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204 Cards in this Set
- Front
- Back
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What are the basic functions of the GI tract?
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motility: propulsion and mixing
secretion of digestive juices digestion of nutrients absorption of nutrients |
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In general, _____stimulation increases the activity of the intrinsic nervous system, whereas, _____stimulation decreases its activity.
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parasympathetic, sympathetic
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Strong stimulation of the _____ nervous system can effectively shut down motility in the gut and can block the movement of nutrients through the GI tract.
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sympathetic
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What is dysphagia?
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Difficulty swallowing
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What is achalasia?
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esophageal motility disorder, loss of peristalsis in lower 2/3 plus impaired LES (lower esophageal sphincter) relaxation
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LES dysfunction or tumors
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can’t deliver bolus to the stomach, just sits in esophagus
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What is a stenosis?
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An abnormal narrowing in a blood vessel or other tubular organ or structure
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Causes of Dysphagia
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fibrosis
compression (tumor) diverticulum (undigested food in pouch) congenital atresia congenital tracheoesophageal fistula (some food goes into lungs) neurological damage to nerves 5, 7, 9, 10 and 12 achalasia (sphincter doesn’t work well so food colelcts and can’t get to stomach) |
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oropharyngeal dysphagia
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nasal regurgitation
airway obstruction with eating coughing when swallowing immediate regurgitation hoarse voice |
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esophageal dysphagia
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no airway distress
late regurgitation chest pain at meals frequent heartburn presence of collagen disease |
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esophatitis
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damage to stratified squamous cells from:
lacerations irritants infection iatrogenic injury |
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Gastroesophageal reflux disease
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The backflow of gastric contents into the esophagus through the LES
Any condition or agent that alters the closure strength and efficacy of the LES or increases intra-abdominal pressure (ex. obesity, pregnancy) may predispose an individual to GERD |
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What is Barrett esophagus?
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metaplastic cells replace squamous cells in inferior part of esophagus
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gastritis
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Present with heartburn, indigestion, epigastric distresss
Up to 2/3 will have no identifiable cause One half will have relief from placebo Symptom profile does not differentiate between GERD, PUD, and non-ulcer dyspepsia (functional) (Represents a range: from inflammation to ulceration; PUD) Physical exam is rarely helpful |
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What are the signs and symptoms of PUD?
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epigastric burning pain
gastric- empty stomach or soon after meal duodenal- 2-3 hrs after meal nausea, abdominal upset, chest pain may be asymptomatic; life threatening GI bleeding occurs without warning |
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What are the components of gastric peptic ulcer disease?
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acid + NSAIDS + H pylori
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What are the components of duodenal peptic ulcer disease?
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acid + H pylori
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What is H pylori?
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gram negative flagellated bacillus that resides between epithelial cells and mucus barrier
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The intestines
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Small: nutrient absorption
Large: water absorption |
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Describe constipation.
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colon absorbs water and electrolytes
stool: hard and dry secondary importance is frequency* relieved by changes in diet and exercise |
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What are the four main types of diarrhea?
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secretory
osmotic exudative motility disturbances |
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Describe secretory diarrhea.
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infectious disorder
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Describe osmotic diarrhea.
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lactase deficiency
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Describe exudative diarrhea.
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inflammatory bowel disease
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Who is more prone to ulcerative colitis and Crohn's disease?
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onset in childhood/young adulthood
more common in females, caucasians, eastern european Jewish |
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ulcerative colitis
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involves only the colon and rectum
mucosal layer is affected HALLMARK- bloody diarrhea and lower abd cramps increased cancer risk after 8-10 yrs |
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Crohn's disease
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intermittent bouts of fever, diarrhea, and RLQ pain
may have RLQ mass, tenderness smoking is strong factor can affect any portion of GI tract |
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bowel obstruction
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pain, distention, vomiting, impaired venous return
small bowel: less urgent/most common large bowel: urgent, danger of cecal perforation/rupture |
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hernia
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intestine protrudes through defect in the inguinal wall of peritoneum into a serosal sac
if blood supply compromised, lead to infection and necrosis |
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What are the most common sites of volvulus (twisting obstruction)?
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cecum and sigmoid colon
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What is intussusception?
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Intestine folds back on itself, mainly caused by tumors
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celiac disease
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gluten sensitivity
genetic + environmental agents gluten is broken down and releases gliadin that sets off the immune response damaged epithelial later allows gliadin to cross into bowel |
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What is diverticulitis?
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microperforation with peridiverticular inflammation
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Who is prone to diverticulitis?
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elderly with LLQ pain, severe constipation, nausea, fever
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Diverticulum
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A single pouchlike herniation through the muscular layer of the colon. Plural = Diverticula
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Diverticulosis
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The presence of one or more diverticula
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Diverticulitis
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Inflammation of one or more diverticula
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Diverticular disease
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Complications related to the presence of diverticuli
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What does the gall bladder do?
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stores and concentrates bile
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What does bile do?
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helps digest fats
helps get rid of cholesterol, bilirubin, and other waste products |
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What is cholecystitis?
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95% associated with stone in cystic duct, often obese female, fever, RUQ pain with scapular or epigastric pain, colicky, nausea and vomiting
Treatment- prompt cholecystectomy (gall bladder removal) |
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acute pancreatitis
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reversible parenchymal injury and inflammation of pancreas
associated with ETOH and stones it is severe epigastric and back pain, nausea, vomiting, steatorrhea |
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Acute pancreatitis can be extremely severe producing systemic inflammatory response leading to:
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disseminated intravascular clotting
acute respiratory distress peripheral vascular collapse death |
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conditions predisposing to pancreatitis
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gallstones, biliary sludge and microlithiasis, alcohol
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pancreatitis
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edema, fat necrosis, acute inflammation and enzyme destruction of tissue and blood vessels; likely autodestruction by inappropriate enzymes activity – probably trypsin
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chronic pancreatitis
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inflammation of pancreas
irreversible destruction of tissue fibrosis and destruction of exocrine pancreas insufficiency, loss of enzymes |
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appendicitis
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obstructions by fecalith (fecal stone) or worms inflammation
inflammation can lead to necrosis, abscess formation and peritonitis |
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appendicitis
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RLQ pain (McBurney's point)
nausea and vomiting fever diarrhea |
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McBurney’s Point
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when you press on this area and lift it up, the pain is worse, NOT ALWAYS PRESENT IN ALL CASES
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Tension
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Spasm, associated with intense peristalsis (irritant, infection, obstruction)
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Ischemia
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Intense constant pain (bowel strangulation, volvulus adhesion)
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inflammation
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First localized to serosa covering inflamed part then extends to abdominal wall causing reflex muscle spasms (rigidity, involuntary guarding)
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Types of acute abdominal pain
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Tension, ischemia, inflammation
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Localization of stomach/duodenum pain:
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mid-epigastric
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Localization of small bowel:
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periumbilical
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Localization of colon:
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low abdomen, midline
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Localization of rectum
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sacrum and perineum
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Localization of gallbladder
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mid-epigastric radiates to RUQ or right scapula
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Localization of pancreas
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mid-epigastric radiates to back
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Localization of appendix
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RLQ, but variable
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Liver’s function as a digestive organ
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bile salt secretion for fat digestion; processing and storage of fats, carbs, and proteins absorbed by the intestines; processing and storage of vitamins and minerals
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Liver’s function as endocrine organ
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Metabolism of glucocorticoids, mineralocorticoids, and sex hormones; regulation of carbs, fat, and protein metabolism
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Liver’s function as hematologic organ
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Temporary storage of blood; synthesis of bilirubin from blood breakdown products; hematopoiesis in certain disease states; synthesis of blood clotting factors
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Liver’s function as excretory organ
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Excretion of bile pigment; excretion of cholesterol via bile; urea synthesis; detoxification of drugs and other foreign substances
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jaundice
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inadequate bile synthesis, flow is obstructed
increased bilirubin (>3 mg/dl) normal .2-1.2 increased RBC breakdown impaired liver uptake of bilirubin impaired excretion of bilirubin |
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indirect bilirubin
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unconjugated
elevated with increased RBC breakdown or impaired liver uptake bound by albumin so no urine bilirubin |
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direct bilirubin
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conjugated
elevated with impaired excretion of bilirubin from liver water soluble, so is found in urine |
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Three types of jaundice
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Prehepatic
Hepatic Posthepatic |
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hemolysis, hematoma reabsorption in mild liver disease, and is characterized by high levels of unconjugated/indirect bilirubin?
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prehepatic jaundice
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any dysfunction in liver cells that disrupts bilirubin metabolism, viral hepatitis, cirrhosis, and is characterized by high levels of conjugated/direct bilirubin?
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hepatic jaundice
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mechanical obstruction of bile ducts, viz tumors and gall stones, and is characterized by conjugated bilirubinemia?
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posthepatic jaundice
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anything that obstructs flow to liver - thrombosis or splenomegly
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pre-hepatic portal hypertension
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What is cirrhosis in relation to portal hypertension?
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intra-hepatic portal hypertension
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What is right heart failure, hepatic vein outflow?
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post-hepatic portal hypertension
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portal hypertension
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acites
esophageal varices splenomegaly |
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What are gastroesophageal varices?
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Uncontrolled bleeding, “caput medusae” ascites
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What is the etiology of acute liver failure?
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Exposure to hepatotoxin or its metabolite (less common than chronic)
Acetomenophen Hepatitis A or B Necrosis occurs |
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cirrhosis of the liver
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12th most common cause of death in US
loss of hepatocellular functions obstruction to blood flow from the gut |
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causes of cirrhosis of the liver
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chronic alcohol use
biliary (obstruction in bile drainage) postnecrotic (viral, toxic hepatitis) cardiac (right heart failure, liver congestion) |
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chronic alcoholic liver disease
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15-20% alcholics develop it
men >4-6, women >3-4 drinks a day fatty liver, hepatitis, cirrhosis |
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hepatic encephalopathy related to chronic alcoholic liver disease
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altered mental status due to accumulation of toxins (NH3)
GI bleed, drugs, increased shunting of blood around liver very bad sign |
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Muscular dystrophy
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Group of genetic disorders
Progressive degeneration and necrosis of muscle fibers Necrotic muscle replaced with fat and connective tissue = enlarged “muscle” -pseudohypertrophy |
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Duchenne’s
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Most common muscular dystrophy
1 in 3500 live male births x-linked recessive trait absence of dystrophin/mutation |
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Manifestations of Duchenne’s
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Normal at birth
Postural muscles weak/problems Confined to wheelchair usually by age 7-12 Respiratory/cardiac muscle involvement Cardiomyopathy; death in early adulthood |
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Myasthenia gravis
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Autoimmune disorder, antibody mediated loss of acetylcholine receptors from neuromuscular junction
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Botulism
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Blocks Ach release, causes paralysis, 50% mortality rate, botox
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Herniated discs
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Structure makes disc able to change shape while absorbing shock during movement
With dysfunction, nucleus prolposus can squeeze out through the annulus or herniated |
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What are three types of spina bifida
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Occulta, meningocele, cystic
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Spinal cord injury
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Severe flexion/extension injury: more common in cervical vertebrae
Compression: common in thoraco-cervical area (bones shatter, squash, burst) |
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Spinal shock
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Immediate response to any spinal injury
Flaccid paralysis; loss of tendon reflexes below injury Absence of visceral/somatic sensations below injury Loss of bowel and bladder function Thermal instability Loss of sympathetic vasomotor tone |
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Consequences of pain
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Affects the immune system
Decreases immune function Decreases the number and activity of natural killer cells |
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Consequences of pain in respiratory/pulmonary system
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Reflex muscle spasm: splinting
Decreases: vital capacity, functional residual capacity, alveolar ventilation Results in atelectasis- pneumonia, hypoxemia |
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Consequences of pain in cardiovascular system
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Sympathetic over-activity
Increases HR, less O2 to heart, peripheral resistance, BP, cardiac output and O2 use Results in hypoxemia, ischemia- heart, periphery\ |
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Psychological consequences of unrelieved pain
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Fear, anxiety, helplessness, hopelessness, distress, decreased will to live, suffering, depression, fear
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What is the new model for pain?
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Focus on cure of pain (treat injury, disease, or illness) and on preemptive analgesia (prevent or palliate all pain)
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4 types of neuronal axons in transduction/nociceptive pain
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A alpha, A beta, Delta, C
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Which nociceptive chemicals activate PAN
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K+, H+, Serotonin, Bradykinin, Histamine
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Which nociceptive chemicals sensitize PAN
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Leukotrienes, prostaglandins, substance P
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Which neuropathic chemicals activate PAN
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Norepinephrine
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Which neuropathic chemicals sensitize PAN
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Prostaglandins, substance P
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Describe neuropathic pain
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Unpleasant burning or searing, deep aching, paroxysmal brief shooting or stabbing pain, all in the absence of any apparent injury
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What are three cardinal symptoms of neuropathic pain?
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Spontaneous pain, hyperalgesia, and allodynia
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What is allodynia
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Pain is experienced after a nonnoxious stimulus
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Types of neurons in the dorsal horn of the spinal cord
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Excitatory interneurons, inhibitory interneurons, projection cells
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What parts function to serve and protect the brain?
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Skull and meninges (dura mater, arachnoid, and pia mater)
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What is the function of the cerebral ventricles
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nutrition, homeostasis, and protection
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What are the functions of the medulla?
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Direct extension of spinal cord
Regulates HR, resp., and BP Nuclei of cranial nerves 6-12 Pyramid deussation 5-HT nuclei sleep-wake cycle |
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What are the functions of the pons
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massive relay between cerebellum and cortex
cranial nerve V NE and 5 – HT nuclei Pyramidal tract |
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What are the functions of the midbrain?
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Cranial nerves II, III, IV
Dopamine nuclei Superior colliculus- vision Inferior colliculus- hearing Large motor tracts |
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Function of diencelphalon – thalamus
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receives almost all afferent sensory flow
receives some efferent motor info topographically organized |
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Function of diencephalon – hypothalamus
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regulates ANS
maintains homeostasis- osmotic pressure, temp regulation putative site of biological shock |
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Function of cerebellum
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precise muscle contraction
balance coordination |
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What are symptoms from damage of upper motor neurons?
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Spasticity and flexion deformities (MS, CVA)
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What are symptoms from damage of lower motor neurons?
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Flaccidity (polio)
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Where are all the upper motor neurons located in the spinal cord?
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Rostral/anterior to the spinal cord ventral horn
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Where are all the lower motor neurons located in the spinal cord?
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Ventral horn of spinal cord to periphery
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Function of basal ganglia
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initiation and control of movement
projects to premotor cortex extrapyramidal some cognitive function provide information to descending motor signals |
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Hippocampus deals with?
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Learning and spatial memory
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Amygdala deals with?
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Memory and appropriate behavior
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12 cranial nerves
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olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, acoustic, glossopharyngeal, vagus, spinal accessory, hypoglossal
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blood brain barrier
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specialized endothelial cells in brain capillaries
develops in newborns around 2-3 months effective lipid soluble barrier |
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Characteristics of electrolytes
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dissociate in solution
formed charged ions; cations and anions |
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Characteristics of non-electrolytes
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do not dissociate in solution
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What is osmosis?
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The movement of water across a semipermeable membrane; water moves down a concentration gradient towards areas of higher solutes through aquaporins
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What is serum osmolality?
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The osmotic pressure of a solution expressed in osmols or milliosmoles per kilogram of water
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What is osmolarity?
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The osmotic pressure of a solution expressed in osmoles or milliosmoles per liter of the solution
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What are the causes of isotonic fluid/saline deficit?
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Diarrhea
Hemorrhage Kidney conditions that cause loss of sodium and water Evaporation and skin damage |
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What are the causes of isotonic fluid/saline excess?
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Inadequate Na+ and H2O elimination
Excessive Na+ and water intake in relation to output Excessive fluid intake Seen in kidney failure and CHF |
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What are the causes of hypernatremia?
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Excessive water loss
Decreased water intake; heat stroke Excessive sodium intake Sodium > 145 mEq/L |
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What are the causes of hyponatremia?
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Sodium loss or water gain
Inadequate sodium intake Sodium < 135 mEq/L |
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What is hypotonic/dilutional hyponatremia?
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Caused by water retention
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What is serum potassium?
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Predominantly intracellular
Largely in muscle Obtained from dietary sources Largely excreted by kidney |
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What is the function of serum potassium and excitable cells?
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Regulates resting membrane potential
Controls opening of sodium channels during action potential Regulates membrane repolarization |
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What is the resting membrane potential (RMP)?
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Ratio between ICF and ECF K+ concentration
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What are the EKG changes from hypokalemia?
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PR prolongation
Depressed S-T segment Low T wave Prominent U wave Leads to ventricular ectopy; fatal rhythms |
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What are the EKG changes from hyperkalemia?
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PR interval prolonged
Low P wave Widened QRS Peaked T wave Leads to conduction delays: ventricular fibrillation |
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What 3 forms do ECF calcium exist?
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Protein bound, complexed, and ionized
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What are the roles of calcium?
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Enzyme reactions
Stabilizes membranes and neuronal excitability Muscle contraction Release of hormones, neurotransmitters Cardiac contractility and automaticity Blood coagulation |
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What are the signs/symptoms and manifestations of hypocalcemia?
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Increased neuromuscular excitability
Cramps, seizure Hypotension, heart arrhythmias Failure to respond to drugs that act through calcium-mediated mechanisms |
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What causes hypercalcemia?
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Increased intestinal absorption
Weakness, lethargy, CNS depression Increased bone resorption (hyperparathyroidism, malignant neoplasms) Decreased/inability of elimination Hypertension, AV block |
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Hypercalcemic crisis?
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Acute increase in serum calcium
Due to malignancies and hyperparathyroidism Polyuria, excessive thirst, fever, altered levels of consciousness, disturbed mental state, cardiac arrest, death |
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What are the principles of acid-base balance?
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Hydrogen ions are necessary for normal functioning
Slight changes in H+ concentration significantly alters functioning The body closely regulates pH |
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pH is maintained by what buffering systems?
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Phosphate buffering
Protein buffering (hemoglobin) Bicarbonate buffering system* pH is maintained by the lungs and the kidneys |
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in the body, pH is viewed as the ratio between what?
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Bicarbonate ions and carbonic acid molecules; this is a buffering system
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the ratio of bicarbonate ions to carbonic acid molecules is what?
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20:1 whenever possible
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when the absolute values change, but the ratio remains 20:1, we say that the body is ___ for the imbalance?
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Compensating
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kidneys regulate ___
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bicarbonate and H+
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lungs regulate ___
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CO2
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interpreting ABGs
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normal: pH = 7.4, resp CO2 = 40, metabolic HCO3- = 24
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Demyelination or axonal degeneration of multiple peripheral nerves.
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polyneuropathies
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polyneuropathies (causes)
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Causes: immune mechanisms (Guillain-Barre), toxic agents (arsenic, lead, alcohol), metabolic diseases (diabetes mellitus).
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polyneuropathies
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symmetric sensory, motor, or mixed sensorimotor deficits
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Guillian Barre Syndrome
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Acute, life threatening peripheral neuropathy
Most common cause of acute, flaccid paralysis in developed nations (now that polio is eliminated) Rapidly progressing ascending limb weakness and loss of tendon reflexes. |
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Guillian Barre Syndrome
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Etiology: immune hypersensitivity that demyelinates nerves.
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Guillian Barre Syndrome
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sensory- paresthesia, numbness, tingling
ANS- postural hypotension, arrhythmias, sweating, urinary retention motor: ascending muscle weakness respiratory paralysis |
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Amyotrophic lateral sclerosis (ALS)
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non-inflammatory, premature aging of upper and lower motor neurons
Middle to later life – death 2-5 years Upper and lower motor neurons affected. Death lower motor neurons leads to denervation atrophy of muscles (amyotrophy); scarring of lateral columns of white matter in SC = lateral sclerosis |
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Amyotrophic lateral sclerosis (ALS)
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Manifestations
Sensory: none Motor: weakness, spasticity, stiffness and impaired fine motor control (UMN) Motor: fasciculations, weakness, atrophy, hyporeflexia, muscle cramps in distal legs More advanced: dysphagia, impaired chewing, speech Respiratory: weak muscles, aspiration |
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Herniated discs
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Location: intervertebral; most critical component of spinal column for load bearing.
Nucleus Pulposus: the soft gelatinous center Annulus fibrosis: the strong, ringlike collar of fibrocartilage that circles the nucleus propulsus |
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Herniated discs
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Manifestations:
Lumbar: Sciatic pain: down back of leg and bottom of foot Intensified by coughing, sneezing, straining, bending Slight motor weakness, paresthesias, tingling Cervical: Pain; may be lateral or midline |
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neural tube disorders
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Abnormal formation or closure of the neural tube
Can affect neural tissue, menninges, muscle, skin, vertebral column 1 in 1000 live births. |
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no symptoms; may have a dimple with hair in it
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Spina bifida occulta
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spina bifida
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Symptoms due to cord abnormalities and infections of the cord.
Motor and sensory dysfunctions in lower limbs Disturbances in bowel and bladder function. |
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spinal cord injury
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Fracture or dislocation of vertabrae that cause injury to the vertebral column or supporting ligaments as well as spinal cord.
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spinal cord injury
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Causes: most injuries a combination of compressive force and bending
Fracture or dislocation of vertabrae: gun shot, car accident Severe flexion/extension injury: head struck from behind or backward. Compression: high velocity blow to the top of the head. |
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Name the types of pain.
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acute, chronic, malignant vs. nociceptive and neuropathic
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nociceptive pain
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Pain resulting from activation of primary afferent nociceptors by mechanical, thermal or chemical stimuli.
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neuropathic pain
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Pain resulting from damage to peripheral nervous or central nervous system tissue or from altered processing of pain in the central nervous system.
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What is the new model for pain?
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focus on cure of pain and on preemptive analgesia
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What are the 4 major steps in the "pain process"?
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1. transduction
2. transmission 3. modulation 4. perception |
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Conversion of a stimulus (mechanical, thermal, chemical) to a neuronal action potential.
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transduction
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What are the ABC's of Pain?
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affective dimension- emotions
behavioral dimension- expression of pain cognitive dimension- beliefs, attitudes, meaning physiological-sensory dimension- pain mechanisms |
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Describe nociceptive pain
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sharp, intense, cutting, burning, acute
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transduction of neuropathic pain
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Unrelieved, persistent noxious stimuli, damage to nerve tissue, and reorganization of the way the central nervous system processes nociception.
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What are the three stages in transmission of nociceptive stimuli?
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projections to CNS
dorsal horn processing propagation through CNS |
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dorsal horn NMDA receptors
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Spread diffusely over dorsal horn
Facilitate pain transmission Activation threshold unchanged for high threshold nociceptive & WDR nociceptive projection cells Central (secondary) hyperalgesia Ketamine reverses NMDA receptor |
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Serum osmolality equation
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(Na+ x 2) + (glucose/18) + (BUN/2.8)
normal range about 230-300 mOSm/kg/liter of water. |
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tonicity
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The tension that effective osmotic pressure exerts on cell size through movement of water across the cell membrane.
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manifestations of isotonic fluid deficit
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- acute weight loss
- compensatory increase in ADH - increased serum osmolality - decreased vascular volume - decreased extracellular fluid volume - impaired temperature regulation |
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manifestations of isotonic fluid excess.
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- acute weight gain
- increased interstitial fluid volume - increased vascular volume |
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manifestations of hypernatremia.
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- elevated serum Na+, serum osmolality, BUN, hematocrit
- thirst and increased ADH - intracellular dehydration - hyperosmolality of ECF; neuron dehydration - extracellular dehydration; decreased vascular volume |
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manifestations of hyponatremia.
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- low serum Na+
- hypo-osmolality: fluid moves into neurons - gastrointestinal |
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insulin, hypokalemic.
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When you give _____, the acidosis is corrected, but the kidney has already excreted the K+ to prevent hyperkalemia, so the patient may become _____.
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manifestations of hypokalemia.
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- impaired ability to concentrate urine
- gastrointestinal: anorexia, nausea, vomiting, constipation - neuromuscular: muscle flabbiness, weakness, fatigue, cramps and tenderness; paresthesias and paralysis - cardiovascular: postural hypotension; increased sensitivity to digoixin; EKG changes; dysrhythmias - CNS: confusion, depression - acid-base: metabolic alkalosis |
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manifestations of hyperkalemia.
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- gastrointestinal: nausea, vomiting, diarrhea, intestinal cramps
- neuromuscular: paresthesias = first sign; weakness, dizziness; muscle cramps - cardiovascular: changes in EKG; risk of cardiac arrest |
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What are the arterial blood gas norms for pH, PaCO2, HCO3-?
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7.35-7.45
35-45 mmHg 22-26 mEq/L |
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What is acidemia?
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arterial blood pH of less than 7.35
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What is acidosis?
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a systemic increase in [H+]
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What is alkalemia?
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arterial blood pH of greater than 7.45
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What is alkalosis?
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a systemic decrease of [H+]
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respiratory, metabolic
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Acid-base imbalances have either a _____ or _____ cause.
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acid accumulation or loss of bicarbonate.
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What is the cause of metabolic acidosis?
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metabolic acidosis
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S/sx: - CNS depression
- headache - cardiac dysrhythmias - Kussmaul resps (compensation) |
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lungs excrete more CO2 (fast)
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What is the compensation for metabolic acidosis?
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acidosis
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An increase in serum K+ is?
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alkalosis
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A decrease in serum K+ is?
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What is the cause of metabolic alkalosis?
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accumulation of bicarbonate or acid loss
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metabolic alkalosis
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S/sx: - CNS irritability
- cardiac dysrhythmias (slow, shallow resp compensation) |
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lungs retain more CO2 (fast)
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What is the compensation for metabolic alkalosis?
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decreased alveolar ventilation
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What is the cause of respiratory acidosis?
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respiratory acidosis
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S/sx: - CNS depression
- headache - cardiac dysrhythmias |
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kidneys increase HCO3- (slow)
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What is the compensation for respiratory acidosis?
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What is the cause of respiratory alkalosis?
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increased alveolar ventilation
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respiratory alkalosis
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S/sx: - CNS irritability
- lightheaded - cardiac dysrhythmias |
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kidneys excrete more HCO3- (slow)
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What is the compensation for respiratory alkalosis?
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