Module 4: Problems of Metabolic Function Flashcards
The Liver: General Overview + Functions (7)
The liver is in the RUQ of the abdomen, and, its functions include:
- Producing bile
- Synthesis of proteins (i.e., albumin – responsible for osmotic pull)
- Detoxifies blood
- Converts glucose to glycogen
- Clearance of bilirubin
- Regulates clotting
- Metabolizes fat, protein, and CHO’s (and lots of medications)
Liver Disease: Assessment
History*:
- Risk for Hepatitis A, B, C
- Alcohol & Drug Use (but, not everyone w/ liver disease has hx of alcoholism!!)
- Sexual history
- Tattoos? (r/t risk for Hep C)
- Biliary tract disorders?
- Blood transfusions?
- Obesity
- Lipids – fatty liver
- Liver injury (i.e., sepsis, large amt. of tylenol)
Physical:
- Fatigue
- Weight changes + GI problems (i.e., vomiting, inability to eat)
- Abdominal pain
- RUQ tenderness
- Bruising & Petechiae (r/t enlarged spleen; destroying platelets)
- Palmar erythema (redness on palms of hands; hormonal)
- GI Bleeding
- Jaundice – r/t build-up of bilirubin! (early s/s!)
- Ascites
- Spider angiomas – inactive hormone circulating in bloodstream
- Caput Medusae – r/t formation of collateral circulation
- Peripheral edema (r/t third spacing)
- Hypotension – protein and fluid leaking out of vasculature; not enough fluid!!
- Asterixis (“flapping hand tremors”)
- Fetor hepaticus (fruity or musty breath)
- Amenorrhea (women)
- Gynecomastia
- Impotence (i.e.. Erectile dysfunction)
- Mental state/Neurological assessment
Liver Disease: Labs
- ALT & AST** (elevated; Messer said, “normal later on in disease” – normal: ALT 7-56 U/L, AST 5-40 U/L)
- AST/ALT ratio (> 1 for alcoholic liver disease)
- Bilirubin** (elevated; normal: 0.1-1.2mg/dL)
- Albumin (low; normal: 3.4-5.4g/dL) – edema
- Platelets (low; normal: 150,000-450,000/uL)
- Lactate Dehydrogenase (LDH)
Liver Disease: Diagnostics
- Ultrasound*
- MRI
- CT
- X-ray
- Biopsy – tricky in the setting of liver failure; huge risk of bleeding!
- EGD – screening for esophageal varices??
- ERCP
Liver Disease: Cirrhosis – General Overview
General Overview
- Widespread scarring throughout liver caused by inflammation – toxins or disease destroy hepatocytes(!!)
- Scar tissue (fibrotic tissue) produce nodules; forms throughout liver –> Blocks blood flow and bile ducts; inability of blood to move through
- Disease usually develops slowly – person is typically not aware they have cirrhosis until symptoms occur, late in disease (+ permanent – too late!)
Various Types of Cirrhosis
- Post-necrotic cirrhosis (i.e., Hepatitis C (or other viral hepatitis); Drug induced (i.e., Tylenol poisoning))
- Laennec’s cirrhosis (i.e., Chronic alcoholism – persistent damage to liver)
- Biliary cirrhosis (i.e., Biliary obstruction; Autoimmune disease)
Compensated v. Decompensated Disease…
- Compensated Disease: Scarring is present but liver can still function; may be able to avoid progression of disease
- Decompensated disease: liver failure with symptoms; too late for change(!!)
Complications of Cirrhosis:
- Portal Hypertension
- Ascites
- Esophageal Varices
- Hepatic Encephalopathy
- Hepatorenal Syndrome
- And, coagulation problems (high risk of bleeding!!), jaundice, and peritonitis*
Liver Disease Complication: Portal Hypertension
- Portal Vein (PV) brings nutrients and toxins from GI tract (and spleen, pancreas and gallbladder) to liver – liver full of nodules, so blood has hard time moving through (leads to pressure in PV!!)
- Increase in pressure in portal vein (> 5 mmHg(!!))
- Blood meets resistance as it tries to flow through liver and backs up into spleen, esophagus(!!), stomach, intestines, abdomen and rectum
- Veins from these areas become dilated; leads to splenomegaly –> thrombocytopenia
- Causes new vessels to form, allowing blood to bypass liver (collateral circulation)
- Allows unfiltered blood to enter circulation(!!) – no bueno!!
Liver Disease Complication: Ascites
- Collection of fluid in peritoneal cavity –> Increased hydrostatic pressure from portal hypertension(!!)
- Plasma protein leaks out of vessels (less plasma protein in blood) – fluid follows plasms protein + builds up in abdomen
- Liver unable to produce albumin appropriately; low albumin levels
- Can cause renal vasoconstriction (big culprit of hepatorenal syndrome!)
Assessment
- Measure abdominal girth
- Daily weights(!!)
- Breathing – ascites can put pressure on lungs
- Balance – impacts posture/center of gravity
- Assess for abdominal and inguinal hernias (r/t increased pressure)
Ascites/Fluid Shifts: Interventions
Nutrition
- Sodium Restriction (1-2 grams)
Paracentesis
- Catheter inserted into peritoneal cavity to remove fluid
- Ultrasound guided
- Tunneled ascites drain (if fluid needs to be removed on regular basis!)
Concern r/t Paracentesis: Spontaneous Bacterial Peritonitis(!!) – Complication Risk
- Lacks an obvious source; fluid harboring bacteria
- Symptoms can be vague and less obvious than “normal” peritonitis (never really normal): low-grade fever, loss of appetite, pain (not usually as severe as “normal” peritonitis), abdominal rigidity, mental status changes, decreased/no bowel sounds
- Interventions: Diagnostic Paracentesis + ABX(!!)
Respiratory Interventions (b/c ascites places pressure on lungs –> Hepatopulmonary syndrome; dyspnea)
- Assess and manage(!!) – HOB elevated, Oxygen therapy
Vitamin Supplements
- Multivitamins
- Thiamine
- Folate
Medications
- Diuretics (a tricky balance! – check elec., get those daily weights!)
Liver Disease Complication: Esophageal Varices
- Caused by portal hypertension (backflow into esophageal vein)
- Esophageal varices become distended and tortuous (WEAK)
- Bleeding from esophageal varices can quickly lead to death; an EMERGENCY(!!) –hematemesis, melena (blood in stool)
- Bleeding may be caused by irritating factors (i.e., heavy liftin’ exercise, dry/hard food, stickin’ tubes down), or, bleeding may occur spontaneously/without aggravation(!!)
Esophageal Varices: Interventions
Screening for varices(!!) – Endoscopy
If varices are present, prevent bleeding(!!)
- Beta Blocker therapy – typically propanol/metoprolol; reduce pressure in portal vein! – Reduces HR and hepatic venous pressure (reduces risk of bleeding)
Managing Bleeding – Bleeding varices causes rapid blood loss –> EMERGENCY; STOP THE BLEED!!
- Endoscopic intervention ASAP (i.e., Ligation – Banding; Sclerotherapy – not used as frequently)
-Balloon Tamponade – Blakemore tube – only used for emergencies; pt. should be on ventilator!; Can potentially cause aspiration and/or esophageal perforation(!!)
- TIPS: Transjugular Intrahepatic Portal-Systemic Shunt – a shunt that bypasses the liver(!!); Performed in Interventional Radiology “IR” – Jugular vein accessed; connects the portal vein to the hepatic vein –> shunts blood from portal vein to hepatic vein (decreases pressure)
Bleeding Support – dump fluids, blood products, and vasopressors
- Vasopressors(!!) – enabling blood to perfuse organs
- Ocreotide – reduces glucagon; allows for less blood flow to GI organs
- IV Protonix
- Fluids(!!)
- Blood products(!!)
- Antibiotics – most GI bleeds for pt. w/ liver failure are precipitated by an infection(!!); know this!
Liver Disease Complication: Hepatic Encephalopathy
Cognitive disorder resulting from liver failure; build up of ammonia (NH3)**; reversible, if caught EARLY!!
May be precipitated by:
- GI bleed
- High protein diet (excess ammonia)
- Infection
- Hypovolemia (r/t third spacing – fluid leaving the vasculature)
- Hypokalemia
- Constipation* (not excreting ammonia from body!)
Signs & Symptoms – Early v. Late
Early Signs:
- Sleep disturbances
- Mood disturbances
- Mental Status changes
- Speech problems
Late Signs
- Altered LOC
- Altered cognition
- Neuromuscular problems
- Coma**
Hepatic Encephalopathy: Interventions
Likely due to ammonia build-up (and other byproducts of protein metabolism); formed in GI tract
- Moderate protein diet (Moderate fats, CHO’s)
- Lactulose(!!) – promotes excretion of ammonia in stool (if pt. can’t drink it, it is given via enema); monitor for skin breakdown, hypovolemia (daily weights, hydration), hypokalemia (monitor potassium)
- Rifaximin (intestinal antiseptic) – destroys normal gut flora + decreases rate of ammonia production
Liver Disease Complication: Hepatorenal Syndrome
Renal vasoconstriction (caused by ascites!!)
Often triggered by
- GI Bleed
- Hepatic encephalopathy
Poor prognosis – often leads to death (renal failure on top of liver failure)
Decreased urinary output (< 500 ml/day)
Elevated Creatinine and BUN
Liver Disease: Goals of Care
- Maintain adequate circulation
- Decrease ascites – keep fluid in veins + arteries(!!)
- Decrease edema
- Prevent respiratory complications from ascites
- Prevent bleeding(!!)
- Cholecystitis: General Overview
Inflammation of the gallbladder (almost ALWAYS caused by gallstones!)
Calculous v. Acalculous:
- Calculous: Chemical irritation and inflammation from gallstones(!!) – block bile duct, cystic duct or gallbladder neck; bile backs into the gallbladder and irritates wall of gallbladder; Ischemia & Infection –> Perforation –> Peritonitis (rigid/board-like)
- Acalculous: Inflammation/No gallstones; Anatomic issues (i.e., kink in neck of gallbladder) and/or flow issues
- Acute + Chronic Cholecystitis: Assessment
- History (focus on pain!)
- Diet (high fat? low fiber?)
- Family/Genetic
- GI symptoms: Abdominal Pain (RUQ); May radiate to right shoulder, rebound tenderness/general abdominal tenderness
- Biliary Colic – stone moving through duct; severe pain - N/V
Assessment r/t Chronic Cholecystitis (less common!!)
- Jaundice
- Clay-colored stools
- Dark Urine
- Fatty stools
- Fever (can also be present w/ acute cholecystitis!)
- Cholecystitis: Diagnostics – Labs + Imaging
Labs
- WBC’s (elevated)
- ALT/AST (liver enzymes – elevated)
- LDH
- Bilirubin
- Amylase & Lipase (increased w/ pancreas involvement)
Imaging
- Abdominal X-Ray (visualize stones, if calcified)
- Ultrasound – identify inflamed gallbladder
- HIDA Scan – bile flow
- ERCP
- MRCP (non-invasive)
Cholecystitis: Interventions
Cholecystectomy (very common!!)
- Laparoscopic is preferred method (AKA Lap Chole)
- Removal of the gallbladder, closure of the cystic duct
- Usually same-day surgery; monitor closely – very common for pt. to feel bloating and right shoulder pain for several days afterwards; walk it off!!
Avoid high-fat foods (in excessive amounts!) – be aware of fat consumption
IV fluids
Drug Therapy
- Opioid pain medication
- NSAIDS (but, potential for GI bleeding!)
- Antiemetics (if appropriate)
Other Options (if not candidate for surgery!)
- Ursodiol/Actigall w/ routine imaging to monitor gallstones
- Extracorpeal shock wave lithotripsy – shakes stones until they break down; many cause flank bruising
- Percutaneous biliary catheter – internal or external; divert bile from liver to duodenum (internal) or to drainage bag (external)
The Pancreas: General Overview + Functions
Endocrine: Produces hormones that regulate blood sugar (insulin, glucagon)
Exocrine(!!): Produces enzymes that help digest our food (amylase - break down of carbs, lipase - break down of fats, protease - break down protein)
So, what happens with the pancreas CAN’T do its job?
- Can’t regulate blood sugar
- Can’t digest food(!!) – leads to “icky belly” (r/t autodigestion of food): bloating, flatulence, diarrhea, foul melling/oily stool (r/t fat released into stool), malnutrition and weight loss (r/t inability to digest food)
Acute Pancreatitis: Pathophysiology
Inflammation of the pancreas
Premature activation of pancreatic enzymes (activated in the pancreas instead of in the intestine)
- These are powerful enzymes(!!); they digest the pancreas (b/c pancreas is not able to handle activated enzymes).
Can be mild or severe – Necrotizing Hemorrhagic Pancreatitis
- Lipolysis –> fatty acids are released and combine with ionized calcium (critically low Ca)
- Proteolysis –> thrombosis and gangrene of pancreas
- Necrosis of blood vessels (via elastase) –> bleeding
- Inflammation –> Leukocytes gather to fix these problems –> pus formation
Acute Pancreatitis: Causes
- Biliary tract disease (gallstones)/Gallbladder disease** – better prognosis(!!)
- Trauma (surgery)
- Alcoholism** – worst prognosis(!!)
Acute Pancreatitis: General Assessment
- Obtain history of gallbladder disease, alcohol use, or precipitating factors
- Assess GI distress, including nausea and vomiting, and diarrhea
- Assess characteristics and level of abdominal pain(!!) – epigastric? occurring when eating? onset/provocation/quality/radiation/severity/time?
- Assess nutritional and fluid status
- Assess respiratory rate and pattern and breath sounds
- Assess for steatorrhea (fat into feces) and malabsorption
- Assess for S/S of diabetes mellitus
- Assess VS
Acute Pancreatitis: Signs + Symptoms
- Pain in mid-epigastric region – “Boring” - bores thought person to their back; gets worse in supine position (unable to digest food)
- Abdominal Distension, Bloating
- Nausea/Vomiting
- Abdominal Guarding – hardening of abdomen
- Diminished/Absent Bowel Sounds
- Fever (if becoming infectious)
- Tachycardia (sepsis?)
- Hypotension
- Breathing problems
- Patient looks sick: may be pale, listless, diaphoretic)
- Cullen’s Sign – superficial edema in umbilicus region; r/t bleeding associated w/ pancreatitis
- Grey-Turner’s Sign – bruising of flank area; associated w/ hemorrhagic pancreatitis
Acute Pancreatitis: Diagnostics
- Serum Amylase (23-85 U/L)*
- Serum Lipase (0-160 U/L)*
- Bilirubin (Total 0.1-1.2 mg/dL)
- Alkaline Phosphatase (25-145 units/L)
- Alanine Aminotransferase (7-40 units/L)
- Serum Glucose (b/c pancreas fxn!)
- WBC’s
- Triglycerides
- Ultrasound
- CT*
- Chest x-ray
