EXAM 5 Flashcards
(458 cards)
1
Q
MOTILITY
A
movement of food through the body from mouth to anus
2
Q
peristalsis
A
involuntary contractions of the intestinal muscles that create wave
movements to propel substances forward
3
Q
sphincter
A
Ring of muscle that closes an opening like at the stomach
4
Q
mastication
A
chewing
5
Q
enteric
A
occuring in the intestines
6
Q
chyme
A
Acidic fluid that moves from the stomach to the small intestine. Consists of gastric juices and partly digested food
7
Q
defacation
A
Discharge of feces from the body
8
Q
intestinal flora
A
Naturally occurring bacteria in the intestine
9
Q
digestion
A
Process of breaking down food into what the body can use and needs
10
Q
Absorption
A
Action of one thing taking up or being taken up by another
11
Q
describe the anatomy of the upper gi tract
A
- 4 layer structure, oral cavity, salivary glands, esophagus, stomach, small intestines- digests food and gets it ready for processing as well as digestion.
12
Q
describe the anatomy of the middle gi tract
A
lower duodenum, 2/3 of transverse colon- processes food that small intestine couldn’t by absorbing minerals and water
13
Q
describe the anatomy of the lower gi tract
A
last 1/3 of transverse colon, upper part of the anal canal- dehydrates and stores fecal material
14
Q
what are the anatomical landmarks of the stomach
A
cardia, fundus, body, pylorus
15
Q
cardia
A
surrounds superior opening,
16
Q
fundus-
A
rounded, gas filled portion superior and left of the cardia,
17
Q
body-
A
large part beneath the fundus.
18
Q
Pylorus-
A
area connecting to the duodenum
19
Q
Saliva-
A
starts digestion, helps chew and swallow, protects teeth,
20
Q
gastric juice-
A
acidic fluid in stomach that promotes digestion,
21
Q
bile-
A
bitter and alkaline fluid that is secreted by the liver and aids digestion,
22
Q
pancreatic fluid-
A
alkaline (bicarbonate)- critical for digestion of protein, fats, and carbs
23
Q
What is the function of the peritoneum?
A
Membrane of smooth tissue that pads and insulates organs and holds them in place. It secretes fluid to reduce friction when organs rub against each other.
24
Q
passage of food through the gi tract
A
Food goes into mouth masticationswallowesophaguslower esophageal sphincterstomachpyloric sphincterenters small intestine small intestine duodenum jejunum ileum ileocecal valve enters large intestine cecum ascending colon transverse colon descending colon rectum internal anal sphincter external anal sphincter
25
6. What are the hormones of the GI tract?
CHOLECYSTOKININ, SECRETIN (GLP-1 AND GIP), GASTRIN, GHRELIN
26
Discuss intestinal flora and the role in digestion and absorption.
Intestinal flora helps supply nutrients, process vitamins and digest cellulose. They have a direct affect on mineral absorption.
27
1. Is the gut of a normal adult sterile?
no
28
2. Where is the largest ecosystem of microbes in the GI tract found?
Large intestine followed by the small intestine
29
3. What role do microorganisms play in the GI tract?
They aid the immune system and ensure the integrity of the mucosal lining.
30
4. What might cause a disruption of intestinal flora and lead to opportunistic infection?
Diet, antibiotics or other meds, or other environmental factors
31
5. Name the three sections of the small intestine.
Duodenum, jejunum, and ileum
32
6. What is the action of pepsin?
Breaks down proteins into peptides and amino acids to be absorbed in the small intestine.
33
7. What is the name of the sphincter located between the stomach and the small intestine?
Pyloric sphincter
34
8. What type of acid-base problem would you anticipate having if you have had frequent prolonged vomiting?
Metabolic alkalosis
35
9. What layer of the GI tract contains blood vessels, nerves, and structures responsible for secretion of digestive enzymes?
submucosa
36
10. What structure covers the larynx and prevents aspiration when swallowing?
epiglottis
37
11. In what part of the GI tract does the majority of nutrient absorption occur?
small intestine
38
12. Does everyone who has gastroesophageal reflux have GERD?
no
39
13. Is there an association between GERD and asthma?
yes
40
14. Why would sitting up help to relieve the symptoms of GERD?
It allows gravity to work to keep contents down when the muscle is too weak and allows backflow.
41
15. What are the complications of GERD?
Esophagitis and barret’s esophagus, gi bleeding, ulcerations, narrowing esophagus
42
why does liver damage cause tarry stools
Liver damage has stopped blood from flowing through the portal vein correctly. This causes the bile to not be broken down as it should be.
43
what do the following symptoms suggest
multiple loose tarry stools, dizzy, rapid hr, weak, thirsty with a Hx of arthiritis treated with daily aleve, advil. pt also sometimes drinks beer and smokes to ease the pain.
There is damage at a cellular level because of what it takes to metabolize these ingested substances. At this point, the patient probably has cirrhosis in it’s late stages.
44
c. What are the two most common causes of peptic ulcer disease?
h. pylori and aspirin/nsaids action of acid and pepsin
45
17. What are some causes of mechanical bowel obstruction?
Adhesions, volvulus, incarcerated inguinal hernia, intussusception
46
18. Why is a patient with C. difficile infection on contact precautions in the hospital?
C diff is airborne transmitted.
47
19. List the functions of the liver.
SECRETION OF BILE, METABOLISM OF BILIRUBIN, VASCULAR/HEMATOLOGIC FUNCTION, METABOLISM OF NUTRIENTS, METABOLIC DETOXIFICATION, STORAGE OF MINERALS AND VITAMINS
48
20. Why do patients develop jaundice?
Usually a sign of liver disease causing a buildup of bilirubin.
49
22. Which blood tests monitor liver function?
Alt, ast, alp, ggt, pt, inr are the typical tests.
50
23. Is liver damage in Cirrhosis reversible?
No, but it can be slowed down
51
24. What are the complications of portal hypertension?
Bleeding in the esophagus and stomach, peritonitis, hepatorenal syndrome
52
25. Compare and contrast cholelithiasis and cholecystitis.
Cholecystitis can be acute or chronic inflammation, usually from an obstruction. Cholelithiasis is gallstones, which are a buildup of cholesterol or bilirubin. Both are due to excessive bilirubin, but cholelithiasis is from bile composition rather than backup. Both are diagnoses with US or CT and both require surgery. Cholelithiasis can be asymptomatic until large enough to cause obstruction, jaundice, or biliary colic. Cholecystitis symptoms may range from RUQ pain, mild fever, n&v, elevated wbc and anorexia to gi discomfort, gallbladder enlargement, and intolerance to certain foods.
53
FUNCTION OF THE KIDNEYS
EXCRETORY AND ENDOCRINE FUNCTION
54
WHAT EXACTLY DO THE KIDNEYS REGULATE
WATER, ELECTROLYTES, AND ACID-BASE BALANCE
55
WHAT DO THE KIDNEYS EXCRETE
FOREIGN CHEMICALS AND METABOLIC WASTE MATERIALS
56
WHAT DO THE KIDNEYS SYNTHESIZE AND ACTIVATE
RENIN, ERYTHROPOIETIN, VITAMIN D, AND PROSTAGLANDINS
57
WHAT ORGANS STORE AND TRANSPORT URINE
URINES, BLADDER, URETHRA
58
WHAT CAN STIMULATE ERYTHROPOIETIN RELEASE FROM THE KIDNEYS
STATES OF DECREASED BLOOD OXYGENATION
59
WHAT IS ERYTHROPOEITIN (EPO)
HORMONE THAT STIMULATES STEM CELLS WITHIN OUR BONE MARROW TO INCREASE RBC PRODUCTION
60
NEPHRON
MAIN FUNCTIONAL UNIT OF THE KIDNEY
61
HOW MANY NEPHRONS DOES EACH KIDNEY HAVE
ABOUT 1.2 MILLION
62
WHAT HAPPENS TO NEPHRONS OVER TIME
THEY DO NOT REGENERATE
DECLINE WITH AGE
63
HOW FAST DOES THE NEPHRON COUNT DECLINE
10% PER DECADE BEGINNING AT AGE 40
64
WHY DO WE HAVE A VERY LARGE RENAL RESERVE
SO THAT OUR KIDNEYS ARE ABLE TO FILTER BLOOD AND FILTER OUT TOXINS, WASTE PRODUCTS, AND FLUIDS VERY EFFECTIVELY
65
HOW MANY NEPHRONS CAN WE LOSE BEFORE WE START SEEING ANY IMPAIRMENT
50%
BUT GENERALLY 75-90% OF NEPHRON LOSS BEFORE WE SEE SERIOUS IMPAIRMENT
66
GLOMERULUS
WHERE THE FILTRATION PRIMARILY OCCURS
MAIN PART THAT ACTUALLY FILTERS THE BLOOD
67
EXPLAIN THE OVERVIEW OF THE NEPHRON BEYOND THE GLOMERULUS
PRIMARILY TUBULAR COMPANENTS WHERE ELECTROLYTES AND OTHER SUBSTANCES THAT ARE NEEDED TO MAINTAIN OUR HOMEOSTASIS ARE REABSORBED BACK IN THE BLOODSTREAM
68
HOW ARE MATERIALS WE DON'T NEED IN THE BODY SECRETED
WITHIN OUR TUBULAR FILTRATE FOR ELIMINATION
69
NEPHRON FUNCTION
1. FILTRATION
2. REABSORPTION
3. SECRETION
70
NEPHRON FILTRATION
OF WATER SOLUBLE SUBSTANCES FROM BLOOD
71
NEPHRON REABSORPTION
OF FILTERED NUTRIENTS, WATER, AND ELECTROLYTES
72
NEPHRON SECRETION
OF WASTES OR EXCESS SUBSTANCES INTO THE FILTRATE
73
DIFFERENT SEGMENTS OF THE NEPHRON SPECIALIZE TO ACCOMPLISH WHAT
ALL NEPHRON FUNCTIONS
74
GLOMERULUS LAYERS
1. CAPILLARY ENDOTHELIUM
2. BASEMENT MEMBRANCE
3. OUTER CAPILLARY ENOTHELIUM PODOCYTES
75
WHAT DOES THE PROXIMAL TUBULE REABSORB
NA
CL
HCO2
K
H2O
GLUCOSE
AMINO ACIDS
76
WHAT DO THE PROXIMAL TUBULES SECRETE
H+
ORGANIC ACID AND BASES
77
WHAT DOES THE THIN DESCENDING LOOP OF HENLE REABSORB
H2O
78
WHAT DOES THE THICK ASCENDING LOOP OF HENLE REABSORB
NA
CL
K
CA
HCO2
MG
79
WHAT DOES THE THICK ASCENDING LOOP OF HENLE SECRETE
H
80
WHAT DOES THE EARLY DISTAL TUBULE REABSORB
NA
CL
CA
MG
81
WHAT DOES THE LATE DISTALE TUBULE AND COLLECTING DUCT INCLUDE
PRINCIPAL CELLS
INTERCALATED CELLS
82
WHAT DO PRINCIPAL CELLS REABSORB
NA
CL
83
WHAT DO PRINCIPAL CELLS SECRETE
K
84
WHAT ARE RESPOONSIBLE FOR ADH MEDIATED H2O REABSORPTION
PRINCIPAL CELLS
85
WHAT DO INTERCALATED CELLS REABSORB
HCO2
K
86
WHAT DO INTERCALATED CELLS SECRETE
H
87
DURING GLOMERULAR FILTRATION, WHAT MOVES FROM THE BLOOD THROUGH THE GLOMERULUS AND INTO THE BOWMAN'S CAPSULE
WATER AND SMALL SOLUTES
*LARGER MOLECULES, PROTEINS, AND BLOOD CELLS ARE UNABLE TO MOVE THROUGH
88
WHAT IS THE RESULTING FLUID OF GLOMERULAR FILTRATION CALLED
GLOMERULAR FILTRATE
89
GLOMERULAR FILTRATION RATE
GFR
125 mL OF GLOMERULAR FILTRATE PRODUCED PER MINUTE
90
HOW MUCH BLOOD PERFUSES THE KIDNEYS
20-25% OF NORMAL CARDIAC OUTPUT
(1000-1300 ML/MIN)
*PROMOTES GLOMERULAR FILTRATION
91
PRIMARY FILTRATION PRESSURES
GLOMERULAR BLOOD HYDROSTATIC PRESSURE
2-3X HIGHER THAN OTHER CAPILLARY BEDS IN THE BODY
92
WHAT HELPS MAINTAIN BLOOD FLOW AND GFR
INTRARENAL AND EXTRARENAL FEEDBACK MECHANISMS
93
Neural/Humoral Controls
| Regulation of Renal Blood Flow -GFR
– Sympathetic stimulation
– Angiotensin II, ADH, prostaglandins
94
Renin angiotensin system
| Regulation of Renal Blood Flow -GFR
Control of blood pressure
95
Autoregulation
| Regulation of Renal Blood Flow -GFR
– Maintain blood flow to provide a constant GFR that allows for solute and water excretion
– Renal systems responds to arterial pressure changes and sodium chloride concentrations
96
INCREASED PROTEIN AND GLUCOSE LOADS
| Regulation of Renal Blood Flow -GFR
Increase GFR
97
What is Glomerular filtration rate used to evaluate
renal tissue function
98
what does decrease in bp do to gfr
decreases hydrostatic pressure that drives filtration
decreases gfr
99
what does an increase in protein and glucose do to gfr
increase gfr
100
what does sympathetic nervous system activation do to gfr
decrease gfr
101
how do hormones like angiotensin II affect gfr
efferent arteriole vasoconstriction increases b/p --> increases gfr
102
how does age affect gfr
loss of nephrons --> decreased gfr
103
how does the presence of prostaglandins affect gfr
increase gfr
104
normal creatinine level
adult:
0.6-1.2 mg/dl
105
what is creatinine
non protein end product of skeletal muscle metabolism
106
to what degree is creatinine eliminated
to the degree renal function will allow
106
how does creatinine indicate renal function
most specific indicator of renal function- estimates function capacity of the kidney
107
normal bun level
8-20 mg/dl in adult
108
urea
byproduct of protein metabolism that is eliminated entirely by the kidney
109
what happens to urea as renal function declines
it accumulates
110
other than renal disease, what else can cause bun elevation
high protein diet
gi bleeding
111
Urinalysis –
gross and microscopic exam of urine to evaluate ph, specific gravity and presence of abnormal substances and formed elements
112
* Gross exam –
| urinalysis
color, clarity, odor, sediment
113
* Microscopic
| urinalysis
– RBC, WBC, epithelial cells, casts, crystals, bacteria, pH
114
* Specific gravity
| urinalysis
– concentration of solutes, hydration status, functional ability of kidney
115
normal specific gravity level in adults
(1.010-1.025)
116
Polyuria
– increased volume of urine voided
117
* Oliguria
– urine output less than 400ml/day
118
* Anuria
– urine output less than 50ml/day
119
* Nocturia
– excessive urination at night
120
* Hematuria
– red blood cells in the urine
121
* Proteinuria
– abnormal amounts of protein inthe urine
122
* Dysuria
– painful or difficult voiding
123
Frequency
– frequent voiding, more thanevery three hours
124
* Urgency
– strong desire to void
125
* Hesitancy
– delay, difficulty in initiating voiding
126
* Enuresis
– involuntary voiding during sleep
127
What is the functional unit of the kidney called?
nephron
128
What structure in the nephron filters blood?
glomerulus
129
What forces drive glomerular filtration?
Capillary hydrostatic pressure (Pc) and Bowman's space oncotic pressure (πi) favor filtration into the tubule, and Bowman's space hydrostatic pressure (Pi) and capillary-oncotic pressure (πc) oppose filtration.
130
What lab test is the most specific indicator of renal function?
urinalysis
131
what age can obstructive renal disorders occur
at any age
132
where can obstructive renal disorders occur
any area of the renal system
133
what are common causes of obstructive renal disorders
– Developmental defects
– Pregnancy
– Benign prostatic hypertrophy
– Infection, inflammation
– Tumors – common cause
– Stones – common cause
134
what are the effects of obstructive renal disorders
urinary stasis --> infection/backpressure --> hydroureter, hydronephrosis
135
Hydronephrosis Pathophysiology
Complete obstruction -> hydronephrosis -> decreased GFR -> ischemia -> increased pressure -> kidney damage
136
Renal Calculi
Crystalline structures that form from components, normally excreted in urine
137
requirements for renal calculi formation
supersaturation
nucleus (nidus)
deficiency of inhibitors
138
why is supersaturation of crystaline structures required for renal calculi formation
supports continued crystallization of stone components
139
why is nucleus (nidus) required for renal calculi formation
for the crystal to form around
140
what inhibitors of stone formation will we se a deficiency of in renal calculi formation
magnesium
citrates
140
types of stones
1. Calcium (oxalate, phosphate or combo) – most common
2. Magnesium ammonium phosphate (struvite)
3. Uric Acid (urate)
4. Cystine
140
clinical manifestations of renal system calculi
1. pain- renal colic or non colicky
2. n&v
3. cool, clammy skin
141
renal colic
| renal calculi pain
(often ureteral) pain, acute, rhythmic progressively, intense, initiates in flank and can radiate.
142
Non-colicky
| renal calculi pain
– pain dull, deep ache in flank, varies in intensity
143
diagnosis
| Renal System Calculi
Clinical symptoms, history to include diet, meds, complicating factors
urinalysis
stone analysis
bun/cr
xray, ct, us, ivp, nuclear scintigraphy
144
what findings on a urinalysis indicate renal system calculi
hematuria, infection, presence of crystals, urine pH
145
treatment
| Renal System Calculi
meds
stone removal
prevention of recurrence
diluting urine
diet
measures to change urine ph
meds to reduce stone causing substances
146
meds used for renal system calculi
pain meds, antiemetics, antibiotics for infections
147
lithotripsy
fragments of stone
urteroscopic removal
148
how do you dilute urine
decrease supersaturation with 2l fluids/day
149
uti
Infection of the urinary system
150
host defenses
| uti
– Washout phenomenon – voiding
– Mucin lining of bladder – barrier protects against invasion of organisms
– Body’s immune defenses
151
– Washout phenomenon
– voiding to reduce/eliminate uti
152
– Mucin lining of bladder
– barrier protects against invasion of organisms
153
Pathogen virulence
| uti
– Bacteria with pili or fimbriae – adhere
– Lipopolysaccarides – bind to host cells and ilicit inflammatory response
– Enzymes that break down RBC, make iron available for bacterial metabolism, multiplication
154
Lipopolysaccarides
| uti
– bind to host cells and ilicit inflammatory response
155
entry
| uti
ascending or bloodborne
156
Escherichia coli
| uti
– common infecting organism, lower UTI
157
is upper or lower uti more serious
upper
158
CAUSES OF UTI
obstruction, reflux (vesicoureteral and urethrovesical), catheters
159
CLINICAL MANIFESTATIONS OF UTI
frequency, dysuria, lower back or abdominal discomfort, chills, fever
160
DIAGNOSIS OF UTI
H&P, ultrasound, CT, renal scans to identify contributing factors, urinalysis, urine culture
161
TREATMENT OF UTI
location of infection, pathogen causing, acute, chronic or recurrent infection, antibiotics, increased fluid intake
162
Vesicoureteral reflux
– abnormal backflow of urine from the bladder into the ureter
163
Glomerulonephritis
– group of diseases that result in inflammation and/or injury to the glomerulus
164
What is the 2nd leading cause of kidney failure
Glomerular Disease
165
what happens in glomerular disease
Disruption of glomerular filtration and alteration of permeability of glomerular capillary membrane
166
is glomerular disease a primary or secondary condition
could be either
167
what are the triggers of glomerular disease
infectious microorganisms, immune mechanisms, environmental agents
168
* Clinical manifestations of glomerular disease
nephritic or nephrotic syndrome.
169
Nephritic syndrome
– inflammatory response --> hematuria, red cell casts in urine, decreased GFR, azotemia, oliguria, hypertension
170
* Nephrotic syndrome
– increased permeability of the glomerulus – massive proteinuria, hypoalbuminemia, generalized edema, lipiduria and hyperlipidemia
171
* Asymptomatic
– hematuria, proteinuria aren’t recognized
172
BOWMAN'S CAPSULE
DOUBLE WALLED CAPSULE ENCASING THE GLOMERULUS
173
INNER CAPILLARY ENDOTHELIUM
INNERMOST STRUCTURE
SINGLE LAYER THICKNESS OF EPITHELIAL CELLS THAT REST ON THE BASEMENT MEMBRANE. THERE ARE A LOT OF SPACES BETWEEN THE CELLS
174
FINISHTRATIONS
SPACES BETWEEN ENDOTHELIAL CELLS OF INNER CAPILLARY ENDOTHELIUM WHERE SUBSTANCES CAN MOVE IN AND OUT
175
BASEMENT MEMBRANE
PREVENTS PLASMA PROTEINS, ERYTHROCYTES, LEUKOCYTES, PLATELETS ETC FROM PASSING THROUGH
176
OUTER CAPILLARY ENDOTHELIUM
SEPERATES THE BLOOD FROM THE CAPILLARIES OR IN THIS CASE FROM THE FILTRATE WITHIN THE BOWMAN'S CAPSULE
177
PODOCYTES
FOOT PROCESSES THAT SURROUND THE GLOMERULUS.
178
SLIP PORES
SPACES BETWEEN THE PODOCYTES
179
WHAT DO PODOCYTES DO
MAKE THE GLOMERULUS VERY PERMEABLE. MORE SO THAN ANY OTHER CAPILLARY
180
WHEN WE SEE GLOMERULUS ISSUES, SPECIFICALLY WITH THE PODOCYTES, WHAT DO WE OFTEN SEE
PROTEIN IN THE URINE
BLOOD CELLS IN THE URINE
181
TUBULAR REABSORPTION
REMOVAL OF MATERIALS FROM THE FILTRATE THAT'S BEEN DEVELOPED WITHIN THE GLOMERULUS
182
TUBULAR SECRETION
FLUIDS AND SUBSTANCES THAT ARE ADDED TO THE FILTRATE AFTER IT HAS BEEN EXTRACTED FROM THE GLOMERULUS
183
FILTRATION IS DRIVEN BY WHAT
HYDROSTATIC PRESSURE SO BLOOD CIRCULATES THROUGH THE CAPILLARIES, BLOOD IS PUSHED AGAINST THE WALLS AND FLUID IS FILTERED OUT
184
HOW DOES STIMULATION OF THE SYMPATHETIC NERVOUS SYSTEM REGULATE GFR
HR INCREASE --> BP INCREASE --> INCREASED CARDIAC OUTPUT --> INCREASE SUPPLY OF BLOOD FLOW TO THE KIDNEY
185
HOW DOES ANGIOTENSIN II AFFECT GFR
STIMULATES THE RELEASE OF ALDOSTERONE IN THE KIDNEYS TO INCREASE BP AND THUS INCREASE BLOOD VOLUME
186
HOW DOES ADH AFFECT GFR
MAKES US HOLD ON TO OUR FLUID WHICH INCREASES CIRCULATING BLOOD VOLUME
187
HOW DO PROSTAGLANDINS AFFECT GFR
DILATING EFFECT INCREASES RENAL BLOOD FLOW AND THUS GFR
188
HOW DOES THE RENIN ANGIOTENSIN SYSTEM AFFECT GFR
CONTROLS BP. HELPS INCREASE BP VIA VASOCONSTRICTION AND RETAIN BLOOD VOLUME
189
WHAT DOES THE GFR DIRECTLY RELATE TO
THE NUMBER OF FUNCTIONING NEPHRONS THAT WE ALSO HAVE IN THE BODY
190
WHAT DOES AN INCREASED CREATININE LEVEL INDICATE
LOW GFR SO WE ARE NOT FILTERING AS EFFECTIVELY
191
BUN
BLOOD UREA NITROGEN LEVEL
192
NORMAL URINE
YELLOW TO AMBER
CLEAR TO SLIGHTLY HAZY
PH 5-6
193
NORMAL URINE PRODUCTION
600-2500 ML/D
194
URINE SHOULD BE NEGATIVE FOR
GLUCOSE
KETONES
BLOOD
PROTEIN
BACTERIA
WBC
CRYSTALS
RBC
BILIRUBIN
195
WHAT DO WBC IN URINE INDICATE
UTI
196
WHAT DOES PROTEIN IN THE URINE INDICATE
PROBLEM OR DAMAGE TO OUR GLOMERULUS
197
WHEN DO WE SEE POLYURIA
DIURETICS
198
WHEN DO WE SEE OLIGURIA
DEHYDRATION
RENAL FAILURE
199
WHEN DO WE SEE ANURIA
CHRONIC RENAL FAILURE
COMPLETE OBSTRUCTION
200
WHAT PERCENT OF CARDIAC OUTPUT DO THE KIDNEYS RECEIVE UNDER NORMAL CIRCUMSTANCES
20-25 % OR ABOUT 1000-13000 ML/MIN
201
WHAT IS A NORMAL GFR
125 ML/MIN
BUT OFTEN JUST LOOKING AT ABOVE 60 OR BELOW 60
202
WHAT FORCES DRIVE GLOMERULAR FILTRATION
BP
PROTEIN AND GLUCOSE LEVELS
RAS SYSTEM
SYMPATHETIC NERVOUS SYSTEM
LOSS OF NEPHRONS
203
WHAT HAPPENS TO URINE OUTPUT WITH SYMPATHETIC NERVOUS SYSTEM STIMULATION AND WHY
INCREASE IN URINE OUTPUT BECAUSE INCREASE IN HR
204
WHAT LAB TEST IS THE MOST SPECIFIC INDICATOR OF RENAL FUNCTION
CREATININE
205
IN RESPONSE TO ACIDOSIS, THE KIDNEYS WILL
PRODUCE AND CONSERVE BICARB AND EXCRETE OUR HYDROGEN ACID
206
WHAT IS THE ACTION OF ALDOSTERONE
MAKES US RETAIN SODIUM THUS WATER RETENTION
207
WHAT ACTION DO NATRIURETIC PEPTIDES HAVE IN THE KIDNEY
PROMOTE RENAL EXCRETION OF SODIUM AND WHERE THAT SALT GOES, WATER WILL FOLLOW
208
IS IT NORMAL TO FIND RBC AND LARGE AMOUNTS OF PROTEIN IN THE URINE
NO
209
WHAT SUBSTANCE PRODUCED BY THE KIDNEY WILL PROMOTE RBC PRODUCTION IN THE BONE MARROW
ERYTHROPOIETIN
210
WHAT CO FACTOR SYNTHESIZED BY THE KIDNEY IS NEEDED TO PROMOTE THE ABSORPTION OF CALCIUM IN THE GI TRACT
VITAMIN D
211
CAUSES OF URINARY OBSTRUCTION
PREGNANCY
TUMOR
KIDNEY STONE
SCAR TISSUE
NEUROGENIC BLADDER
BLADDER OUTFLOW OBSTRUCTION
URETEROVESICAL JUNCTION STRUCTURE
212
STAGHORN STONES
LARGE STONES THAT FILL THE RENAL PELVIS AND AT LEAST ONE RENAL CALYCES
MOST COMMONLY STRUVITE AND LINKED TO UTI
213
68 y/o, Fx tibia, immobilized for two weeks, Hx of stones. He has excruciating left flank pain. Pt. states pain comes and goes and it intensifies
.– Type of pain – colicky or non-colicky?
– Suggestion as to location of stones?
– Type of stone?
A. COLICKY
B. KIDNEY OR UPPER URETER OF LEFT KIDNEY
C. USUALLY CALCIUM PHOSPHATE
214
Who is more at risk for a UTI (female or a male)? Why?
FEMALE, SHORTER URETHRA
215
Why are fluids recommended in the treatment of UTI’s?
WASHOUT PHENOMENON
216
What factors increase the risk of a UTI in an older adult?
MALNUTRITION
DECREASED NEPHRONS
SEDENTARY LIFESTYLE
LOWER ESTROGEN LEVELS
217
Why are UTI’s difficult to diagnose in elderly?
UNABLE TO ACCURATELY REPORT
LOWER NORMAL BODY TEMP
PREVALENCE OF ASYMPTOMATIC BACTERIA
218
CLINICAL MANIFESTATIONS OF NEPHRITIC SYNDROME
inflammatory response -->hematuria, red cell casts in urine, decreased GFR, azotemia, oliguria, hypertension
219
CLINICAL MANIFESTATIONS OF NEPHROTIC SYNDROME
increased permeability ofthe glomerulus – massive protein uria,hypoalbuminemia, generalized edema, lipiduria and hyperlipidemia
220
CLINICAL MANIFESTATIONS OF ASYMPTOMATIC GLOMERULAR DISEASE
hematuria, proteinuria aren’t recognized
221
WITH NEPHRITIC SYNDROMES, IS GLOMERULAR INFLAMMATION ACUTE OR CHRONIC
ACUTE
222
WHAT HAPPENS WHEN NEPHRITIC SYNDROMES CAUSE OCCLUSION OF THE CAPILLARY LUMEN
decrease incapillary permeability, capillary wall damage
– Sudden onset of hematuria, with red blood cell casts
223
WHAT DO WE SEE WHEN NEPHRITIC SYNDROMES CAUSE A DECREASED GFR
fluid accumulation, edema, hypertension
* Varying degrees of proteinuria
224
225
WHEN GLOMERULAR DAMAGE CAUSES HYPOPROTEINEMIA, WHAT 2 THINGS HAPPEN
| NEPHROTIC SYNDROME
1. EDEMA
2. HYPERLIPIDEMIA
226
HYPOPROTEINEMIA
INCREASED PERMEABILITY TO PROTEINS FROM GLOMERULAR DAMAGE
227
PREOTEINURIA LEVELS
>3.5 G/D
228
WHY DOES HYPOPROTEINEMIA CAUSE EDEMA
DCREASED PLASMA ONCOTIC PRESSURE
229
WHY DOES HYPOPROTEINEMIA CAUSE HYPERLIPIDEMIA
COMPENSATORY SYNTHESIS OF PROTEINS BY THE LIVER
230
Tx OF GLOMERULONEPHRITIS
* Focus on cause
* Steroids – inflammation, plasmaphresis
* Dietary, fluid management
* Treament of HPT
* If kidney failure – dialysis or transplant
231
PROGRESSION OF Diabetic Glomerulosclerosis
Diabetic nephropathy --> glomerulosclerosis --> chronic kidney disease
* Result of the effects of elevated glucose on the glomerulus
232
PATHO OF DIABETIC GLOMERULOSCLEROSIS
Widespread thickening of the basement membrane, early increase in GFR --> over time reduces GFR
233
EARLY CHANGE INDICATING DIABETIC GLOMERULOSCLEROSIS
MICROALBUMINEMIA
234
Tx of Diabetic Glomerulosclerosis
– Control blood glucose levels
– ACE inhibitors or ARBs
– Control of blood pressure
– Smoking cessation
235
Tubulointerstital Diseases
Affect renal tubule structures and interstitial tissues surrounding tubules
236
* Acute tubular necrosis
a kidney disorder involving damage to the tubule cells of the kidneys, which can lead to acute kidney failure.
237
* Acute/chronic pyelonephritis
a sudden and severe kidney infection. It causes the kidneys to swell and may permanently damage them. Pyelonephritis can be life-threatening. When repeated or persistent attacks occur, the condition is called chronic pyelonephritis.
238
Pyelonephritis
Infection of the renal parenchyma, pelvis
ACUTE OR CHRONIC
CAN ASCEND OR BE HEMATOGENOUS
239
PREDISPOSING FACTORS OF PYELONEPHRITIS
vesicoureteral reflux, pregnancy, neurogenic bladder, catheterization instrumentation
240
Pyleonephritis – Clinical Manifestations
| ACUTE
Chills, fever
* Headache
* Flank,back pain
* Dysuria, frequency urgency
* Malaise
* Costovertebral angle tenderness
241
Pyleonephritis – Clinical Manifestations
| CHRONIC
* History of recurrent UTI
* Can be same as for acute or
* Polyuria
* Nocturia
* Mild proteinuria
* Hypertension
242
Wilms tumor (nephroblastoma)
| RENAL CARCINOMA
– Children 3-5 years.
– Associated with chromosomal abnormality (5%)
– Abdominal mass, hypertension, abd. pain, vomiting
– Diagnosis: ultrasound, CT
– Treatment – surgery, chemo, radiation
243
RENAL CELL CARCINOMA
– Adults 60-70’s
– Hematuria, flank pain, palpable flank mass
– Diagnosis: ultrasound, CT
– Treatment: surgical resection
244
Acute Kidney Injury
Sudden severe decrease inrenal function that ispotentially reversible
245
PRERENAL
| ACUTE KIDNEY INJURY TYPES
decreased blood flow to kidney
246
Intrarenal (intrinsic)
| ACUTE KIDNEY INJURY TYPES
- damage to the structures within the kidney (nephrons)
247
Postrenal
| ACUTE KIDNEY INJURY TYPES
– interference with urine outflow
248
WHAT CAUSES INTRINSIC ACUTE KIDNEY INJURY
DAMAGE TO THE STRUCTURES WITHIN THE KIDNEY
249
WHAT CAUSES PRERENAL ACUTE KIDNEY INJURY
MARKED DECREASE IN RENAL BLOOD FLOW
250
WHAT CAUSES POSTRENAL ACUTE KIDNEY INJURY
OBSTRUCTION OF URINE OUTFLOW FROM THE KIDNEY
251
Decreased renal perfusion
| PRERENAL AKI
– Hypovolemia – hemorrhage, dehydration
– Decreased cardiac output – heart failure, anaphylactic or septic shock
252
CAN PRERENAL AKI BE REVERSED
YES, IF CAUSE IS QUICKLY IDENTIFIED AND TREATED
253
NEPHRONS
| PRERENAL AKI
functional, but decreased blood flow results in decreased GFR. (results with prolonged mean arterial pressure <70 mm Hg.)
254
What is an indicator of tissue perfusion that might provide a cue about a pre-renal problem?
PROTEIN IN THE URINE INDICATED NEPHRON DAMAGE
255
Intrarenal (Intrinsic)
| AKI
* Damage to the renal parenchyma (nephron -glomerulus or tubules injured)
* Longer course of recovery, or progression to chronic renal failure
256
CAUSES OF INTRARENAL (INTRINSIC) AKI
– Prolonged ischemia
– Exposure to nephrotoxic agents
– Intratubular obstruction (myoglobinuria, myeloma)
– Inflammatory process – glomerulonephritis, pyelonephritis
257
Acute Tubular Injury or Necrosis Intrarenal
Destruction of the tubular epithelial cells leading to acute impairment of renal function
258
Acute Tubular Injury or Necrosis Intrarenal
| CAUSES
extensive surgery, severe hypovolemia, sepsis, trauma, burns, intratubular obstructions – myoglobin or hemoglobinuria
259
ATN - Patho
Ischemic/toxic insult->
tubular epithelial cellinjury ->
release “debris” intotubular lumen-> lumen obstructed -> tubular pressure increases -> pressure in Bowman’s capsule increases -> glomerular filtration slowed ->Pressure not relieved ->“back leak” into the interstitium -> decreased perfusion -> kidneys become hypoxic
260
Postrenal AKI
Outflow obstruction within the urinary collecting system distal to the kidneys (ureters, bladder, urethra)
261
Postrenal AKI CAUSES
BPH, stones, UTI, tumors, strictures, altered bladder contraction
262
POSTRENAL AKI PROGRESSION
Obstruction -> increased interstitial pressure -> elevated Bowman’s capsule pressure-> impedes filtration -> GFR decreased
263
POSTRENAL AKI TREATMENT
REMOVAL OF OBSTRUCTION
264
Onset
| AKI PHASES
– precipitation event until tubular injury
265
* Oliguric (anuric)
| AKI PHASES
– GFR falls, nitrogenous wastes accumulate (azotemia), hyperkalemia urine output decreases (oliguria, anuria) -> fluid retention
266
* Diuretic
| AKI PHASES
– GFR increases, healing, urine output increases
267
* Recovery
| AKI PHASES
– tubular edema resolves, GFR improves (70-80% of normal), urine output and blood levels of nitrogenous wastes return to normal
* Note – some damage may persist
268
Hallmarks of Acute Kidney Injury
* Decreased glomerular filtration rate
* Azotemia
* Decreased urine output (oliguria, anuria)
269
RISK FACTORS OF AKI
Pre-existing renal impairment, atherosclerosis, hypertension, diabetes, HF, age
270
MORTALITY OF AKI
15-60%
271
AKI NURSING CONSIDERATIONS
Prevention
* Early diagnosis – identify the cause, watch for symptoms
* Monitor urine output
* Urine tests – UA, specific gravity, osmo
* Blood tests – BUN, Cr, electrolytes
* Adequate nutrition and rest
272
HOW DO YOU PROTECT THE KIDNEY IN AKI
– Prevention of infections
– Monitor use of nephrotoxic drugs (ie: aminoglycosides, radiocontrast agents etc.)
* Dialysis or continuous renal replacement therapy (CRRT)
273
Does Kidney failure equal end stage renal disease
no
274
what is chronic renal failure
Progressive loss of renal function over months to years due to permanent loss of nephrons
275
is chronic renal failure reversible
not as reversible as aki
276
can chronic renal failure be slowed
yes
277
when does chronic renal failure become irreversible
end stage renal disease
278
two main causes of chronic renal failure
diabetes and hypertension
279
mortality rate of chronic renal failure
100% without dialysis or transplant
280
stages of chronic kidney disease correspond to
degree of nephron loss
281
stage 1 of chronic kidney disease
kidney damage with normal or increased gfr >90 ml/min
282
stage 2 chronic kidney disease
decreased gfr
kidney damage with mild decrease in gfr
60-89 ml/min
283
stage 3 of chronic kidney disease
gfr <60 ml/min for 3 months or longer
moderate decrease in gfr- 30-59 ml/min
284
stage 4 chronic kidney disease
gfr <60 ml/min for 3 months or longer
severe decrease in gfr 15-29 ml/min
285
stage 5 of chronic kidney disease
kidney failure
<15 ml/min
286
nervous system
| systemic effects of uremia
changes in alertness, level of consciousness, neuropathy -->muscle weakness, restless leg syndrome
287
cardiovascular
| systemic effects of uremia
decreased cardiac output, pericarditis, hpt
288
hematologic
| systemic effects of uremia
anemia, bleeding tendencies
289
immune
| systemic effects of uremia
infection
290
gi
| systemic effects of uremia
anorexia, n&v
291
skin
| systemic effects of uremia
pruritus, uremic frost
292
other
| systemic effects of uremia
sexual dysfunction
293
why are chronic renal failure patients at risk for hypertension
Diseased kidneys are less able to help regulate blood pressure. As a result, blood pressure increases.
294
why are chronic renal failure patients at risk for hyperkalemia
Reductions in urinary potassium excretion that occur in CKD can lead to an inability to maintain potassium homeostasis.
295
why are chronic renal failure patients at risk for anemia
their kidneys cannot make enough erythropoietin which causes their red blood cells to drop and anemia. Most such patients develop anemia, which can happen early in the illness and worsen with time.
296
why are chronic renal failure patients at risk for acidosis
the kidneys can't remove enough acid, which can lead to metabolic acidosis. The normal level of serum bicarbonate is 22-29 mEq/L. Kidney experts recommend that patients not have their serum bicarbonate levels fall below 22 mEq/L
297
why are chronic renal failure patients at risk for uremia
uremic solutes accumulate in the circulation owing to deficient renal clearance. Some of these products are considered uremic toxins and are believed to contribute to the uremic syndrome.
298
why are chronic renal failure patients at risk for hyperparathyroidism
Defect in the activation of vitamin D in the kidneys due to chronic kidney disease (CKD) leads to hypocalcemia and hyperphosphatemia, resulting in a compensatory increase in parathyroid gland cellularity and parathyroid hormone production and causing secondary hyperparathyroidism (SHP)
299
What happens to H ions in renal failure? how does this affect ph
H+ retention in CKD decreases the pH of the kidney interstitial and intracellular compartments,
300
Why do patients with uremia experience neuropathy and severe muscle weakness?
Kidney disease and dialysis can lead to neuropathy pain and muscle atrophy. The exact reasons for this are unknown but several possible causes exist. They include vitamin and mineral imbalances, added pressure from dialysis, and overlapping conditions.
301
treatment of chronic kidney disease
slow progression
transplantation
dialysis
302
types of dialysis
hemodialysis
peritoneal
continuous renal replacement therapy
303
hemodialysis
a machine filters wastes, salts and fluid from your blood when your kidneys are no longer healthy enough to do this work adequately.
304
peritoneal dialysis
During peritoneal dialysis, a cleansing fluid called dialysate passes through a catheter tube into part of the abdomen known as the peritoneal cavity. The dialysate absorbs waste products from blood vessels in the lining of the abdomen, called the peritoneum. Then the fluid is drawn back out of the body and discarded.
305
crrt dialysis
CRRT is a slower type of dialysis that puts less stress on the heart. Instead of doing it over four hours, CRRT is done 24 hours a day
306
kidney transplant
* Patients with ESRD
* Availability of organs
* Two types of donors– Living related– Cadaver
* Renal transplant success superior to any other organ transplant
307
FUNCTIONS OF THE GI SYSTEM
1. PROVIDE NUTRIENTS FOR THE BODY THROUGH
A. GI MOTILITY
B. SECRETION OF DIGESTIVE JUICES, ENZYMES, AND HORMONES
C. DIGESTION OF NUTRIENTS
D. ABSORPTION OF NUTRIENTS
308
GI MOTILITY
PROPULSIVE AND MIXING MOVEMENTS
309
MUCOSA
| LAYERS OF THE GI TRACT
1. EPITHELLIUM
2. LAMINA PROPRIA
3. MUSCULAR MUCOSAE
*INNERMOST LAYER
*ABSORPTIVE FUNCTION OCCURS HERE
310
SUBMUCOSA
| GI TRACT LAYERS
RIGHT BELOW THE MUCOSA
311
THIRD LAYER OF THE GI TRACT
MUSCULARIS PROPRIA- INNER CIRCULAR MUSCLE LAYER, INTERMUSCULAR SPACE, AND OUTER LONGITUDINAL MUSCLE LAYER
312
4TH LAYER OF THE GI TRACT
SEROSA
312
WHAT DOES THE MUSCULARIS EXTERNA INCLUDE
LONGITUDINAL MUSCLE
CIRCULAR MUSCLE
313
WHAT IS THE SEROSA MADE OF
CONNECTIVE TISSUE
314
MESOTHELIUM OF THE GI TRACT
SEROSA
315
WHAT DOES GI MOTILITY DO
PROPELS FOODS AND FLUIDS THROUGH THE SYSTEM
INTESTINAL SMOOTH MUSCLE- INTRINSIC PACEMAKER- SLOW WAVE ACTIVITY
316
WHAT REGULATES GI MOTILITY
ANS AND LOCAL (ENTERIC) SYSTEMS
317
WHAT ENTERIC SYSTEM REGULATES THE GI SYSTEM
AUERBACH'S PLEXUS
MEISSNER'S PLEXUS
318
AUERBACH'S PLEXUS
CONTROLS MOTILITY
319
MEISSNER'S PLEXUS
CONTROLS SECRETION AND BLOOD FLOW
320
PARASYMPATHETIC SYSTEM AND THE GI SYSTEM
VAGUS NERVE --> INCREASE MOTILITY --> SECRETORY ACTIVITIES
321
SYMPATHETIC NERVOUS SYSTEM AND THE GI SYSTEM
aravertebral, celiac, superior and inferior mesenteric ganglia --> sphincter control, decrease motility and secretory activities
322
Cholecystokinin
stimulates contraction of gallbladder, secretion of pancreatic enzymes, slows gastric emptying
323
SECRETIN
Stimulates secretion of bicarb solution from pancreas and liver
324
Glucagon-like peptide I (GLP-1)
| Incretin hormones
augments insulin release, suppresses glucagon release, slows gastric emptying, decreases appetite
325
Glucose dependent insulinotropic polypeptide (GIP) – augments insulinrelease
| Incretin hormones
– augments insulin release
326
GASTRIN
Stimulates gastric acid, pepsinogen secretion, increases gastric blood flow, stimulates smooth muscle contraction and growth of mucosa
327
GHRELIN
STIMULATES SECRETION OF GROWTH HORMONE, STIMULATES APPETITE
328
WHAT DOE EPITHELIAL CELLS SECRETE
MUCOUS FOR PROTECTION
329
WHAT DO PARIETAL (OXYNTIC) CELLS SECRETE
HCL AND INTRINSIC FACTOR
330
WHAT DO CHIEF (PEPTIC) CELLS SECRETE
PEPSINOGEN
331
WHAT DO G CELLS SECRETE
GASTRIN
332
Prostaglandins - Serve a protective function in the stomach and duodenum by:
1. STIMULATING THE SECRETION OF MUCOUS AND BICARB
2. SUPRESSING THE SECRETION OF GASTRIC ACID
3. PROMOTING SUBMUCOUSAL BLOOD FLOW BY VASODILATION (PROMOTES EPITHELIAL CELL REGENERATION
333
WHAT SUBSTANCES CAN BE DAMAGING TO THE MUCOUSAL BARRIER
NASAIDS, HELIOBACTER PYLORI, ALCOHOL, BILE SALTS
THEY ALLOW THE HYDROGEN ION ENTRY INTO THE TISSUE THAT RESULTS IN TISSUE DAMAGE
334
IS THE GUT STERILE
NO
335
WHY DOES THE STOMACH AND SMALL INTESTINE ONLY CONTAIN A FEW SPECIES OF MICROORGANISMS
VERY ACIDIC. MANY DON'T SURVIVE ALL THE WAY TO THE SMALL INTESTINE
336
WHERE IS THE LARGEST ECOSYSTEM OF MICROBES IN THE GI TRACT FOUND
COLON: PART OF THE LARGE INTESTINE. PRIMARILY ANAROBIC. 300-500 SPECIES
337
WHAT ROLE DO THE MICROORGANISMS PLAY IN THE GI TRACT
HELP FERMENT DIETARY RESIDUE, HELPS PREVENT EXOGENOUS INFECTION
338
WHAT MIGHT CAUSE A DISRUPTION OF INTESTINAL FLORA AND LEAD TO OPPORTUNISTIC INFECTION
ANTIOBIOTICS- SPECIFICALLY BROAD SPECTRUM
339
GI IMMUNITY
DAILY CONTACT WITH EXTERNAL ENVIRONMENT
PATHOGENS AND TOXIC SUBSTANCES
GI IMMUNE STRUCTURES HELP TO PREVENT SUBSTANCES FROM ENTERING BLOOD/LYMPH
340
FACTORS OF GI IMMUNITY
LOW PH IN THE STOMACH
IMMUNOGLOBULINS IN MUCOUS
GALT
MICROFOLD CELLS
341
GALT
GUT ASSOCIATED LYMPHOID TISSUES
PEYER'S PATCHES
LYMPHOCYTES THROUGHOUT GUT
342
Name the three sections of the small intestine
1. DUODENUM
2. JEJUNUM
3. ILEUM
343
What happens when you don’t have intrinsic factor?
ISSUES ABSORBING VITAMINS LIKE B12 LEADING TO ANEMIAS
344
What is the action of pepsin?
AID IN DIGESTION
SPECIFICALLY BREAKING DOWN PROTEINS
345
What is the name of the sphincter located between the stomach and the small intestine?
PYLORIC SPHINCTER
346
What type of acid-base problem would you anticipate having if you have had frequent prolonged vomiting?
METABOLIC ALKALOSIS
347
What layer of the GI tract contains blood vessels, nerves and structures responsible for secretion of digestive enzymes
SUBMUCOSAL
348
What is the form that protein needs to be in order to be used by the body?
AMINO ACIDS
THIS IS WHAT PEPSIN BREAKS IT INTO
349
What are the four parts of the colon?
1. SIGMOID
2. ASCENDING
3. TRANSVERSE
4. DESCENDING
350
What structure covers the larynx and prevents aspiration when swallowing?
EPIGLOTTIS
351
In what part of the GI tract does the majority of nutrient absorption occur?
SMALL INTESTINE
352
Liver
- Secretion of bile - HEPATOCYTES
- GETS LIKE 20% OF CARDIAC OUTPUT
- Metabolism of bilirubin
- Vascular/hematologic function
- Metabolism of nutrients
- Metabolic detoxification
- Storage of mineral and vitamins
353
Gallbladder
Stores and concentrates bile between meals
Bile from liver via hepatic ducts
354
Pancreas
Secretes enzymes and alkaline fluids that digest proteins, carbs, and fats
355
Choleresis
=bile secretion
356
WHAT DOES BILE CONTAIN
bile salts required for intestinal emulsification and absorption of fats
357
FAT SOLUABLE VITAMINS
D, E, K, A
358
HOW MUCH BILE DOES THE LIVER SECRETE A DAY
700-1200 ML/DAY
359
WHAT IS BILIRUBIN A BYPRODUCT OF
DESTRUCTION OF OLD RB'S
Gives bile its color and produces yellow tinge of jaundice
360
HOW IS BILIRUBIN EXRETED
MOSTLY IN URINE
361
KUPFFER CELLS
MACROPHAGES THAT TAKE UP AND DESTROY AGED RBCs AND CONVERT THEM TO BILIRUBIN
362
Vascular/Hematologic Functions
| LIVER
Stores large volumes of blood
Kupffer cells important in destroying intestinal bacteria and preventing infection
Synthesizes prothrombin, fibrinogen, and factors I, II,VII, IX, and X
Vit K depends on adequate bile production
363
Anorexia
– loss of appetite, lack of desire to eat, despite the normal physiologic stimuli
364
Factors influencing appetite:
hunger, smell, emotions, drugs, disease states
365
Nausea
– unpleasant, subjective, conscious sensation resulting from stimulus of the medullary vomiting center
366
Common cause of nausea:
distention of duodenum
367
nausea is Accompanied by autonomic nervous system responses:
watery saliva, pallor, sweating, elevated heart rate
368
regulation of vomiting
in medulla
Chemoreceptor trigger zone, Vomiting center
369
stimuli that can result in vomiting
Distention or irritation of the stomach, small intestine
Stimulation of the vestibular system in the inner ear (motion sickness, ear infection etc.)
Blood-borne emetics/toxins (chemotherapy, opioids, ipecac)
Sensory input (sight, smell, pain)
Hypoxia (decreased CO, shock, increased intracranial pressure)
370
vomiting patho
Airway closed, forceful contraction of diaphragm/abd. muscle, gastroesophageal sphincters relax
371
dysphagia
Difficulty swallowing
May include inability to initiate swallowing or sensation that swallowed foods “stick
372
causes of dysphagia
Problem in food delivery into esophagus (neuromuscular incoordination)
Problem with transport down the esophagus (altered peristaltic activity)
Problem with entry into stomach (LES dysfunction or obstructing lesions)
373
DIARRHEA
Increase in the frequency and fluidity of bowel movements. Symptom of GI disease
374
types of acute diarrhea
inflammatory
noninflammatory
375
causes of diarrhea
nfection, maldigestion, inflammation, functional disorders
376
complications of diarrhea
dehydration
electrolyte imbalances
377
management of diarrhea
Diagnosis and treatment of the underlying cause
Replacement of lost water and electrolytes
Relief of cramping
Reducing the passage of unformed stools
378
CONSTIPATION
Small, infrequent, incomplete or difficult passage of stool
379
Impaction:
firm, immovable mass of stool that becomes stationary in the GI
380
Constipation causes
Low residue (fiber) diet
Lack of exercise (sedentary lifestyle, bedrest)
Slowed peristalsis (elderly, excessive use of opioids)
Conditions that alter GI motility (spinal cord injuries, MS, endocrine)
- Medications (opioids, anticholinergics
381
GASTROESOPHAGEAL REFLUX
Symptoms or mucosal damage caused by abnormal reflux of gastric contents into esophagus
Weakening of lower esophageal sphincter
382
Persistent reflux =
esophagitis, reflux disease
383
gerd
Weak, incompetent LES
Irritation effects of refluxate (ph <4.0)
Decreased clearance of refluxate from the esophagus
Mucousal injury, hyperemia, inflammation
Progressive disease -> erosive esophagitis Barrett’s esophagus
384
barrett’s esophagus
– metaplasia squamous mucosa, replaced by abnormal columnar epithelial cells
increased cancer risk
385
gerd Clinical manifestations:
heartburn
regurgitation
belching
pain
bleeding
respiratory symptoms
386
gerd Tx
Weight reduction
Avoid large meals
Decrease in foods/activities that decrease LES tone (caffeine, fats, chocolate, ETOH, smoking)
Avoid activities that increase IAP (lifting)
Positioning (elevate HOB, upright after eating)
Medications
Surgical intervention
387
does everyone who has gastroesophagealreflux have GERD?
no
388
Is there an association between GERD and asthma?
yes
389
why would sitting up help to relieve the symptoms of gerd
gravity, keeps it down
390
what are the complications of gerd
burning of esophagus
pain
391
BALANCING THE SCALE- GASTRIC MUCOSAL BARRIER
| agressive factors
age
smoking
alcohol
bile acids from duodenal reflux
h pylori
nsaids
acid
pepsin
392
gastric mucosal barrier
| defensive factors
mucus
bicarb
blood flow
prostaglandins
393
esophagitis
inflammation of esophagus from gerd
394
pyloris
heartburn
395
Hematemesis
– bloody vomitus (bright red or coffee ground)
396
Melena
– blood in the stool (bright red to tarry black)
397
Occult blood
– blood in the stool that is not apparently visible
398
Hematochesia
– fresh blood from the stool
399
causes of acute gastritis
ingestion of alcohol, aspirin/NSAIDS, viral, bacterial or chemical toxins, glucocorticoids, profound stress
400
causes of chronic gastritis
helicobacter pylori, atrophic (autoimmune, environmental), chemical gastropathy (alkaline reflux)
401
clinical manifestations of gastritis
Anorexia, nausea, vomiting, occ. Blood, Hematemesis, abd. pain
402
Tx of acute gastritis
remove causative agent
403
Tx of chronic gastritis
reat H. pylori (antimicrobials)
404
PEPTIC ULCER DISEASE
Disorders of the GI tract (stomach, duodenum) caused by action of acid and pepsin
Range -> slight injury -> severe ulceration
Can affect one or multiple layers
Imbalance of defensive (protective) factors vs. aggressive factors
405
Two major causes of gastric irritation and ulceration
– H. pylori, aspirin, other NSAIDS
406
peptic ulcer disease- clinical manifestations
Epigastric burning, discomfort, pain
Nausea
Abdominal upset
407
peptic ulcer disease-diagnosis
H&P, endoscopy, H.pylori test labs, radiographic studies
408
Tx of peptic ulcer disease
Pharmacologic – eradicate cause, relieve ulcer symptoms, heal the ulcer
Prevent complications
Avoidance of injurious agents
Diet: avoid foods that cause symptoms
409
complications of peptic ulcer disease
hemorrhage, gastric outlet obstruction, perforation
410
INFLAMMATORY BOWEL DISEASE
| 2 diseases
crohns disease
ulcerative colitis
411
inflammatory bowel disease
| chronic illness
remissions and exacerbations
412
onset of ibd
childhood to young adulthood
413
causes of ibd
autoimmune, genetic predisposition, environmental trigger - microbial flora
414
how is ibd diagnosed
colonoscopy
415
ulcerative colitis
| ibd
Ulcerative, exudative
Primarily mucousal
Continuous lesions
Rectum, left colon
Diarrhea - common
Rectal bleeding -common
Fistulas, strictures, abscesses -rare
Increased risk of colon cancer
416
chron's disease
Granulomatous
Primarily submucousal
Skips lesions - cobblestone
Primary ileum, then colon
Diarrhea – common;
Rectal bleeding - rare
Strictures, fistulas, abscesses -common
Cancer risk- uncommon
417
ibd diagnosis
History/physical, colon/sigmoidoscopy, biopsy, stool exams
418
Tx of ibd
Reduction of inflammation (control not cure)
medications
Maintaining adequate nutrition
Preventing complications
Surgical intervention
Removal of diseased portion of bowel
419
diverticular disease
Outpouchings through the muscular layer of the colon wall
Often found in descending/sigmoid colon
420
diverticular disease
| patho
high intraluminal pressure on areas of bowel wall weakness
421
diverticular disease
| causes
ow fiber diet, lack of exercise, poor bowel habits, aging
422
diverticular disease
| progression
Inflamed diverticula -> diverticulitis -> fever, lower abd. pain ->abscess development, peritonitis, obstruction
423
diverticular disease
| Tx
diet,“itis” -> antibiotic, fluids, electrolytes, surgery –unresolved symptoms, complications
424
intestinal obstruction
Partial or complete blockage of the small or large intestinal lumen –impaired movement
425
types of intestinal obstruction
mechanical
paralytic
426
intestinal obstruction
| clinical manifestations
* Mechanical: increased bowel sounds, abd. pain, colicky, nausea
* Paralytic: absence of bowel sounds
* Both: pain, constipation, abd. distention, vomiting
427
intestinal obstruction
| diagnosis
h and p
abd xray
ct
us
428
intestinal obstruction
| complications
edema
ischemia
necrosis
perforation
429
intestinal obstruction
| Tx
decompression or surgical intervention, correction of fluid and electrolyte imbalances
430
PERITONITIS
Inflammatory response of the serous membrane
431
peritonitis
| causes
chemical irritation
bacteria
432
peritonitis
| symptoms
pain, tenderness, rigid/boardlike abdomen, vomiting, fever, tachycardia, hypotension, elevated WBC, hiccups, paralytic ileus
433
peritonitis
| rx
correct cause, antibiotics, decompression, fluid and electrolyte replacement, nothing by mouth, pain control
434
COLORECTAL CANCER
2nd leading cause of cancer deaths in US
Seen in those in 40’s, mean age 68 men, 72 women
Adenomatous polyps thought to be a precursor
435
polyp
benign neoplasm, from mucosal epithelium of the intestine
436
cause of colorextal cancer
unknown, incidence
increases with age, familial risk, diet, ulcerative colitis
437
screening for colorectal cancer
40 – digital rectal exam annually
50 – fecal occult blood test annually, sigmoidoscopy every five years , barium enema every five years or colonoscopy every 10.
High risk – screen earlier
Colonoscopy with positive screen
438
hepatitis
Inflammation/infection of the liver by hepatotoxic viruses
439
types of hepatitis
A (spread by fecal-oral route)
B (spread by blood, body secretions/oral/sexual contact)
C (spread by blood)
440
clinical minifestations of hepatitis
N/V/D, elevated liver enzymes, elevated bilirubin, liver tenderness
441
Tx of hepatitis
antivirals, minimize risk factors, prevention via immunizations
442
LIVER—CIRRHOSIS
End stage liver disease with loss of functional liver tissue
443
LIVER—CIRRHOSIS
| causes
Causes: etoh, hepatitis, toxicity from drugs/chemicals
444
LIVER—CIRRHOSIS
| clinical manifestations
vary, asymptomatic to end stage liver failure
Weight loss, anorexia, weakness, diarrhea, hepatomegaly, jaundice, portal hypertension
445
portal hypertension
increased resistance to flow in the portal venous system
446
LIVER—CIRRHOSIS
| complications
include ascites, splenomegaly, hepatic encephalopathy ,and esophageal varices
447
Cholecystitis
| gallbladder
acute or chronic inflammation of the gallbladder (commonly due to obstruction of gallbladder outlet
448
acute Cholecystitis s/s
| gallbladder
RUQ/epigastric pain, mild fever, anorexia, nausea, vomiting, elevated WBC, elevated liver enzymes, elevated bilirubin
449
chronic Cholecystitis s/s
| gallbladder
more vague—intolerance of fatty foods, belching, GI discomfort, possible enlargement of gallbladder
450
diagnosis of gallbladder
US, CT scans; treated by surgical cholecystectomy if needed
451
Cholelithiasis
gallstones
Generally caused by buildup of cholesterol or bilirubin
452
Cholelithiasis
| contributing factors
* Contributing factors: abnormal bile composition and bile stasis
453
Cholelithiasis
| s/s
many are asymptomatic until stones are large, may see obstruction, jaundice, biliary colic
454
