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49 Cards in this Set
- Front
- Back
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largest gland in the body
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the liver
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functions of the liver
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There are 100's but major ones are
1) glucose metabolism 2) AMMONIA conversion 3) protein metabolism 4) fat metabolism 5) Vitamins and IRON 6) Bile Formation 7) Bilirubin Excretion 8) drug metabolism |
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so explain the functions a little
1) glucose metabolism 2) AMMONIA conversion 3) protein metabolism 4) fat metabolism 5) Vitamins and IRON 6) Bile Formation 7) Bilirubin Excretion 8) drug metabolism |
a) Glucose= glycogen- stored in hepatocytes
b) glycogenisis= glycogen back into usable glucose c) gluconeogenesis= glucose made from amino acids/lactate (hypoglycemia) ------------------------------------- -Ammonia is byproduct of gluconeogenesis -also made by bacteria in GI tract w/digestion of protein and blood products *converted into UREA which is excreted in urine --------------------------------------- coagulation factors a) VII, IX, X, b) Prothrombin (w/vit K) c) Albumin --------------------------------------- a) Ketones= result of fatty acid breakdown b) cholesterol and other lipid formation -------------------------------------- A,D,E,K,B12, iron and copper -stored in gallbladder empties into sm intestines -emulsifies fats and stimulates peristalsis --------------------------------------- -bile then reabsorbed in distal ileum *enterohepatic circulation -pigment form hemoglobin breakdown by reticuloendothelial sys (Kupffer) -unconjugated bilirubin=cannot be excr |
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Liver palpation
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-tenderness=acute enlargement (drug induced/acetaminophen most often)
-non tender= chronic enlargement (malnutrition/alcoholism most often) -if very tender can also lightly tap (maybe b4 palpation) *note size (from lower costal margin), tenderness, smooth/nodulare,etc |
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AST or SGOT
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(Serum aminotransferase study)
10-40 (4.8-19 U/L) -primarly elevated with liver damage/trauma |
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ALT or SGPT
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(Serum aminotransferase study)
5-35 (2.4-17 U/L) -present in tissues w/high metabolic activity -can be elevated w/liver, heart, skeletal muscle, and kidney issues |
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increased serum bilrubin
conjugated (direct) |
may be biliary obstruction
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increased serum bilrubin
unconjugated (indirect) |
hemolysis or hepatic damage
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Jaundice
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-can see changes when serum bilirubin is 2.5mg/dL or higher
-hyperbilirubinemia may cause pigment stones in gallbladder -4 major types 1) Hemolytic 2) Hepatocellular 3) Obstructive 4) hereditary hyperbilirubinemia |
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Hemolytic Jaundice
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-RBC are destroyed so fast that liver cannot clear bilirubin
-liver is still functioning but cannot keep up w/the demand -so serum levels of unconjugated bilirubin are high free bilirubin (unconjugated) levels >20-25mg/dL= risk of brainstem damage -high fecal/urine urobilinogen BUT NO bilirubin in urine -no symptoms unless levels are SUPER HIGH |
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Hepatocellular Jaundice
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-DAMAGED liver cells cannot clear bilirubin from blood
- anorexia, nausea, malaise, fatigue, possible wt loss -serum bilirubin and urine urine bilinogen elevated -elevated ALT and AST |
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Obstructive Jaundice
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-occlusion of bile, it backed up in liver, reabsorbed by the blood
*choleststic agents= statis and inspissation of bile d/t the drugs -excreted by urine= deep orange and foamy -light or clay colored stools -puritis, dyspepsia, intolerance to fatty foods -mild elevation of AST, ALT, and GGT -elevated bilirubin and alkaline phosphataste |
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hereditary hyperbilirubinemia
Jaundice |
-Gilbert’s syndrome (no liver damage)
-Dubin-Johnson syndrome (w/pigment) -Rotor’s syndrome (w/out pigment) “benign” cholestatic jaundice of pregnancy retention of bilirubin d/t hormones) |
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Cirrhosis
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-chronic dz characterized by replacement of normal tissue w/ fibrosis
-most often d/t alcohol or low protein diet but has many other factors -insidious onset S/S -hobnail appearance to cirrhotic liver -acute pain d/t stretching of Glisson’s capsule and enlargement (1st) -atrophy and nodular edges (later stages) DX; -decreased serum albumin -elevated serum globulin -elevated serum alkaline phosphatase, AST, ALT, GGT -decreased serum cholinesterase -prolonged prothrombin time 3 types |
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3 types of cirrhosis
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1) alcoholic cirrhosis
2) postnecrotic cirrhosis 3) biliary cirrhosis |
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alcoholic cirrhosis
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AKA Laennec’s (micronodular)
Scar tissue around portal areas –most common |
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postnecrotic cirrhosis
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(macronodular)
Broad bands of scar tissue late result of previous acute viral hepatitis |
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Biliary cirrhosis
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Scarring in liver around bile ducts
-often d/t obstruction/infection (more rare) |
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Child-Pugh classification
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used to evaluate severity of cirrhosis
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Bacterial peritonitis
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AKA spontaneous bacterial peritonitis (SBP)
-may occur w/cirrhosis and/or ascites even in absence of infection -hepatorenal syndrome is most severe complication = renal failure w/out patho changes to kidneys dehydration, obstruction, etc unresponsive to fluid or diuretics |
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Complications of cirrhosis
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Portal hypertension
Ascites Esophageal Varices Hepatic Encephalopathy -Coma Edema/bleeding Vitamin Deficiency(avitaminoses) Glucose metabolism Estrogen Puritus |
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Portal HTN
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increased pressure in portal venous system d/t blood flow obstruction in liver
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Ascites
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-failure of liver to metabolize aldosterone=increased Na and water retention
=Na/water retention, increased intravascular fluid/lymph flow, decreased synthesis of albumin result in 3rd space shifting into peritoneal space LARGE AMOUNTS OF PROTIEN RICH FLUID IN ABDOMEN S/S: -increased abdominal girth (X marks the spot) -weight gain (meaure I+O and daily wt) -SOB -striae and distended veins on abdomen -umbilical hernias -fluid and electrolyte imbalance -flanks buldge in supine position -percussion may yield shifting dullness -fluid wave DIET: -low salt (2g) –careful to avoid ammonia and K * when K goes down=ammonia goes up -liberal use of milk products -avoid alcohol TX: -diuretics (Aldactone-K sparing) -wt loss not to exceed 1-2k w/ peripheral edema or 0.5-0.75 w/out edema -bed rest (upright position=rennin angiotensin alosterone sys activation) -paracentesis (pg1126) w/IV salt poor albumin or other colloid (Y tube 18G+) -TIPS (transjugular intrahepatic portosystemic shunt |
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Patho of Ascites
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Cirrhosis w/ portal hypertension
| splanchnic arterial vasodilation | decreased circulating blood volume | activation of rennin-angiotensisn and sympathetic nervous sys and ADH | kidney retains sodium (water follows) | hypervolemia | persistant activation of systems (Na/water retention/edema/ascites) | continued arterial i=underfilling (cycle repeats) |
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Esophageal Varices
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-varicosities veins/hemorrhoids that drain N2 portal sys d/t increased pressure
-venous blood from intestinal tract seeks alternate path to return to R atrium -prone to rupture and HEMORRAGE -bleeding =increased nitrogen=increased ammonia=increased risk encephalopathy -almost always caused by portal HTN S/S -hematemeis, melena, deterioration in mental and physical status -dilated abdominal veins (caput medusae) -hemorrhoids, ascites -splenomegaly -increased portal venous pressure -SHOCK=cool-clammy skin, hypotension, tachycardia -endoscopy to ID site (hold fluids until gag reflex returns) TX: -estimate circulating blood volume -BP via arterial catheter -O2 -IV fluids w/electrolytes and volume expanders -I+O (catheter) |
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Patho bleeding esophageal varices
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Portal HTN
| pressure gradient of 12mmHg+ between portal vein and inferior vena cava (portal pressure gradient) | venous collaterals develops from high portal sys pressure to systemic veins in esophageal plexus, hemmorrhoidal plexus, and retroperitoneal veins | abnormal varicoid vessels form in any of the above locations | vessles may rupture=LIFE THREATENING HEMORRHAGE |
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Hepatic Encephalopathy and Coma
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AKA portosystemic encephalopathy (PSE)
NEUROPSYCHOLOGIC s/s of liver failure/portal HTN,and shunting of blood 1) inability of liver to detoxify toxic byproducts of metabolism 2) portal-systemic shunting allows portal blood (toxins) to enter systemic AMMONIA= enters brain, stimulates peripheral benzo-type receptors on astrocyte cells, thus increases neurosteriod synthesis=stimulates GABA GABA=depression of CNS S/S: -mental changes and motor disturbance that get worse w/time -confused, unkempt -doll eyes -sleep during day w/insomnia at night (difficult to awaken) -disoriented to place and time -may lapse into frank coma or have seizures -involuntary movements -hyperactive DTR that progress to flaccidness -EEG= generalized slowing, increased amplitude, and TRIPHASIC waves TX: -Neuro status –assessed -monitor serum ammonia -I&O, daily wt -low protein diet (1.0-1.5g/kg)/(vegetable protein if needs <1g) -gastric suction -provide safe environment and normal sleep/wake cycle |
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Asterixis
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AKA as liver flap often seen in stage II
-arm out w/hand help upward, will flap forward then return to normal position -seen w/encephalopathy |
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Constructional apraxia
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-inability to produce a simple figure
(ask to draw same figure everyday) -seen w/encephalopathy |
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Fetor hepaticus
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-sweet, slightly fecal odor to breath
(cut grass/ acetone/ wine) -seen w/encephalopathy |
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Drugs for encephalopathy
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-Lactulose (Cephulac)-reduces ammonia level via BM (2-3 soft/day optimal)
*watery stools may indicate med overdose -IV glucose= minimizes protein breakdown -antibiotics reduce gut bacteria Neomycin, metronidazole (Flagyl), rafaximin (Xifaxan) -Benzodiazeine antagonists –flumazenil (Romazicon) |
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Edema and bleeding w/cirrhosis
why |
-Generalized edema d/t hypoalbuminemia / facial edema is uncommon
-reduced clotting factors may cause bleeding issues TX: -soft bristled toothbrush, electric razors, safety prevention |
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Vitamin Deficiency w/cirrhosis
why |
-fat soluble vitamins and fats d/t reduced bile (salts)
-vit K may cause lack of clotting factors *supplement w/ vit A, B complex, C ,K, and folic acid -use water-soluble forms of fat soluble vitamins if steatorrhea is present |
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s/s of Vitamin Deficiency
Vit A Thiamine Riboflavin Pyridoxine Vit C Vit K Folic Acid |
Night blindness, eye/skin changes
---------------------------------- Beriberi, polyneuritis, and Wernicke-Korsakoff psychosis -------------------------------------- Lesions on skin, MM -------------------------------------- Lesions on skin,MM and neurological changes -------------------------------------- Hemorrhagic lesions and scurvy -------------------------------------- Hypoprothrombinemia=spontaneous bleeding and ecchymoses --------------------------------------- Macrocytic anemia |
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Cirrhosis and estrogen
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-failure of liver to inactive estrogens=
-gynecomastia, amenorrhea, testicular atrophy, loss of pupic hair (men), etc |
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Puritis and cirrhosis
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-puritus d/t retention of bile salts
-spider angiomas (esp above the waist) most often w/cirrhosis -“liver palms” AKA palmar erythema TX: -avoid irritating soaps and adhesive tapes/etc |
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Fulminant Hepatic Failure
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-clinical syndrome of sudden and severe impaired liver F in previously healthy pt
-starts w/jaundice and progresses to encephalopathy -viral hepatitis is a common cause -more deadly but 50% chance of cure Antidotes: -acetominophen= N-acetylcysteine -mushrooms= penicillin |
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Liver abscesses
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2 types:
1) amebic-most common in developing countries d/t poor sanitation 2) pyogenic-less common BUT more common in developed places -fluid filled cavity d/t infection anywhere along GI tract that gets into liver S/S: VAGUE-may just look like the flu but monitor for worsening pain after dx |
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Gallbladder
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-stores BILE (when sphincter of Oddi is closed between meals)
-reabsorbs much of the water so bile becomes concentrated -released when food inters the duodenum *response d/t choleecystokinin-pancreozymin (CCK-PZ) –intestinal hormone |
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Bile
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-emulsifies fats in distal ileum and stimulates peristalsis
-bile then reabsorbed in distal ileum via portal blood and returned o liver =enterohepatic circulation Composed of: H20, Na, K, Chl, bicarb, lecithin, fatty acids, cholesterol, and BILIRUBIN(50%) |
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Exocrine function of Pancreas
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pancreatic enzymes :
-very high in BICARB =neutralize acids in duodenum secretin= stimulates release of BICARB -amylase= carbs -tripsin= proteins -lipase= fats (CCK-PZ)= triggers release of enzymes as does the vagus nerve |
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Endocrine function of Pancreas
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The islets of Langerhans composed of alpha, beta, and delta cells
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Alpha cells
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Secrete GLUCAGON
-effect is opposite of insulin = raises blood sugar by converting glycogen N2 glucose -secreted when blood suagr is low |
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Beta cells
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Secrete INSULIN
-lowers blood glucose by shifting glucose INTO the cells -also promotes storage of fat in adipose cells and protein synthesis -if insulin is low glucose will be excreted in urine (as in DM) -secreted when blood sugar is high |
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Delta cells
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Secrete SOMATOSTATIN
-lowers blood sugar -inhibits release of growth hormone from pituitary and glucagons from pancreas |
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Blood glucose
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60- 100 =WNL
-decreased=insulin -increased =glucagons, epinephrine, adrenocorticosteriods, growth/ thyroid H’s |
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Cholecystitis
Calculous Acalculous |
Inflammation of the gallbladder
-pain, tenderness, rigidity of upper right abdomen -may radiate to midsternal area or right shoulder -may also see N/V and s/s of acute inflammation --------------------------------------- Gall stone obstructs bile flow +bile starts to digest bladder may cause gangrene -any bacterial infections are often enteric in origin -------------------------------------- It’s not a stone causing the obstruction but something else - d/t sx, trauma, burns, multiple blood transfusions, increased bile viscosity |
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Cholelithiasis
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Calculi (gallstones) form from solidified constitutes of bile
-risk increases w/age 2 types: 1) pigment stones -more rare- cannot be dissolved -d/t unconjugated bilirubin -sm. Dark clusters 2) cholesterol -usually cholesterol is dissolved by acids -lrg. Pale yellow s/s: -fullness, abdominal distention, URQ pain, worse after a fatty meal -if distended and touching abdominal wall=pain on deep inspiration -jaundice -dark urine and light stools -vitamin deficiency (ADEK) possible bleeding issues DX: -ultrasound is the best= after fasting to cause distention TX: -cholecystectomy-removal of gallbladder -laproscopic sx prevents paralytic ileus and is more commonly done -low fat diet -avoid alcohol/ gas forming vegetables -meds to dissolve po/injected -shock/pulse therapy |
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Cholelithiasis risk factors
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-5 F’s= fair, fat, forty, female, fertile
-women esp after age 40 -multiple children -obesity -use of estrogen/ birth control -rapid wt loss or frequent changes in wt -DM or cystic fibrosis |
