enter the intestinal tract and causes build up.
Hemolytic jaundice
(prehepatic jaundice) – excessive hemolysis (destruction) of red blood cells
Jaundice manifestations
Dark urine due to conjugated bilirubin (water soluble).
Light color stools due to complete obstruction of bile flow from the liver to duodenum.
Fever, chills and pain (bacterial inflammation of the liver, e.g. viral hepatitis)
Discoloration in sclera of the eye, then progresses to skin.
Pruritus (itching) due to bilirubin in the skin
Hepatorenal Syndrome
functional renal failure that develops as a complication of advanced liver failure.
Not caused by primary renal disease
Caused by portal hypertension and other circulatory alterations associated with advanced liver disease.
Viral Hepatitis
Viral Hepatitis: relatively common systemic disease that affects the liver
All 5 types (A, B C, D E) can cause acute, icteric illness
pathologic lesions can cause: necrosis, scarring and Kupffer cell hyperplasia
Hep Prodromal phase
2 weeks after exposure and ends w/ appearance of jaundice; marked by fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgesia, cough, and low-grade fever; infection is highly transmissible during this phase
Hep Icteric phase
1-2 weeks after prodromal phase; lasts 2-6 weeks
jaundice, dark urine, clay-colored stools
liver is enlarged–causes pain (actual phase of illness)
hep recovery phase
begins with resolution of jaundice, 6-8 weeks after exposure
symptoms diminish, but liver remains enlarged and tender; back to normal 2-12 weeks after onset of jaundice
Chronic active hepatitis
persistence of clinical manifestations and liver inflammation after acute stages of HBV and HCV infection
Cirrhosis
irreversible inflammatory, fibrotic liver disease–leading cause of death in US; alcoholic liver disease
cirrhosis manifestations
fatty infiltration: no specific symptoms or abnormal liver function test results
liver: usually enlarged
anorexia, nausea, jaundice and edema develop w/ advanced fatty infiltration or onset of alcoholic steatohepatitis
Cholesterol gallstones
form in bile that is supersaturated w/ cholesterol from liver
Pigmented stones:
form from increased levels of unconjugated bilirubin, which binds with calcium
Cholelithiasis (gallstones) manifestations
cholelthiasis: asymtomatic
***abdominal pain and jaundice are cardinal
manifestations of cholelthiasis
vague symptoms: heartburn, flatulence, epigastric discomfort, food intolerances (fat and cabbage)
cause: lodging of one or more gallstones in the cystic or common duct
jaundice=stone in common bile duct
Cholecystitis
acute or chronic = both forms are almost always caused by gallstone lodged in cystic duct
Cholecystitis manifestations
ischemia, necrosis and perforation from pressure against distended wall of gallbladder (decrease in blood flow)
fever, leukocytosis, rebound tenderness, abdominal muscle guarding
serum bilirubin and alkaline phosphatase levels may be elevated
esophageal cancer risk factors
>65 years old, Male Tobacco use Alcoholism Malnutrition Chronic reflux Hiatal hernia Obesity
esophageal cancer manifestations
chest pain
dysphagia
heartburn (pyrosis)
**Esophageal carcinoma is asymptomatic during the early stages and presents at an advanced stage. Esophageal cancer metastasizes rapidly with a poor prognosis.
stomach cancer risk factors
Salty foods
Nitrates-nitrosamines
stomach cancer manifestations
anorexia malaise weight loss upper abdominal pain vomiting Occult blood
colorectal cancer risk factors
Polyps
Ulcerative colitits
Diverticulitis
High carb, high fat, low fiber diets
colorectal manifestations
Pain Mass Anemia Bloody stool Obstruction Distention
liver cancer risk factors
HBV (hep B), HCV (hep C)
Cirrhosis
Intestinal parasite
Aflatoxin from moldy peanuts
liver cancer manifestations
Pain Anorexia Bloating Weight loss Portal Hypertension Ascites Jaundice
pancreatic cancer risk factors
Chronic pancreatitis
Cigarette use
Alcohol
Diabetic women
pancreatic cancer manifestations
Weight loss Weakness Nausea/vomiting Abdominal pain Depression +/- Jaundice Insulin-secreting tumors with s/s of hypoglycemia
