Abdominal Disorders Flashcards
Liver functions (10)
- Synthesize plasma (albumin/globulins)
- Nutrient metabolism (Glycogen to glucose)
- Sunthesize bile
- Provides for fat/vitamin storage (B12/iron/copper)
- Eliminate bilirubin
- Steroid hormons/polypeptides inactivate
- Kupffer’s cells (break down drugs/toxins)
- Coagulation factors
- Fat metabolism
- Detoxify ammonia
Hepatitis
Define
Inflammation of the liver
(virus,bacteria, drugs )
* obstructs ducts/circulation
* impedes liver function
* necrosis of tissue
Hepatitis
Treatment
supportive care
* rest
* nutrition
* avoid stress
* avoid hepatotoxic substance
Cirrhosis
Define
chronic liver inflammation
caused by chronic alcohol abusehepatitis/biliary obstruction
Cirrhosis
Pathophysiology
- Initially fatty infilitration/obstruction
- oxidation of alcohol yield acetaldehyde
(damages hydrochondria / necrosis) - necrotic tissue becomes scar tissue –> distorting blood flow
results in dysfunction and liver failure
CAUSING
portal hypertension
Portal vein hypertension
venous congestion and dilation
nutrient rich blood shunted away from liver
* results in poor metabolism of nutrients, drugs, toxins
* vascular changes –> varicose veins
Impaired liver function
Edema
decreased osmotic pressure by lack of plasma proteins
Impaired liver function
ALL
- edema
- jaundice
- malnutrition
- hyperlipidemia
- hormones
- unstable glucose
- bruising/hemorrhage
- cognitive change
- hepatic encephalopathy
Impaired liver function
Jaundice
increased bilirubin
Impaired liver function
Fatigue, malnutrition
liver cannot process nutrient rich blood
Impaired liver function
hormones
Inappropriate ADH/aldosterone levels
Impaired liver function
ALT/AST
high levels – feedback function no longer valid
Impaired liver function
glucose
poor carbohydrate metabolism
Impaired liver function
cognitive change
somnolence/agitation
irritability/hostility
Liver disease labs
- ↑ALT/AST
- ↑ammonia
- ↑ bilirubin
- ↑ PT/PTT
- decreased protein
- decreased h/h
Hepatic encephalopathy
Define
accumulation of neurotoxins ammonia
progress with change in personality, irritability
* aserixis –> hand flapping –> cannot keep hand still
Hepatic encephalopathy
Management
maintain safe environment
* remove/decrease nitrogenous waste
* Lactulose (clear toxin)
* Xifaxan (prevents bacterial action)
Ascites
Define
accumulation of fluid in peritoneum
decreased colloid pressure
↓
increased hydrostatic pressure
↓
ald/ASH remain in blood –> retain fluid
↓
increase abd girl, fluid wave
↓
respiratory distress
Acites
Treatment
- Bed-rest
- Low sodium-diet
- Diuretics
- Paracentesis (hypotension/infection)
Ascites
LeVeen shunt
relieves resistant ascities
complications sepsis, peritonitis, occlusion
Ascites
Trans jugular Intrahepatic Porto system shunt
- decompress portal venous system
- decrease portal hypertension
- stop/reduce ascites
Contraindications –> CHF
Circulatory Effects of Cirrhosis `
enlarged liver
↓
increased resistance to blood flow
↓
increased PHT
↓
varices develop in esophageal/gastic/ hemorrhoidal veins
Esophagogastic varices
Engorged and distended blood vessels of the esophagus and proximal stomach that develop as a result of portal hypertension.
Varices
Complications
- Acute GI hemorrhage
- Life-threatening (severe can rupture)
- treatment/management similar to acute GI bleed
Acute Gastrointestinal Bleeding
three disease
- peptic ulcer disease
- stress-related erosive
- esophageal varices
Peptic ulcer disease
Define
results from breakdown of gastromucosal lining
Normal protection of gastic mucosa
- glyocoprotein
- gastic mucosal blood supply
- cells connected by tight junctions
Peptic ulcer disease
2 main causes
- NSAIDs
- H. pylori
breakdown barriers
Stress-related erosive syndrome
Define
increased gastric acid production resulting in decreased blood flow (ischemia)
Stress-related erosive syndrome
at risk
ventilation patients
shock
burns
trauma
major surgery
stress
GI bleed
Assessment - coffee ground
more gastic content in contact with blood
GI bleed
Assessment - maroon
less gastric contact with blood
GI bleed
Assessment - hematemesis
vomiting bright red blood
GI bleed
Assessment - hematochezia
bright red blood from profuse bleeding from lower gi per rectum
GI bleed
Assessment - melena
tarry stool d/t old blood moving through GI tract
GI bleeding
early sign
postural hypotension
GI bleeding
later signs
- decreased h/h
- tachycardia
- pale, SOB
- axiety
- elevated BUN with normal creatinine
GI bleeding
Management
- Fluid resuscitation
- Packed RBC
- Endoscopy
- Billroth I + II
GI bleeding
Sclerotherapy
Creates inflammatory reaction that induces vasoconstriction and results in the formation of venous thrombus.
GI bleeding
Band ligation
hematemesis could be loss of clip
Bleeding Esophageal Varices
Baloon tamponade
esophagogastric tubes
internal pressure within varices
- Aspiration
- Asphyxiation
- esophageal erosion
deflate q12h to allow perfusion (bleeding status)
Vasopressin
GI bleeding
given IV to constrict splanchnic
* decrease portal HTN
* systemic ischemia
* short term use with lowest dose
Somatostatin/octreotide
GI bleed
decrease portal venous pressure
H2 antagonist
pepcid/zantac
GI bleed
prophylaxis
block acid secretion
Proton pump inhibitor
omeprazole, protonix
GI bleed
treat the bleed –> help healing
block final stage in acid production
Antacid
GI bleed
neutralize acid/ bind phosphates in GI
Blocking agent
carafate
GI bleed
cover ulcer sit with protective bonding
Pancreas
Exocrine functions
digestive enzymes
acinar cells secrete: amylase/lipase
Pancreas
Endocrine functions
hormones
islets of langerhans: glucagon, insulin, somatosatin
Pancreatitis Exocrine
digest protein, fat, starch
↓
enzymes activated in duodenum
↓
bile obstruction
↓
premature activation
↓
autodigestion
↓
break down tissue
Acute Pancreatits
Pathophysiology
- autodigestion
- increasing capillary permeability (edema)
- fibers of blood vessels (hemorrhage)
- cell membranes
- lipase moves into systemic circulation
↓
fat necrosis
Acute Pancreatitis
Assessment
- epigastric to midabd pain
- nausea/vomiting
- grey turner (L)
- cullen sign(L)
- edema
Acute Pancreatitis
Lab results
- ↑amylase/lipase
- hypocalcemia
- ↑glycemia/bilirubinemia
Acute Pancreatitis
Diagnostic procedures
CT scan
ABD IS
Acute Pancreatitis
Treatment
pain relief
fetal position
rest –> NPO FULL WEEK
*TPN
* I/O
CT imagining revealed a pus-like pseudocyst. What order would the nurse anticipate to be ordered?
Antibiotic for peritonitis prophylaxis
Acute Pancreatitis
Patient is at risk for:
- third spacing
- hemorrhage
- SIRS
- Shock
- coagulation issues
Hyperglycemic Hypersmolar State
Define
extremely high levels of plasma glucose leading to osmotic diuresis
Hyperglycemic Hypersmolar State
Etiology
Still has some insulin
pancreas produces insufficent amount of insulin for high glucose
dehydration d/y hyperglycemia
Hyperglycemic Hypersmolar State
Causes
- infection
- CVA, MI, trauma
- Steroids, beta-blocker, dobutamine, phenytoin
Hyperglycemic Hypersmolar State
Pathophysiology
- reduced insulin allows more glucose to accumulate
- triggers glucagon release
- glucose increase = osmolality increase
- body pulls intracellular into vascular
- excessive fluid loss = hypovolemia
reduced kidney perfusion/oliguria
Hyperglycemic Hypersmolar State
Assessment
s/s ignored
* polyuria
* polydipsia
* weight loss
* weakness
* dehydration
Hyperglycemic Hypersmolar State
Labs
- Glucose over 600
- Serum osmolality over 320
- pH >7.3
- bicarb over 15
- ketonuria
- elevated hematocrit
- low potassium
Hyperglycemic Hypersmolar State
Treatment
- rapid rehydration
- hypotonic then isotonic (9-12L)
- insulin replacement - low dose
- correct electrolytes (K+)
Monitor K+ - treat cause
What should you do before giving insulin for a patient in Hyperglycemic Hypersmolar State?
CHECK POTASSIUM
(if low insulin will make it lower)
Solid organs
BLEED
* spleen
* liver
* kidney
* pancreas
Hollow organs
generally do not bleed
* stomach
* gallbladder
* duodenum
* small intestines
Abdominal trauma
Assessment
- location
- cullen/grey
- hematoma
- distension
- auscultation
- rebound tenderness
- subcutaneous emphysema
Abdominal trauma
Diagnostics
- NG/urinary cath COLOR
- H/H, amylase
- CT
- Ultrasound
- Perioneal lavage –> DPL
- Laparoscopy
Abdominal trauma
Medical management
Non-op –> management
OP –> nonstable hemodynamics
Intestinal injuries require surgical intervention
Spleen
Define
Most likely to be injured
lymphoid tissues serves as reservor
* control leukocyte production
* recycles iron/rbc
* antibody production
Spleen Injury
Assessment
- LUQ pain, radiating to left shoulder (Kehr’s)
- Peritoneal irritation, hypotension, tachcardia
- increase WBC
- less effective RBC
Spleen Injury
Treatment
Pain control
Antibiotics
Surgery (splenectomy)