Download Tuesday, January 06, 1998: (Day 1) Syllabus and course policy. No

Tuesday, January 06, 1998: (Day 1)
Syllabus and course policy.
No Lecture.
Friday, January 09, 1998: (Day 2)
Went over pre-test GI/GU
1) Briefly outline an organized procedure for the evaluation of abdominal complaints.
 OPPQRST, abdominal regional exam, x-ray (KUB, thoracic and lumbar), lab tests.
 KUB look for calcium build up or aneurysms. Look for organ #, placement and size.
2) List some signs and symptoms of gastrointestinal disease.
 Malnutrition, cramping abdominal pain, colicystitis with sharp pain that peaks and fades.
 Colicky pain is seen in patient with unsatisfied contractions. Usually related to obstruction.
Biliary colic with bile stone, colic in intestine with iliocecal valve.
 Burning pain with ulcers.
 Constant pain with destructive tumors and metastasis
 Constipation and diarrhea, nausea and vomiting, Bloating and swelling, fever
3) Describe the pathway a button would take if swallowed. (You are to list normal anatomy in order of
appearance.)
 Lips, teeth, tongue, nasopharnyx and oropharnyx combine to form pharnyx proper  epiglottis
closes to protect trachea  esophagus  Gastroesphageal sphincter (poorly developed sphincter)
 stomach (fundus, pyloric, antrum)  pyloric valve (highly developed sphincter)  duoedenum
with the ampulla of vader (conjoined of 3 different ducts)  jejunum (With tinea colae)  ileum
 ileocecal valve  ascending colon (cecum is proximal portion of ascending colon)  hepatic
flexure to transverse colon  splenic flexure to descending colon  sigmoid colon  rectum 
anus
4) Calcification in the right upper quadrant could be from which sources?
 Kidney stones, colic system stone, sclerosing of vesels
5) List some organs that play an ancillary role in the physiology of the gastrointestinal tract.
 Liver, gall bladder, pancreas, secretory glands, salivary gland,
6) List several kidney functions.
 Electrolyte balance, blood pressure regulation, filtration,
7) List some signs and symptoms of GU complaints
 Burning and painful urination, colicy pain from kidney stones. Nocturia, swelling, prostate based
problem. Difficulty in voiding
8) List 4 studies to evaluate the GU system.
9) List 4 disease processes that may be associated with abnormal urinalysis.
Monday, January 12, 1998: (Day 3)
Kidney
 Talk about macro and micro features of the kidney
 Renin angiotensin sytem is an important function of kidney. It is extremely self serving process of the
kidney. Its job is to maintain flow rates of glomerulus. It is very potent and important.
 Produces hemopoietin to maintain the red cell mass of the body.
 Glomerulus is a vascular system that is designed to leak to produce mechanical filtration. Lets things
up to 7 or 8 Daltons through the membrane.
 99.98% of water delivered to kidney can be recovered but you can overwhelm kidney with work.
 Cortex is where bowmans capsule lives.
 Deep in the kidney is where the deep descending loop lives and has very specialized functions
 Medullary problems primarily hit tubules.
 Proximal tubule lies in cortical region.
 Reabsorb bicarbonate, sodium, potassium, chloride, urea, amino acids, water and glucose. In many
cases absorbed 100% in proximal tubules. Bicarbonate is absorbed 99%
 Secreted directly into proximal tubule, creatinine,
 Distal tubule is where nitrogenous waste enters urine so that it cannot be processed.
 Uric acid can be introduced directly into proximal tubule.
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Hormones that regulate renal function:
 Parathormone: enhances the absorption of calcium. Allows osteoclasts to work easier.
 Fundamental role of parathormone is to maintain calcium in the serum.
 Improves recovery of calcium out of urine.
 Increase level of active form of vitimin D in liver
 Increase uptake of calcuim from GI tract.
 Aldosterone changes permeability of distal tubule.
 Increase aldosterone will allow more potassium to leave with the urine.
 ADH
 Levels increase produce hypertonic urine
 Levels decrease have hypotonic urein
 Erythropoietin
 Released by juxtaglomeruleral cells and stimulates red cell production.
 Renin
 Released by juxtaglomerular cells after they have been wakened by macula densa.
 Renin angiotensin
 MD (macula densa) notes passage of chloride through tubules. When MD sense decline in
chloride ions, it tells juxtaglomerular cells to release renin. Renin meets angiotensinogen and a
cleaving operation takes places to produce angiotensin I (not an active molecule yet). Another
cleaving takes place and produces angiotensin. Close down peripheral vessels and makes more
blood go to core and increases glomerular filtration in bowmans capsule
 Angiotensin II levels rise you have direct vaso-reaction response. Can stimulate aldosterone
function which brings more sodium and water in and makes potassium leave.
3 Basic Pressures regulate blood flow through glomerulus
1. Hydrostatic pressure in the glomerulus has greater effect of regulation kidney. Most important.
2. Proper osmotic pressure in the glomerulus. (low)
3. Proper hydrostatic pressure in bowmans capsule (low pressure).
Peritubular capillaries introduce substances in and supply nutrition to that region of the organism
(mitochondria)
Renal failure is back up of flow in the kidney.
Tuesday, January 13, 1998: (Day 4)
 Maximum Tubular load: the maximum amount of a rate of a substance that can be filtered and totally
reabsorbed. The best example of this is glucose.
 When you see glucose enter urine, it is on of two things
1. Diabetic patient with no insulin to remove glucose within the serum.
2. Damage kidney to remove nephrons.
 Albumin is the only protein that gets totally resorbed. Usually protein usually does not make it
through bownans capsule.
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Creatine and uric acid
 Two products commonly used to asses renal function
 Creatinine produced by phosphorolation pathway.
 Skeletal muscle is the only source of this and is delivered to kidney as waste product.
 Only filtration and secretion can affect serum creatinine levels.
 Patients hydration state does not have a remarkable impact on this level
 Once at the kidney, 99.99% will be excrete.
Creatinine clerance test
Assess the ability of volume of plasma to be cleared of creatinine.
Takes at least 50% reduction in tubular mass (kidney function) before test becomes positive
If it happens quicker smaller amounts of compromise will be detected.
Normal range is .5-1.5mg/dl. (small numbers but big range)
Increased creatinie levels happen in some muscle diseases. Examples are gigantism.
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Nephritis or renal failure can make creatinine levels increase.
Muscular dystrophy is the only thing that will decrease creatinine levels.
If creatinine levels get too high, 10mg/dl it is the panic value and they need dialysis immediately.
If creatinine levels increase, urea levels will also be increased.
BUN
 Elevetaed levels of urea also call azotea?
 Urea is liver byproduct of protein metabolism
 Urea carried to kideys as waste product.
 Normal range is 10-20mg/dl.
 Panic level is 100mg/dl.
 Liver failure decreases BUN levels.
 Overhydration
 Dehydration produces slow tubular flow and produces greater opportunity for equilibration.
 Elevated levels of urea are much more devastating than creatanine levels
 Decreased serum levels of urea
 Liver failure, catabolism cannot take place and urea is not formed
 Overhydration
 Flows more briskly through tubules and
 Increased serum levels of urea
 Renal failure: decreased function will not accept or remove as much urea. It could be the
bowmans capsule or it could get hung up in the tubule.
 Dehydration can increase serum BUN levels. Less fluid delivered to nephron and less fluid filterd
allowing more time for equibliration that is going to allow more to return to vascular supply.
 Urinary obstruction works through pressure mechanism. Fully dialate renal pelvis, calyx,
collecting ducts. Pressure rises is distal and proximal tubules, bowmans capsule ect. now kidney
tries to restore flow rate with renin angiotensin system and will increase hydrostatic pressure, there
is no net flow.. this equals renal failure.
 Hypotension produces renal failure. CHF, Renal Artery stenosis, extrinsic pressure from tumor.
Decrease ability of renal system to be perfused by blood. Causes regional or systemic
hypertension.
 Panic value for urea is 100mg/d.
BUN-Creatinine Ratio
Normal Ratio: B:C = 20:1
Renal failure, dehydration and cardiovascular ratio can increase the ratio.
Dehydration:
 Has no affect on creatinine levels
 Increases ratio by duplicating urea. Slow tubular flow allows more urea to exit the tubule and go back
into blood stream.
 Have a quick rise in urea with no rise in creatinine
Less than 20:1 Ratio only accomplished by renal failure
 Kidney is not accepting any of the waste products.
 Both numbers higher than normal but creatinine will accumulate. End up with net decline in ratio.
 Can produce a high and low B:C ratio
Azotea is increased level of urea in the blood stream. Three causes discussed below.
 Pre-renal: Prior to blood reaching kidney. Best example is renal artery stenosis. Cannot deliver blood
to the kidney to be filtered and the kidney dies. Causes rise in BUN
 Renal: Nephritis, acute tubular necrosis, acute glomerular nephritis.
 Post-renal: After kidney. Examples are prostatic enlargement leading to renal stenosis, stone in a
ureter, medications for migraine headaches. Other could be cervical tumors, prostate cancer, ect.
 Will probably ask question that we must know anatomy to know if it is pre, post or renal Causes.
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Renin Angiotensin system:
 Macula Densa cells are the lookout for chloride ions. Usually have hypotension or hypoperfusion that
limits chloride through tubules. When MD cells recognize lack of chloride it releases renin. Renin
looks for angiotensinogen and cleaves to convert to angiotensin I. Angiotensin I gets converted to
Angiotensin II in the lungs. Angiotension II is vasoactive product with local effect at kidney. Cause
more blood to perfuse through the kidney.
 Angiotensin II also releases aldosterone to cause sodium recovery with water.
 Antihypertensive medication
Friday, January 16, 1998: (Day 5)
Review of Renin- Angiotensin
Hypotension  Macula Densa Cells Excited  Juxtaglomerular cells release Renin  Looks for
Angiotensinogen  Angiotensinagen meets renin to make  Angiotensin I  Angiotenin II is produced
by cleavage process in lungs. This is a vasoctive substance.
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Angiotensin II is so vasoactive it is protected by two steps to get there.
Effects of angiotensin is to stimulate aldosterone release. This will reabsorb Na+ and Water.
Another Job of angiottensin II is to increase glomerular filtraton rate. Increase tubular flow rate.
Patients who only take heart pill and not diuretic, they will have increased volume loads and become
puffy.
Review of Urinalysis
3 parts of a urinalysis
1. Visual inspection (color) which is subjective. Color, clarity, odor. Ketones are what make urine
smell, Ring compounds.
2. Dipstick (quantitative, and qualitative components)
3. Microscopic examination looking for nothing in normal urine.
4. Culturing is an alternate step of testing. Decide this early and do it quickly so it is not
contaminated and it is tested very quickly because bacteria can proliferate very quickly in standing
urine. Must freeze if it is not tested immediately. Must use aseptic techinque.
UA Findings in Subjective category
 Red: Blood (New blood, gross hematuria)
 Black: Blood (within bladder or urethra that has been there for a while and had time to break down.);
Ocranosis comes out of patient yellow and turns black.
 Tea colored: Hyperbilirubenimea.
 Bright yellow: Hypervitiminosis. This is not a problem.
UA Findings in Objective Category:
 200 mg of protein is allowed in urine. It did not come through glomerulus, it is a process of cells
degrading in the tubules as a natural process. Tamm-Horsfall Protein: Normal protein shed through
the process of maturation and turn over
 4-5 grams in proteniuria: nephrotic syndrome where protein came through glomerulus.
 Hematuria and pyuria will registar as protein on dipstick
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pH normal is 5.5-6
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Casts: form in tubules.
 Normal tubular flow rate and overwhelm them with protein (nephrotic syndrome)
 Low tubular flow rates that we might see in glomerular nephritis or blockage
 Cellular, coursely granular, waxy will tell us about how long the cast has been there.
 Waxy has been there for weeks.
 Cellular is most immature and just packed in
 Usually see cell membrane first and organelles give coarsely granular appearance. As they
degrade you get more granular and finely granular. Epithelial cells then mature into a more waxy
cast. This is the end stage of a once cellular cast.
 Fatty casts are the end stage of a once protenatious cast.
 Mixed Casts (WBC, protein, cells) we are looking for an upper urinary tract infection.
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Crystals
 Calcium Oxolate:
 See renal stones that are oxalate in origin
 Dietary problems are diets high in citrus fruits, asparagus ect.
 Uric acid is defect in metabolism of purines.
 Iatrogenic condition may be chemotherapy demonstrating uric acid crystal formation.
 Triple phosphate (coffin lids or rectangle shape) found in alkaline urine. Can exist in urinary tract
infections that can produce stone diseases.
Hematuria:
 RBC’s in the urine
 Two general varieties
 Gross (visible to unaided eye)
 Gross hematuria is common
 Microscopic (invisible to unaided eye)
 Microscopic hematuria occurs in 3-4% of the population
 Significant hematuria is 3= RBC’s/HPF in a centrifuged specimen
Common causes:
 Urinary tract infections
 Prostatic diseases
 Neoplasm
 Urinary stones
 Trauma
 Renal diseases
 Drugs.
 Cystitis is more common in women than men
 Benign prostatic hpertrophy:
 Affects an average of 23% of males by age 45 and 88% by age 90
 Caused by persistent contraction of the detrusor muscles causing enlargement and dilatation of the
mucosal vessels
 Bleeding occurs by leaking of RBC’s
 Prostatitis
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Neoplasm
Incidence increases after age 40
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Friday, January 16, 1998: (Day 6)
Second and Third Hours: Notes are in a folder in the library about hematuria.
Benign prostetic hematuria the patient does not feel pain
Prostatitis, the patient feels pain the whole time you are doing the digital rectal exam.
Strep glomerularnephritis is autoimmune. It ends up plugging up glomerulus and making it useless.
IVP: intravenous pyleogram. Inject media and do a study on the kidney
Synography: sound waves go through acoustic window of liver and gives size of kidney and can determine
solid from cystic mass.
Cystoscopy to determine stenosis or fibrotic tissue from previous urinary tract infections.
Infarcts in the kidney often for a wedge shape of cell death due to arborization (tree like branching).
Drug therapy may cause complications of GU system long after the course of the medication was taken.
Ebb and flow of colicy pain is unsatisfied flow. Pushing against a closed valve. There is an increase of
stretch at the point of the blockage.
Triple catch test is used for men.
Get 3 sterile containers and be educated on sterile technique.
All 3 cups is bladder carcinoma
Retrieve 3rd cup after rectal/prostate exam.
First cup is urethra
Women get 2 cups for this test. (They don’t have a prostate)
Get paper in file about testing procedures on GU disease
 Concentration-Dilution is a very important test. Provides most sensitive means of early or mild
impairment of renal physiology. Patient with completely normal concentration ability is not likely to
have serious kidney disease.
 Acid Base Function Features: 90% of bicarbonate is recovered in proximal tubules. 10% is allowed to
remain in the tubule to neutralize Hydrogen in the tubule. The 10% remaining is a buffer.
 Common mistake is you forget kidney is barrier between urine and blood stream. The kidney
undergoes kidney acidosis and then it backs up into the body and produces metabolic acidosis.
 Proximal renal acidosis. More generally can have a cortical kidney disruption.
Tuesday, January 20, 1998: (Day 7)
Renal Failure: Acute and Chronic.
 Acute: The more rapidly you loose renal function, the less there needs to be to see symptoms.
 Chronic: you can loose more of kidney before symptoms
 3 categories are pre-renal, renal, and post-renal.
Pre-Renal causes of renal failure:
 Hypotension and Hypertension
 Polychthemia Vera
Post Renal Failure
 Stone: Ureter stone dilates because of the pressure. Renal pelvis dialtes, swelling of collecting ducts
and it leads all the way back to bowman’s capsule and the glomerulus to destroy the pressure gradient.
 Autonephrectomy is most serious complication. The organ dies.
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Renal Causes:
 Acute glomerular nephritis
 Young people
 Males more often than females
 Usually hypersensitivity reaction from previous upper respiratory infection. Strep just a few
weeks ago. Basically gum up the works. Some glomeruli are stopped up and some let everything
through.
 Most common is URI
 Wounds with trauma and strep involved
 Diabetic patients
 Malaria ect. (exotic causes)
 Latent period may be 1-4 weeks.
 When they develop renal failure (3rd or 4th leading causes for pediatric admission to hospital) they
have clinical features such as tiredness, acheyness in peripheral joints. Then develop anorexia and
nausea and vomiting as urea levels rise. Later see fever (younger = quicker).
 Weight gain has happened at a certain stage (?)
 Casts are common due to incompetence of glomerulus and decreased flow. RBC and WBC casts
are found probably due to strong immune response.
 Protein uria: can loose small to massive amounts of protein. .2g/day is normal, can loose up to
6g/day
 Treatment is metabolic support. Look at panic values. 90% with renal causes of acute renal
failure recover.
 Chronic renal failure is progressive and all you can hope for is slowing down.
 Anti-infammatories are used.
Acute glomerular necrosis
Friday, January 23, 1998: (Day 8)
UTI: We do these on test one and test two because it is so common
Renal causes of kidney failure:
 Pre-renal, Renal, Post-Renal: try and categorize problem
 Pre renal and post renal have IVP and Retrograde IVP
 IVP involves contrast material into patients vien and then should see renal blush then outward inward
of kidney.
 See failure of enhancement in the kidney it serves as a twin differential: 1. Proper blood supply to
kidney? Or 2. Such high intrinsic renal pressure that there was eqilibration in the kidney.
 Retrograde IVP is introduced by catheter and works it’s way one ureter and can determine post renal.
 Use these two tests together to go from both ends to middle to determine post or renal
Renal causes
Acute glomerular nephritis
Recap
 Young person problem but does not exclude older adults.
 Male greater than female but not too significant
 Essence of AGN: Upper respiratory infection with hypersensitivity reaction. Antigen antibody
reaction at glomerular membrane.
Acute Renal Failure:
 Very survivable. There is probably residual damage but not measurable partly due to insensitivity of
test and the redundancy of GU system.
 Clinically may see: Fatigue and malaise. Maliaise is a step beyond fatigue, it is a general ill feeling.
Flue symptoms may be reported by patients. Oliguria may be seen and on occasion you may see
Aneuria. Edema comes with fluid coming in and nothing going out.
 Makes people puffy and loose wight is protein deficiency. Patient demonstraes hypoalbuninemia.
This may be a common feature but it is a very different disease. Be aware.
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Acute Tubular Necrosis:
Recap
 Two major categories
1. Ischemia
 Most common cause of acute tubular necrosis
 Usually caused by hypotension
 Will affect capillaries in basement membrane (glomerulus) and then after that the tubular
cells.
 ATN is worse than AGN
 # of nephrons involved determines severity. 50% or more tubules damaged it will be
permanently impaired kidney.
 Shock: blood pressure low for about an hour
 Burns: massive (30% body surface is minimum) loose lots of protein and have lots of
migration of tissue. Protein removed leads to low blood volume, low tubular rates ect.
 Pregnancy: Eclampsia? Catecholimine release leading to hypotension. Mechanical could be
full uterus compressing on renal arteries.
 Dehydration caused by drug use could cause low blood volume and increased viscosity of
blood.
Early Stage:
 Oliguria present and may get to aneuria.
 Anything below 100 ml in aneuria
 Mechanical plugging of tubules leads to oligura
 Simple inflammation can close off tubules and lead to oliguria.
He talked about some lab stuff and I missed it
Late tubular necrosis
 Observe Edema. If ambulatory check ankles
 Oliguria is present but not as bad.
 As urea levels persist, more serious clinical presentations such as nausea and vomiting.
Adynamic ileus. Anorexia because of supression of the urge to eat. Asotemia and acidosis
are combined features of anorexia. Lethargy and weakness, increased thirst.
 In late late stages see Cardiovascular problems b/c of more fluid trying to return to hear.
Fluid in lungs and patients life is in jeopardy.
 Arrhythmia’s produced by acidosis and increased levels of serum potassium. Postassium
intoxication is there because of renal failure and
 Metabolic acidosis squeezes out more potassium.
 Infection is complication of acute tubular necrosis
 Neurological effects such as seizures are complications.
2. Toxins:
 Found in industrialized sector: mercury (fish), ethylene glycol (still a common problem at
harbor light clinic ‘2 cases’), Carbon tetrachloride (dry cleaning 15-20 years ago).
 Ibuprofen (older bottle) maximum daily dose is lower today because it can cause overdose. It
may cause renal failure if you overdose.
 Exogenous toxins: aminoglycosides, materials absorbed through skin, ingestion (mushroom).
Streptomyacin, heavy metals (iron, bismuth, zink), and radio-contrast agents.
 Endogenous: Hb no longer contained by RBC (hemolysis), Myoglobin from crushing
injuries and will ppt and obstruct (mechanical, tubular problem)
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Afternoon (2nd hour)
Differences between AGN & ATN
Sign of recovery of ATN is diuresis. They are still not out of the woods. They can still loose a good
amount of water along with sodium
AGN has higher mortality rate
ATN has worse effect during pregnancy than on non-pregnant person.
Azotemia levels will rise. Creatinine and BUN will improve over a month or month and a half during
recovery.
CHRONIC RENAL FAILURE:
 Similar to acute except you are looking at longer onset time
 Some same have acute renal failure that lingers so long it turns chronic. Repetitive events of acute
renal failure have accumulated enough damage to move on to chronic renal failure.
 Four Big Causes:
1. Diabetic Nephropathy (28%)
2. Hypertension (24%)
3. Glomerular Nephritis (includes acute and other glomerular insults)
4. Polycystic Disease: Patient develops more numerous and large retention cysts. Fluid is not
compressible and eventually perencymal tissue gets squeezed and gives up.
Clinical Features:
Similar to acute renal failure
Early Stage:
 Diuresis: liberate more urine that is isothenuria (fixed specific gravity over and over again because
they are acting as a mechanical filter with no concentration ability)
 Dehydration because of polyurea. It is ok to add and replace fluids.
 Will excrete potassium to maintain low levels in the blood.
Late Stage:
 Looks more like acute renal failure than early chronic renal failure. Early chronic renal falure has a
different presentation
 Do not want to add fluid because they cannot eliminate
 Hypercalemia will result because potassium is not excreted in enough quantity. Acidosis will lead to
hyperkalemia. Reduce dietary intake of potassium.
General:
 Increase Accumulation of BUN as GFR declines. Will see patient get more thirsty at this point. This
is due to uremia elevation
 Hyponutria: distal tubule, sodium loss, causes people to be thirsty.
 Increaded thirst throughtou
 Oliguria will continue untill they reach dialysis or transplant.
 Renal tubular acidosis is seen in renal tubular failure. Renal tubular acidosis is defined as more acid
load than acid handling ability.
Systemic Manifestations of Chronic Renal Failure:
 Fluid overload situation. Diuretics are not helpful because the tissue that diuretics affect are no longer
working.
 Hypertensive effects:
 CHF is a possibility as a combination of hypertension and Edema.
 Pulmonary edema is a late problem. They may survive this event and maybe even a second but they
are in huge trouble
 Pericarditis probably due to irritating effects of uremic acid.
 Digestive effects of anorexia, nausea, vomiting, adynamic ileus, mouth ulcers.
 Osteoporosis because of renal osteo dystrophy. (secondary hyperparathyroidism)
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Third Hour:
Leaving class early today
White powder on skin is excess urea crystals forming on skin. Look in moist areas
Chronic renal failure treatment
 Limit load on kidney.
 In early it is ok to treat with fluids. Once they retain urine, limit intake.
 Aluminum antacid supplementation is good idea. Antacid phosphate concentrate leaves GI tract with
rest of fecal material.
 If they live long enough they will get to dialysis only or dialysis to transplant.
 Willingness to modify lifestyle is a must for a transplant recipient. Overall health status, drinker or
non-drinker, money, how did you get in that situation.
Monday, January 26, 1998: (Day 9)
Upper UTI: will be no dysuria or painful symptoms related to urination. Many urinary tract infections are
from outside sources. If it goes on long enough you may demonstrate urinary symptoms.
Upper urinary tract (pure):
 See cast formation, (cellular, wbc, rbc, bacterial, ect…)
 Produces sicker patient
Taking shitty notes today
Causes of UTI:
 Urinary stasis: 80-85% of time related to E. Coli
 Erythral procedure patient is a route that bacteria can be introduced
 Urethral trauma causes swelling (honeymoon cystitis attributed to frequent sexual activity) simple
way to prevent is to void the bladder after sexual intercourse.
 Pregnancy is lumped into honeymoon cystitis. This is more of a space occupying phenomenon.
 Diabetes mellitus: small amounts of bacteria can be made very vigorous with the presence of glucose
in the urine. Bacteria can get out of control.
 Bladder distension will lead to net constriction of vessels. If this persists by obstruction or voluntarily
 Any obstruction can be a problem.
 Hypertension will lead to decreased urinary flow and will affect upper tract and make casts
 Neurogenic can cause urinary stasis and cause bacteria to grow.
 Congenial anomalies related to duplex ureter. Two renal pelvis with one calliculi.
 Foul fecal smelling discharge due to inflammatory bowl disease. Fistula formation
Kidney infections
 Renal medulla is more often involved in infections. This is due to ascending infections.
 Overall the medulla does not have copious vascular supply that the cortex has.
 Osmolality is higher in medulla and WBC does not do as good of a job here.
 Acute Glamerulus nephritis does not fall into this category because it is an autoimmune response
 Reflux infections are most common cause
End Test I Material
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