EXAM 5 Flashcards
MOTILITY
movement of food through the body from mouth to anus
peristalsis
involuntary contractions of the intestinal muscles that create wave
movements to propel substances forward
sphincter
Ring of muscle that closes an opening like at the stomach
mastication
chewing
enteric
occuring in the intestines
chyme
Acidic fluid that moves from the stomach to the small intestine. Consists of gastric juices and partly digested food
defacation
Discharge of feces from the body
intestinal flora
Naturally occurring bacteria in the intestine
digestion
Process of breaking down food into what the body can use and needs
Absorption
Action of one thing taking up or being taken up by another
describe the anatomy of the upper gi tract
- 4 layer structure, oral cavity, salivary glands, esophagus, stomach, small intestines- digests food and gets it ready for processing as well as digestion.
describe the anatomy of the middle gi tract
lower duodenum, 2/3 of transverse colon- processes food that small intestine couldn’t by absorbing minerals and water
describe the anatomy of the lower gi tract
last 1/3 of transverse colon, upper part of the anal canal- dehydrates and stores fecal material
what are the anatomical landmarks of the stomach
cardia, fundus, body, pylorus
cardia
surrounds superior opening,
fundus-
rounded, gas filled portion superior and left of the cardia,
body-
large part beneath the fundus.
Pylorus-
area connecting to the duodenum
Saliva-
starts digestion, helps chew and swallow, protects teeth,
gastric juice-
acidic fluid in stomach that promotes digestion,
bile-
bitter and alkaline fluid that is secreted by the liver and aids digestion,
pancreatic fluid-
alkaline (bicarbonate)- critical for digestion of protein, fats, and carbs
What is the function of the peritoneum?
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.
passage of food through the gi tract
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
- What are the hormones of the GI tract?
CHOLECYSTOKININ, SECRETIN (GLP-1 AND GIP), GASTRIN, GHRELIN
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.
- Is the gut of a normal adult sterile?
no
- Where is the largest ecosystem of microbes in the GI tract found?
Large intestine followed by the small intestine
- What role do microorganisms play in the GI tract?
They aid the immune system and ensure the integrity of the mucosal lining.
- What might cause a disruption of intestinal flora and lead to opportunistic infection?
Diet, antibiotics or other meds, or other environmental factors
- Name the three sections of the small intestine.
Duodenum, jejunum, and ileum
- What is the action of pepsin?
Breaks down proteins into peptides and amino acids to be absorbed in the small intestine.
- What is the name of the sphincter located between the stomach and the small intestine?
Pyloric sphincter
- What type of acid-base problem would you anticipate having if you have had frequent prolonged vomiting?
Metabolic alkalosis
- What layer of the GI tract contains blood vessels, nerves, and structures responsible for secretion of digestive enzymes?
submucosa
- What structure covers the larynx and prevents aspiration when swallowing?
epiglottis
- In what part of the GI tract does the majority of nutrient absorption occur?
small intestine
- Does everyone who has gastroesophageal reflux have GERD?
no
- Is there an association between GERD and asthma?
yes
- 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.
- What are the complications of GERD?
Esophagitis and barret’s esophagus, gi bleeding, ulcerations, narrowing esophagus
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.
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.
c. What are the two most common causes of peptic ulcer disease?
h. pylori and aspirin/nsaids action of acid and pepsin
- What are some causes of mechanical bowel obstruction?
Adhesions, volvulus, incarcerated inguinal hernia, intussusception
- Why is a patient with C. difficile infection on contact precautions in the hospital?
C diff is airborne transmitted.
- 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
- Why do patients develop jaundice?
Usually a sign of liver disease causing a buildup of bilirubin.
- Which blood tests monitor liver function?
Alt, ast, alp, ggt, pt, inr are the typical tests.
- Is liver damage in Cirrhosis reversible?
No, but it can be slowed down
- What are the complications of portal hypertension?
Bleeding in the esophagus and stomach, peritonitis, hepatorenal syndrome
- 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.
FUNCTION OF THE KIDNEYS
EXCRETORY AND ENDOCRINE FUNCTION
WHAT EXACTLY DO THE KIDNEYS REGULATE
WATER, ELECTROLYTES, AND ACID-BASE BALANCE
WHAT DO THE KIDNEYS EXCRETE
FOREIGN CHEMICALS AND METABOLIC WASTE MATERIALS
WHAT DO THE KIDNEYS SYNTHESIZE AND ACTIVATE
RENIN, ERYTHROPOIETIN, VITAMIN D, AND PROSTAGLANDINS
WHAT ORGANS STORE AND TRANSPORT URINE
URINES, BLADDER, URETHRA
WHAT CAN STIMULATE ERYTHROPOIETIN RELEASE FROM THE KIDNEYS
STATES OF DECREASED BLOOD OXYGENATION
WHAT IS ERYTHROPOEITIN (EPO)
HORMONE THAT STIMULATES STEM CELLS WITHIN OUR BONE MARROW TO INCREASE RBC PRODUCTION
NEPHRON
MAIN FUNCTIONAL UNIT OF THE KIDNEY
HOW MANY NEPHRONS DOES EACH KIDNEY HAVE
ABOUT 1.2 MILLION
WHAT HAPPENS TO NEPHRONS OVER TIME
THEY DO NOT REGENERATE
DECLINE WITH AGE
HOW FAST DOES THE NEPHRON COUNT DECLINE
10% PER DECADE BEGINNING AT AGE 40
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
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
GLOMERULUS
WHERE THE FILTRATION PRIMARILY OCCURS
MAIN PART THAT ACTUALLY FILTERS THE BLOOD
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
HOW ARE MATERIALS WE DON’T NEED IN THE BODY SECRETED
WITHIN OUR TUBULAR FILTRATE FOR ELIMINATION
NEPHRON FUNCTION
- FILTRATION
- REABSORPTION
- SECRETION
NEPHRON FILTRATION
OF WATER SOLUBLE SUBSTANCES FROM BLOOD
NEPHRON REABSORPTION
OF FILTERED NUTRIENTS, WATER, AND ELECTROLYTES
NEPHRON SECRETION
OF WASTES OR EXCESS SUBSTANCES INTO THE FILTRATE
DIFFERENT SEGMENTS OF THE NEPHRON SPECIALIZE TO ACCOMPLISH WHAT
ALL NEPHRON FUNCTIONS
GLOMERULUS LAYERS
- CAPILLARY ENDOTHELIUM
- BASEMENT MEMBRANCE
- OUTER CAPILLARY ENOTHELIUM PODOCYTES
WHAT DOES THE PROXIMAL TUBULE REABSORB
NA
CL
HCO2
K
H2O
GLUCOSE
AMINO ACIDS
WHAT DO THE PROXIMAL TUBULES SECRETE
H+
ORGANIC ACID AND BASES
WHAT DOES THE THIN DESCENDING LOOP OF HENLE REABSORB
H2O
WHAT DOES THE THICK ASCENDING LOOP OF HENLE REABSORB
NA
CL
K
CA
HCO2
MG
WHAT DOES THE THICK ASCENDING LOOP OF HENLE SECRETE
H
WHAT DOES THE EARLY DISTAL TUBULE REABSORB
NA
CL
CA
MG
WHAT DOES THE LATE DISTALE TUBULE AND COLLECTING DUCT INCLUDE
PRINCIPAL CELLS
INTERCALATED CELLS
WHAT DO PRINCIPAL CELLS REABSORB
NA
CL
WHAT DO PRINCIPAL CELLS SECRETE
K
WHAT ARE RESPOONSIBLE FOR ADH MEDIATED H2O REABSORPTION
PRINCIPAL CELLS
WHAT DO INTERCALATED CELLS REABSORB
HCO2
K
WHAT DO INTERCALATED CELLS SECRETE
H
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
WHAT IS THE RESULTING FLUID OF GLOMERULAR FILTRATION CALLED
GLOMERULAR FILTRATE
GLOMERULAR FILTRATION RATE
GFR
125 mL OF GLOMERULAR FILTRATE PRODUCED PER MINUTE
HOW MUCH BLOOD PERFUSES THE KIDNEYS
20-25% OF NORMAL CARDIAC OUTPUT
(1000-1300 ML/MIN)
*PROMOTES GLOMERULAR FILTRATION
PRIMARY FILTRATION PRESSURES
GLOMERULAR BLOOD HYDROSTATIC PRESSURE
2-3X HIGHER THAN OTHER CAPILLARY BEDS IN THE BODY
WHAT HELPS MAINTAIN BLOOD FLOW AND GFR
INTRARENAL AND EXTRARENAL FEEDBACK MECHANISMS
Neural/Humoral Controls
Regulation of Renal Blood Flow -GFR
– Sympathetic stimulation
– Angiotensin II, ADH, prostaglandins
Renin angiotensin system
Regulation of Renal Blood Flow -GFR
Control of blood pressure
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
INCREASED PROTEIN AND GLUCOSE LOADS
Regulation of Renal Blood Flow -GFR
Increase GFR
What is Glomerular filtration rate used to evaluate
renal tissue function
what does decrease in bp do to gfr
decreases hydrostatic pressure that drives filtration
decreases gfr
what does an increase in protein and glucose do to gfr
increase gfr
what does sympathetic nervous system activation do to gfr
decrease gfr
how do hormones like angiotensin II affect gfr
efferent arteriole vasoconstriction increases b/p –> increases gfr
how does age affect gfr
loss of nephrons –> decreased gfr
how does the presence of prostaglandins affect gfr
increase gfr
normal creatinine level
adult:
0.6-1.2 mg/dl
what is creatinine
non protein end product of skeletal muscle metabolism
to what degree is creatinine eliminated
to the degree renal function will allow
how does creatinine indicate renal function
most specific indicator of renal function- estimates function capacity of the kidney
normal bun level
8-20 mg/dl in adult
urea
byproduct of protein metabolism that is eliminated entirely by the kidney
what happens to urea as renal function declines
it accumulates
other than renal disease, what else can cause bun elevation
high protein diet
gi bleeding
Urinalysis –
gross and microscopic exam of urine to evaluate ph, specific gravity and presence of abnormal substances and formed elements
- Gross exam –
urinalysis
color, clarity, odor, sediment
- Microscopic
urinalysis
– RBC, WBC, epithelial cells, casts, crystals, bacteria, pH
- Specific gravity
urinalysis
– concentration of solutes, hydration status, functional ability of kidney
normal specific gravity level in adults
(1.010-1.025)
Polyuria
– increased volume of urine voided
- Oliguria
– urine output less than 400ml/day
- Anuria
– urine output less than 50ml/day
- Nocturia
– excessive urination at night
- Hematuria
– red blood cells in the urine
- Proteinuria
– abnormal amounts of protein inthe urine
- Dysuria
– painful or difficult voiding
Frequency
– frequent voiding, more thanevery three hours
- Urgency
– strong desire to void
- Hesitancy
– delay, difficulty in initiating voiding
- Enuresis
– involuntary voiding during sleep
What is the functional unit of the kidney called?
nephron
What structure in the nephron filters blood?
glomerulus
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.
What lab test is the most specific indicator of renal function?
urinalysis
what age can obstructive renal disorders occur
at any age
where can obstructive renal disorders occur
any area of the renal system
what are common causes of obstructive renal disorders
– Developmental defects
– Pregnancy
– Benign prostatic hypertrophy
– Infection, inflammation
– Tumors – common cause
– Stones – common cause
what are the effects of obstructive renal disorders
urinary stasis –> infection/backpressure –> hydroureter, hydronephrosis
Hydronephrosis Pathophysiology
Complete obstruction -> hydronephrosis -> decreased GFR -> ischemia -> increased pressure -> kidney damage
Renal Calculi
Crystalline structures that form from components, normally excreted in urine
requirements for renal calculi formation
supersaturation
nucleus (nidus)
deficiency of inhibitors
why is supersaturation of crystaline structures required for renal calculi formation
supports continued crystallization of stone components
why is nucleus (nidus) required for renal calculi formation
for the crystal to form around
what inhibitors of stone formation will we se a deficiency of in renal calculi formation
magnesium
citrates
types of stones
- Calcium (oxalate, phosphate or combo) – most common
- Magnesium ammonium phosphate (struvite)
- Uric Acid (urate)
- Cystine
clinical manifestations of renal system calculi
- pain- renal colic or non colicky
- n&v
- cool, clammy skin
renal colic
renal calculi pain
(often ureteral) pain, acute, rhythmic progressively, intense, initiates in flank and can radiate.
Non-colicky
renal calculi pain
– pain dull, deep ache in flank, varies in intensity
diagnosis
Renal System Calculi
Clinical symptoms, history to include diet, meds, complicating factors
urinalysis
stone analysis
bun/cr
xray, ct, us, ivp, nuclear scintigraphy
what findings on a urinalysis indicate renal system calculi
hematuria, infection, presence of crystals, urine pH
treatment
Renal System Calculi
meds
stone removal
prevention of recurrence
diluting urine
diet
measures to change urine ph
meds to reduce stone causing substances
meds used for renal system calculi
pain meds, antiemetics, antibiotics for infections
lithotripsy
fragments of stone
urteroscopic removal
how do you dilute urine
decrease supersaturation with 2l fluids/day
uti
Infection of the urinary system
host defenses
uti
– Washout phenomenon – voiding
– Mucin lining of bladder – barrier protects against invasion of organisms
– Body’s immune defenses
– Washout phenomenon
– voiding to reduce/eliminate uti
– Mucin lining of bladder
– barrier protects against invasion of organisms
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
Lipopolysaccarides
uti
– bind to host cells and ilicit inflammatory response
entry
uti
ascending or bloodborne
Escherichia coli
uti
– common infecting organism, lower UTI
is upper or lower uti more serious
upper
CAUSES OF UTI
obstruction, reflux (vesicoureteral and urethrovesical), catheters
CLINICAL MANIFESTATIONS OF UTI
frequency, dysuria, lower back or abdominal discomfort, chills, fever
DIAGNOSIS OF UTI
H&P, ultrasound, CT, renal scans to identify contributing factors, urinalysis, urine culture
TREATMENT OF UTI
location of infection, pathogen causing, acute, chronic or recurrent infection, antibiotics, increased fluid intake
Vesicoureteral reflux
– abnormal backflow of urine from the bladder into the ureter
Glomerulonephritis
– group of diseases that result in inflammation and/or injury to the glomerulus
What is the 2nd leading cause of kidney failure
Glomerular Disease
what happens in glomerular disease
Disruption of glomerular filtration and alteration of permeability of glomerular capillary membrane
is glomerular disease a primary or secondary condition
could be either
what are the triggers of glomerular disease
infectious microorganisms, immune mechanisms, environmental agents
- Clinical manifestations of glomerular disease
nephritic or nephrotic syndrome.
Nephritic syndrome
– inflammatory response –> hematuria, red cell casts in urine, decreased GFR, azotemia, oliguria, hypertension
- Nephrotic syndrome
– increased permeability of the glomerulus – massive proteinuria, hypoalbuminemia, generalized edema, lipiduria and hyperlipidemia
- Asymptomatic
– hematuria, proteinuria aren’t recognized
BOWMAN’S CAPSULE
DOUBLE WALLED CAPSULE ENCASING THE GLOMERULUS
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
FINISHTRATIONS
SPACES BETWEEN ENDOTHELIAL CELLS OF INNER CAPILLARY ENDOTHELIUM WHERE SUBSTANCES CAN MOVE IN AND OUT
BASEMENT MEMBRANE
PREVENTS PLASMA PROTEINS, ERYTHROCYTES, LEUKOCYTES, PLATELETS ETC FROM PASSING THROUGH
OUTER CAPILLARY ENDOTHELIUM
SEPERATES THE BLOOD FROM THE CAPILLARIES OR IN THIS CASE FROM THE FILTRATE WITHIN THE BOWMAN’S CAPSULE
PODOCYTES
FOOT PROCESSES THAT SURROUND THE GLOMERULUS.
SLIP PORES
SPACES BETWEEN THE PODOCYTES
WHAT DO PODOCYTES DO
MAKE THE GLOMERULUS VERY PERMEABLE. MORE SO THAN ANY OTHER CAPILLARY
WHEN WE SEE GLOMERULUS ISSUES, SPECIFICALLY WITH THE PODOCYTES, WHAT DO WE OFTEN SEE
PROTEIN IN THE URINE
BLOOD CELLS IN THE URINE
TUBULAR REABSORPTION
REMOVAL OF MATERIALS FROM THE FILTRATE THAT’S BEEN DEVELOPED WITHIN THE GLOMERULUS
TUBULAR SECRETION
FLUIDS AND SUBSTANCES THAT ARE ADDED TO THE FILTRATE AFTER IT HAS BEEN EXTRACTED FROM THE GLOMERULUS
FILTRATION IS DRIVEN BY WHAT
HYDROSTATIC PRESSURE SO BLOOD CIRCULATES THROUGH THE CAPILLARIES, BLOOD IS PUSHED AGAINST THE WALLS AND FLUID IS FILTERED OUT
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
HOW DOES ANGIOTENSIN II AFFECT GFR
STIMULATES THE RELEASE OF ALDOSTERONE IN THE KIDNEYS TO INCREASE BP AND THUS INCREASE BLOOD VOLUME
HOW DOES ADH AFFECT GFR
MAKES US HOLD ON TO OUR FLUID WHICH INCREASES CIRCULATING BLOOD VOLUME
HOW DO PROSTAGLANDINS AFFECT GFR
DILATING EFFECT INCREASES RENAL BLOOD FLOW AND THUS GFR
HOW DOES THE RENIN ANGIOTENSIN SYSTEM AFFECT GFR
CONTROLS BP. HELPS INCREASE BP VIA VASOCONSTRICTION AND RETAIN BLOOD VOLUME
WHAT DOES THE GFR DIRECTLY RELATE TO
THE NUMBER OF FUNCTIONING NEPHRONS THAT WE ALSO HAVE IN THE BODY
WHAT DOES AN INCREASED CREATININE LEVEL INDICATE
LOW GFR SO WE ARE NOT FILTERING AS EFFECTIVELY
BUN
BLOOD UREA NITROGEN LEVEL
NORMAL URINE
YELLOW TO AMBER
CLEAR TO SLIGHTLY HAZY
PH 5-6
NORMAL URINE PRODUCTION
600-2500 ML/D
URINE SHOULD BE NEGATIVE FOR
GLUCOSE
KETONES
BLOOD
PROTEIN
BACTERIA
WBC
CRYSTALS
RBC
BILIRUBIN
WHAT DO WBC IN URINE INDICATE
UTI
WHAT DOES PROTEIN IN THE URINE INDICATE
PROBLEM OR DAMAGE TO OUR GLOMERULUS
WHEN DO WE SEE POLYURIA
DIURETICS
WHEN DO WE SEE OLIGURIA
DEHYDRATION
RENAL FAILURE
WHEN DO WE SEE ANURIA
CHRONIC RENAL FAILURE
COMPLETE OBSTRUCTION
WHAT PERCENT OF CARDIAC OUTPUT DO THE KIDNEYS RECEIVE UNDER NORMAL CIRCUMSTANCES
20-25 % OR ABOUT 1000-13000 ML/MIN
WHAT IS A NORMAL GFR
125 ML/MIN
BUT OFTEN JUST LOOKING AT ABOVE 60 OR BELOW 60
WHAT FORCES DRIVE GLOMERULAR FILTRATION
BP
PROTEIN AND GLUCOSE LEVELS
RAS SYSTEM
SYMPATHETIC NERVOUS SYSTEM
LOSS OF NEPHRONS
WHAT HAPPENS TO URINE OUTPUT WITH SYMPATHETIC NERVOUS SYSTEM STIMULATION AND WHY
INCREASE IN URINE OUTPUT BECAUSE INCREASE IN HR
WHAT LAB TEST IS THE MOST SPECIFIC INDICATOR OF RENAL FUNCTION
CREATININE
IN RESPONSE TO ACIDOSIS, THE KIDNEYS WILL
PRODUCE AND CONSERVE BICARB AND EXCRETE OUR HYDROGEN ACID
WHAT IS THE ACTION OF ALDOSTERONE
MAKES US RETAIN SODIUM THUS WATER RETENTION
WHAT ACTION DO NATRIURETIC PEPTIDES HAVE IN THE KIDNEY
PROMOTE RENAL EXCRETION OF SODIUM AND WHERE THAT SALT GOES, WATER WILL FOLLOW
IS IT NORMAL TO FIND RBC AND LARGE AMOUNTS OF PROTEIN IN THE URINE
NO
WHAT SUBSTANCE PRODUCED BY THE KIDNEY WILL PROMOTE RBC PRODUCTION IN THE BONE MARROW
ERYTHROPOIETIN
WHAT CO FACTOR SYNTHESIZED BY THE KIDNEY IS NEEDED TO PROMOTE THE ABSORPTION OF CALCIUM IN THE GI TRACT
VITAMIN D
CAUSES OF URINARY OBSTRUCTION
PREGNANCY
TUMOR
KIDNEY STONE
SCAR TISSUE
NEUROGENIC BLADDER
BLADDER OUTFLOW OBSTRUCTION
URETEROVESICAL JUNCTION STRUCTURE
STAGHORN STONES
LARGE STONES THAT FILL THE RENAL PELVIS AND AT LEAST ONE RENAL CALYCES
MOST COMMONLY STRUVITE AND LINKED TO UTI
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
Who is more at risk for a UTI (female or a male)? Why?
FEMALE, SHORTER URETHRA
Why are fluids recommended in the treatment of UTI’s?
WASHOUT PHENOMENON
What factors increase the risk of a UTI in an older adult?
MALNUTRITION
DECREASED NEPHRONS
SEDENTARY LIFESTYLE
LOWER ESTROGEN LEVELS
Why are UTI’s difficult to diagnose in elderly?
UNABLE TO ACCURATELY REPORT
LOWER NORMAL BODY TEMP
PREVALENCE OF ASYMPTOMATIC BACTERIA
CLINICAL MANIFESTATIONS OF NEPHRITIC SYNDROME
inflammatory response –>hematuria, red cell casts in urine, decreased GFR, azotemia, oliguria, hypertension
CLINICAL MANIFESTATIONS OF NEPHROTIC SYNDROME
increased permeability ofthe glomerulus – massive protein uria,hypoalbuminemia, generalized edema, lipiduria and hyperlipidemia
CLINICAL MANIFESTATIONS OF ASYMPTOMATIC GLOMERULAR DISEASE
hematuria, proteinuria aren’t recognized
WITH NEPHRITIC SYNDROMES, IS GLOMERULAR INFLAMMATION ACUTE OR CHRONIC
ACUTE
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
WHAT DO WE SEE WHEN NEPHRITIC SYNDROMES CAUSE A DECREASED GFR
fluid accumulation, edema, hypertension
* Varying degrees of proteinuria
WHEN GLOMERULAR DAMAGE CAUSES HYPOPROTEINEMIA, WHAT 2 THINGS HAPPEN
NEPHROTIC SYNDROME
- EDEMA
- HYPERLIPIDEMIA
HYPOPROTEINEMIA
INCREASED PERMEABILITY TO PROTEINS FROM GLOMERULAR DAMAGE
PREOTEINURIA LEVELS
> 3.5 G/D
WHY DOES HYPOPROTEINEMIA CAUSE EDEMA
DCREASED PLASMA ONCOTIC PRESSURE
WHY DOES HYPOPROTEINEMIA CAUSE HYPERLIPIDEMIA
COMPENSATORY SYNTHESIS OF PROTEINS BY THE LIVER
Tx OF GLOMERULONEPHRITIS
- Focus on cause
- Steroids – inflammation, plasmaphresis
- Dietary, fluid management
- Treament of HPT
- If kidney failure – dialysis or transplant
PROGRESSION OF Diabetic Glomerulosclerosis
Diabetic nephropathy –> glomerulosclerosis –> chronic kidney disease
* Result of the effects of elevated glucose on the glomerulus
PATHO OF DIABETIC GLOMERULOSCLEROSIS
Widespread thickening of the basement membrane, early increase in GFR –> over time reduces GFR
EARLY CHANGE INDICATING DIABETIC GLOMERULOSCLEROSIS
MICROALBUMINEMIA
Tx of Diabetic Glomerulosclerosis
– Control blood glucose levels
– ACE inhibitors or ARBs
– Control of blood pressure
– Smoking cessation
Tubulointerstital Diseases
Affect renal tubule structures and interstitial tissues surrounding tubules
- Acute tubular necrosis
a kidney disorder involving damage to the tubule cells of the kidneys, which can lead to acute kidney failure.
- 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.
Pyelonephritis
Infection of the renal parenchyma, pelvis
ACUTE OR CHRONIC
CAN ASCEND OR BE HEMATOGENOUS
PREDISPOSING FACTORS OF PYELONEPHRITIS
vesicoureteral reflux, pregnancy, neurogenic bladder, catheterization instrumentation
Pyleonephritis – Clinical Manifestations
ACUTE
Chills, fever
* Headache
* Flank,back pain
* Dysuria, frequency urgency
* Malaise
* Costovertebral angle tenderness
Pyleonephritis – Clinical Manifestations
CHRONIC
- History of recurrent UTI
- Can be same as for acute or
- Polyuria
- Nocturia
- Mild proteinuria
- Hypertension
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
RENAL CELL CARCINOMA
– Adults 60-70’s
– Hematuria, flank pain, palpable flank mass
– Diagnosis: ultrasound, CT
– Treatment: surgical resection
Acute Kidney Injury
Sudden severe decrease inrenal function that ispotentially reversible
PRERENAL
ACUTE KIDNEY INJURY TYPES
decreased blood flow to kidney
Intrarenal (intrinsic)
ACUTE KIDNEY INJURY TYPES
- damage to the structures within the kidney (nephrons)
Postrenal
ACUTE KIDNEY INJURY TYPES
– interference with urine outflow
WHAT CAUSES INTRINSIC ACUTE KIDNEY INJURY
DAMAGE TO THE STRUCTURES WITHIN THE KIDNEY
WHAT CAUSES PRERENAL ACUTE KIDNEY INJURY
MARKED DECREASE IN RENAL BLOOD FLOW
WHAT CAUSES POSTRENAL ACUTE KIDNEY INJURY
OBSTRUCTION OF URINE OUTFLOW FROM THE KIDNEY
Decreased renal perfusion
PRERENAL AKI
– Hypovolemia – hemorrhage, dehydration
– Decreased cardiac output – heart failure, anaphylactic or septic shock
CAN PRERENAL AKI BE REVERSED
YES, IF CAUSE IS QUICKLY IDENTIFIED AND TREATED
NEPHRONS
PRERENAL AKI
functional, but decreased blood flow results in decreased GFR. (results with prolonged mean arterial pressure <70 mm Hg.)
What is an indicator of tissue perfusion that might provide a cue about a pre-renal problem?
PROTEIN IN THE URINE INDICATED NEPHRON DAMAGE
Intrarenal (Intrinsic)
AKI
- Damage to the renal parenchyma (nephron -glomerulus or tubules injured)
- Longer course of recovery, or progression to chronic renal failure
CAUSES OF INTRARENAL (INTRINSIC) AKI
– Prolonged ischemia
– Exposure to nephrotoxic agents
– Intratubular obstruction (myoglobinuria, myeloma)
– Inflammatory process – glomerulonephritis, pyelonephritis
Acute Tubular Injury or Necrosis Intrarenal
Destruction of the tubular epithelial cells leading to acute impairment of renal function
Acute Tubular Injury or Necrosis Intrarenal
CAUSES
extensive surgery, severe hypovolemia, sepsis, trauma, burns, intratubular obstructions – myoglobin or hemoglobinuria
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
Postrenal AKI
Outflow obstruction within the urinary collecting system distal to the kidneys (ureters, bladder, urethra)
Postrenal AKI CAUSES
BPH, stones, UTI, tumors, strictures, altered bladder contraction
POSTRENAL AKI PROGRESSION
Obstruction -> increased interstitial pressure -> elevated Bowman’s capsule pressure-> impedes filtration -> GFR decreased
POSTRENAL AKI TREATMENT
REMOVAL OF OBSTRUCTION
Onset
AKI PHASES
– precipitation event until tubular injury
- Oliguric (anuric)
AKI PHASES
– GFR falls, nitrogenous wastes accumulate (azotemia), hyperkalemia urine output decreases (oliguria, anuria) -> fluid retention
- Diuretic
AKI PHASES
– GFR increases, healing, urine output increases
- 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
Hallmarks of Acute Kidney Injury
- Decreased glomerular filtration rate
- Azotemia
- Decreased urine output (oliguria, anuria)
RISK FACTORS OF AKI
Pre-existing renal impairment, atherosclerosis, hypertension, diabetes, HF, age
MORTALITY OF AKI
15-60%
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
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)
Does Kidney failure equal end stage renal disease
no
what is chronic renal failure
Progressive loss of renal function over months to years due to permanent loss of nephrons
is chronic renal failure reversible
not as reversible as aki
can chronic renal failure be slowed
yes
when does chronic renal failure become irreversible
end stage renal disease
two main causes of chronic renal failure
diabetes and hypertension
mortality rate of chronic renal failure
100% without dialysis or transplant
stages of chronic kidney disease correspond to
degree of nephron loss
stage 1 of chronic kidney disease
kidney damage with normal or increased gfr >90 ml/min
stage 2 chronic kidney disease
decreased gfr
kidney damage with mild decrease in gfr
60-89 ml/min
stage 3 of chronic kidney disease
gfr <60 ml/min for 3 months or longer
moderate decrease in gfr- 30-59 ml/min
stage 4 chronic kidney disease
gfr <60 ml/min for 3 months or longer
severe decrease in gfr 15-29 ml/min
stage 5 of chronic kidney disease
kidney failure
<15 ml/min
nervous system
systemic effects of uremia
changes in alertness, level of consciousness, neuropathy –>muscle weakness, restless leg syndrome
cardiovascular
systemic effects of uremia
decreased cardiac output, pericarditis, hpt
hematologic
systemic effects of uremia
anemia, bleeding tendencies
immune
systemic effects of uremia
infection
gi
systemic effects of uremia
anorexia, n&v
skin
systemic effects of uremia
pruritus, uremic frost
other
systemic effects of uremia
sexual dysfunction
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.
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.
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.
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
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.
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)
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,
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.
treatment of chronic kidney disease
slow progression
transplantation
dialysis
types of dialysis
hemodialysis
peritoneal
continuous renal replacement therapy
hemodialysis
a machine filters wastes, salts and fluid from your blood when your kidneys are no longer healthy enough to do this work adequately.
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.
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
kidney transplant
- Patients with ESRD
- Availability of organs
- Two types of donors– Living related– Cadaver
- Renal transplant success superior to any other organ transplant
FUNCTIONS OF THE GI SYSTEM
- 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
GI MOTILITY
PROPULSIVE AND MIXING MOVEMENTS
MUCOSA
LAYERS OF THE GI TRACT
- EPITHELLIUM
- LAMINA PROPRIA
- MUSCULAR MUCOSAE
*INNERMOST LAYER
*ABSORPTIVE FUNCTION OCCURS HERE
SUBMUCOSA
GI TRACT LAYERS
RIGHT BELOW THE MUCOSA
THIRD LAYER OF THE GI TRACT
MUSCULARIS PROPRIA- INNER CIRCULAR MUSCLE LAYER, INTERMUSCULAR SPACE, AND OUTER LONGITUDINAL MUSCLE LAYER
4TH LAYER OF THE GI TRACT
SEROSA
WHAT DOES THE MUSCULARIS EXTERNA INCLUDE
LONGITUDINAL MUSCLE
CIRCULAR MUSCLE
WHAT IS THE SEROSA MADE OF
CONNECTIVE TISSUE
MESOTHELIUM OF THE GI TRACT
SEROSA
WHAT DOES GI MOTILITY DO
PROPELS FOODS AND FLUIDS THROUGH THE SYSTEM
INTESTINAL SMOOTH MUSCLE- INTRINSIC PACEMAKER- SLOW WAVE ACTIVITY
WHAT REGULATES GI MOTILITY
ANS AND LOCAL (ENTERIC) SYSTEMS
WHAT ENTERIC SYSTEM REGULATES THE GI SYSTEM
AUERBACH’S PLEXUS
MEISSNER’S PLEXUS
AUERBACH’S PLEXUS
CONTROLS MOTILITY
MEISSNER’S PLEXUS
CONTROLS SECRETION AND BLOOD FLOW
PARASYMPATHETIC SYSTEM AND THE GI SYSTEM
VAGUS NERVE –> INCREASE MOTILITY –> SECRETORY ACTIVITIES
SYMPATHETIC NERVOUS SYSTEM AND THE GI SYSTEM
aravertebral, celiac, superior and inferior mesenteric ganglia –> sphincter control, decrease motility and secretory activities
Cholecystokinin
stimulates contraction of gallbladder, secretion of pancreatic enzymes, slows gastric emptying
SECRETIN
Stimulates secretion of bicarb solution from pancreas and liver
Glucagon-like peptide I (GLP-1)
Incretin hormones
augments insulin release, suppresses glucagon release, slows gastric emptying, decreases appetite
Glucose dependent insulinotropic polypeptide (GIP) – augments insulinrelease
Incretin hormones
– augments insulin release
GASTRIN
Stimulates gastric acid, pepsinogen secretion, increases gastric blood flow, stimulates smooth muscle contraction and growth of mucosa
GHRELIN
STIMULATES SECRETION OF GROWTH HORMONE, STIMULATES APPETITE
WHAT DOE EPITHELIAL CELLS SECRETE
MUCOUS FOR PROTECTION
WHAT DO PARIETAL (OXYNTIC) CELLS SECRETE
HCL AND INTRINSIC FACTOR
WHAT DO CHIEF (PEPTIC) CELLS SECRETE
PEPSINOGEN
WHAT DO G CELLS SECRETE
GASTRIN
Prostaglandins - Serve a protective function in the stomach and duodenum by:
- STIMULATING THE SECRETION OF MUCOUS AND BICARB
- SUPRESSING THE SECRETION OF GASTRIC ACID
- PROMOTING SUBMUCOUSAL BLOOD FLOW BY VASODILATION (PROMOTES EPITHELIAL CELL REGENERATION
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
IS THE GUT STERILE
NO
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
WHERE IS THE LARGEST ECOSYSTEM OF MICROBES IN THE GI TRACT FOUND
COLON: PART OF THE LARGE INTESTINE. PRIMARILY ANAROBIC. 300-500 SPECIES
WHAT ROLE DO THE MICROORGANISMS PLAY IN THE GI TRACT
HELP FERMENT DIETARY RESIDUE, HELPS PREVENT EXOGENOUS INFECTION
WHAT MIGHT CAUSE A DISRUPTION OF INTESTINAL FLORA AND LEAD TO OPPORTUNISTIC INFECTION
ANTIOBIOTICS- SPECIFICALLY BROAD SPECTRUM
GI IMMUNITY
DAILY CONTACT WITH EXTERNAL ENVIRONMENT
PATHOGENS AND TOXIC SUBSTANCES
GI IMMUNE STRUCTURES HELP TO PREVENT SUBSTANCES FROM ENTERING BLOOD/LYMPH
FACTORS OF GI IMMUNITY
LOW PH IN THE STOMACH
IMMUNOGLOBULINS IN MUCOUS
GALT
MICROFOLD CELLS
GALT
GUT ASSOCIATED LYMPHOID TISSUES
PEYER’S PATCHES
LYMPHOCYTES THROUGHOUT GUT
Name the three sections of the small intestine
- DUODENUM
- JEJUNUM
- ILEUM
What happens when you don’t have intrinsic factor?
ISSUES ABSORBING VITAMINS LIKE B12 LEADING TO ANEMIAS
What is the action of pepsin?
AID IN DIGESTION
SPECIFICALLY BREAKING DOWN PROTEINS
What is the name of the sphincter located between the stomach and the small intestine?
PYLORIC SPHINCTER
What type of acid-base problem would you anticipate having if you have had frequent prolonged vomiting?
METABOLIC ALKALOSIS
What layer of the GI tract contains blood vessels, nerves and structures responsible for secretion of digestive enzymes
SUBMUCOSAL
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
What are the four parts of the colon?
- SIGMOID
- ASCENDING
- TRANSVERSE
- DESCENDING
What structure covers the larynx and prevents aspiration when swallowing?
EPIGLOTTIS
In what part of the GI tract does the majority of nutrient absorption occur?
SMALL INTESTINE
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
Gallbladder
Stores and concentrates bile between meals
Bile from liver via hepatic ducts
Pancreas
Secretes enzymes and alkaline fluids that digest proteins, carbs, and fats
Choleresis
=bile secretion
WHAT DOES BILE CONTAIN
bile salts required for intestinal emulsification and absorption of fats
FAT SOLUABLE VITAMINS
D, E, K, A
HOW MUCH BILE DOES THE LIVER SECRETE A DAY
700-1200 ML/DAY
WHAT IS BILIRUBIN A BYPRODUCT OF
DESTRUCTION OF OLD RB’S
Gives bile its color and produces yellow tinge of jaundice
HOW IS BILIRUBIN EXRETED
MOSTLY IN URINE
KUPFFER CELLS
MACROPHAGES THAT TAKE UP AND DESTROY AGED RBCs AND CONVERT THEM TO BILIRUBIN
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
Anorexia
– loss of appetite, lack of desire to eat, despite the normal physiologic stimuli
Factors influencing appetite:
hunger, smell, emotions, drugs, disease states
Nausea
– unpleasant, subjective, conscious sensation resulting from stimulus of the medullary vomiting center
Common cause of nausea:
distention of duodenum
nausea is Accompanied by autonomic nervous system responses:
watery saliva, pallor, sweating, elevated heart rate
regulation of vomiting
in medulla
Chemoreceptor trigger zone, Vomiting center
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)
vomiting patho
Airway closed, forceful contraction of diaphragm/abd. muscle, gastroesophageal sphincters relax
dysphagia
Difficulty swallowing
May include inability to initiate swallowing or sensation that swallowed foods “stick
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)
DIARRHEA
Increase in the frequency and fluidity of bowel movements. Symptom of GI disease
types of acute diarrhea
inflammatory
noninflammatory
causes of diarrhea
nfection, maldigestion, inflammation, functional disorders
complications of diarrhea
dehydration
electrolyte imbalances
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
CONSTIPATION
Small, infrequent, incomplete or difficult passage of stool
Impaction:
firm, immovable mass of stool that becomes stationary in the GI
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
GASTROESOPHAGEAL REFLUX
Symptoms or mucosal damage caused by abnormal reflux of gastric contents into esophagus
Weakening of lower esophageal sphincter
Persistent reflux =
esophagitis, reflux disease
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
barrett’s esophagus
– metaplasia squamous mucosa, replaced by abnormal columnar epithelial cells
increased cancer risk
gerd Clinical manifestations:
heartburn
regurgitation
belching
pain
bleeding
respiratory symptoms
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
does everyone who has gastroesophagealreflux have GERD?
no
Is there an association between GERD and asthma?
yes
why would sitting up help to relieve the symptoms of gerd
gravity, keeps it down
what are the complications of gerd
burning of esophagus
pain
BALANCING THE SCALE- GASTRIC MUCOSAL BARRIER
agressive factors
age
smoking
alcohol
bile acids from duodenal reflux
h pylori
nsaids
acid
pepsin
gastric mucosal barrier
defensive factors
mucus
bicarb
blood flow
prostaglandins
esophagitis
inflammation of esophagus from gerd
pyloris
heartburn
Hematemesis
– bloody vomitus (bright red or coffee ground)
Melena
– blood in the stool (bright red to tarry black)
Occult blood
– blood in the stool that is not apparently visible
Hematochesia
– fresh blood from the stool
causes of acute gastritis
ingestion of alcohol, aspirin/NSAIDS, viral, bacterial or chemical toxins, glucocorticoids, profound stress
causes of chronic gastritis
helicobacter pylori, atrophic (autoimmune, environmental), chemical gastropathy (alkaline reflux)
clinical manifestations of gastritis
Anorexia, nausea, vomiting, occ. Blood, Hematemesis, abd. pain
Tx of acute gastritis
remove causative agent
Tx of chronic gastritis
reat H. pylori (antimicrobials)
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
Two major causes of gastric irritation and ulceration
– H. pylori, aspirin, other NSAIDS
peptic ulcer disease- clinical manifestations
Epigastric burning, discomfort, pain
Nausea
Abdominal upset
peptic ulcer disease-diagnosis
H&P, endoscopy, H.pylori test labs, radiographic studies
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
complications of peptic ulcer disease
hemorrhage, gastric outlet obstruction, perforation
INFLAMMATORY BOWEL DISEASE
2 diseases
crohns disease
ulcerative colitis
inflammatory bowel disease
chronic illness
remissions and exacerbations
onset of ibd
childhood to young adulthood
causes of ibd
autoimmune, genetic predisposition, environmental trigger - microbial flora
how is ibd diagnosed
colonoscopy
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
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
ibd diagnosis
History/physical, colon/sigmoidoscopy, biopsy, stool exams
Tx of ibd
Reduction of inflammation (control not cure)
medications
Maintaining adequate nutrition
Preventing complications
Surgical intervention
Removal of diseased portion of bowel
diverticular disease
Outpouchings through the muscular layer of the colon wall
Often found in descending/sigmoid colon
diverticular disease
patho
high intraluminal pressure on areas of bowel wall weakness
diverticular disease
causes
ow fiber diet, lack of exercise, poor bowel habits, aging
diverticular disease
progression
Inflamed diverticula -> diverticulitis -> fever, lower abd. pain ->abscess development, peritonitis, obstruction
diverticular disease
Tx
diet,“itis” -> antibiotic, fluids, electrolytes, surgery –unresolved symptoms, complications
intestinal obstruction
Partial or complete blockage of the small or large intestinal lumen –impaired movement
types of intestinal obstruction
mechanical
paralytic
intestinal obstruction
clinical manifestations
- Mechanical: increased bowel sounds, abd. pain, colicky, nausea
- Paralytic: absence of bowel sounds
- Both: pain, constipation, abd. distention, vomiting
intestinal obstruction
diagnosis
h and p
abd xray
ct
us
intestinal obstruction
complications
edema
ischemia
necrosis
perforation
intestinal obstruction
Tx
decompression or surgical intervention, correction of fluid and electrolyte imbalances
PERITONITIS
Inflammatory response of the serous membrane
peritonitis
causes
chemical irritation
bacteria
peritonitis
symptoms
pain, tenderness, rigid/boardlike abdomen, vomiting, fever, tachycardia, hypotension, elevated WBC, hiccups, paralytic ileus
peritonitis
rx
correct cause, antibiotics, decompression, fluid and electrolyte replacement, nothing by mouth, pain control
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
polyp
benign neoplasm, from mucosal epithelium of the intestine
cause of colorextal cancer
unknown, incidence
increases with age, familial risk, diet, ulcerative colitis
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
hepatitis
Inflammation/infection of the liver by hepatotoxic viruses
types of hepatitis
A (spread by fecal-oral route)
B (spread by blood, body secretions/oral/sexual contact)
C (spread by blood)
clinical minifestations of hepatitis
N/V/D, elevated liver enzymes, elevated bilirubin, liver tenderness
Tx of hepatitis
antivirals, minimize risk factors, prevention via immunizations
LIVER—CIRRHOSIS
End stage liver disease with loss of functional liver tissue
LIVER—CIRRHOSIS
causes
Causes: etoh, hepatitis, toxicity from drugs/chemicals
LIVER—CIRRHOSIS
clinical manifestations
vary, asymptomatic to end stage liver failure
Weight loss, anorexia, weakness, diarrhea, hepatomegaly, jaundice, portal hypertension
portal hypertension
increased resistance to flow in the portal venous system
LIVER—CIRRHOSIS
complications
include ascites, splenomegaly, hepatic encephalopathy ,and esophageal varices
Cholecystitis
gallbladder
acute or chronic inflammation of the gallbladder (commonly due to obstruction of gallbladder outlet
acute Cholecystitis s/s
gallbladder
RUQ/epigastric pain, mild fever, anorexia, nausea, vomiting, elevated WBC, elevated liver enzymes, elevated bilirubin
chronic Cholecystitis s/s
gallbladder
more vague—intolerance of fatty foods, belching, GI discomfort, possible enlargement of gallbladder
diagnosis of gallbladder
US, CT scans; treated by surgical cholecystectomy if needed
Cholelithiasis
gallstones
Generally caused by buildup of cholesterol or bilirubin
Cholelithiasis
contributing factors
- Contributing factors: abnormal bile composition and bile stasis
Cholelithiasis
s/s
many are asymptomatic until stones are large, may see obstruction, jaundice, biliary colic
