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.