!!Exam 3 Patho final review

Enteral Nutrition

• least expensive and least invasive

• preserves their gut and decreases risk of bowel necrosis

• Indication:

  • abnormal esophageal/ stomach peristalsis

  • altered anatomy secondary to surgery

  • depressed consciousness

  • impaired digestive capacity

Enteral Nutrition (interactions)

• Interactions: stop feeds for 2 hours before and after administration or change route to IV

  • Phenytoin (delayed)

  • Tetracylines (inactivated)

  • increased absorption of corticosteroids, vitamin A and D

Enteral Nutrition (Adverse Events)

• Diarrhea (talk to provider about slowing down the rate)

• Dumping Syndrome ( nutrients are moved to quickly from stomach to small intestine) 

  • N/V/D, cramping, sweating, heart racing

• Aspiration Pneumonia (possible if during feedings they’re lying down or their head isn’t elevated

Nursing Implications: Enteral Nutrition

• feedings are started slowly and rate increases gradually

• Monitor: daily weights and Intake/Output

Parental Nutrition

• totally digested nutrients directly enter the circulatory system

• the entire GI system is bypassed, eliminating the need for absorption, metabolism, or bowel elimination

• Types: Peripheral and Total (central)

Peripheral Parenteral Nutrition (PPN)

• short term, less than 2 weeks

• mild to moderate nutritional deficiencies

• replacement of nutrients from present oral intake (doesn’t provide complete nutrients)

• solution is less than 10 % dextrose

• risk of phlebitis and fluid overload

Total Parental Nutrition (TPN)

• given via CVC (large central vein)

• provides complete nutrience needed for survival (long term)

• solution contains max 35% dextrose (hypertonic)

Indications:

• nonfunctioning GI tract

• short bowel syndrome

• bowel rest required

• severe malnutrition or malabsorption

• nutritional support needed for over 7-10 days

Total Parental Nutrition (TPN): Risks

• infection

• trauma from CVL placement— pneumothorax

• metabolic alterations (hyperglycemia)- check blood glucose often

Nursing Implications: TPN

• monitor: 

  • blood glucose

  • start IVF with 5-10% dextrose if TPN stopped to prevent hypoglycemia

Obesity

• body weight beyond physical requirement

• abnormal increase and accumulation of fat cels

• increase in number (hyperplasia) and size (hypertrophy)

Metabolic Syndrome

increased risk of cardiovascular disease, stroke and diabetes

5 critera: 3/5 to be diagnosed

• increased waist circumference, triglycerides, BP, fasting glucose

• decreased HDL

health risks associated with obesity

• increased mortality, especially with increased visceral fat

• reduced quality of life

• most conditions can improve with weight loss

• increased risk of heart attack and stroke, HTN

• greater risk of type 2 diabetes

• GERD, gallstones, Nonalcoholic steatohepatitis

• sleep apnea

• osteoarthritis

• cancer

Gastric cells

• parietal cells (secrete hydrochloric acid)

• chief cells (secrete pesinogen —> pepsin)

• goblet cells: secrete mucous

N/V (definitions and causes)

• nausea: subjective feeling

• vomiting (emesis): forceful ejection of partially digested food and secretion

• causes:

  • GI disorders/infections

  • CNS or cardiac problems

  • hormonal/ endocrine 

  • med induced 

  • motion related

  • psychological factors

N/V (patho)

• medulla of the brain (vomiting center): receives stimuli from body to initiate vomiting reflex

  • GI tract, kidneys, heart or brain send messages

• Brain stem (chemoreceptor trigger zone (CTZ)): responds from drugs, toxin, motion

  • stimulates SNS and PNS

N/V Complications

• dehydration and electrolyte imbalance (decreased K)

• metabolic Alkalosis

• Hypovolemic shock

Gastroesophageal Reflux Disease (GERD)

• acute/chronic syndrome with varying intensity and frequency

• backflow of gastric or duodenal contents into the esophagus

• leads to irritation and inflammation of esophagus

Causes of GERD

• incompetent or relaxed LES

• pyloric stenosis

• Hiatal Hernia

• Motility Disorder— delayed gastric emptying

• obesity

Diagnosis of GERD

• hx and physical

• upper endoscopy (EGD) with biopsy

• barium swallow/ upper GI series

• ambulatory pH monitoring

GERD: Manifestations

• heart burn after eating (pyrosis): releived with antacids

• pain or discomfort in upper abdomen (dyspepsia)

• burping: sometimes causing bitter liquid entering mouth (regurgitation)

• difficulty swalloing

• breathing problems

GERD: complications

• Esophagitis: inflammation, dysphagia — ulcerations may lead to scarring, stricture, dysphagia

• Barret Esophagus: metaplasia (pre cancerous cellular changes)—- increased risk of cancer

• Asthma, Pneumonia, Chronic Bronchitis: aerosolized acid goes into lungs

• Dental Erosion

GERD: Medical Management

• drug therapy focuses on:

  • decrease volume and acidity of reflux

  • improving LES function

  • protecting esophageal mucose

• PPIs and H2 blockers

• antacids, cholinergic (PNS), cytoprotective, prokinetics

Hiatal Hernia

• portion of stomach protrudes thru diaphragm into esophagus

  • sliding: most common, part of stomach can slide back and fourth

  • rolling (parasophageal): more dangerous, can strangulate

• contributing factors: 

  • structural (weakened muscles in diaphragm and esophagastric opening)

  • increase abdominal pressure

• diagnostic test and manifestations are similar to GERD 

• may require surgery

Peptic Ulcers

• #1 cause= H pylori, #2 cause= NSAID use

• may be asymptomatic and never have ulcers

• resistant bacteria able to withstand highly acidic environments

• leads to mucosal damage and increase gastric secretion

Peptic Ulcer Complications

• hemorrhage

• pyloric obstruction

• perforation and penetration

• malabsorption

• dumping syndrome

Gastric Ulcers

• antrum, prevalent in ages 50-60 , more in women than men

• high mortality rate/recurrence rate and cancer risk

• increase frequency of obstructions

manifestations

• pain worse with eating (1-2 hours after meal

• burning or gaseous pain

Duodenal Ulcers

• pain relieved BY EATING

• prevalent in ages 35-45

• often associated with chronic diseases such as COPD, pancreatitis, renal failure

• may occur, disappear and reoccur

• increase risk of GI bleed (instead of perforation)

Duodenal Ulcer Manifestations

• pain improves with eating (pain occurs 2-5 hours after meal)

• burning or cramping in mid epigastric area or back

• may be silent

• bloating, N/V, early satiety

Triple therapy for H pylori

• 7-14 days

• PPI

• amoxicillin

• clarithromycin

• optional: bismuth

Perforation

• medical emergency

• GI contents enter sterile peritoneal cavity

• Severe Upper abdominal pain— may be referred to shoulder 

• tender abdomen, board like

• bowel sounds absent; N/V

• symptoms of shock

• possible Peritonitis (check temperature and BP)

Hemorrhage

• medical emergency

• risk of hypovolemic shock

• symptoms: sudden severe pain, hematemesis, melena (digested blood), occult bleeding

Diarrhea (causes and risk factors)

• 3 or more stools/day

• causes: infection (most common), viruses, E coli, Giordia Lamblia, C diff, Laxative use, food intolerance, malabsorption

• Risk factors: advanced age, decreased gastric acidity (PPI and decrease HCl), immmunocompromise

Diarrhea (manifestation and complications)

• stool may contain leukocyte and blood and mucus

• risk of dehydration, electrolyte imbalance, acid base imbalances

Irritable Bowel Syndrome (IBS)

• functional bowel disorder

• chronic and recurrent abdominal pain

• disordered bowel movements

• diagnosis of exclusion

• constipation, diarrhea or both

Irritable Bowel Syndrome (IBS): symptoms

• irregular BM

• bloating and excess gas

• passing mucus via the rectum or while passing stool

• abdominal crmaps accompanied by pain

• onset of sudden need to use the loo

Irritable Bowel Syndrome (IBS): Management

• deal with psychological factors; CBT - relaxation techniques

• dietary changes

• meds (antidepressants, bowel meds, antispasmodics)

• identify triggers

Celiac Disease

malabsorption disorders

• autoimmune response to gliadin

• causes damage to small intestinal mucosa

• Diagnosis:

  • IgA anti-tissue transglutaminase

  • confirmed with EGD biopsy

Celiac Disease: Manifestation

• diarrhea

• steatorrhea

• abdominal pain/ distention

• flatulence

• weight loss

• dermatitis herpetiformis

Appendicitis

infection/inflammation

• most common emergent abdominal surgery

• common in ages 10-30

• inflammation leads to —→ distention, accumulation of mucus and bacteria leads to gangrene, and perforation leads to peritonitis

• Meds: analgesics, antiemetic, ABX, IV fluid

Appendicitis: Manifestations

• RLQ pain( may begin with central/umbilical pain, increase pain with cough, sneeze, deep breath)

• fever

• muscle guarding

• rebound tenderness

• rigid abdomen

• position of comfort: supine with right leg flexed

• Psoas sign= pain with extension of Right Leg

Diverticulosis

infection/inflammation

• diverticula= outpouchings of colonic mucosa

• diverticulosis= diverticula NOT inflammed; asymptomatic

• Causes & Risk Factors:

  • genetics, environment

  • chronic constipation and lack of fiber

  • obesity and inactivity

  • smoking and alcohol use

  • NSAID use

Diverticulitis

infection/ inflammation

• diverticulitis= inflamed, possibly infection diverticula

• Manifestations: LLQ pain, change in BMs, Nausea, Fever, palpable mass, Rectal bleeding

Intestinal Obstruction

• mechanical: (physical blockage) herniation, adhesions, intussusceptions, volvulus

• nonmechanical: decreased or absent bowel sounds, due to altered PNS innervation

  • paralytic ileus due to surgery, peritonitis, inflammatory disorders, electrolyte imbalances, spinal injuries

Small Bowel Obstruction Symptoms

• rapid onset

• crampy, wave like colicky

• no feces or flatus

• projectile vomiting

• severe dehydration

• electrolyte imbalances

• minimal to moderate distention

Large Bowel Obstruction Symptoms

#1 cause of cancer

• severe distention

• gradual onset

• less dehydration

• some have only constipation

• ribbon like or liquid stool

• anemia, weight loss, anorexia

• perforation may occur 43

Inflammatory Bowel Disease— IBD

• chronic inflammation of GI tract (autoimmune disorder)

• periods of exacerbation and remission

• begins in teens/early adults or 60s (2nd peak)

• genetic component

• affects 1 or more layers of bowel wall

2 main types

• chrons

• ulcerative colitis

IBD: diagnosis

• colonoscopy

• CT or MRI

• stool studies: blood 

• blood tests: antibody test

  • increase ESR, CRP, WBC

  • decreased albumin

  • electrolyte disturbance

Chrons Disease

• skip lesions

• cobblestone appearance

• bowel wall thickened, fibrotic— narrowed lumen

• manifestations:

  • RLQ psin, worse AFTER meals

  • abdominal tenderness

  • diarrhea with steatorrhea (<6 /day)

  • blood may be present in stool

  • severe malabsorption can lead to weight loss (small intestine is affected)

Chrons disease: complications

• adhesions and abscesses

• fistula

• peritonitis

• 60-70% require surgery

• up to 50% loss of small bowel can be tolerated

Ulcerative Colitis (UC)

• contiguous lesions (start in rectum and travel up)

• multiple ulcerations, diffuse inflammation

• bowel narrows, shortens and thickens

manifestations:

• 6+ stools/day

• Bloody diarrhea

• associated fatigue, anemia, pallor

• LLQ pain

• intermittent tenesmus (bowel emergency)

Ulcerative Colitis (UC): complication

• toxic megacolon

• perforation

• bleeding

• increase risk of colon cancer (both UC and chrons)

Stomas

• preop and post op care

• ileostomy= high risk of dehydration

• emotional support

• skin and stoma care

• diet and fluid intake

risk factors for gallbladder disease

• female

• multiparity

• over 40

• estrogen therapy

• sedentary

• family history

• obesity

Cholelithiasis

• stones in gallbladder

• bile secreted by liver becomes supersaturated with cholesterol

• imbalance of : cholesterol, bile salts, calcium

• leads to precipitation

• either stay in gallbladder or migrate to cystic or common bile duct—→ pain and obstruction

Cholecystitis

• inflammation of gallbladder

• usually associated with gallstones also sludge

• no pain to severe

• pain increases when stones are moving or causing obstruction

  • tachycardia, diaphoresis, prostration

  • RUQ (may referred to right shoulder and scapula)

  • 3-6 hours after high fat meal or when patient lies down

• severe: steatorrhea, bleeding tendencies, N/V/D, pruritis, jaundice

Diadnostic findings in Cholecystitis

• increased: WBC, urine and serum bilirubin, liver enzymes, serum amylase (if pancreatic involvement)

Cholecystitis Meds

• ABX for possible infection

• opioids

• anticholinergics (decrease GI secretions and counteract smooth muscle spasm)

Pancreatitis

acute inflammation

• spillage of pancreatic enzymes into surrounding tissues (auto digestion and severe pain_

  • activated pancreatic enzymes cause injury to pancreatic cells

• varies from mild edema to severe necrosis

causes:

• gallbladder disease (females)

• chronic alcohol use (males)

Pancreatitis Manifestation

• LUQ or mid epigastric (radiates to back)

• worse with eating

• N/V

• jaundice

• crackles in lungs

• hypocalcemia

• cullens sign (blue gray discolor around umbilicus)

• turners sign (ecchymosis on flank)

Pancreatitis Lab findings

• elevated:

  • amylase

  • lipase

  • bilirubin

  • WBC

  • liver enzymes

  • glucose

  • tryglycerides

• decreases: calcium

acute pancreatitis complications

pseudocyst

• encapsulated fluid surrounds pancreas

• abdominal pain, palpable ass

• resolves spontaneously or may perforate and cause peritonitis

Hepatitis Types/Routes

fecal oral transmission

• types A (vaccine)

  • mild flu like symptoms, doesnt become chronic

• Types E (non vaccine)

  • rarely chronic

blood borne

• types B (vaccine)

  • acute and chronic, health care workers at risk, iv drug users

• types C: (cure, no vaccine)

  • acute and chronic, 15-20 year period between transmission and liver damage

• types D (hep b vaccine)

  • only occurs in people with past or current Hep B

Hepatitis Patho

• hepatocytes are destroyed in large amounts

• decreased liver functioning

  • decreased production of clotting factors, bile, protein

  • decreased ability to metabolize drugs, hormones, metabolites

Hepatitis Complications

• fibrosis/ scarring progressing to cirrhosis

• cancer

• portal hypertension

Hepatitis: Acute Phase Manifestation

• lasts up to 6 months

• many are asymptomatic

• fatigue, anorexia

• hepatomegaly and splenomegaly

• RUQ TENDERNESS

• flu like symptoms

• muscle and joint pain

• with or without jaundice

Hepatitis: Convalescent Phase Manifestations

• begins as jaundic is disappearing

• lasts approx 2-4 months

• hepatomegaly persists; splenomegaly resolves

• malaise and easily fatigued

Cirrhosis

hepatocytes replaced by nonfunctional scare tissue (fibrosis)

• obstructs blood flow thru liver

  • portal hypertension

  • esophageal varices

• many causes: Hep C, alcohol use, steatohepatitis

• diagnosis: hepatic function test, fibroscan, biopsy

Cirrhosis Manifestations

• red palms (palmar erythema)

• asterixis (flapping tremor)

• fetor hepaticus (must breath odor)

• caput medusae (network of large, swollen veins on abdomen

• spider angioma (central red spot with thin branching blood vessels

Cirrhosis Pharmacologic treatments

• no cure

• vitamin and mineral supplement

• diuretics

• lactulose (binds with ammonia)

Cirrhosis Complications

• portal hypertension

• ascites

• esophageal varices

• hepatic encephalopathy

Portal Hypertension

• obstruction of hepatic blood flow (in and out of liver)

  • due to liver scarring blocking blood flow

• portal vein brings blood from digestive tract to liver

consequences

• splenomegaly, ascites

• collateral (backup) circulation develops

• weaker and smaller vessels resulting in caput medusae and esophageal varices

Esophageal varices

• swollen fragile blood vessels

• prone to rupture

• pt presents with melena or hematemesis

• hemorrhage can be life threatening

  • hypotension and tachycardia

Ascites

• result of third spacing of lfuid into abdomen

  • increased pressure from portal hypertension

• may cause respiratory destress

• Meds: diuretics

hepatic Encephalopathy

• scarred liver cannot convert ammonia to urea

• results in cerebral edema

manifestations

• personality changes

• lethargy

• sleep disturbances

• LATER: slow speech, coma, convulsions

Treatment: lactulose to remove ammonia from body

Sprains and Strains

do not involve fractures

• sprains: ligaments (twisted or wrenched)

• strain: tendons (stretched)

Sprains and Strains (manifestations, diagnosis, complications)

• pain, edema, decreased function and bruising

• diagnosis: X ray

• complications

  • avulsion fracture

  • subluxation or dislocation

  • hemarthrosis

  • surgical repair

displacement of bone (types, symptoms, complications, diagnosis)

• dislocation: complete displacement or separation of the articular surfaces of the joint

• subluxation: partial or incomplete dislocation of the joint surface

symptoms

• deformity, pain, tenderness, loss of function, swelling

complications

• intraarticular fractures and avascular necrosis

diagnosis

• X ray and or aspiration

Carpal Tunnel

compression of median nerve

• tinel and phalens sign

• impaired sensation

• pain, numbness

• weakness

• late: atrophy, dysfunction

Tinel and phalens sign

Tinel = tap on median nerve

• causes tingling in median nerve distribution

Phalen

• tingling in same area produced by holding hands in position

Fractures

disruption or break in bone

• traumatic or pathologic

• open: broken skin

• closed: intact skin

• complete: completely through the bone

• incomplete: partly across the bone

direction of fracture line: linear, oblique, spiral

Fracture manifestations

• pain

• point tenderness

• edema

• deformity

• crepitation

• muscle spasm

• loss of function

• guarding

Fracture reduction

• closed reduction

  • nonsurgical, manual realignment of bone fragments

  • traction applied

• open reduction

  • surgical incision and fixation

  • reduced risks related to immobility

Fracture healing process

1. fracture hematoma (blood clot forms)

2. granulation tissue (absorption of products in necrosis, hematoma converted to granulation tissue)

3. callus formation (minerals and new bone matrix deposited, callus can be seen on x ray)

4. ossification (callus hardens)- cast may be removed

5. consolidation (distance btwn fragments decrease)

6. remodeling (excess bone tissue is resorbed)

complications of fractures

• compartment syndrome

• fat emboli

• rhabomyolysis

compartment syndrome

swelling and increased pressure within a limited space

• the fascia has limited ability to stretch, continued swelling causes pressure

• compromises nerovascular function

causes

• decreased compartment size or increased compartment content

• early intervention vital, can occur early or be delayed

• ischemia can occur within 4 hours of onset

compartment syndrome Manifestations

7 P’s

• pain out of proportion

• pressure

• paresthesia

• pallor

• paralysis

• pulselessness

• cold

Fat embolism

• rare complciation 10% mortality rate

• fat globules from within bone travel to circulation

• delayed onset 24-48 hours after injury

• impairs perfusion

  • chest pain, dyspnea

  • confusion

  • petechial rash on chest, neck, axilla

Rhabdomyolysis

• breakdown of damaged skeletal muscle to myoglobin

• cannot pass through nephron

• result: obstructed renal tubules—> acute tubular necrosis

• signs: dark to reddish brown urine

Fracture examples

• colles: distal radius

• pelvic: high mortality, risk of bleeding

• hip fracture

Osteomyelitis

severe infection of bone, bone marrow and surrounding soft tissue (mainly affects children)— causes increase pressure in bone

• most common pathogen: Staph A

pathogen enters body either

• directly (80%) due to a locally spreading infection

• indirectly (20%) through blood

routes of entry: open wound, foreign body, chronic diabetic or pressure wounds

• sequestra : dead bone that separated from living bone

• involucrum: new bone

Osteomalacia

result of vitamin D deficiency

• bone loses calcium and becomes soft

• metabolic bone disease

osteoporosis

chronic progressive metabolic bone disease marked by low bone mass and deterioration of bone tissue that leads to increased bone fragility

• bone loss exceeds bone production

• metabolic bone disease

• known at the silent thief (major contributor to fractures)

• more common in women

• peak bone mass 9achieved by 20)

• bone loss after age 35-40

• rapid bone loss for women at menopause

• kyphosis

• bisphosphonates!!

Osteoarthritis

gradual loss of articular cartilage = narrowed joint space/cartilage destruction “wear and tear”

formation of osteophytes at joint margins (bone spurs, not normal)

• not systemic

• progressive

• microscopic inflammation only

• affects synovial joints

• irreversible

Osteoarthritis Risk factors/causes

• advanced age

• obesity

• manual labor

• post menopausal women

• previous injury

• meds

• congenital abnormalities

Osteoarthritis Manifestations

• mild to severe pain— worsens with activity

• joint stiffness — improves within 30 minutes in morning

• asymmetric

• crepitus

• leads to loss of function

Osteoarthritis Joint deformities

• varus deformity

• valgus deformity

• Heberdens nodes (distal interphalangeal joints)

• Bouchards nodes (proximal interphalandeal joints)

Osteoarthritis Diagnostic criteria

X ray

• detect joint space narrowing, increased bone density, osteophytes

• early joint changes

• synovial fluid analysis: fluid is clear yellow with no signs of inflammation

• labs= normal

Osteoarthritis management

• mild to moderate joint pain: acetaminophen

• moderate to severe: NSAIDs

chronic pain = try not to use opioids, causes tolerance

• intraarticular corticosteroid injections

Rheumatoid Arthritis

autoimmune disorder, chronic, progressive, remission and exacerbations, systemic

• more common in women, peak incidence 30-50 years old

• overreactive inflammatory response

• type 3 hypersensitivity

• Rheumatoid factor antibody made against the IgG antibodies

• immune complexes formed

immune complex consequences

activation of complement and inflammatory response

• t helper cells CD4 activated, stimulating immune cells to secrete pro inflammatory cytokines (IL1 , IL6 , TNF)

end result: thickened synovial membrane and damaged cartilage

• chronic inflammation