Exam 3 Flashcards
hepatitis
inflammation of the liver
non-infectious hepatitis: how long does it last
can be acute, less than 6 months
causes of non-infectious hepatitis (6)
-ETOH
-Other toxins: Bacterial, fungal, or parasitic toxic exposure
-Autoimmune diseases - primarily biliary atresia cirrhosis, -hemochromatosis
-Congenital wilson’s disease
-R-sided HF - d/t back up of fluid
-non-ETOH fatty liver (NASH)
infectious hepatitis causes
can be acute or chronic d/t:
-Hep viruses
-Herpes
-Epstein Barr
-Coxsackievirus
-Varicella-zoster
signs and symptoms of hepatitis (beginning) (8)
Yellowing skin and eyes
Extreme fatigue
Low grade fever
Loss of appetite
N/V
Dark urine
Light colored stool
Diarrhea
s/s that hepatitis is progressing towards cirrhosis
-jaundice d/t cirrhosis and portal HTN
-hepatomegaly d/t HTN or extra fluid
-ascites
-muscle wasting
-hypoalbuminemia
-Na retention
-vitamin deficiencies
-bruising and bleeding
-sparse body hair
-caput medusa
-dark amber urine d/t bilirubin
-clay colored stool b/c of bilirubin
-palmer erythema
why does hypoalbuminemia occur in patients with hepatitis
d/t liver’s impaired ability to synthesize proteins
Edema/third spacing d/t decreased oncotic pressure
Skin is shiny, soft and pitting
signs of hepatomegaly
RUQ tenderness
Can palpate borders - will feel lumpy due to nodules
what is cheilosis
happens to lips - swelling / fissures on lips
Vit B2 deficiency, sign of hepatitis
glossitis (what is it and how do you tx?)
inflammation of the tongue
happens with vit deficiences in hepatitis
tx: antibiotics , avoid spicy/hot food, good oral care
why do patients with hepatitis bruise and bleed more
Impaired clotting factors
sequestration of platelets in the spleen
what is caput medusa and what causes it
superficial varicose veins on abdomen
May have arterial bruit
d/t portal htn and congestion
when do patients with hepatitis start showing s/s?
65-75% of hepatocytes are destroyed or dysfunctioning
when does liver failure occur
when there is a loss of 60% or greater hepatocytes
what would you include in an assessment for hepatitis
ask about
Alcohol use, ecstasy, needle sharing (IV drug abuse)
Transfusion history
OTC drugs
Occupation and travel exposure
Safe sex
what lab values do you draw for the synthetic functions of the liver
albumin, PT
what is albumin responsible for
colloid/osmotic pressure, keeps intravascular volume in vessels
normal albumin level
3.5-5.3 gm/dl
what is PT
measures liver’s ability to synthesize clotting factors
normal PT / INR
Normal PT 11-13
Normal INR - 0.8-1.1
Dysfunctional liver → PT increases, at risk for bleeding
what values of albumin and PT/INR will happen in liver failure
decrease albumin and increase PT/INR (longer to clot, more bleeding)
what are the hepatocellular damage markers
AST
ALT
what is AST and normal values
aspartate transaminase
Normal: 6-40 iu/l
enzyme that usually helps metabolize amino acids
Go up when there is damage
what is ALT and normal values
alanine transaminase
Normal: 30-120 units/L
Helps metabolize proteins
Go up when liver is damaged
when are AST and ALT released
released when hepatocytes are injured or die
Numbers should come down if treated and working
how do you evaluate cholestasis (excretory function, slowing or stalling of bile flow through your biliary system)
alkaline phosphatase
bilirubin
what is alkaline phosphatase + normal levels
Increased when bile duct is damaged or obstruction so bile can’t get out
Normal: 44-147 iu/L
Later marker than AST and ALT
what is bilirubin
Made during normal breakdown of blood cells
Can increase with liver dysfunction or bile duct issues
total bili normal levels + jaundice levels
Normal 0.1-1.2 mg/dL
Become jaundice when bili > 2.5 mg/dL
direct bili normal levels
< 0.3 mg/dL
what is nursing mgmt for hepatitis?
supportive care (rest, nutrition, avoiding further liver injury)
daily weights, measure abdominal girth
when does a patient with hepatitis need to be hospitalized
-unstable hemodyanmics
-encephalopathy
-poor fluid/food intake
-ascites
-respiratory issues
what diet should a pt with hepatitis have
High calorie low protein diet, small frequent meals
how do you treat ammonia
Lactulose for ammonia - acidifies the colon to prevent absorption of ammonia
draws ammonia from the blood into the colon where it is removed from the body
how are you going to treat pt with hepatitis
-Lactulose for ammonia - acidifies the colon to prevent absorption of ammonia
-Antibiotics to clear colon of bacteria that produces ammonia
-cholestyramine to treat pruritus
-Need antiemetics to combat N/V
-IV fluid - has to be saline - Can’t metabolize ringers → makes ph imbalance worse
what causes hepatic encephalopathy
increased ammonia
tx with lactulose
pt teaching for hepatitis
Infection
Modes of transmission
diet/fluid restrictions
Total cessation of alcohol (if alcohol related)
what are the 4 categories of cirrhosis
Laennec’s (portal)
Post necrotic cirrhosis
biliary
cardiac
Laennec’s (portal) cirrhosis
Seen in alcoholic cirrhosis or severe malnutrition
Middle aged males 40-60 years
post necrotic cirrhosis
cirrhosis following submassive necrosis of the liver (subacute yellowatrophy) due to toxic or viral hepatitis
biliary cirrhosis (what causes it and what are the characteristics)
Caused by obstruction or infection of major extra or intrahepatic bile ducts
characteristics: Jaundice, abdominal pain, steatorrhea, enlargement of liver and spleen
cardiac cirrhosis
d/t intractable heart failure
what causes cirrhosis (6)
chronic Hepatitis Virus,
alcohol abuse,
nonalcoholic steatohepatitis,
hereditary hemochromatosis,
Wilson’s disease, and
alpha1-antitrypsin deficiency
how does cirrhosis occur
Inflammation, fibrotic changes, and increased intrahepatic vascular resistance cause compression of the liver lobule, leading to increased resistance or obstruction of normal blood flow through the liver, which is normally a low-pressure system
Leads to splenomegaly, varices, hemorrhoids, cardiac dysfunction, fatigue, unstable glucose levels
s/s of cirrhosis
Lower extremity edema, ascites and hypotension
decreased synthesis of albumin leads to interstitial edema and deceased plasma volume
Clotting dysfunction-bruising to hemorrhage low-grade DIC
physical findings of cirrhosis (3)
LE edema
Ascites
hypotension
lab data for cirrhosis (albumin, bili, Na/H2O)
decreased albumin
increased bili
Liver can’t eliminate solute free water → decrease in sodium concentration in serum –> more retention of water –> more edema
tx for cirrhosis
Antibiotics to clear colon of bacteria that produces ammonia
Hepatic encephalopathy: Tx: lactulose
IV lasix for ascites -Normal saline!
antihypertensives to prevent rupture of varices
Beta blockers and nitrates
If bleeding —> will need packed RBCs
is there a cure for cirrhosis
no
what is supportive care for cirrhosis
Treat symptoms
Daily weights, strict Is and Os
Measure abdominal girth with ascites everyday
Check urine output to make sure it is adequate
Blood tests everyday - electrolytes, plts, H&H, coags
Neuro assessment
Monitor nutrition
Ascites will lead to resp issues
how can you manage ascites
paracentesis
when is a VP Shunt used in ascites
when resistant to other therapies
drains peritoneal fluid from the peritoneum into veins, usually the internal jugular vein or the superior vena cava
what is TIPs
transjugular intrahepatic portosystemic shunt
Used to decompress portal venous system
Portal vein → bypass liver circulation to hepatic vein → can lead to metabolic encephalopathy
Point is to reduce portal HTN → decrease size of varices and decrease bleeding
how to manage ascites (3)
first step - IV lasix
second - paracentesis
third - VP Shunt
complications of VP shunt
infection, occlusion of tube - can thrombose, can make esophageal varices more engorged and cause hemorrhaging
normal ammonia levels
9.5 - 49 mcg/dl
if blood ammonia increases, what happens?
Decreased LOC
Neuromuscular disturbances
Asterixis - push back/ flex hand and it flaps
Hyperreflexia
Impaired thinking
Changes in memory, personality, concentration, reaction times
what can cause hepatic encephalopathy
Can be d/t use of TIPS,VP shunt, GI bleed from esophageal varices → create nitrogen load → leads to bacterial deamination = amino acids break down → converted to ammonia
how to tx hepatic encephalopathy
Low protein diet
Medications -
-Lactulose: Decreases colonic pH to decrease absorption of ammonia by facilitating BM
-Neomycin (antibiotic)
-Metronidazole (flagyl) - 500mg q8 (IV, PO)
—All 3 focus on clearing nitrogen out of gut
Asterixis
very early sign of hepatic encephalopathy - ask patient to hold hand out and like stopping traffic and watch for involuntary flapping motion
balloon tamponade
usually refers to the use of balloons inserted into the esophagus, stomach or uterus, and inflated to alleviate or stop refractory bleeding
nursing care for balloon tamponade
Can only be inflated for 24-48 hours, bc can cause necrosis, perforation, ulcerations, 12-24 after hemostasis
Pressure to 25-39mmHg
HOB > 30 degrees to prevent reflux
why is respiratory assessment so important with balloon tamponade
tube can move and obstruct airway-if this happens cut tube to deflate gastric balloon quickly, bleeding assessment-can cause perf or esophageal rupture
what are the exocrine cells of the pancreas
Aciner cells - synthesize and secrete digestive enzymes to assist in the breakdown of starch, fat and proteins
empty secretions into pancreatic ductal system → joins common bile duct
what are the endocrine cells of the pancreas
Islets of langerhans: secrete insulin, glucagon, and somatostatin
causes of acute pancreatitis
-heavy alcohol use (40%)
-gallstones (40%)
-others (10%) - trauma, infection, shock, medications, biliary tract disease, cancer, atresia
how do gallstones cause acute pancreatitis
blocks pancreatic secretions from emptying into duodenum → reflux of bile initiates inflammatory process
More common in women (Fat, Female, Forty, Farting)
what are the two types of acute pancreatitis
Interstitial: mild form, lasts 1-2 weeks, no organ dysfunction, reversible, no serious complications
Necrotizing: 10-20% of cases progress to this
necrotizing acute pancreatitis
Causes irreversible damage to pancreas and surrounding tissues
Poor prognosis for patient → sepsis, MODs, high mortality rate
Ill from every system standpoint
Cellular necrosis and hemorrhage inside the pancreas
what are the results of the inflammatory response in acute pancreatitis (necrotizing)
Hypovolemia from capillary permeability,
acute respiratory distress syndrome, DIC,
renal failure,
cardiovascular failure,
GI hemorrhage
what will you ask your patient about when it comes to history for acute pancreatitis
Ask about alcohol and gallbladder disease
Diabetes
Medications
Any biliary tract disease?
Any jaundice?
Anorexia
N/V
Abdominal distension
what is the hallmark sign of pancreatitis
Present with epigastric to LUQ pain
Pain = deep, sharp, constant, radiating through to the back and up to the chest
Increases within minutes of eating food high in fat content
pain is worst lying down (do not lay them in supine)
Nonspecific
10/10, severe
additional signs of pancreatitis
abdominal guarding on exam
low grade fever, jaundice
Diarrhea
Bleeding
Foul smelling bowel movement
Dehydrated quickly
decreased BP → increased HR
If islets of langerhans are damaged during necrosis → patient will develop diabetes
amylase + normal levels
convert starch and glycogen into simple sugars
Normal 23-85 (up to 140) u/L
will amylase increase or decrease in pancreatitis
elevation 3x normal
lipase
fats → fatty acids and glycerol
Normal: 0-160 u/l
what is the most sensitive indicator for acute pancreatitis
lipase
will BUN increase or decrease with pancreatitis
increase - suggests hypovolemia
will AST increase or decrease with pancreatitis
increase indicates damage to liver cells
will ALT increase or decrease with pancreatitis
indicative of gallstone pancreatitis
Increase
will WBC increase or decrease with pancreatitis
increase d/t inflammation
what do you need for diagnosis pancreatitis
Amylase and/or lipase are 3x normal
Characteristic pain
Abdominal imaging
what is the priority in the ED for pancreatitis
Priority = Volume resuscitation - a lot of NS and electrolyte (esp hypocalcemia)
then…
-pain relief
-stabilization of VS
-anticholinergics to decreases GI motility and pancreatic enzyme release
-Antispasmodics – relaxes the smooth muscle, relaxes sphincter of Oddi
-H2 blockers/PPI – decrease GI acid secretions
-When being fed, need pancreatic enzymes to aid in digestion of fats and proteins
-Antibiotics – if have necrotizing pancreatitis
priorities for pancreatitis in the ICU
Fluid resuscitation
Inotropic support
Respiratory support
Renal therapy
Nutritional support - Not TPN
Pharm therapy
Surgical intervention
what is MRCP and what is it used for
magnetic resonance cholangiopancreatography
Can detect gallstones down to 3mm in diameter and remove them
High quality
what does hypocalcemia indicate in pancreatitis
can indicate presence of pancreatic fat necrosis
Calcium binds with fatty acids during necrosis process
why would a patient with pancreatitis be hyperglycemic
decreased release from damaged beta cells → increase glucagon release + increased stress response from inflammation
will TGLs increase or decrease with pancreatitis
elevate - over 1000 mg/dl
3 pain control methods for pancreatitis
High fowlers
IV narcotics
NG tube to decompress belly
pancreatic rest for pancreatitis
NGT on low intermittent to decompress the stomach and to decrease stimulation of secretin which stimulates production of pancreatic secretions
signs of severe hemorrhagic pancreatitis
Turner’s Sign – bruising of the flanks, retroperitoneal hemorrhage
Cullen’s Sign – edema and bruising around the umbilicus
signs of hypocalcemia
Chvosteks & Trousseaus
Chvostek’s Sign
twitching of the facial muscles in response to tapping over the area of the facial nerve
hypocalcemia
Trousseau’s sign
carpopedal spasm caused by inflating the BP cuff to a level above the systolic pressure for 3 minutes
type 1 DM
no production of insulin
type 2 DM
insulin resistance, which is hyperglycemia, hyperinsulinemia, and consequent Beta cell exhaustion
complications of diabetes
Blindness - retinopathy, cataracts
Stroke
Premature CAD
HTN - Atherosclerotic changes in heart, brain, kidneys
Gastroparesis
Diarrhea (especially due to medications like metformin)
Fertility issues, impotence
Increased risk of infections
Peripheral Vascular disease - Poor wound healing, Amputation
Peripheral neuropathy
3 hallmarks of DKA
hyperglycemia that causes hyperosmolarity
metabolic acidosis
fluid/electrolyte disturbance / volume depletion from osmotic diuresis
most common cause of DKA
infection (30-50%, UTIs, pneumonias in older adults)
why are ketones produced in DKA
Ketones are produced when body is forced to use fat to create energy because lack of insulin that is converting glucose to energy
Fat is turned into ketones = acids → accumulate in bloodstream
other causes of DKA
Inadequate insulin therapy
Stroke, MI, pancreatitis
Alcohol/drug abuse
Trauma
Meds: diuretics, corticosteroids, beta blockers, some antipsychotics/anti seizures
is DKA more common with type 1 or 2
type 1
DKA nursing care assessment: history
Diabetic regime
Weight loss
Thirst
Urinary frequency
Bloating
Any anorexia?
s/s of DKA
kussmaul respirations
fruity breath d/t acetone
abdominal pain with N/V
Polyuria
Polydipsia
Abdominal distension
Dry mucous membranes - dehydration
Decreased perfusion
Hypotension
Tachycardia = compensatory
Altered mental status - somnolence, stupor, coma
Fever = sign of underlying problem being an infection
BG level in DKA
> 250 - 1200 mg/dl
average = 600
anion gap
specialized blood tests that lets us know about metabolic acidosis
Look at difference b/w sodium + potassium on one side and Cl and HCO3 on the other
Less than 11 = normal
how to improve circulatory volume and perfusion in DKA
NS 1L/hr in ED and ICU
Until HR and BP returns to normal
BP over 90/100
HR to come down
correcting electrolyte imbalances with DKA
potassium phosphate (once you get lab values)
bicarb (if ph is less than 7)
