Exam 5 Flashcards
(317 cards)
1
Q
What is the function of the mouth
A
-digestion starts
-breaks up food
-language
2
Q
What is the function of the salivary glands
A
-saliva moistens and lubricates food
-amylase digests polysaccharides
3
Q
What is the function of the pharynx
A
swallows
4
Q
What is the function of the esophagus
A
transports food
5
Q
What is the function of the stomach
A
-stores and churns food
-pepsin digests protein
-HCl activates enzymes, breaks up food, kills germs
-mucus protects stomach wall
-limited absorption
6
Q
What is the function of the liver
A
-breaks down and builds up biological molecules
-stores vitamins and iron
-destroys old blood cells
-destroys poisons
-bile aids digestion
7
Q
What is the function of the gallbladder
A
-hormones regulate BG levels
-bicarbonates neutralize stomach acid
-trypsin and chymotrypsin digest proteins
-amylase digests polysaccharides
-lipase digests lipids
8
Q
What is the function of the small intestine
A
-completes digestion
-mucus protects
gut wall
-absorbs nutrients, most water
-peptidase digests proteins
-sucrases digest sugars
-amylase digests polysaccharides
9
Q
What is the function of the large intestine
A
-reabsorbs some water and ions
-forms and stores feces
10
Q
What is the function of the rectum
A
stores and expels feces
11
Q
What is the function of the anus
A
opening for elimination of feces
12
Q
Dysphagia
A
difficulty swallowing
13
Q
Dysphagia etiology
A
-neuromuscular dysfunction
-structural dysfunction
14
Q
dysphagia complications
A
-malnutrition
-aspiration
15
Q
Dysphagia S&S
A
-pain/cough with swallowing
-choking/aspiration
-malnutrition
-weight loss
-regurgitation
-pooling of food
-drooling
16
Q
Dysphagia treatment
A
-thickener
-aspiration precautions
-keep head up
-surgical correction
-dont use straw, increases risk for aspiration
17
Q
esophageal pain types
A
-pyrosis (heartburn)
-pain in middle of chest (mimics angina pectoris, may radiate)
18
Q
esophageal pain pathophysiology of pyrosis
A
reflux gastric contents into esophagus
-feeling of heartburn
19
Q
esophageal pain pathophysiology chest pain
A
-esophageal distention
-powerful esophageal muscle contraction
20
Q
esophageal pain S&S
A
-chest pain
-SOB
-retrosternal burning
-water brash (regurgitation sour or tasteless saliva into mouth)
-nausea
21
Q
esophageal pain treatment
A
-prevention
-causative agent specific
22
Q
diarrhea
A
increase in frequency and fluidity of bowel movements
23
Q
what are some causes of acute diarrhea
A
-infection
-stress
-food allergy
-leakage stool around an impaction
24
Q
chronic diarrhea
A
-greater than 4 weeks
-malabsorption
-chronic infection
25
diarrhea pathophysiology
-motility disturbance: decrease contact time of chyme with small intestine
-exudative: inflammatory process of mucous, blood, protein
-toxins stimulate intestinal fluid secretion impairing absorption
-increased amount poorly absorbed solutes
26
constipation
-small, infrequent or difficult bowel movements
-fewer than 3 stools per week
27
constipation etiology
-low fiber diet
-slow peristalsis
28
constipation risk factors
slow peristalsis in elderly, post op, narcotic users
29
constipation complications
lead to impaction
30
gastroesophageal reflux disease (GERD)
-backward flow of gastric contents into esophagus
-may or may not produce symptoms
-#1 cause esophageal pain
-leads to metaplasia
31
gastroesophageal reflux disease (GERD) pathophysiology
-incomplete closure lower esophageal sphincter
-increased abdominal pressure
-drugs
32
GERD incomplete closure lower esophageal sphincter may be affected by
-fatty foods
-caffeine
-ETOH (alcohol)
-smoking
-sleep position
-obesity
33
GERD increased abdominal pressure is affected by
-pregnancy
-hiatal hernias
-tight clothing
34
drugs causing GERD
-beta agonist
-CCB
-nitrates, anticholinergics
35
GERD S&S
-heartburn (dyspepsia)
-regurgitation
-dysphagia
-chronic cough, asthma, aspiration pneumonia
-chest pain after meal
36
GERD complications
-bleeding
-esophageal strictures (ulcers)
-barrett esophagus (from metaplastic mucosa)
-cough, asthma, laryngitis
37
GERD treatment
-increase function of lower esophageal sphincter: HOB elevated
-surgical repair
-H2 blockers, PPI
-avoid alcohol, fatty foods, eating before bed, quit smoking, small meals. increase fluid
38
Hiatal hernia
-cause not understood
-associates with conditions of increased intra abdominal pressure: ascites, pregnancy, obesity, chronic straining/coughing
39
Hiatal hernia pathophysiology
defect in diaphragm allowing portion of stomach to pass into thorax
40
Hiatal hernia S&S
-ulcerations
-predisposed to GERD: heartburn, chest pain, dysphagia
41
Hiatal hernia complications
incarcerated hernia- strangulated: rare and life threatening, portion of stomach caught above diaphragm and occluded
42
Hiatal hernia treatment
-alleviate symptoms, avoid food late at night, elevate head (same as GERD)
-surgery for incarceration and intractable reflux
43
Gastritis
inflammation stomach lining
44
What can cause Acute gastritis
-overuse alcohol
-aspirin
-NSAIDS
-tobacco
45
Chronic gastritis
precursor to cancer
-helicobacter pylori
46
Acute gastritis pathophysiology
self limiting
47
Chronic gastritis pathophysiology
Helicobacter pylori promotes inflammation in gastric mucosa, interferes with prostaglandins which normally provide protection
48
Gastritis S&S
-anorexia
-nausea
-vomiting
-hematemesis (vomit blood)
-dyspepsia (burps burn)
-postprandial discomfort (after eating)
-chronic gastritis: pernicious anemia
49
Gastritis complication
acid makes hole in stomach if untreated
50
Gastritis treatment
-remove causative agent
-small meals, lower gastric pH, avoid irritants
-antibiotic to get rid of helicobacter pylori
51
Gastroenteritis
(food poisoning)
-irritation stomach and small intestine lining from pathogen or toxin
-norovirus is common cause
-usually self limiting
52
Acute gastroenteritis pathophysiology
-direct pathogen or toxin invasion in GI tract causing inflammation
-ingested bacteria
-imbalance normal flora: predisposes travelers gastroenteritis
53
Chronic gastroenteritis pathophysiology
-result to another GI disorder such as ulcerative colitis or Crohn's
54
Gastroenteritis S&S
-fluid and electrolyte imbalance signs (dry)
-abdominal discomfort
-pain
-nausea, vomiting, diarrhea
-12-72 hr course
-elevated temp and malaise
55
Gastroenteritis complications
dehydration and electrolyte imbalance
56
Gastroenteritis treatment
fluid replacement and electrolyte replacement
57
Peptic ulcer disease (PUD)
-from acid and pepsin
-injuries in esophagus, stomach, duodenum, jejunum
-slight to mucosal injury ulcerations in severity
58
Peptic ulcer disease (PUD) etiology
-H pylori
-aspirin/NSAIDS
-caffeine
-diet/stress
-smoking
59
Peptic ulcer disease (PUD) stomach pathophysiology
-hypersecretion HCL acid
-breaks in lining may be exacerbated by meds
-10 min pain onset
60
Peptic ulcer disease (PUD) duodenum pathophysiology
-excessive secretion acid
-couple hours till pain onset
61
Peptic ulcer disease (PUD) S&S
-epigastric pain
-nausea
-abdominal upset
-chest pain
62
Peptic ulcer disease (PUD) complications
GI bleeding from it eroding to blood vessel
-upper stomach: dark tarry stool
-lower stomach: bright red stool
63
Peptic ulcer disease (PUD) treatment
-PPI (protonic pump inhibitor)
-eradication H pylori
-coating agents
-smoking cessation
-avoid aspirin/NSAIDS
-avoid stress and dietary irritants
64
Ulcerative colitis (UC)
-inflammatory disease of mucosa of rectum and colon
-affects epithelial layer
-remission/exacerbations
-mostly lg intestine
65
ulcerative colitis (UC) etiology
poorly understood
-genetic: Jewish
-environmental
-immunological
-stress doesnt cause but increases severity of attack
66
ulcerative colitis (UC) pathophysiology
-immunological changes in cytotoxic T cells
-leukocytes invade and crypt abscesses develop
-abscesses drain, become necrotic and ulcerate
-sloughing: bloody, mucous filled stools
-increased risk colorectal cancer
67
Ulcerative colitis (US) S&S
-abdominal pain
-blood, mucous filled diarrhea (brighter red)
-rectal bleeding
-weight loss
-anorexia
-anemia
-dehydration
68
Ulcerative colitis (UC) treatment
-steroids: short term
-immunosuppressive therapy
-antibiotics
-colectomy and ileectomy
69
Crohns diseases
-inflammation extends through all layers intestinal wall
-commonly effects terminal ileum
-mostly sm intestine
-diagnosed by age 20
-cause unknown
70
Crohns disease risk factors
-genetics
-ethnicity: Caucasians
-Jewish
-smoking
-urban dwellers
71
Crohns disease pathophysiology
-lymph nodes in GI tract enlarge blocking flow
-inflammation leads to deep linear ulcer and crypt abscess
-thickened with fibrous scarring
-bowel becomes incapable of absorbing intestinal contents (cant absorb food)
72
Crohns disease S&S
-constant abdominal pain in RLQ during flareups!
-diarrhea
-abscesses
-weight loss
-nutrient deficiencies
-fluid imbalance
-fever
-distention
-arthritis
-uveitis: eyes
-cheilitis: lips
-dermatological lesions: erythema nodosum
(more systemic than ulcerative colitis)
73
Crohns disease complications
-Perianal fissures
-Fistulas
74
Crohns disease treatment
-antitumor necrosis factor
-corticosteroids
-antidiarrheals
-opoids
-stress reduction
-vitamin supplements
-limit fruits, veggies, high fiber, dairy, spicy fatty foods, carbonates and caffeinated drinks
75
Enterocolitis/Pseudomembranous colitis
-c diff diarrhea
-inflammation and necrosis large intestine
-"antibiotic associated colitis"
-can be from surgery/cancer as well
76
Enterocolitis/Pseudomembranous colitis pathophysiology
-antibiotic exposure: kills microflora then C diff toxins infect
-bacterial toxins
-colon develops "pseudo membrane" with leukocytes, mucous, fibrin, inflammatory cells
-mucosal necrosis
77
Enterocolitis/Pseudomembranous colitis S&S
-diarrhea (often bloody)
-abdominal pain
-increased HR first sign
-major cause of fever among hospitalized patients receiving antibiotics!
78
Enterocolitis/Pseudomembranous colitis complications
perforation
79
Enterocolitis/Pseudomembranous colitis treatment
-stop antibiotic
-oral flagyl or vancomycin
-supportive care
80
appendicitis
-inflammation of vermiform appendix
81
appendicitis risk factors
-peak age 10-19yrs
-more common in men
-low fiber diet
82
appendicitis pathophysiology
-caused by obstruction
-inflammation can lead to necrosis of appendix and lack of perfusion
-infection
-perforation
-peritonitis (inflammation peritoneum from bacteria or irritating substances)
83
appendicitis S&S
-generalized periumbilical for 1-3 days
-pain localizes to RLQ (McBurneys point!)
-rebound tenderness!
-nausea
-diarrhea
-anorexia
-fever: increased WBC!
84
appendicitis treatment
-removal
-open surgery of ruptured or perforated
-laparoscopic is preferred removal
-antibiotic therapy
-fluid replacement
-fever still persists for 1-2 days after surgery
85
irritable bowel syndrome (IBS) risk factors
-more common females
-onset before age 35
86
irritable bowel syndrome (IBS) pathophysiology
-poorly understood
-disorder of motility
-increased wave activity in colin
-heightened sensory response to distention and stimulation
-greater visceral pain sensitivity
-no test to determine
87
irritable bowel syndrome (IBS) S&S
-alternating diarrhea/constipation
-abdominal pain
-different variations
-mucous in stool
88
irritable bowel syndrome (IBS) treatment
-anti diarrheal agents
-anti spasmodic agents
-increase fiber
-hydration
89
colon polyps
-protrusion into lumen of GI tract (unknown cause)
-benign or not yet malignant lesion
-found in colonoscopy
-chunk of tissue
90
colon polyps treatment
removal upon identification
91
colon cancer risk factors
-over age 40
-high fat, low fiber diet
-obesity and insulin resistance
-inactivity
-african american
-tobacco
-heredity!
-ulcerative colitis, chrons disease, polyps (remove to prevent cancer)
92
Colon Cancer Pathophysiology
unknown
93
colon cancer S&S for right side of colon
-obstruction
-abdominal cramping/fullness
-ribbon or pencil like stools
-blood or mucous in stool
94
Colon cancer S&S for rectum
-change in bowel habits
-rectal fullness (late)
95
Colon cancer treatment
-surgical removal so need colostomy from portion of colon being removed
-chemo
-radiation
-prevention: screening age 50
96
warning signs GI tract cancer
-black tarry or bloody stool
-pencil shaped stool
-change in bowel habits
97
bowel obstruction internal etiology
tumors, fecal impactions, inflammation, strictures
98
bowel obstruction external etiology
-adhesions, hernias
99
bowel obstruction non mechanical etiology
loss or decreased peristalsis
100
bowel obstruction pathophysiology
-intestinal contents accumulate above obstruction causing failure to absorb contents and abdominal distention
-loss fluid from vascular space
-fluid/electrolyte and acid/base imbalance
101
bowel obstruction complications
-hypovolemic shock then death
-necrosis and perforation if blood flows cut off
102
bowel obstruction S&S
-N/V
-hiccups
-no gas and obstipation
-pain
-distention: rounded and tight!
-high pitched bowel sounds or absent bowel sounds!
-dehydration
-hypotension
-shock
103
bowel obstruction treatment
-NG tubes
-fluid and electrolyte replacement
-pain management
-surgical correction
-dont give narcotics
104
peritonitis etiology
-contamination peritoneal cavity
-perforation visceral organs
-ascending infections
-hematopoietic/lymphatic spread
-leakage during surgery
105
Peritonitis Pathophysiology
inflammation of peritoneum causes vasodilation/capillary permeability and fluid shifts to peritoneal cavity
-fluid/electrolyte and pH imbalances
106
peritonitis complications
hypovolemic or septic shock, multiple system organ failure and death
107
peritonitis S&S
-rigid board like abdomen from fluid or blood!
-shoulder and thorax pain!
-rebound tenderness!
-no gas or BM!
-N/V
-high fever
-decreased bowel sounds
-increased HR and WBS
-hiccups
-signs of shock
108
peritonitis treatment
-remove cause with surgery
-antibiotics
-fluids
-increase BP meds
109
role of bile
-aid in digestion of lipids
-transport waste products: bilirubin, cholesterol, IgA, toxins
110
bile is formed in the
liver
111
bile is stored in the
gallbladder and bile ducts
112
Cholelithiasis etiology
-gallstones composed of mainly cholesterol
-many asymptomatic
113
Cholelithiasis risk factors
forty, fat, fair, female
114
Cholelithiasis pathophysiology
-supersaturation of bile with cholesterol
115
Cholelithiasis S&S
-persistent RUQ abdominal pain (biliary colic) from obstruction of cystic duct by gallstone
-sometimes radiates to back
-N/V
-often precipitates by fatty meal followed by abdominal pain
116
Cholelithiasis diagnosis
ultrasound
117
Cholelithiasis treatment
-Surgery: cholecystectomy
-Lithotripsy: mechanical breakdown of stones
118
Cholecystitis
inflammation of gallbladder wall following stimulating event
119
Cholecystitis pathophysiology
-obstruction of cystic duct which passes into bile duct from gallbladder
-stasis of bile
120
Cholecystitis complications
if left untreated the gangrene of gallbladder wall may rupture
121
Cholecystitis S&S
-acute severe right upper abdominal pain
-fever
-nausea, vomiting, eructation (burping)
-heartburn
122
Cholecystitis treatment
-pre treatment with antibiotics
-percutaneous catheter or endoscopic drainage with stent placement
-open or laparoscopic surgery
123
Chronic Cholecystitis
-chronic inflammation of gallbladder
-diabetes and obesity are predisposing factors
-sporadic symptoms
124
acute pancreatitis predisposing factors
-biliary tract disease
-elevated triglycerides
-alcohol abuse
-infectious origin
-hypercalcemia
insecticides
125
acute pancreatitis pathophysiology
obstruction pancreatic duct by stone or other cause
-outflow of pancreas gets blocks and enzymes stay and break down pancreas
126
acute pancreatitis S&S
-increasing pain in LUQ
-radiates to back
-guarded position
-cullens sign: blueish coloration around umbilicus
-grey turner sign: red/brown discoloration at flank
127
acute pancreatitis diagnosis
serum lipase and amylase
-ultrasound
128
acute pancreatitis treatment
-NPO: nasogastric suctioning, TPN
-IV fluids
-pain management
129
chronic pancreatitis etiology
vast majority of cases are related to alcohol abuse. African americans are most likely race. It is due to chronic inflammatory lesions within the pancreas and destruction of endocrine and exocrine parenchyma.
130
Chronic pancreatitis clinical manifestations
Malabsorption of fats and fat soluble vitamins
131
What is treatment for chronic pancreatitis
Endocrine and exocrine insufficiency management: oral hypoglycemics, insulin, low fat diet, and pancreatic enzyme replacement
132
What are risk factors for pancreatic cancer
smoking, alcohol abuse, diabetes, high fat diet, excessive salt intake, nitrates, and older age
133
What are clinical manifestations for pancreatic cancer
It has an insidious onset, with dull epigastric or back pain. Jaundice, weight loss/anorexia, and nausea/vomiting
134
How is pancreatic cancer treated
Has a 99% mortality rate. Pain control, supportive care, and chemo/radiation
135
Describe the livers dual blood supply
25% comes from hepatic artery while 75% comes from the portal vein that drains capillary bed of alimentary canal and pancreas. This blood drains into the hepatic vein then onto the inferior vena cava
136
Name 7 manifestations of liver disease attributable to hepatocellular failure
Jaundice, decreased clotting factors, hypoalbuminemia, glucose imbalance, decreased absorption of vitamins D and K, feminization, and hepatic encephalopathy
137
Name 5 manifestations of liver disease attributed to portal hypertension (disruption of blood flow)
This is GI congestion leading to: esophageal varices, gastric varices, hemorrhoids, splenomegaly, and ascites
138
What is the etiology of jaundice
Yellow/green staining of tissues by bilirubin due to impaired bilirubin metabolism. One of the most characteristic signs of liver dysfunction
139
Describe pathogenesis of jaundice throughout pre-hepatic, hepatic, and post-hepatic
Pre-hepatic:
hemolysis and ineffective erythropoiesis
Hepatic:
Impaired liver function
post-hepatic:
defective transport of bile salts and obstruction
140
Describe the etiology and pathogenesis of portal hypertension
elevated pressure in the portal system leads to sluggish or obstructed flow through the portal vein/system. Venous drainage of much of the GI tract is congested. Usually the result of alcoholic or post hepatic cirrhosis (in western society)
141
Describe the clinical manifestations of portal hypertension
caput medusae (superficial periumbilical varices) as well as esophageal, gastric, and rectal varices
142
What is the etiology/pathogenesis of gastroesophageal varices
Collateral venous pathway that occurs due to portal hypertension. As portal pressure elevates, becomes vulnerable to rupture. Main cause of death in chronic cirrhosis
143
What are clinical manifestations of gastroesophageal varices
Hematemesis, melena, rapid intestinal transit and vigorous bleading
144
How do we treat gastroesophageal varices
fluid resuscitation (normal saline). Medications to lower portal pressure or reduce flow to susceptible organs: vasopressin, nitroglycerin, and somatostatin.
145
Describe hepatic encephalopathy etiology/pathogenesis
exact cause unclear. Hepatic failure or severe chronic liver disease. Associated with elevated ammonia levels. Asterixis (classic physical finding) is a "liver flap" spastic jerking of hands when in forced extended position
146
Describe clinical manifestations of hepatic encephalopathy from Grade 1-Grade 4
Grade 1: mild confusion, no flap. Grade 2: drowsy, confused, flap present Grade 3: stuporous, marked confusion, flap present Grade 4: coma, no flap
147
How do we treat hepatic enecphalopathy
identify precipitating factors: GI bleeding. Reduce dietary protein intake. Diuretics to enhance elimination of nitrogenous wastes. Osmotic cathartic (lactulose) and antibiotics to reduce normal flora to reduce protein breakdown
148
Describe ascites etiology and pathogenesis
Accumulation of fluid in peritoneal cavity
Advanced liver disease:
Portal hypertension
Hypoalbuminemia
Intraabdominal accumulation of sodium, water, and protein
Also caused by:
Malignancy
Infection
Pancreatitis
Nephrosis
Cardiac failure
149
List clinical manifestations of ascites
Abdominal distention
Difficulty breathing
Abdominal or umbilical herniation
150
What is the treatment for ascites
Reduce dietary sodium
Diuretics
Bedrest
Therapeutic paracentesis
151
What is the etiology for cirrhosis
Irreversible end stage of multiple liver diseases
Severe acute hepatitis
Chronic hepatitis
Alcoholism
Toxic hepatitis
Hepatitis C
Nonalcoholic fatty liver disease – related to DM, obesity, hypertriglycemia
152
What is the pathogenesis of cirrhosis
Fibrosis and wide spread scarring secondary to inflammation
Results in permanent alteration of hepatic blood flow
Decreased liver function results
153
What are clinical manifestations of cirrhosis
Jaundice
Portal hypertension
Esophageal varices
Ascites
Hepatic encephalopathy
154
What is the treatment for cirrhosis
Nutritional supplements
Antacids
Diuretics
155
What is an alcoholic fatty liver and describe some treatments
Abnormal deposits of fat in liver cells
More fat than liver can metabolize
Most from ETOH (5 beers or glasses of wine per day) but also:
Diabetes
Obesity
TPN
Drugs
Normally asymptomatic
Treatment:
Stop alcohol intake
Nutritional support
If left untreated may go on to progressive liver fibrosis and cirrhosis
156
What is alcoholic hepatitis and give some treatments
Active inflammation Associated with “binges” Ranges from mild to very severe
Liver shows signs of hepatocyte necrosis
Treatment:
Stop alcohol intake
Nutritional support
Steroids
Complicated by DTs
157
Describe the etiology of hepatitis A (enteric)
Transmission
Fecal-oral
Sexual (oral-anal contact)
Common in areas of overcrowding
Day care centers
Institutional settings
158
What is the pathogenesis of hepatitis A virus (enteric)
Despite the cause, changes to the liver are usually similar in each type of viral hepatitis
Liver call destruction
Self-destruction of cells
Tissue death
Anorexia
Jaundice
Hepatomegaly
159
What is treatment for hepatitis A virus
Vaccination
Added to routine childhood vaccines in 2006
May be vaccinated after exposure
Prevention
Handwashing
Prognosis good
160
Give the etiology for hepatitis B
Transmission by parenteral contact with
blood
blood products
contaminated needles
sexual contact
perinatal
161
Give treatment for hepatitis B (serum)
Supportive
Hepatitis B immune globulin
May be given within 7 days of exposure
Recommended as part of childhood vaccination regimen
Recommended for high-risk individuals:
Multiple sex partners
Male homosexuals
Illicit drug users
Hemodialysis patients
Health care workers
Prognosis worsens with age and debility
162
Give clinical manifestations of hepatitis B (serum)
More insidious onset
Similar to Hepatitis A but may involve:
Urticaria & other rashes
Arthralgia
Angioedema
Glomerulonephritis
163
Give the etiology for hepatitis C virus
Important occupational risk for health care workers
Transmission similar to Hepatitis B
IV drug use
Blood transfusions prior to availability of screening test
Intranasal cocaine use
164
Give treatment for hepatitis C virus
Interferon alfa
Developing drug therapies
Supportive
Rest
Nutritional support
Prognosis moderate
165
Give etiology for hepatitis D virus
Requires an infection with Hepatitis B to survive
Transmission by parenteral routes
Exposure to blood and blood products
IV drug users
Hemophiliacs
166
What is the treatment for hepatitis D
No specific treatment for Hepatitis D
Prognosis fair, worsens with chronic disease
Prevention
Safe sexual practice
Screening of blood products
Avoidance of IV drug use
Vaccination with Hepatitis B vaccine
167
Give etiology for hepatitis E virus
Transmission fecal-oral (especially contaminated water)
Most common cause of acute hepatitis in developing countries
Cases in the US typically follow travel
India
Africa
Asia
Central America
168
Give treatment for hepatitis E virus
Supportive
No vaccine
Prevention
Avoid undercooked foods
Careful handwashing
Drink safe water and beverages
Canned
Bottled
Purified
169
Renal disorder is associated with pain in what area of the back?
costovertebral angle
170
An infection of the renal pelvis and interstitium is known as:
pyeolonephritis (caused by streptococcus)
171
A classic manifestation of chronic pyelonephritis is:
atrophic kidneys with diffuse scarring
172
The most common physiologic abnormality found in patients with a renal stone is:
hypercalcemia
173
glomerulonephritis results from:
antigen-antibody complexes
174
Autosomal Dominant Polycystic Kidney Disease (ADPKD):
> presents with pain being the most frequent client complaint
> results from formation of cysts that involve the entire nephron
> results in urinary tract infections, often due to Enterobacter organisms
175
What are some predisposing factors associated with pyelonephritis?
urinary obstruction, pregnancy, diabetes, catheterization, neurogenic bladder
176
Complete urinary obstruction causes:
> increased urinary stasis (inactivity)
> increased urinary frequency
> decreased glomerular filtration rate
> increased predisposition to infection
177
Clinical manifestations of glomerulonephritis include:
proteinurea, periorbital edema, coffee-colored urine
178
What clinical findings suggest a diagnosis of nephritic syndrome?
hypercoagulability, hypoalbuminemia, hyperproteinemia, hyperlipidemia, edema
179
Kidneys are responsible for:
maintaining fluid and electrolyte homeostasis
180
What are the functions of the renal system?
> maintain fluid, electrolyte, and acid-base balance
> detoxifying the blood and eliminating wastes
> regulating blood pressure
> production of erythropoietin (red blood cell growth catalyst)
> activation of Vitamin D to facilitate absorption of calcium
181
How many liters of blood are filtered by the kidney per hour? What percentage is returned to the body?
7 L; 99 percent
182
Why is renin released?
to cause vasoconstriction to increase BP
183
Functions of the renal system
Maintain fluid, electrolyte, and acid-base balance
Detoxifying the blood and eliminating wastes
Regulating blood pressure (increase in volume = increase in pressure)
Production of erythropoietin (renal failure will be enemic)
Activation of Vitamin D to facilitate absorption of calcium (chronic renal failure have bone disorders)
184
If kidneys are failing which metabolic dysfunction will you have?
Metabolic acidosis
185
What are the parts of the urinary system?
kidneys, ureters, bladder, urethra
186
What are the three principle areas of renal parenchyma?
> pelvis: large collecting area for urine
> medulla: pyramids
> cortex: glomeruli, nephron tubules
187
What is the nephron?
functional unit of the kidney
188
How much urine filters through the kidneys per hour?
7 liter per hour
189
What are the three major functions of the nephron?
> filtration of water soluble substances from the blood
> reabsorption of filtered nutrients, water, and electrolyes
> secretion of waste products
190
What are the functions of the glomerulus?
> site of fluid filtration from blood to the nephron
> more permeable than other capillaries in the body
> prevents passage of blood cells and proteins
191
What is the glomelular filtration rate (GFR)?
> 125 mL/min
> each glomeruli can regulate its own GFR (effective as long as SBP is 90-180)
> one of the most important factors of blood volume
192
best way to measure GFR
> creatinine clearance is a good measure of GFR
kidneys dont reabsorb it, how much runs through per minute gives gfr
193
Describe the proximal convoluted tubule?
> reabsorbs about 2/3 of the filtered water and electrolytes
> reabsorbs all of the glucose, amino acids, and vitamins
194
if there is sugar in blood stream?
lots of sugar in your blood and kidney gets rid of it
>200
195
Describe the Loop of Henle.
> overall process includes pushing fluid into interstitial space to further concentrate filtrate
196
Descending loop of henle
transports water
delivers concentrated filtrate to ascending loop
197
Ascending loop of henle
> ascending loop: actively transports Na+, Cl-, K+; increased interstitial osmolarity
198
Describe the distal convoluted tube.
> "fine tune" of sodium and water reabsorption: ADH (antidiuretic hormone- vasopressin), aldosterone
> site from which filtrate enters the collecting tubule
199
What does ADH do in the distal convoluted tube?
monitors the osmolality (thickness) of your blood and causes you to retain water to thin out your blood
200
What does aldosterone in the distal convoluted tube do?
makes you hold onto sodium and water
201
best way to measure urine output
catheter
202
Describe the collecting tubule.
> distal tubules empty into the single larger collecting tubule
> merges into larger collecting ducts
> more than 99% of the original filtrate is reabsorbed by the time it reaches the renal pelvis
> creates 30-60 mL of urine/hour
203
Describe BUN. (meaning, normal value, what it measures, what it can also reflect)
Blood urea nitrogen - byproduct of protein metabolism that can be affected by diet, GI bleed causing blood cells to be digested
> normal value: 10-29 mg/dl
> indirect measure of overall hydration
> can also reflect diet, GI bleeding, tissue breakdown
204
Describe creatinine.
> reflects GFR
> most commonly used "quick" method to estimate renal function
byproduct of muscle metabolism and ONLY excreted by kidneys
205
What are normal values for creatinine?
> female: 0.5-1.1 mg/dL
> male: 0.6-1.2 mg/dL - higher muscle mall
206
Describe urinalysis.
Normal urine is clear, pale yellow to amber, slightly acidic, may contain a few cells
207
What causes glycosuria?
exceeding the threshold for glucose reabsorption
208
What is the main driving force for glomerular filtration?
hydrostatic pressure in the glomerular capillaries
209
What would increase GFR?
fluid volume excess
hydro-static pressure in glomerular capillaries is main force driving force for glomerular filtration
210
Serum creatinine may be increased by:
muscle breakdown
211
What is the etiology of cystic kidney disease? (cause, two types)
> genetically transmitted
> autosomal recessive (evident in childhood) or autosomal dominant (occur later in life) polycystic kidney disease
> involves one or both kidneys -- cyst may be found in other organs
> Develops more quickly in men
212
ARPKD etiology - cause
> identified in neonatal period
> kidneys retain shape but are enlarged
> dilated collecting ducts
> abnormal portal (liver) ducts
213
ARPKD clinical manifestations that can lead
> respiratory distress
> palpable - feelable- kidneys
> systemic hypertension even as a baby
pulmonary hypoplasia - not enough cells of pulmonary system
214
ARPKD diagnosis
> recessive pattern of inheritance in the family
> liver biopsy
> CT, MRI, ultrasound will be similar to ADPKD
215
ADPKD etiology
> most common
> no gender/ race risk factor
> usually diagnosed at 40-59 yrs old
> kidneys cannot concentrate urine
> cysts multiply and expand: kidney size increases, decline in GFR, decreased renal perfusion, local ischemia (cyst can rupture, cause kidney ischemia)
> involvement of other organs, most commonly the liver
216
ADPKD clinical manifestations
inability to concentrate urine, hypertension, proteinuria, hematuria (blood in urine), pain (from cyst rupturing or kidney stones), kidney stones, UTI, cyst infections
217
ADPKD diagnosis
> genetic history
> ultrasound
218
ADPKD treatment
> supportive: control BP, manage other conditions
> dialysis
> kidney transplant
219
Renal Cell Carcinoma
> 2-3% of all malignancies in the US
> 85% all renal cancers
>39000 new cases annually
>13000 deaths annualy
> 2x more common in men
> 20% higher incidence in African Americans
> mean 5 year survival for advanced RCC is <10%
220
RCC etiology
> risk increased 3-4x when a 1st degree relative has the disease
> primary risk factors: cigarette smoking, obesity, hypertension (quit smoking and lose weight RF goes dow)
221
RCC clinical manifestations - S/S
> often asymptomatic until late - hard to catch early because kidneys have large reserve to function even if large portion is damanged
> costovertebral angle tenderness - bottom of ribs meet spine on the back - land mark for kidneys - very painful
> hematuria
> palpable abdominal mass
> bone pain, SOB, chest pain, from *metastatic - spreading* disease late
222
RCC treatment
> surgical removal
> metastasis usually unresponsive to chemotherapy (metastasis occurs in 1/3 cases
223
What are the four RCC stages?
I: tumor w/in capsule
II: tumor invades perirenal fat
III: tumor extends into renal vein or regional lymphatics
IV: metastasis (other kidney, bone, liver, lungs, heart)
224
What prevents against kidney infection?
normal host defenses:
> acidic pH and urea in urine
> prostatic secretions in men
> urethral secretions in womean
> microurition - unidirectional flow - voiding/peeing in one direction to flush out
> epithelial cells trap bacteria and provide additional protective barrier
225
How does decreased estrogen increase risk for infection?
larger urethra with thinner membranes
226
What are the risk factors for renal system infection?
> increasing age
> vesicoureteral reflus of urine
> congenital abnormalities
> female gender
> pregnancy
> neurogenic bladder (bladder can't empty due to a neurological condition)
> urinary obstruction
> obesity
> diabetes
> uncircumcised male children
> instrumentation (catheters)
227
Risk factors of acute pyelonephritis
> pregnancy is a major risk factor
> highest incidence in young women, infants, and the elderly
> usually unilateral
> right kidney involved >50 percent of the time
228
What usually causes acute pyelonephritis?
Ecoli
229
Pathogenesis of acute pyelonephritis
> usually an "ascending" infection
> can arrive via bloodstream
> bacteria binds to epithelial cells
> inflammatory response/damage to parenchymal tissue
230
What is acute pyelonephritis?
common bacterial infection of the renal pelvis and kidney
231
What are the clinical manifestions of acute pyelonephritis?
> sudden onset
> fever/chills
> nausea, vomiting, anorexia
>CVA tenderness
> dysuria (painful urination), urgency, frequency
> complications: septic shock, ARDS (adult respiratory distress syndrome)
> chronic kidney disease due to scarring
232
What is the treatment for acute pyelonephritis?
> diagnosis made via urinalysis (bacteria, RBCs, WBCs)
> antibiotic therapy for 7-10 days usually outpatient
> may be hospitalized for more severe cases (urine culture, IV antibiotics, IV fluids)
233
What is chronic pyelonephritis?
continuing pyogenic infection of the kidney that occurs almost exclusively in patients with major anatomic abnormalities
234
What is the etiology of chronic pyelonephritis?
> small atrophied kidneys with diffuse scarring
> risk factors: vesicoureteral reflux, urinary obstruction, neurogenic bladder
235
Pathogenesis of chronic pyelonephritis
> chronic or recurrent infections
> chronic interstitial inflammation
> reduction in the number of functional nephrons
end stage renal failure is worst thing that can happen
236
clinical manifestations of chronic pyelonephritis
> minimal symptoms
> flank pain less intense than in acute pyelonephritis
> incidental diagnosis at times (hypertension, UTI, elevated creatinine levels)
237
treatment of chronic pyelonephritis
> correction of underlying problem
> antibiotic therapy (prolonged)
> support existing renal function
238
Renal obstruction does what?
> interferes with the flow of urine
> can occur at any point within the system
> causes urinary stasis
> predisposes to UTIs
> can lead to post renal acute renal failure and acute tubular necrosis
239
renal obstruction etiology
> congenital: anatomical malformation
> acquired: calculi (low urine output, abnormal pH, medications), tumors
240
renal obstruction pathogenisis
> changes secondary to obstruction depend on location and size of obstruction
> hydrostatic pressure increases proximal to the obstruction
> dilation follows with reduction in GFR
> eventually portions of the kidney become ischemic
241
Obstruction of renal S/S
Depends on location and degree of obstruction:
Bilateral
Weight gain
Nausea
Anorexia
Malaise
Headaches
Increased abdominal girth
Edema
242
What is hydroureter?
complete obstruction of ureter leads to:
Hydronephrosis
Decreased GFR
Ischemic kidney damage
243
urinary tract obstructions of the pelvis, ureter-intrinsic, ureter-extrinsic, bladder, urethra, prostate
> pelvis: calculi, tumors, ureteropelvic stricture
> ureter-intrinsic: calculi, tumors, clots, sloughed papillae, inflammation
> ureter-extrinsic: pregnancy, tumors, retroperitoneal fibrosis
> bladder: calculi, tumors, functional (neurogenic)
> urethra: posterior valve stricture, tumors (rarely)
> prostate: hyperplasia, carcinoma, prostatitis
244
Urintary tract obstruction clinical manifestations
> depends on location and degree of obstruction
> bilateral: weight gain, nausea, anorexia, malaise, headaches, increased abdominal girth, edema
> hydroureter: complete obstruction of ureter
> hydronephrosis
> decreased GFR
> ischemic kidney damage
245
Urinary tract obstruction treatment
> depends on cause
> location of obstruction
> size
> lithotripsy (shock waves)
246
What is the two-word technical term for kidney stones?
renal calculi
or named for where they are
247
What causes the pain?
movement with peristalsis
248
What adverse effects could arise if a renal calculi completely blocks a ureter?
hydronephrosis, where the urine backs up into the kidney
249
Why is it important to increase fluid intake to 8-10 glasses?
to flush out stones
250
What is a primary glomerular disorder?
primary glomerulopathies: only the kidney is involved
251
What is a secondary glomerulopathy?
injury due to drug exposure, infection, systemic, or vascular pathology
252
Glomerular disorders are responsible for?
end stage renal disease; glomerular disorders account for 90%
253
What may glomerular damage result in?
hematuria, proteinuria, abnormal casts (composed of WBCs, RBCs, or kidney cells), decreased GFR, edema, hypertension
254
What are glomerulopathies?
things that are wrong with the glomerulus
255
How are glomerulopathies typically classified?
by the degree of proteinuria
256
What is nephritic syndrome (inflammation)?
hematuria, *mild to moderate proteinuria main thing to know*
, decreased GFR, hypertension, edema of hands and face, elevated creatinine, and may lead to renal failure
257
What is nephrotic syndrome?
protein loss through hyperexcretion
258
Acute glomerulonephritis (inflammation and glomerular damage) etiology
> more common in men
> a leading cause of ESRD (end stage renal disease)
> wide variety of triggers (bacterial, viral, parasitic, systemic disease
259
acute glomerulonephritis clinical manifestations
> dark urine
> proteinuria
> edema
> hypertension
> oliguria: <400 mL in 24 hours (not enough)
> increased BUN/creatinine
260
acute glomerulonephritis diagnosis
> patient history
> clinical manifestations
> BUN and creatinine levels
> urinalysis
261
acute glomerulonephritis treatments
> supportive care
> may include temporary dialysis
262
nephrotic syndrome (too much protein excretion) etiology
> greater than 3-3.5 grams of protein loss per day
> common systemic disease cause: diabetes mellitus
> genetically linked in children
263
nephrotic syndrome clinical manifestations
> hypoalbuminemia
> hyperlipidemia (increased lipid production)
> edema
> hypercoagulability (proteinuria causes decrease in proteins that maintain blood levels, so the body releases clotting factors to compensate)
264
nephrotic syndrome treatment
> diuretics
> lipid lowering meds
> immunosuppressive therapy
> hypertensive therapy
treat problem thats causing glomerus to be too permeable
265
chronic glomerulonephritic
> pathologic process same as acute
> progresses into chronic end stage renal disease (ESRD)
> nephrons atrophy, become scarred and non-functioning
266
The condition characterized by oliguria and hematuria is:
acute glomerulonephritis
267
Nephrotic syndrome does not usually cause:
hematuria
268
It is true that polycystic kidney disease is _________ transmitted
genetically
269
Acute kidney injury was formerly known as what?
acute renal failure
270
AKI (acute kidney injury)
> potentially reversible
> characterized by abrupt deterioration of renal function
> increase in serum creatinine 0.5 mg/dL
> mortality rates very high in critically ill patients
271
What is oliguria?
uop of less than 400 mL/24 hours
272
What is anuria?
uop of less than 100 mL/24 hours
273
AKI risk increases with what comorbitities?
diabetes, heart failure, liver failure, hypertension, atherosclerosis, advanced age (GFR at 80 is half of what it was at 30)
274
What are the 3 broad categories of acute renal failure?
pre-renal - (perfusion problem)
post-renal
intra-renal
275
What is meant by pre-renal kidney injury?
> decreased perfusion to the kidney
> could be due to drug use (ACEI, ARB, NSAIDS - vasodilating drugs)
> decrease in blood volume (dehydration, vomiting, hemorrhage, diuretics, burns, large volumes of fluid in interstitial space or peritoneal space)
276
pre-renal injury pathogenesis
> decreased perfusion = decreased GFR
> autoregulatory mechanisms protect the renal parenchyma to a point
> correction of underlying problem will prevent tissue damage if done quickly
> if uncorrected: hypoperfusion=ischemia of renal parenchyma=acute tubular necrosis
277
What does post-renal kidney injury mean?
> obstruction of normal urine outlfow
> S&S of fluid overload present
> most common causes: BPH (enlarged prostate), kinked or obstructed catheters, tumors, strictures, calculi
278
In post-renal kidney injury, what happens to the unaffected kidney?
it increases production to compensate
279
Which kidney injury is easiest to treat?
post-renal kidney injury
280
What is intra-renal kidney injury?
> caused by dysfunction of the nephrons (vascular, interstitial, glumerular, tubular)
inside the kidneys
281
What is ATN? What causes it? What does it cause?
Acute Tubular Necrosis
> drug induced
> ischemia, contrast media, nephrotoxins, sepsis
282
What are the phases of ATN?
> prodromal phase: insult has occurred, duration will vary
>oliguric phase: up to 8 weeks, diuresis occurs but tubular function remains impaired (50-400 mL/day), uremic syndrome (decreasesd GFR = oliguria)
>postoliguric phase: 1 week- 1 year, normal creatinine is marker for full recovery
283
What is the treatment for AKI?
> identify risk factors
> treat hypoperfusion promptly
> nephrology consult
> nutrition
284
Describe chronic kidney disease
progressive and irrevocable loss of functioning nephrons
285
In chronic kidney disease, how many nephrons may be lost before symptoms manifest?
75%
286
What is the final outcome of chronic kidney disease?
ESRD imporant
biggest risk factors are DM and HTN
287
What are risk factors for CKD?
diabetes and hypertension
288
Stages of CKD
> decreased renal reserve: <75%
> renal insufficiency: 75-90%
> ESRD: >90% loss
289
Complications of CKD
> cardiovascular disease (hypertension and heart failure)
> uremic syndrome (inability to eliminate waste)
> metabolic acidosis
> electrolyte imbalances
> renal osteodystrophy (high phosphate, low calcium), fractures
> malnutrition
> anemia
> pain
> depression
290
CKD treatment
treat symptoms (sodium bicarbonate for metabolic acidosis, vitamin D for deficiency, etc)
> hemodialysis
> peritoneal dialysis
> kidney transplant
291
Describe micturition (urniation)
> often taken for granted but requires CNS, ANS, and PNS
> continent ability means control of voiding patterns
292
What is normal bladder capacity?
300-500 mL
293
What is normal post-void residual volume?
50-100 mL
294
When does the urge to void usually happen?
150-250 mL
295
What is the process of catheterization?
one provider has to watch and do a check-off while the other provider performs the procedure
296
What is a CAUTI?
Catheter-Associated Urinary Tract Infection
> most common nosocomial infection today
> sentinel event/never event
> evidence based bundles of care: aseptic technique, discontinue ASAP, catheter care, must justify insertion and continued use
297
What is cystitis?
bladder infection
298
etiology of cystitis
> bacteria normally cleared by flushing of urine
> more common in females due to shorter urethra
> risk factors: obstruction, instrumentation, pregnancy, obesity, catheterization
299
Cystitis risk factors
Obstruction
Instrumentation
Pregnancy
Obesity
Catheterization
300
cystitis pathogenesis
> inflammatory response secondary to bacterial invasion
> E. coli responsible for most infections
> typically travel "up": sexual activity, poor hygiene, contraceptive use (diaphragm)
301
clinical manifestations of cystitis?
frequency, urgency, dysuria, pain, hematuria, cloudy urine, odor
302
cystitis treatments
> prevention
> antibiotic therapy
303
Micturition requires what NS
Central nervous system
Autonomic nervous system
Peripheral nervous system
304
Normal bladder capacity? When do you need to pee?
300-500 mL
pee at 150-250 mL
post residual 50-100 mL
305
What is incontinence?
involuntary urine loss
> 2x more common in women
> prevalence increases w/age
> by age 50, 30% females have it
> In 2000, $20 billion spent on incontinence
306
Risk factors for incontinence
> pregnancy, vaginal delivery
> impaired cognition
> immobility
> diabetes
> spinal cord injuries
> UTI
> pelvic muscle weakness
307
pathogenesis of incontinence
normal functioning requires: CNS, bladder/urethral function, cognition
308
What is a neurogenic bladder?
a disruption in the nervous control of micturition (stroke, parkinsonism, spinal cord injuries/defects)
309
What are the types of incontinence?
> urge - over active bladder
> stress
> mixed
> overflow
> functional
310
Incontinence treatment
> review of contributing factors
> behavioral (pelvic floor muscle training)
> pharmacologic
> surgical (bladder sling, artificial urinary sphincter)
311
Describe urge incontinence
> most common in older men
> urgency/leakage of urine
> overactive detrusor muscle that contracts
> causes: aging, bladder infections, tumors/radiation, calculi, idiopathic
312
Describe stress incontinence
> most prevalent
> small amounts of urine lost with increased abdominal pressure (sneezing, laughing, coughing, heavy lifting)
> weakened pelvic floor
> childbearing
313
Describe mixed incontinence
> combo of stress and urge
> common in older women
> greater volume of urine leakage can disrupt ADLs
314
Describe overflow incontinence
> bladder becomes overfull
> causes: obstruction, bladder weakness
315
Describe functional incontinence
> physical or environmental limitations that prevent access "in time" Lack of facilities
Cognitive deficits
Physical limitations
Health care workers play a critical role in manipulating the environment!!
316
Treatment of incontinence
Review of contributing factors
Behavioral
Pelvic floor muscle training
Pharmacologic
Surgical
Bladder sling
Artificial urinary sphincter
317
