Exam 3 Flashcards
what is the function of the liver
- metabolism of glucose, proteins, lipids, vitamins
- detoxification
- synthesis of clotting factors
- synthesis of bile acids
what is hepatitis
diffuse inflammation of the liver
what is the time line for non infectious
can be acute, lasting less than 6 months or can develop into chronic hepatitis
what causes non-infectious hepatitis
excessive ETOH, toxic exposures, autoimmune diseases, bacterial, fungal, parasitic
what is infectious hepatitis
acute or chronic caused by viral syndromes of herpes, Epstein Barr, varciella Zoster
what history should be considered for hepatitis
ask about ETOH and illicit drug usage, use of Rxs or OTC meds, tranfusion hx, occupational or travel history
what are the symptoms of hepatitis
yellowing of skin
dark urine
clay colored stool
N/V
loss of apetite
extreme fatigue
what other physical findings may be seen with hepatitis
bruising and bleeding tendencies
tongue changes
nutritional changes
spider nevi
sparse body hair
aterial brewery
what marks hepatitis on labs
albumin decreases
AST/ ALT increased
bilirubin increased
elevating cholestasis
what would be used to measure liver capacity to synthesize clotting factors
PT
what does management look like for hepatitis patient
volume status
diet
antimetics
IV fluids
what can the liver not metabolize
lactate and leads to metabolic acidosis
why do you need to watch volume status
daily weights due to the low colloid osmotic pressure so leads to leaking of intravenous fluid to interstitial spaces
what type of diet would you want to give someone with heptatitis
high calorie, low protein
what drug gets rid of urea
lactulose
What type of acid/base imbalance would exist with hepatitis
metabolic acidosis
What is cirrhosis
severe scarring of the liver that can occur due to hepatitis or chronic alcoholism
what causes cirrhosis
chronic hepatitis virus
alcohol abuse
nonalcoholic steatohepatitis
hereditary hemochromatosis
Wilson’s disease and alpha1-antitrypsin deficiency
what are the symptoms of cirrhosis
low blood pressure
lightheadedness
postural hypertension
positive orthostatic
edema
worsening signs of volume overload
three hallmark signs of cirrhosis
ascites
edema
hypotension
what are the labs associated with cirrhosis
low albumin
increased AP
increased AST and ALT
increased coagulants
increased bili
hypo-osmolality
high ammonia levels
what is supportive care for cirrhosis
there is no cure, reaction to the ongoing signs and symptoms = monitor BP, oxygenation, strict IO, neuro assessments
how do you manage ascites
paracentesis
what is used as a therapy when treatments are not working for cirrhosis
VP shunt
TIPS
transjugular intrahepatic portosystemic shunt
what is hepatic encephalopathy
related to the accumulation of toxins (amonia) and changes in neurologic levels
is hepatic encephalopathy reversible
yes
what is seen in a patient
a decrease in neurological function that is subtle including memory, personality, concentration, reaction times
what is. an early sign of hepatic encephalopathy
Asterixisis
what is Asterixisis
a clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements
how long can a balloon tamponade be inflated
24 to 48 hours (due to necrosis or ulcerations)
what is the priority assessment with balloon tamponade
respiratory (if the balloon migrates up)
what is the pressure of a balloon tamponade
25 to 39 mmHg
what should the head of the bed be with balloon tamponade
> 30 degrees
what is Hepatorenal Syndrome
Most frequently fatal complication of cirrhosis
Development of renal failure in pts with severe liver disease in the absence of other identifiable causes for renal pathology.
what is compensatory mechanisms related to Hepatorenal Syndrome
get extreme systemic vasodilation which decreases circulating blood volume; compensatory action is CO increases and maximal renal vasoconstriction occurs which reduces renal perfusion and results in renal failure
what symtpoms will a patient with Hepatorenal Syndrome present with
Reduced renal blood flow
Ascites
Jaundice
Hypotension
Decreasing urine output
Increased serum creatine
SBP = spontaneous bacterial peritonitis
what is the treatment for Hepatorenal Syndrome
liver renal transplant
what is the MELD score
used to predict a 3 month mortality of patients with severe cirrhosis and resulting in kidney failure
postoperative phase of transplant
the nursing focuses on hemodynamic stability, adequate oxygenation, fluid and electrolyte balance
following a transplant what drugs may be needed
vasopressors and fluid boluses may be required the first 24 to 48 hours related to high cardiac outputs and low systemic vascular resistance
what does the exocrine fucntion of the pancreas include
acinar cells
what do acinar cells do
digest proteins, fats, starch
what does the endocrine function of the pancreas include
islets of langerhans
what do the islets of langerhans do
secrete insulin, glucagon, pancreatic polypetide hormones
what does insulin do
increase uptake of glucose into the cells, promotes glycogenesis, lowers blood sugar levels
what does glucagon do
increases blood sugar levels
what is main consideration with pancreatitis
PAIN
what are other nursing considerations for pancreatitis
altered tissue perfusion
impaired gas exchange
decreased cardiac output
fluid volume deficit
infection
knowledge deficit
altered nutrition
what is acute pancreatitis
acute inflammation of the pancreas
what causes acute pancreatitis mainly
gallstones
why do gallstones cause pancreatitis
block the pancreatic secretions from emptying into the duodenum and this causes inflammation (the reflux of bile causes the inflammation)
what is the second most cause of acute pancreatitis
alcohol (direct toxic effect)
what are the two types of acute pancreatitis
- interstitial
- necrotizing
what is interstitial pancreatitis
mild form of acute inflammtion
how long does interstitial pancreatitis last
self limiting with full recovery
last a few weeks and then goes away
what happens to a patient that develops necrotizing acute pancreatitis
irreversible damage caused by this and Most patients end up with sepsis, then MODS
what should you ask a patient about when gathering history related to acute pancreatitis
alcohol consumption
diabetes
gallbladder disease
medications
recent anorexia, N/V, weight loss
what is the hallmark sign of acute pancreatitis
Pain
where is pain felt with acute pancreatitis
persistent epigastric to the left upper quadrant, constant and radiating to the back, can be described as non-specific, severe pain (10/10)
what other S/S are seen with acute pancreatitis
abdominal guarding
Illeus
Diarrhea
Bleeding
Foul smelling bowels
dehydration
decreased BP (increased HR)
what is a key lab value for acute pancreatitis
amylase and lipase elevation 3 times normal
normal amylase level is
23 to 85 unites per liter
normal lipase levels
0 to 160 U/L
how will acute pancreatitis impact BUN
increased
what does an increased BUN suggest
hypovolemia
AST and ALT in relation to acute pancreatitis
Increased
AST suggests
indicates damage to liver cells
WBC related to
inflammation
the three diagnostic criteria for acute pancreatitis
(i) abdominal pain consistent with the disease
(ii) serum amylase and/or lipase greater than three times the upper limit of normal, and/or
(iii) characteristic findings from abdominal imaging
acute pancreatitis patient enters the ED
establish the diagnosis
if the patient is determined to have AP what is next step to be done in ED
volume resuscitation then stabilization of vital signs
the priority pain relief drug for AP is
opioids (dilaudid / morphine)
why would an AP patient get anti- cholinergic
decrease Gi motility and pancreatic enzyme release
why would an AP patient get anti-sporadics
relax the smooth muscles
why would an AP patient get H2 blockers
decrease GI acid secretions
if the patient has necrotizing pancreatitis what medication may they require
antibiotics
three complications of liver disease
- cirrhosis
- Hepatic Encephalopathy
- Hepto-renal syndrome
Laenacks Cirrhosis
seen in middle age men who are alcoholics
Post Necrotic Cirrhosis
cirrhosis that develops after sub massive necrosis of liver due to nasty toxin or viral hepatitis, not common
Biliary Cirrhosis
obstruction or infection of extra or intra hepatic bile ducts so bile cant drain, marked by jaundice, abdominal pain, steatorrhea, enlargement of liver and spleen
cardiac cirrhosis
related to recurrent and tractable CHF (from left sided heart failure moves into right sided heart failure), output decreases and perfusion decreases
acute pancreatitis is a _________ problem
exocrine
diabetes mellitus is a ____________ problem
endocrine
N/V can lead to what electrolyte imbalance
hypokalemia
what electrolyte imbalance may be seen with acute pancreatitis due to loss of fat
hypocalemia
Endoscopic retrograde cholangiopancreatography (ERCP)
Procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas
when may a patient need ERCP to be performed
Necessary if massive pancreatic necrosis and patient has worsening clinical picture (tachycardia, other organ failure, supplemental O2 required and not maintaining good O2, intubation required)
what are some complications of ERCP
can precipitate acute pancreatitis and introduce infection to sterile area, risks/complications include bleeding and using contrast dye (dye load)
severe hemorrhagic pancreatitis two signs
- Turner’s Sign
- Cullen’s Sign
turner’s sign
bruising of the flanks, retroperitoneal hemorrhage
cullen’s sign
edema and brusing around the umbillicus
chvostek’s sign
twitching of the facial muscles in response to tapping over the area of the facial nerve
○ Trousseau’s Sign
carpopedal spasm caused by inflating the BP cuff to a level above the systolic pressure for 3 minutes, more sensitive to hypocalcemia
type 1 diabetes
autoimmune, no insulin production, often first diagnosis of diabetes comes with an episode of DKA especially in children
type 2 diabetes
insulin resistance, hyperglycemia, hyperinsulinemic, beta cells don’t work well
complications of diabetes
○ Diabetic retinopathy: #1 cause of blindness
○ Premature coronary artery disease
○ HTN
○ Autonomic dysfunction with gastroparesis
○ Diarrhea
○ Nephropathy
○ Infertility issues
○ Increased risk of infection
○ Hyperlipidemia
○ Peripheral vascular disease
○ Poor wound healing - osteomyelitis
metabolic syndrome
High triglyceride
low HDL
HTN
Hyperglycemia
Central Obesity
When do we do impaired glucose tolerance test?
pregnant
nursing diagnosis to consider
Fluid Volume Deficit
Decreased Cardiac Output
Altered Nutrition
Risk for altered tissue perfusion: cerebral
DKA is common with what type of diabetes
Type 1
what is the most common cause of DKA
infection
other factors that can lead to DKA (beyond #1 reason)
drugs, trauma, stroke, MI, Pancreatitis
biggest concern with DKA
Blood glucose level and dehydration
three hallmark signs of DKA
polyuria, polydipsia, polyphagia
what is the cornerstone of management with DKA
Insulin therapy
hyperglycemia leads to
hyperosmolality
the accumulation of keto-acids leads to
metabolic acidosis
what is the breathing seen with DKA patients
kussmaul respiratory pattern (to compensate for metabolic acidosis)
what are the other symptoms would be seen with DKA
fruity breath
dry mucous membranes
flushed skin
hypotension
tachycardia
poor ski turgor
what medications may be used for DKA
diuretics, beta blockers, corticosteroids, anti-psychotics
two priority management for DKA
fluid resuscitation and insulin therapy
HHS is more common with what type of diabetic
Type 2
HHS is secondary to
some sort of physiologic stress
examples of some sort of physiologic stress
illness, infections, trauma, UTI, surgery
HHS is known for
marked hyperglycemia
hyperosmolality
no ketoacidosis
DKA or HHS lead to more mortality
HHS
what is the typical HHS patient present with
Older adult pt with type 2 diabetes, drowsy, eating less, sleeping more, impaired neuralgic function
the BG of a patient with HHS is
BG 400-4000 (mean is 1100 mg/dL),
sodium levels of HHS patient is
high NA and serum osmolarity
is a HHS acidotic
NO
what will not be considered with HHS patient
pH, anion gap, bicarb, ketones
what is the priority management of HHS
Fluid resuscitation and insulin therapy are two priorities in management
what is more dangerous hypoglycemia or hyperglycemia
hypoglycemia
hypoglycemia can lead to
death, coma, injury
what causes hypoglycemia
stress, weight loss, insulin shock, excessive alcohol, sepsis
hypoglycemia is a _______ mimicer
stroke
signs of hypoglycemia
hypothermia
tachypnea
tachycardia
HTN
dysrthmias
diaphoresis
hunger
what is the role of your skin barrier
protects against infections
prevents fluid losses
controls body temperature
produces vitamin D
Allograft
AKA homograft, temporary wound covering, donor is cadaver, temporary
Xenograft
AKA heterograft, skin taken from another species usually pigs, temporary
Autograft
skin taken from themselves, permanent
Physiologic Dressing
allograft, xenograft, autograft are all examples of physiologic dressing
Eschar
AKA scab, dark dead slothy layer of skin/tissue, associated with escharotomy, can strangle circulation
granulation
when taking off eschar, healthy pink skin is called granulation skin, when you see it you know burn is ready for permanent graft
Debridement
removal of eschar, can happen naturally, with enzymes, or done surgically by burn nurse
Escharotomy
incision into eschar to expose healthy skin to relieve pressure that may result in strangulation of circulation
most severe types of burns
combination of partial and full thickness
Superficial burn
Only involve epidermis !!!!
○Has a dry appearance without blistering
○Skin appears pink, red, blanches when you apply pressure (when release it fills up again)
○May be mild edema
examples of superficial burn
sunburn, splashes from hot liquid
partial thickness superficial includes
epidermis and superficial dermis
