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Pathophysiology > Patho Exam #3 > Flashcards

Patho Exam #3 Flashcards

1
Q

Anatomy

A
  • Oral Cavity: intakes and passage of food
  • Esophagus: passage of food, no digestion, no enzymes
  • Stomach: mechanical churning of food, beginning breakdown of food, gastric/enzyme “juices”
  • Small intestine: most absorption
  • Large intestine: absorb water, salts, vitamins, elimination of undigestible food and residue
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2
Q

Carbohydrate Digestion

A 
•Mouth: salivary amylase
•Duodenum: pancreatic amylase
oPolysaccharides → disaccharides
•Brush border enzymes
oDisaccharides → monosaccharides
oMonosaccharides absorbed in blood
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3
Q

Protein Digestion

A 
•Stomach: pepsinogen 
  oActivated pepsin by acid in stomach
  oBreaks protein into polypeptides
•Duodenum: pancreatic trypsinogen
  oActivated to trypsin in duodenum
  oBreaks proteins into polypeptides
•Brush border enzymes
  oBreaks polypeptides into 2-3 amino acid peptides
oPeptides absorbed into blood
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4
Q

Fat Digestion

A
  • Duodenum: bile; emulsifies fats
  • Duodenum: pancreatic lipase; breaks triglycerides into glycerol and fatty acids
  • Jejunum: packages digested fats as chylomicrons; passed to the lymph
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5
Q

Hemorrhage above stomach

A

frank hematemesis: bright red blood in vomit

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6
Q

Hemorrhage into the stomach with partial digestion of blood

A

coffee-ground vomitus

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7
Q

Hemorrhage in the intestine with blood mixing into stools

A

occult blood

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8
Q

Hemorrhage into the intestines with large volumes of blood

A

melena

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9
Q

Hemorrhage in the rectum

A

red blood coating stools

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10
Q

Clinical Manifestations in GI Dysfunction: Abdominal pain

A

oSymptom of a number of GI disorders
oParietal pain
oVisceral pain
oReferred pain

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11
Q

Clinical Manifestations in GI Dysfunction: GI bleeding

A

oMortality rate 6-10%
oIncrease in older adults, especially in older women
oAssociated with NSAIDS (Non-steroidal anti-inflammatory drug)
oCan be caused by ibuprofen

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12
Q

Clinical Manifestations in GI Dysfunction: Upper GI bleeding

A

oEsophagus, stomach, duodenum
oMost severe is by sudden onset
oArteriole: bright red
oVenous: darker red

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13
Q

Clinical Manifestations in GI Dysfunction: Lower GI bleeding

A

bleeding from jejunum, ileum, colon, or rectum

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14
Q

Hematemesis

A

bleeding in vomit, somewhere above the stomach, Upper GI

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15
Q

Hematochezia

A

upper GI bleed can manifest itself in stool, bright red stools, several areas can be bleeding

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16
Q

Melena

A

lower GI, bleeding into intestine with large amounts of blood

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17
Q

Occult bleeding

A

smear stool and get it tested, lower GI

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18
Q

Dysphagia

A

difficulty swallowing

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19
Q

Achalasia

A

smooth muscle in esophagus and lower esophageal sphincter (in relaxed state); Esophagus can slide up and down

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20
Q

Gastroesophageal reflux disease (GRD)

A

oSymptom of secondary problem
oLower ES weaker and allows gastric contents to go up esophagus
o14-20% people suffer from this once a week
oBurning tight sensation
oReflux of chime from stomach to esophagus
oIf causes inflammation to esophagus, called reflux esophagus
oNormal functioning lower esophageal sphincter maintains a zone of high pressure to prevent chime reflux
oCauses: conditions that increase abdominal pressure can contribute to GER
Diet, stress, overeating, smoking, eating too fast, obesity, pregnancy, chocolate, caffeine, anticholergics
oManifestations: heartburn (burning tight sensation below the lower sternum), regurgitation of chyme, and upper abdominal pain within 1 hour

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21
Q

Acute Gastroenteritis

A
  • Acute inflammation of GI mucosa
  • 2nd leading cause of morbidity in US
  • Occurs in all age groups
  • Epidemic outbreaks due to ingested contaminated foods
  • Viral gastroenteritis more common in winter months due to closeness (people are mostly inside and in close proximity)
  • Self-limiting: can only treat symptoms
  • Very young, elderly and those with concomitant chronic debilitating disease are at a high risk for increased mortality
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22
Q

Acute Gastroenteritis: Etiology

A

o Commonly due to infectious agents such as bacteria, virus, parasites
Bacteria: exotoxins induce hypersecretion and peristalsis – causing diarrhea and/or vomiting
Staphylococcus: 1-6 hours
E. coli: 24-72 hours
Shigella/Salmonella: 8-24 hours
Botulism: 12-36 hours
Giardia lablia: 7-21 days

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23
Q

Acute Gastroenteritis: Signs and Symptoms

A 
Abrupt onset of nausea or vomiting
 	Explosive flatulence
 	Crampy abdominal pain
 	Frequent, watery stools
 	Myalgia: muscle aches
 	Headache
 	Fever: moderate to high for viral
 	Generalized weakness and malaise
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24
Q

Acute Gastroenteritis: Diagnostic Tests

A

CBC: normal
Stool guiac: occult, hemoccult
Stool culture: chronic gastritis can break down mucosa in stomach, can be more prone to have ulcers

Caused by renal failure, sepsis, and burn victims

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25
Q

Peptic Ulcer Disease

A

• Break or ulceration in the protective mucosal lining of the lower esophagus, stomach or duodenum
• Acute and chronic ulcers
• Superficial: erosions
• Deep: true ulcers
• Duodenal ulcers: most common type
o Developmental factors
Helicobacter pylori infection: toxins and enzymes that promote inflammation and ulceration; major cause of ulcers
o Hypersecretion of stomach acid and pepsin
o Use of NSAIDS; second most common cause of ulcers
o High gastrin levels
o Acid production by cigarette smoking

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26
Q

Appendicitis

A

• Right lower quadrant pain, holds bacteria
o Rebound tenderness
o Serious complication is sepsis (peritonitis)
o Hardened feces

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27
Q

Appendicitis: etiology

A

o Obstruction with hardened feces, stricture, inflammation due to infection, foreign body or neoplasm
o Occurs in all age groups but commonly in males between 10-30
o Higher mortality rate due to complications in children, adolescents and persons over 55
o RUPTURE → PERITONITIS → DEATH

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28
Q

Appendicitis: Signs and Symptoms

A

o Acute onset periumbilical or epigastric pain which ranges from mild diffuse to severe
o Anorexia, nausea, and vomiting usually subsequent to pain onset
o Shifting of pain to right lower quadrant (McBurney’s point) after several hours
o Pain aggravated by walking or coughing
o Spasm of abdominal muscle
o Constipation usual
o Diarrhea rare
o Elderly may present with mild symptoms or unexplained weakness, anorexia, tachycardia, and abdominal distention with little pain
o Occasional radiation of pain into ipsilateral testicle or labia

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29
Q

Appendicitis

A

o Generally may or may not APPEAR SICK
o Fever 100-102
o Slight tachycardia related to pain and fever
o Abdominal point and rebound tenderness in RLQ
o Decreased or absent bowel sounds
• Diagnostics
o CBC with differential: shows leukocytosis with increased bands
o X-ray may show fecalith

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30
Q

Liver functions

A
  • Bile production
  • Protein processing and metabolism
  • Glycogen synthesis
  • Fat synthesis and metabolism
  • Detoxification/filtration
  • Clotting factor synthesis
  • Storage
  • Heat production
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31
Q

Metabolic Functions of the Liver

A

• Carbohydrate, protein, and lipid metabolism
• Sugars → stored as glycogen, converted to glucose, used to make fats
• Proteins → synthesized from amino acids; ammonia made into urea
• Fats → oxidized for energy, synthesized, packaged into lipoproteins
• Drug and hormone metabolism
o Biotransformation into water-soluble forms
o Detoxification or inactivation
• Bile production
• Hematologic disorders
o Anemia, thrombocytopenia, coagulation defects, leukopenia

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32
Q

Liver failure

A

• Skin disorders
o Jaundice, red palms, spider nevi
• Hepatorenal syndrome
o Azotemia (itching of the skin), increased plasma creatinine, oliguria
• Hepatic encephalopathy: amniotic levels reach toxic level
o Asterixis, confusion, coma, convulsions

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33
Q

Hepatitis

A 
• Inflammation of the liver caused by an infectious agent or response to exposure to a toxin
• Manifestations
o Vascular congestions
o Cellular swelling 
o Decreased hepatocyte function
o Mechanical impairment of circulation
o Toxin exposure
 	Direct or indirect hepatocyte damage
34
Q

Hepatitis A Virus (HAV)

A
  • “Infectious hepatitis”
  • Most common hepatitis in the world (61,000)
  • Found in underdeveloped countries
  • Fecal-oral route
  • Oral contamination
  • Small RNA virus
  • Usually benign
  • Self-limiting
  • Incubation 2-8 weeks
35
Q

Hepatitis B virus (HBV)

A
  • “Serum hepatitis:” blood and body fluids (saliva)
  • DNA virus
  • Parental and sexual contact
  • Acute hepatitis
  • Incubation 4-26 weeks
  • Persistent antigenemia
  • Chronic → cirrhosis
  • Percutaneously (drug use)
  • Perinatal
  • Needle sticks
  • More infectious that HIV
36
Q

Hepatitis C virus (HCV)

A
  • Common infection
  • 20% end up with cirrhosis in liver within 20 years
  • HIV patients
  • High risk of sexual behavior
  • Body piercing, tattooing
  • 170 million infected
  • Chronic infection
  • 30,000 diagnosed per year
  • “Non-A, non-b”
  • 90-95% transfusion hepatitis
  • Inoculations and blood transfusions
  • RNA-virus, unstable
  • Associates with cirrhosis and hepatocellular carcinoma
  • Incubation period 2-26 weeks
  • No immunity
  • Percutaneously: IV drug use
  • Hemodialysis
37
Q

Hepatitis D (HDV)

A
  • Chronic progression blood-borne disease
  • Terminates in cirrhosis
  • Common in Mediterranean countries, Africa, Middle East and rare in US
  • HBV can later form
  • Coinfection of HDV and HBV can make infection infectious
38
Q

Hepatitis E virus (HEV)

A
  • Water-borne infection
  • Enteric transmission
  • Self-limiting
  • Common in Asia, Indian continent, Mexico, sub-Saharan Africa
39
Q

Hepatitis G

A
  • Viral agent similar to HCV
  • Transfusion transmitted
  • Non-pathogenic
40
Q

Chronic Viral Hepatitis

A
  • Caused by HBV, HCV, and HDV
  • Principal cause of chronic liver disease, cirrhosis, and hepatocellular cancer in the world
  • Chief reason for liver transplantation in adults
41
Q

Cirrhosis

A

• Irreversible inflammatory disease that disrupts liver function and even structure
• Chronic progressive disease
• Decreased hepatic function caused by nodular and fibrotic tissue synthesis (fibrosis)
• Bilary channels become obstructed and cause portal hypertension. Because of the hypertension, blood can be shunted away from the liver, and a hypoxic necrosis develops
• Alcoholic: oxidation of alcohol damages hepatocytes
• Bilary (bile canaliculi)
o Cirrhosis begins in the bile canaliculi ducts
o Primary bilary cirrhosis (autoimmune)
o Secondary bilary cirrhosis (obstruction)
• 9th leading cause of death
• People 35-54 4th leading cause of death
• Twice as common in men

42
Q

Alcoholic Liver Disease

A

• Fatty liver (steatosis)
o Liver cells contain fat deposits; liver is enlarged
• Alcohol hepatitis: liver inflammation and liver cell failure
• Cirrhosis – scar tissue partially blocks sinusoids and bile canaliculi

43
Q

Cholectasis and Intrahepatic Bilary Disorders

A

• Bile flow in the liver slows down
• Bile accumulates and forms plugs in the ducts
o Ducts rapture and damage liver cells
Alkaline phosphatase released into blood
• Liver is unable to continue processing bilirubin
o Increased bile acids in the blood and skin
Pruritus

44
Q

Cholecytitis

A

• Inflammation of the gall bladder, usually as a result of stone formation (cholelithiasis). Infection may or may not be present. Bile is trapped in the gall bladder, acting as a chemical irritant. Gall bladder ischemia and necrosis can occur. Stone may obstruct bilary tract

45
Q

Choleithiasis (gallstones)

A

o Cholesterol, calcium salts, or mixed
o Obese
o Native Americans

46
Q

Acute and chronic cholecystitis

A

nflammation caused by irritation due to concentrated bile

47
Q

Choledocholithiasis

A

stones in the common bile duct

48
Q

Cholangitis

A

inflammation of the common bile duct

49
Q

sBilary Reflux

A
  • Gallbladder contracts
  • Bile is sent down common bile duct
  • Blockage forms in ampulla of Vater: bile cannot enter duodenum
  • Bile goes up pancreatic duct
  • Bile in pancreas disrupts tissues; digestive enzymes activated
50
Q

Disorders of the Pancreas

A

• Pancreatitis
• Activated enzymes begin to digest the pancreas cells
o Severe pain results
o Inflammation produces large volumes of serous exudate hypovolemia (autodigestion)
• Enzymes (amylase, lipase) appear in the blood
• Areas of dead cells undergo fat necrosis
o Calcium from the blood deposits in them
Hypocalcemia

51
Q

Pancreatitis

A

• Inflammation of the pancreas
• Associated with several other clinical disorders
o Caused by an injury or damage to pancreatic cells and ducts, causing a leakage of pancreatic enzymes into the pancreatic tissue
• Manifestations and evaluation
o Epigastric pain retaining to the back
o Fever and leukocytosis
o Hypotension and hypovolemia
Enzymes increase vascular permeability
o Characterized by an increase in a patient’s serum amylase level
• 3 times higher rate in African Americans than Caucasians
• Alcohol related
• Seen more in females: biliary tract problem

52
Q

Chronic Pancreatitis and Pancreatic Cancer

A

• Related to alcohol abuse
• Have signs and symptoms similar to acute pancreatitis
• Often have:
o Digestive problems because of inability to deliver enzymes to the duodenum
o Glucose control problems because of damage to islets of Langerhans
o Signs of biliary obstruction because of underlying bile tract disorders or duct compression by tumors

53
Q

Nephron Function

A

• Filters plasma
• Reabsorbs and secretes
o Tubular reabsorption and sercretion
• Forms a filtrate to protein-free fluid
• Regulates the filtrate to maintain fluid volume, electrolytes, and pH
• Glomerular filtration
o Net filtration pressure
Glomerular capillary oncotic/hydrostatic pressure
Bowman capsule oncotic/hydrostatic pressure
o Filtration rate
180 L/day

54
Q

Glomerular Filtration Rate

A

125 mL/min & 1.5 L/day

55
Q

Kidney Functions

A 
• Filters the blood
• Remove water-soluble wastes
• Help control blood pressure and composition
• Help maintain RBC levels
• Maintain homeostasis of the blood
o Balance water
o Balance sodium
o Balance potassium
o Balance acidity
56
Q

Components of Urine Formation

A
  • Filtration
  • Reabsorption
  • Secretion
  • Excretion
57
Q

Kidney stones

A

o Calculi or urinary stones
Masses of crystals, protein, or other substances that form within and may obstruct the urinary tract
o Risk factors
Gender, race, geographic location, seasonal factors, fluid intake, diet, and occupation
o Kidney stones are classified according to the minerals comprising the stones
o More common in women

58
Q

Renal Calculi (Kidney Stones)

A

• Saturation theory: urine is supersaturated with stone components
• Matrix theory: organic materials act as nidus for stone formation
o Precipitation of a salt from liquid to solid state
Temperature and pH
• Inhibitor theory: a deficiency of substances that inhibit stone formation
• Four types of kidney stones:
o Calcium stones (ex: oxalate or phosphate); most common
70-80% of all of stones that require treatment
o Magnesium ammonium phosphate stones (struvite)
o Uric acid stones
o Cystine stones
• Contributing factors
o High purines and gout

59
Q

Kidney Stones

A

• Most common sign is pain in lower back
• Manifestation
o Renal colic: stretching of tubules where stone is stuck
• Evaluation
o Stone and urine analysis
o IV pyelogram: ask patient if they are allergic to iodine
o Kidney, ureter, bladder x-ray (KUB)
o Spinal abdominal CT
• Treatment
o High fluid intake, decreasing dietary intake of stone-forming substances stone removal (if stone doesn’t pass on its own)
Lithotripsy: laser beam that breaks up stone and makes it easier to pass

60
Q

Urinary Tract Infections

A

• 2nd most common bacterial disease
• Most common in women and pregnant women
• More than 8 million office visits/year
• Greater than 100,000 people hospitalized each year
• Gram-negative bacteria
• Systitis: lower UTI that is localized in the bladder; inflammation in the bladder
• Upper UTI: kidney involvement
• Bacteria usually enter through the urethra
• Host defenses include:
o Washout phenomenon
o Protective mucus
o Local immune responses and IgA
o Normal bacterial flora
• E. coli most common pathogen

61
Q

UTI Signs & Symptoms

A
  • Burning/itching
  • Frequent feeling that they have to use the restroom
  • Blood in urine
  • Dysuria: pain in urination
  • Confusion in elderly
  • Urine cloudy and have sediment
  • Urinalysis (UA) and urine culture and sensitivity
62
Q

When Kidneys Fail

A

• Less waste is removed
• More waste remains in the blood
• Nitrogenous compounds build up in the blood
o BUN: Blood urea nitrogen
o Creatinine: renal function approx. by: initial creatinine level/current creatinine level

63
Q

Acute Renal Failure: Prerenal

A

o Decreased blood supply
Shock, dehydration, vasoconstriction
o Oliguria: less than 30 mL/hour
o Glomerular filtration rate (GFR) declines because of decrease in filtration pressure
o Cause is pre- (before) kidney (blood flow to kidney related)
o Most common cause
o Caused by impaired renal blood flow

64
Q

Acute Renal Failure: Intrinsic (Intrarenal)

A 
o Acute tubular necrosis (ATN): most common cause of intrarenal renal failure
o Ischemia occurs
o Usually post-op
o Sepsis/trauma/burns
o Within the kidney
o Postischemic or nephrotoxic
65
Q

Acute Renal Failure: Postrenal

A

o Urine flow is blocked
Stones, tumors, enlarged prostate
o BPH: benign prostatic hypertrophy: enlarged prostate
o After kidney cause – structural
o Occurs within urinary tract obstructions that affect the kidneys bilaterally

66
Q

Phases of ARF

A 
• Oliguria phase: less than 30 mL/hour
o Seen as kidney disease worsens
o Lasts several hours or 1-3 weeks
• Diuretic phase
o Increase of urine volume
o Monitor fluid and electrolyte status
o Renal tubules still damaged, but person begins to recover
• Recovery phase
o Can take 3-12 months to recover
o GFR back to baseline status
67
Q

Chronic Renal Failure (CRF)

A 
• Progressive, irreversible loss of renal function that affects nearly all organ systems
• GFR: less than 60 mL/min
• Stages
o Chronic renal insufficiency
o Chronic renal failure
o End-stage renal failure: GFR drops to 15 mL/min
• Proteinuria and uremia
• Creatinine and urea clearance
• Fluid and electrolyte balance
o Sodium and water balance
o Phosphate and calcium balance
o Potassium balance
o Acid-base balance
• Fewer nephrons are functioning
• Remaining nephrons must filter more
o Hyperperfusion
o Hypertrophy
68
Q

Development of CRF

A

• Diminished renal reserve
o Nephrons are working as hard as they can
• Renal insufficiency
o Neprons can no longer regulate urine density
• Renal failure
o Neprons can no longer keep blood composition normal
• End-stage renal disease

69
Q

Uremia

A 
• Urine in the blood
• Renal filtering function decreases
o Altered fluid and electrolyte balance
 	Acidosis, hyperkalemia, salt wasting, hypertension
• Wastes build up in blood
o Increased creatinine and BUN
 	Toxic to CNS, RBCs, platelets
• Kidney metabolic functions decrease
o Decreased erythropoietin
o Decreased Vitamin D activation
70
Q

Hemodialysis

A
  • Filtering blood
  • Diffusion of dissolved particles from one compartment to the other through semi-permeable membrane
  • Cleanses accumulated wastes, removes excess fluids, metabolic by-products
  • Maintains/restores buffer system & electrolyte levels
71
Q

Peritoneal Dialysis

A

• Dialyzing membrane
• Uses diffusion and osmosis principles to exchange fluid and solutes
• Peritoneal cavity is rich in capillaries so excellent blood supply for exchange
• Contraindications: peritonitis, recent abdominal surgery, abdominal adhesions, impending transplant
• Types
o Continuous ambulatory peritoneal dialysis dialysis (CAPD)
o Automated peritoneal dialysis (CCPD)

72
Q

Complications of Peritoneal Dialysis

A
  • Peritonitis
  • Abdominal pain
  • Insufficient flow
  • Leakage around catheter site
73
Q

Nursing Implementation

A
  • Monitor vital signs, lab values, weights, I&O, adequate nutrition
  • Monitor patency of access device
  • Hold antihypertensives and sedatives prior to procedure
  • Hold medications which can be filtered out during dialysis
  • Monitor for post-procedure complications
74
Q

Complications of Dialysis

A
  • Hypotension & shock
  • Muscle cramps
  • Electrolyte changes
  • Sepsis
  • Blood loss
  • Hepatitis
75
Q

Fracture Classifications

A

Complete (broken all the way through) or incomplete (damaged but still in one piece)
 Closed (skin hasn’t been compromised) or open (bone sticking out of skin)
Comminuted: two or more fragments that are broken
Linear: parallel fracture to bone
Oblique: slanted
Spiral: when bone is twisted apart
Transverse: straight across bone

76
Q

Fracture Classifications 2

A

• Greenstick: chunk of bone missing, bone bends and cracks
• Torus: (buckling) incomplete fractures of shaft of long bone caused by impaction
• Bowing: incomplete fractures of long bones in children
• Pathologic: caused by disease that led to weakness of bone structure
• Stress: tiny cracks in a bone due to overuse
o Fatigue and insufficiency
o Transchondral: in articular surface of bone

77
Q

Bone fractures

A

broken bone can cause damage to the surrounding tissue, the periosteum, and the blood vessels in the cortex and marrow
Hematoma formation
Bone tissue destruction triggers an inflammatory response
Procallus formation

78
Q

Manifestations of Fractures

A
  • Unnatural alignment, swelling, muscle spasm, tenderness, pain, impaired sensation, and possible muscle spasms
  • Deformation and weakness
  • Change in alignment
79
Q

Treatment of Fractures

A

• Closed manipulation, traction, and open reduction
• Internal and external fixation
• Improper reduction or immobilization
o Nonunion, delayed union, and malunion

80
Q

Osteoporosis

A 
• Porous bone
• Poorly mineralized bone
• Bone density
o Normal bone: 833 mg/cm2
o Osteopenic bone: 833 – 648 mg/cm2
o Osteoporosis: <648 mg/cm2
• Demonstrated by reduced bone mass/density and an imbalance of bone reabsorption and formation
• Bone histology is usually normal but it lacks structural integrity
• 80% women
• Asian background
• Insufficient dietary calcium
81
Q

Potential Causes of Osteoporosis

A
  • Decreased levels of estrogen and testosterone
  • Decreased activity level
  • Inadequate levels of vitamins D and C, or Mg++
  • Corticosteroids and cancer treatments
  • Usually in bigger joints
82
Q

Osteomyelitis

A

• Most often caused by a Staphyloccal infection
• Most common cause is open wound (exogenous); also can be from a blood-borne (endogenous) infection
• Manifestations
o Acute and chronic inflammation, fever, pain, necrotic bone
o Night sweats, nausea
o Constant bone pain
o Unrelieved by rest
• Treatment
o Antibiotics, debridement, surgery, hyperbaric oxygen therapy
o Vigorous antibiotics for several weeks
o Surgical removal of tissue
o Hyperbaric oxygen therapy

Pathophysiology (2 decks)

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