1. health and fitness
2. disease

GI-GU – 9/9/08
Co-management, Refer, Self-Treat
3 keys to the class…when to co-manage, when to self-treat (in office), when to refer
*** 5 exams with the final exam not cumulative and less than 1/5 of the material ***
*** Cecil’s is a reference book (you may not need to purchase it…use it only as a reference) ***
*** Take a look at various paper’s for each exam…In the front is the testable material and the back is the additional info,
usually not tested on ***
*** First test is 5-6 weeks away and then every 2-3 weeks ***
*** Tests are usually 8:15 Tuesday – They will be multiple choice and fill in the blanks ***
*** 5 Exams each are 20% ***
PRE-TEST
Briefly outline an organized procedure for the evaluation of abdominal complaints.
History: It will give us a ton of information. Somethings come fast, somethings come slow. History allows us to find
out ths infomraiton. We want family history, history of chief complaint, and past medical history.
Exam: Abdominal exam (inspection, auscultation, palpation)…We always want to inspect first, ausultate second and
palpate third…We listen for bowel sounds and bruits. Peristalsis is segmentally controlled stretch receptors.
Activatin of receptors sends signals to cord and the message ascends to brain. The brain then sends the signal via
parasympathetics triggering peristalctic wave to squeeze fecal material proximal to distal, pushing feces downstream
into a new section wchih dilates and causes a stretch reaction. The stretch receptors cannot tell the difference from
inside-out stretch to outside in stretch, so a stretch to the body via palpation can create bowel sounds which mask what
we attempt to hear. So we look first, listen second and palpate third. We need to pay attention to lack of sounds, and
that occurs by absence of bowel sounds. We always listen to multiple sites in each quadrant. To document a
peristalsis it takes 5 minutes.
We then go into light palpation. We check for spasm. Spasm is a reflex action. Spasm attempts to hold in place the
structures. WE then go into deep palpation. After deep palpation, we go into percussion. Percussion is one of the
least reliable. When we deal with fluid/ascites, we deal with percussion. We can also do KUB. KUB films is usually
lower to increase contrast and observation of kidneys. Ascites can give us a bigger liver by percussion, but the
radiograph gives us the observable size. Ascites percusses big and shows as normal size liver. True enlargement
percusses big and looks big.
List some signs and symptoms of GI disease.
Blood in the stool. There are various relationships of blood in the stool. Occult blood in the stool cannot be seen. We
can use a hema-occult/GUIAC test. GUIAC mixed with hemoglobin and hydrogen peroxide turns blue. Frank blood
in the stool comes in 2 colors (red – source is likely to be distal like the sigmoid colon and beyond) & (black-melena
stool – black tarry stool, the source is more proximal and is mixed in). The hypertonic, black stool liberates blood and
it degrades to a black color.
Another sign and symptom of GI disease is pain. Cramping or colicky pain can ensue. Cramping/colicky pain is
linked with unsatisfied contraction. BIliary colic, renal colic or GI colic are 3 types. Cramping pain can be
explained by obstruction. All the systems are in place and the system is interfered with. This is not very satisfying.
Tyring to clear the area with an obstruction is unsatisfied contraction. Each system is intact, but something prevents
its operation. This information helps to limit, making the diagnosis.
Indigestion…Irregularity in bowel movements, reverse peristalsis, vomiting, diarrhea, cramping, acid reflux (burning
pain),
Nauseua…It can exist alone or with other symptoms. Nausea can relieve pain and discomfort
Low Back Pain: Sclerotogenous pain with referral can happen. You can poke around the abdomen and sometimes
generate the low back pain.
Abnormal Bowel Sounds: Absence of bowel sounds is a problem.
Gas: Belching or flatulence…Ask the patient what is normal for them…A long list of things cause flatulence (celiac
disease – icomplete digestion due to organ problems….enzyme deficiency (cannot break things down –
flatulence)…Bad food can cause flatulence
Obstruction:
Sharp Pain: It hurts right here (pt. points to one spot)…What you don’t want to hear is that it hurt right here and then
all of a sudden just got better (indicates bursting) – subsequently this may cause peritonitis
Diarrhea: Frequent watery stools
Weight Loss: Ask about how they lost the weight? Ask about time frame? Ask about if weight loss was intended?
Colon Cancer: The #2 cause of death in the United States.
Abdominal Swelling: Puffy and maybe not limited to the stomach. Ascites and lymphedema and common reasons.
Abdominal and LE retention is usually lymphedema. The more distributed the gain the greater the chance of proximal
lymphatic obstruction.
Hepatomegaly can lift the ribs up.
Anorexia: Appetite suppression is true anorexia. Anorexia nervosa does not show appetite suppression. Anorexia
nervosa shows body image distortion. You see too skinny and they look at themself as I need to lose more.
Painful Defacation: Anal Fissures can be a cause as well as perinanal abscess or tearing of the sigmoid colon. They
can have a large, hard stool which can tear the sigmoid as it forces stool through. Anal fissures can be painful.
Cholecystitis: Pain follows an activity. Inspiration and expriation changes intra-abdominal pressure. Cholecystitis
inflames the gallbladder. Usually a fat load provokes a prominent contraction of gallbladder.
Pus in the Stool: Invasion of the wall of the intestine. The further down, the more likely you’ll observe the pus.
Infections affect nobody and no boundaries.
Hurts to Swallow: Esophageal ulcer…Hurts and eating makes it feel better (stomach ulcer)…Hurts 45-50 minutes
after eating (small intestine and duodenum)….Usually esophageal and pyloric ulcers are predictable.
Lower L Quadrant Pain: Diverticulitis
Lower R Quadrant Pain: Appendicitis
Fatigue: Anemia (loss of cells by GI)….
Gallstone: R Upper Quadrant Pain
Pancreatitis: Severe Pain with posture of bending forward. The pancreas is more posterior in the abdominal
cavity…Inflammed pancreas do not like to lie down, so they like to lay down.
Hernias:
Difficulty Swallowing: One of the more common signs and symptoms.
Describe the pathway a button would take if swallowed. (Normal Anatomy)
1. Oral Cavity,
2. Throat – Pharynx (Oro, Naso, Pharynx Proper) – everything travels down the pharynx…The epiglottis, protects the
trachea
3. Esophagus, Trachea and Epiglottis (Upper Esophagus is under somatic control vs. the lower esophagus is under
autonomic control)
4. LES – Lower Esophageal Sphincter (also called GE junction – gastro-esophageal junction)…The sphincter is a bad
one and that is why we have GERD
5. Stomach (the last part of the stomach is called the antrum)…The antrum is a busy area for disease
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Pyloric Sphincter – Good sphincter…Slowly allows release of contents…Reactive to stomach contents…Heavy fat
meals are delayed due to the pyloric sphincter…Water is allowed to pass through easily…It is under neurologic and
hormonal control
Duodenum – C-Sweep of Duodenum (first return to mid-line)… Pancreas is cradled in the middle of the C-sweep
Jejunum (no valve between duodenum and jejunum)
Ileum (No valve between jejunum and ileum)
Iliocecal Valve – Pretty good valve (
Cecum
Ascending Colon
Transverse Colon (we can differentiate where it changes over based on direction…The colon is kept up by suspensory
ligaments…The suspensory ligament end signals the beginning of the ascending colon)…The transverse colon can
loop
Splenic Flexure & Descending Colon
Sigmoid
Rectum
Anus
Calcification in the R Upper Quadrant could be from which sources?
Calcified Gallstones, Kidney Stones, Athersclerosis (renal artery, hepatic artery), costal cartilage (physiologic calcification),
Dystrophic Calcification (liver, pancreas, kidney)…Pancreatic calcification is very devastating (no good reason for
calcification in the pancreas)…Ureter (stone), Supra-Renal/Adrenal Gland Calcification
Duodenum (calcium pills can pass through and break up)
LUQ : Similar concept, but add spleen, aorta calcification
RLQ & LLQ are smaller lists of calcifications
List some organs that play an ancillary role in the physiology of the GI tract?
Pancreas (enzymes)
Kidney (hydration status)
Parotid Gland
Teeth (mechanically break down food exposing food for chemical action)
List Several Kidney Functions.
Filter Waste from Blood: Filter blood and filter out toxins and waste products
Water Balance and Regulation: Conservation or Removal of water…Kidney can recover 99% of what you drink (at best)
Electrolyte Balance: Gets rid or keeps potassium, hydrogen, etc.
RAA System: Dehydration, thick blood shows reduction in GFR…The kidney needs blood to pass through it so that it creates
high BP to increase pressure in the efferent tubule to increase GFR
Vitamin D Activation: We need active vitamin D. Bad kidneys and we lose ability to make D.
Erythropoietin: They have anemia of underproduction iwhtouh kidneys.
GU Signs and Symptoms
Blood: Occult and Frank Hematuria. It has to deal with quantity and resent event. High vs. low also has to deal with
casts. Casts are from the tubular cells of the kidney (only).
LBP: Tends to be unilateral in presentation when from kidney stone.
Puss: Cloudy urine in color. Can be infection. Urethral infection presents with frequency, urgency, painful urination,
and cannot fully void.
Incontinence:
Murphy’s Punch: Hydronephrosis and pyelonephritis
Polyuria: Many trips to the bathroom….Diuresis: A large volume of urination….Polyuria is increased frequency vs.
iduresis is increased volume (more than 2 L a day)
Odor; Pee in a cup. The doctor tests color, clarity and odor. Ketones can cause change in urine scent. Asparagus and
cabbage can change the odor.
Color: Pale to Straw Yellow is normal. You don’t want to see brown urine (hematuria).
Glucose: Often linked to polyuria, nocturia. Poluria and nocturia is linked with diuresis.
Hesitancy: Troube to initiate flow and stop flow (mechanical problem aand can be BPH or prostate cancer in males)
Dehydration: Dark Urine (polyuria, polydipsia, heat and humidity)
Painful Urination:
Urgency, Hurt when they fill, Hurt whey they empty: Hurts in all 3 phases indicates bladder infection…urethritis
only hurts for brief time. Higher up indicates flank pain and upper UTI.
Hypospadias: New born problem.
List 4 Studies used to evaluate the GU system.
KUB (drop KVP and increase the mass), Dip Stick (urine is a fluid biopsy), Physical Exam, Diagnostic Ultrasound, PSA Test,
Urethrocystocope - Cystoscopy (flexible fiberoptic) , Contrast Studies (Excretory Urogram), MRI (kidneys are nicely imaged
on MRI…MRI’s can comment on physiology), CT Scan (Helical CT’s are faster, relatively inexpensive and give good slices),
Manometers (pressure testing)
List 4 Disease Processes that may be associated with anormal urinalysis.
Diabetes, Glomerulonephritis (casts produced and renal cells), Pyelonephritis, Prostatic Cancer (history is important)
GI-GU – 9/15/08
KIDNEY
Cortical region (outer)
Medullar region (inner area)
These are the 2 big regions of the kidney. All of the glomeruli lie within the cortical region and all bowman’s capsule is in
the same area. We have varying prox and distal convoluted tubule in the cortical area.
We have some unusual circumstances that damage both areas of the kidney.
Layered Organization of the Kidney
1.Bulk of the functional unit as the combo of Glomerulus, Bowman,s PcT, DCT and loop of henle between = functional unit to
perform filtration and concentration
2. PCt and DCT, Bowmna’s and Glomerulus – The bulk of the loop dives deep into the medullary cavity
It takes billions of units working together to perform bodily functions.
Glomerulus (wrap around area in the pictures)….Show a hand in glove relationship. The Glomerulus is part of the circulatory
system and specifically the arterial system. Filtered by the kidney is blood IN the Glomerulus, this is a specialized
vascular structure designed to leak. We don’t want leakage anywhere else in the vascular system.
Size
The afferent arteriole is the entrance. The efferent arteriole is the eixt and should hae less particles. The Glomerulus is binary
(it fits through the hole or it doesn’t). We have moleculues of all sizes (we lose waste and “cherished” moleculues). We do
need a system to return moleculues. Particularly, bicarbonate is important. 7-8,000 Daltons is the cutoff for what makes
it through and what doesn’t make it through.
Lipids and lipoproteins can be very large (20,000 or more Daltons). 7-8,000 allows waste to go through. We do have a way
later to recover molecules we need.
For our purposes, 100% of glomeruli lie in cortical region
Arterial vs. Venous System
Some differences: Tunica Media (resistance and elasticitiy – it changes diameter and reacts)….The Tunica Media is not
important in the Glomerulus (designed to leak). Another difference between the environments of venous vs. arterial is
pressure. The highest pressure is the arterial. Moving products from Glomerulus to Boman’s (venous like – low pressure)
there must be a gradient. The Glomerulus pushes by higher pressure. The pressure behind moves particiles.
Glomerulus
1. Kitchen Tools (Glomerular Like) – Strainer
2. Bowman’s Caspule – Captures everything that comes out…Bowman’s takes what the Glomerulus dishes
out…Funnel (Bear Bong)…Funnel’s are not selective (just like Bowman’s)
PCT
Very important component. Without the PCT, kidney function cannot be accomplished. Passive and active transport take
place here. Active transport requires energy. Mitochondria creates the energy to drive active processes forward. The more
mitochondria the greater the engery requirement and the greater the active transport. The mitochondria density in the PCt is
great as the PCt is the most active component on the kidney.
The segregation process begins in the PCT. Waste re-enters the vascular tree. Waste comes back into the system and is not
desirable. The waste molecule most notable urea is destabilizing to normal membranes. It renders the cells leaky (urea).
Not everything that comes back through the wall of the PCT is desirable, but it does occur. Urea comes back in the blood. It
can be normal or abnormal amounts in the blood.
Sodium, potassium, cholidrd, glucose, bicarbonate are important items to retain. The PCt also allows for entrance of waste
molecules.
Non-glomerular but enter through Tubular Wall
Creatinine,
UA
Hydrogen: REpresetns acid load (hydrogen load)
Thin Loop of Henle
Thick walled and thin walled portion exist in the loop. The loop is divided by size (thick and thin). Thin loop dives the
deepest into the kidney The thin loop leaks as well. Water mostly leaks from the think loop. The htin loop is called the
concentrating segment. It does not have mitochondria. Passive methods help to drive the process. Water moves by
osmolality. We pack particles in the parenchymal tissue in the thin loop. Semipermeable membranes with hyper and
hypotonic areas show equilibration. The deeper into the kidney the more particiles the hiher the osmolality, the better the
system is at recovering water.
When the body needs to recover water, it recovers 99.998%. It only wastes .002% under great demand.
The think loop is the concentraring segment.
Thick Loop of Henle
Called the Diluting Segment. This may be some of the stone prevention function. Kidney stones are not tolerated very
well. The thick loop appears to be a defensive mechanism. There is still a net recovery of water, but diluting still occurs.
DCT
By function…DCT needs to be separated into proxima and distal parts (proximal-DCT & distal-DCT). The first ½ functions
like the thick loop of Henle. The first 1/2 fine tunes the hydration state of waste. The distal-DCT functions like the collecting
duct. It reacts to ADH and aldosterone. It fine tunes the molecules of the system. The oollecting duct works like/with the
DCT.
The DCT has receptors for ADH and aldosterone (particulalr). It eliminates potassium and hydrogen. Hydrogen as an acid
load, is introduced into filtrate by the DCT.
5 Hormones
1). Parathormone: Raises blood calcium when calcium is required. Has 3 effects under normal conditions: 1). Improved
recovery of calcium from filtrate and tubular processes 2). Activating Vitamin D drive forward to increase 1,25
dihydroxycholecalciferol
3). Softening on the bonds of crystal matrix of bone…There are no receptors for Parathormone on osteoclasts, but there are
receptors in bone….Improves solubility of bone and allows osteoclasts to now work more effectively on bone (recovery
increasesd amounts of calcium per unit time)
Primary HPT, Secondary HPT, Tertiary HPT
We will spend the least amount of time on primary.Secondary HPT has gensis of renal failure. Tertieray is bad renal failure
requiring dialysis (wasting of calcium).
2). Aldosterone: Linked with Sodium…Aldosterone elevations show more recovery of sodium from urine. We also see
potassium increased excretion. Both moledules are + charged, so we maintain electric charge in our bodies.
3). ADH: ADH increases in dehydrated states and resists diuresis. Eelevates in times of need to conserve water. We see
return from collecting ducts and DCT of water
4). REnin: REnin is derived from the kidney. Activation of the RAA (REnin-Angiotensin-Aldosterone) system shows
increased aldosterone at the end of the process.
5). Erythropoietin: Loss of 1 kidney showed a secondary conseuquence of anemia. The erythropoietin is derived in the cells
of the juxtagolmerular apparatus.
3 Pressures
1. Hydrostatic Glomerulus: Hydrostatic pressure in the Glomerulus is very important. Hydrostatic pressure must cause
leakage.
2. Hydrostatic Bowman’s: In Bowman’s capsule, the pressure should be low (to receive )vs. glomerulues it should be high
enough (to leak)
3. Osmotic (Glomerulus) : Low enough to let water go (in Bowman’s)…In teory we want the funnel empty. Osmotic Gl
Hypertension (GFR increases, tubular flow rates increase, urinary output goes up)
Heart Damage – Hypotension (pressure down, tubular rates down, urinary output down, GFR decreases)
Dehydration – Osmotic pressure increases (GFRdecreases, tubular flow rate decreases, urinary rate decrease???)
Overhydration – (GFR increase, flow rate increase, urinary output increase)
Hypertension is the 2nd most common cause of chronic renal failure. Early is diuresis and late is oliguria with hypertension.
Peritubular Capillaries
3 Main functions: 1
Non glomerular filtrate (hydrogen (mostly DCT), creatinine, ) all sourced from the peritubular capillaries
Surface is the lining of the tubule.
Kidney Functions
1. Filter and eliminate waste
2. Maintain Fluid Balance
3. Maintain electrolye balance
4. Maintain acid/base balance (linked with electrolyte balance)
5. Recover “Cherished” Filtrate
6. Maintain adequate red cell production
Filtration Function
Size is 7-8,000 Daltons.
Tests of Renal Function
The tests are not routinely abnormal until a significant amount of damage is done to the kidney system. Generally speaking,
we recognize ½ the renal function is lost before the tests become abnormal. Some patients lose function slowly over a period
of time and the body tries to adapt to diminished capacity. Some patients will have already lost 2/3 of function by the time the
test is +.
People who lost function quickly, we may see them with about 30% of function. 30% or 1/3 may catch the condition in this
scenario.
66% may be lost in a chronic condition.
Bicarb
Bicarb is recovered by passive processes. It is very important to acid/base balance. We do not recover 100% of the
bicarb. Bicarb is a buffer. 10% of all bicarb remains in urine. It is usually consumed by the acid load. Even the aicd load in
urine, would be ore acidic if not for bicarb in the urine.
If we need to get all the bicarb back, there would be an active process. We don’t need it, so we are designed to have passive
process.
Sodium
Active and Passive transport underlie the importantce. We need 2 processes to recover sodium.
Water, Potassium
Passive processes in the PCT.
Amino Acides and Glucose
We can recover 100% and sometimes more than 100%. WE can evern recover abnormally high amounts back into
blood. AA’s in urine indicate a very sick system. Glucose in urine indicates spillover with exceddignly high lvels in the
blood.
2 Waste Molecules
1. Urea:
2. Creatinine: A product of ADP + …It happens in the muscle. We only produce small amounts with normal amounts of .51.5 mg/dL. We see creatine phosphate + ADP ------ ATP + creatinine (waste molecule to be eliminated). Creatinine that
makes it into Bowman’s capsule is passed into the urine and toilet bowl. This is not the case for urea.. Creatininie is a good
marker because it behaves differently than urea. WE have a creatinine clearance system and not a urea clearance system.
There are too many variables in the urea system, but the creatining is easier to track and record. The creatinine cleareance
test is due to pressure changes.
Blood Levels of Creatine Elevation
We think about renal failure with this patient. Another condition could be nephritis (inflammation of the nephron)
with a wide range of etiologies (endotoxins, exotins, etc). ending with inflammation plugging the tubules. We can even
see immunoglobulins in the tubular cells. The last reason for elevation is a very large increase in muscle mass. It
typically takes gigantisum to produce routine elevation of creatinine.
Renal Failure comes in 2 types
1). Oliguria = Less than 500 mL output in 1 day…
a). Anuria = 100 mL or less in 1 day
2). Diuresis = Over 2 L of urinary output in 1 day
WE expect to see elevation of creatinine in oliguria states.
When creatining levels are less than normal, there is no renal reason for it to occur. Therfore, muscle wasting is happiening.
ALS, myasthenia gravis, etc. decreases muscle mass and they can’t even generate .5 mg/dL.
Urea
The source is liver metabolism. Specialically protein catabolism. There is a range of 10-20 mg/dL for normal. The peak is
3x higher than the base value. Decrease in BUN (Blood Urea Nitorgen) we must consider renal failure. We have to also
consider: liver disease, overhydration. Reduction in urea
Overhydration affects only urea (decreased BUN), not creatinine. Creatnine is impervious to hydratiaon state.
Increased BUN = 1). Renal Failure (Oliguria form of renal failure)…Blocking urinary output (like BPH or prestate cancer) can
increase hydrostatic pressure in Bowman’s and decrease GFR.
Dehydration affects and increases BUN.
Hypotension, Renal Artery Stenosis (elevate urea levels)
Renal Failure= Elevate waste molecules (oliguric state)
Urinary Obstruction = Urethral Obstruction (tumor blocking L Ureter with normal R Ureter and you;ll be able to
handle excess waste load and show normal function, but blocking the urethral will block both kidney’s and you’ll see
a change in the system)
Overhydration vs. Dehydration = Overhydration makes osmotic pressure in Glomerulus decrease, increases GFR,
increases tubular flow rates,. Urea upsets membranes and causes more leaking. Urea leaks back into the system.
Overhydration moves urine through system (flowing), and we see reduction in te amount of urea back in the
blood because we decrease contact time. We have a higher percentage of rurea in urine that can’t leak back
(due to time)
Dehydration (drops hydrostatic pressure, increases osmotic pressure, lowers GFR, lowers tubular
rates)…Dehydration has a slow rate and urine loses a higher percentage of its urea, so wel’’ll see a higher
BUN rate.
Hypotension: Could be local event. A 90% occlusion of renal artery diameter decreases flow, pressure and affects the
hydrostatic pressrure in glomerlules. It increases GFR, etc. Systemic Hypotneion affects boh renal aretiers and the
system.e
Panic Value Urea: 100 mg/dL (need dialysis)
Panic Value Creatinine: 10 mg/dL
BUN/Creatinine Ratio
20:1 – Think B before C (BUN:Creatinine Ratio)
Greater than 20:1 = Renal Failure palys a role, dehydration plays a role, CV Failure (increases
ratio)…Elevation of the ratio proportionally can show 20:1 ratio and “hide disease”. Creatinine handles urea vs.
creatinine …Creatiinine goes to the toilet bowl (urine) vs. urine (houdinin molecule)….Urea can leak out its container
and escape. Ureas is called also POW (escape molecule).
Less than 20:1 = Renal Failure (More than 1 kind or renal failure – Oliguria and Diuresis --- Oliguric forms shows
accumulatin of both molecules but quicker accumulation of urea. Oliguric shows BUN Elevation. Decreased ratio
shows diuresis (hypertensive, diabetic or overheydrate – lots of fluid raises hydrostatic pressure and reduces osmotic
pressure that allows water and solutes by caysing higher percentage of urea lost per unit time and showing lower
ration). Suppressed ratio = diuresis.
9/16/08
Renal Failure
We must recognize that interference with any 1 of the normal 5 functions of the kidney represents renal failure.
Oliguric & Diuresis
These are the 2 forms of renal failure
Azotemia = Elevation of BUN
Divided anatomicall in pre-renal, renal and post-renal.
Pre-Renal Azotemial
Heart disease…Heart disease that creates hypotension decreases hydrostatic pressure, decreases GFR, affects tubular
flow rates, and adds leaking back into blood. Urea comes from urine and goes back into the blood. Hypotension
leads to a series of events that leads to BUN elevation.
Hypertension does not produce azotemia. Increased BP, Increased GFR, increase tubular flow rates and higher
amount of urine goes to the bladder. The normal value of urea is suppressed. Urea does not leak back into the blood
and BUN drops with hypertension.
Heart disease drops BP reducing hydrotstic pressure in the Glomerulus.
Renal Azotemia
Post Renal Azotemia
Typically obstruction that works its way back. This can occur with BPH, prostate tumor, etc. The collecting
system becomes engorged, content in Bowman’s capsule occurs (abnormal to have content there), so hydrostatic in
Bowman’s is too high resisting in flow from Glomerulus, GFR is low, urea escapes and goes back to blood We
can’t force new urea in because of Bowman’s capsule pressure and we see rapid rise in BUN.
*** Know the 3 types of azotemia and conditions that create azotemia….3 types = pre, post and renal….Conditions
that create hypotension are heart diease causes ***
RAA System
Stimulation
RAA is stimulated by: Drop in BP, Hypovolemia, Rise in Sympathetics. Blood passes via the afferent arteriole.
The JG cells is where the macula densa cells live. The macula densa cells are counter cells, that count chloride ions.
Decreased chloride ions in circulation is associated with drops in pressures and GFR and kiendy finciton. The
macula densa cells stimulate the JG cells. JG cells release rennin and rennin increases. Renin now goes into
circulation.
REnin (kidney) interacts angiotensinogen and opens a binding site and undergoes a name change to angiotensin
1. Angiotensin 1 is now in circulaitn and finds its way to pulmonary vessels to find ACE (lung). ACE is
angiontensin converting enzyme. ACE is a cleavage molecule that opens a binding site to angiotensin 2.
Angtiotensin 2 is vasoactive on the afferent dilates and efferent arteriorles constrict creating a high pressure
zone in the Glomerulus (increases hydrostatic in the Glomerulus, increases GFR and increases tubular flow
rates and chloride flows quicker to macula densa cells satisfying the macula densa’s count). The second effect
of angiotensin 2 is to stimulate aldosterone release. Aldosterone works on the DCT-DCT and the collecting
duct with the net effect of sodium recovery. The point of the process is to recover water. Sodium attracts and
recovers water. Aldosterone leads to recovery of sodium, which leads to recovery of water. This expalnds fluid
volume, increasing BP< increasing tubular flow, GFR and hydrostatic pressure. This also impacts the macula
densa’s need for chloride
*** Know the system well ***
Glucose
A). Goes into the Glomerulus. Glucose is less than 7000 daltons and pases through the system going into Bowman’s capsule.
We recover glucose. We use an active transport molecule putting glucose back into the stream.
B). The more numerous the levels of glucose (serum elevation), they still pass to Bowman’s capsule. We can respond to the
demand and pass most molecules back into blood.
C). Excessive glucose in circulatin still passes through to Bowman’s capsule. If we exceed the work capacity of the the PCT,
we see glucose spilling in the urine. Blood values can be elevated in condition #2, but nothing escapes into the urine indicating
good kidney function. If we see glucosuria and glucosemia, we know the patient can’t handle the sugar load and are spilling
into the urine. We could have a good kidney that is not able to do its job. Diabetic nephropathy is a serious problem. Diabetes
is independent of how well or poorly controlled the diabetes is. Pts. With diabetes are mre likely to spill sugar decreasing work
cppacity. We must decide whtere this is an overwhelmed system or an overwhelmend, damaged sysem.
Reserve Capacity vs. Threshold
If it takes 50% loss of renal function, to see abnormal renal tests, that translates to 1 extra kidney. So we can give up a kidney
(kidney transplant). Renal size and function post-srugery, we can see the kidney at least 20% more function and 20% more
size. The kidney grows in size and increases function.
Reserve capacity decreases with dieaese. The difference between normal and abnormal test result gets closer and closer.
The two concepts are not the same.
Hypertension
The standard in allopathic medicine is medicine (diuretics, anti-hypertensive medications). The 2 drugs are: 1).
Antihypertensives (as a consequence they gained fluid quick)…Increasing fluid volume increases pressure 2). Fluid
Pill/Diuretic (was used to remove the fluid to decrease BP).
Pulmonary edema and CHF shows as sings of coughing upon sleeping with dyspnea and change of position relieves the
coughing and dyspnea as well as swelling of the ankles/pitting edema.
As a consequence of only taking a hypertensive: Dropping BP, drops GFR, drops Tubular flow rates, induces oliguria (as a
consequence of the hypertensives). The macula densa stimulate JG cells to send out rennin --- angiotensinogen (liver) ---angiotensin 1 ---- ACE (lungs) ----- Angiotensin 2 (vascoatcive function on the afferent and efferent arterioles to change
pressure in Glomerulus & aldosterone to bring back sodium and water) – elevating volume and pressure – now creating
dependent edema. Now most people are single drug formulations which create the same side effect.
Urinalysis
There are times when urine analusis is preferree over blood tests
UTI’s require urinalsis
Patient comfort and convenience are a considereation
Cost is a factor. Urine exams are musch less expansive than blood exams
Even when
Urinalysis Types of Urine Specimens
First Morning: Often makes the best sample…If they can’t come in first thing in the morning, have them collect the sample
and drop it off
Random: Done spur of the moment…A little more likely for false - results
Timed: Ex. create a dehydration state and check the UA for abnormal findings
Double-Voided (& Triple Void): Sample sub-divided to see what anatomy is the source of the problem. Often they look for
blood or bacteria
Culture and Sensitivity: What is the strain of bacteria and what is the culture sensitive to.
Urinalysis Collection Methods
Routine Void
Mid stream/clean catch
24 hour collection
Urethral Catheterization
Suprpubic aspiration
Pediatric Colleciton Bags
Routine void, mid stream/clean catch, 24 hour collection = In most states scope of practice
Urinalysis Specimen Handling Imperatives
100-200 mL is a typical minimum
Plastic containers with screw top lids
Sterile wrap containers for clean catch or any sample designated for culture
24 hour cample containers are brown (opaque) to avoid exposure to light, hold 3L, air tight lid, and require the use of
preservatives
Levels of Analysis
All samples inspected for: color, clarity, odor
Reagent Strips
Single to multiple reagents on a plastic strip
Rapid Interpretation testing
This is the basic urine study, ideal for screens.
Dipstick Urinalysis
Appearance and color are examined first
The urine sample should demonstrate clarity
What a sample lacks clarity it is due to particles suspended in the sample
Proteins, pus, RBC’s, and bacteria are common cuases of cloudy urine. --- A little fuzzy = minimal particulate…Very fuzzy = a
lot of particulate…Fatty meals can even show some cloudiness in urine.
Recent or retrograde ejaculation may be a cause of cloudy urine
At times a diet high in fats may also produce a cloudy urine
Alteration in the color may result from various medications, vitamine preparations and bleeding into the urinary tract
Certain foods like carrots, rhubarb, and beets may produce a change in urine color
Carrots may change urine to a dark yellow, beets produce a red color, while rhubarb produces reddish or brownish urine.
Table 13-3 Frequently Used Drugs that may affect Urine Color
*** Don’t have to know this for the exam, just know that there are reference lists out there ***
Dipstick Urinalysis: Proteinuria
Evaluation of protein is a sensitive indicator of kidney function
Normally, protein is not present in the urine
The Glomerulus acts as a filter which prevents the loss of protein into urine filtrate
It is tpical for small amounts of albumin to pass through the Glomerulus only to be recovered from the proximal tubule.
Albumin and small Amino Acids can make it through the Glomerulus, but the PCT should recover albumin, red cells, and even
the AA’s. The content of blood in the afferent arteriole is different than blood from the efferent arteriole. We don’t want the
same amount of blood and would miss filtration function. Osmolality should not change between the arterioles. The
milliosmoles per kg should be the same due to proportionate loss. We should maintain osmotic equality. Osmotic pressure is
maintained by proteins. We need circulating proteins (large and small weighted) to keep fluids in the proper location.
Anything other than albumin or AA’s in the urine, assume a problem with the Glomerulus. The Glomerulus has the task of
separating out proteins.
When albumin or other larger proteins are found in urine that suggests injury to the Glomerulus.
Large amounts of protein may be lost from the kidneys
This may lead to reduced vascular volume and lead to edema
Quantification of protein loss is best done following a 24 hour collection.(This is the best way to get a handle on the process)
Any loss of protein greater than 3 grams is concerning. (Normal protein loss is 200 mg per day so 3000 mg is a huge loss)
A patient that loses 3-5 grams of proteins has diuresis and loss of blood volume (hypotension). This has bad consequences on
the body.
Urinalysis: Interfering Facotrs Producing Proeinuria
Transiet proteinuria may be associated with severe emotional stress, excessive exercise and cold baths.
Diets high in protein (ex. Atkin’s Diet – Can show protein in urine)
Highly concentrated urine (exceeds PCT’s ability)
Hemoglobinuria, Acetazolamide, Aminoglycosides, Amphotericin, Cephalosporin, Oxacillin, Penicillin G, Penicillamine,
Sallicylates, Sulfoamides, and Vancomycin are a few drugs able to produce proteinuria.
Urinalysis: Dip Stick Specific Gravity
Specific gravity is a measure of the concentration of particles, including wastes and electrolytes in the urine
High specific gravity indicates
Urinalysis: Microscopic Exam
Typical urine sample is free of sediment.
It is described as acellular and aseptic under normal conditions
Crystals, casts, WBC’s and RBC’s are searched for.
Crystals found in urine indicate a great potential for stone formation.
Casts are formed exclusively in the tubules . Presences of casts indicate tubular or peritubular disease.
Hyaline casts are collections of protein.
Cellular casts are collections of various living cells: WBC’s, Epithelial Cells, RBC’s (all 3 are classic examples)
If we just see White cells in urine, think sample contamination first.
Casts are markers. The casts constituent overwhelms the tubules. The cells stick together and take up the shape of the tubule.
Casts tell us the problem is an URTI. White cells stuck together is immature. Coarsly granular casts hang around for 1-2
weeks in length. A finely granular casts persist for 2-3 weeks.
Cast appearance may be described as cellular, granular and finely granular (most immature ---- most mature)
Noting the appearcne can grade the age of the cast
Epithelial casts that shed into the tubular space may undergo degnereation into fatty casts
*** See the test #1 folder in the library ***
Lab Investigation of Renal Disease --- Summary of Fundamental Considerations
BUN, Plasma Creatinine, Creatinine Clearance
Quantitative Tests: GFR (Serum Creatinine Clearance), Tubular Function (Concentratinig ability or adi/base study, Glucose
REabsorption, Special studies where indicated)
Urinalysis
Only rarely will a patient who demonstrates normal results in these tests have significant renal disease. Gnereally speaking,
about 50% renal function must be lost before you can appreciate it with a screening test. Slow loss it’ll take 66% loss to find
the problem. Fast loss, it’ll take 33% to determine the problem.
Normal glomerular basement membrane produces an almost completely protein-free filtrate. The small amounts of protein that
are normally filtered (largely albumin & minimally AA’s) are reabsorbed by the PCT (and put back into the blood stream).
Normally less than 200 mg of protein is excreted daily.
Proteinuria generally signifies some type of glomerular abnormality and should not be ignored. Even a 1+ on routine
urinalysis should be investigated by a quantitative determination of protein in a 24 hour urine collection. Other causes of
urinary protein include bleddingi n the urinary tract, prolonged standing and exercise.
Non-glomerular load = Does not come from Glomerulus…The strtum corneum is mostly dead cells, that protect the more
immature layers. Skin is a form of mucosal tissues. Tubular cells are multi-layered and cannot be shed to the exterior. So the
cells are shed into urine. Part of the 200 mg is actually dead tubular cells that can be flushed away in urine. The cells are shed
to allow new cells foto replace them.
Tamm Horsefall Protiens are the shed cells.
Normal is less than 200 mg/day. Most is Tamm Horsfall proteins (glomerular filtrate is protein free)
Most accurate is the 24 hour collection.
Proteinuria ----- Precipitation in Tubules ----- Hyaline Casts (Source is the Glomerulus)
Glomerular Loss of RBC’s ---- RBC casts ----- Hemoglobin casts
Loss of WBC’s into tubule ----- Leukocyt (pus) casts (first thing to degrade is the cell wall = immature….granular casts that are
smooth are mature)
Epithelial Desquamation ---- cellular casts ----- finely or coarsely granular casts ----- waxy casts (end stage of this)
Blood may enter the urinary stream anywhere from the Glomerulus to the urethral measuts. Do not overlook essential
hematuria (may be unilateral), use of anticoagulant, and blood dyscrasias. The presence of blood casts (RBC or liberated
hemoglobin) points to intrarenal oriin. Investigation of hematuria may require IV urography, cystoscopy, renal biopsy,
ultrasound, coagulation studies, sickle cell testing and urine culture.
Microscopic amounts of blood are necessary and can trigger a quick response (quicker than indicated on the dipstick box).
+ test for Hematuria = Repeat the test…(may reasons can cause blood in the urine)….
Basic Considerations
GFR is by far the most important assessment of kidney function. GFR in normal adult male is about 125 ml/min.
Females, smaller people and aged have lower rates.
Important: More than 2/3 of the GFR may be lost in chronic renal disease before symptoms appear and lab studies (other than
GFR) become abnormal.
A patient with 90% loss in renal function appraches “end-stage renal disease” and will soon require dialysis or transplant.
The GFR estimation allows “staging” of renal dysfunction and quantitative assessment of its course.
If there is 90% loss of function, the patient will probably need dialysis. You try to find the best host for a dialysis or for a
transplant. You need to do everything that you can as a patient and a doctor to get the transplant. That includes asking the
patient to exercise, stop smoking, etc. Part of the issue is the topic of “return on investment.” A family with good financial
support may move up on the list, because they have a better ability to treat and receive care for the new kidney.
GFR testing is not abnormal till 50% renal function is lost. Patients can test normal but be symptomatic. The sick can have
non-testable levels of disease.
Rationale of GFR Tests
Requirements:
1. A substance whose molecular weight is small enough tht is passes through the glomerular filter at the same rate as
water and which is not reabsorbed, secreted, or metabolically altered by the renal tubule.
2. Measurement of the concentration of this substance in the plasma (P)
3. The measurement of the concentrationin the urine (U)
4. Measruemtn of the rate of urine flow per minute (V)
Calculation filtered = amount excreted
P x GFR = U x V
GFR = U/P x V
Substances used to test glomerular filtration includes inulin, creatinine, and urea (with creatinee being the most practical).
Assessments of the kidney’s concentration-dilution functions provide the most sensitive means of detecting early or mild
impairment of renal physiology. A patient with completely normal concentrationg ability is unlikely to have serious kidney
malfunction of any type.
Value of Test
The normal ability to concentrate urine requires:
1). Copious GFR (good flow)
2). A proper amount and distribution of renal blood flow
3). Adequate tubular mass
4). Healthy tubular cells
Loss of concentrating ability: Hypokalemia, hypercalcemia, absence of ADH, diminished gFR, Amyloidosis, Increased solute
load, Loop Diuretics, Disturbed medullary circulation plus any disease resulting in chronic renal failure
Note: The countercurrent multiplier mechanism in the loop of Henle (red) is responsible for the generation of a hypertonic
urine. The energy to operate this mechanism comes primarily from the reabsorption of salt without water in the thick
ascending limb of Henl’s Loop. This mechanicsm with help from the distal portions of the nephron also permits the generation
of urine.
9/22/08
Testing Tubular REabsorption
Rationale: in the presence of ADH, the walls of the collecting dcuts become highly permeable to water, allowing somotic
equilibrium between the tubular urine and adhacent intersitital fluid because of the couttercurrent multiplier, the osmoliaity of
th intersititial fluid in the renal medulla rises progressively form the corticomedullary unction ot the tip of the papulla. The
maximum level at the latter defines the maxiumu urinary osmoliality.
Level of the maxiumum osmolality (about 1200 mOsm/kg) – The tubular system is to recover fluid enhanced under conidiotns
Schematic gradient of interstitial fluid (osmolality in renal medulla)
Osomolality at the level is isotoni to the blood (about 286 mOsm/kg) --- Bowman’s, PCT, osmolar environment is neutral and
doesn’t move stuff in or out….
Method: Nothing is given by mouth after 6 PM the night prior to the collection of urine samples. Dehydration stimulates
maximal endogenous ADH secretion oand urine is collected at 9, 10, and 11 am the following morning. In chronic nephritis,
water reabsorption is reduced by damaged tuules. Failure to concentrate also occurs in neprogenic dieabetes insipidus although
ADH secretion is normal and in diabetes insipidus because of inadequate ADH production due to posterior pituitary
dysfunction.
Note: Miaximum osmolality also declines with ae and ther is considerable idnificual variation amount normals. Up to 75% of
the maxium osmolaity expected for a given age group is considred normal.
A significant amount of damage to the GFR must be present to find the levels on a test.
Acid –Base Function: Basic Features
Arterial bicarbonate concentration = about 25 mEq/L
GFR = about 180 L/day
Therefore, the filtered load of bicarb = about 4,500 mEq/day
About 90% of this is reabsorbed by the mechanism of H+ secretion by the tubule, which titrates bicarbonate to CO2
In the distal tubule, H+ secretion reclaims the remainder of the bicarbonate (the requirements of acid-base balance are also met
here b further H+ secretion in the form of titratable acidity plus ammonium ion secretion)
Acid outuput by the kidney is limited by two factors:
1. The maximum number of moles of H+ which may be secreted by the tubules
2. The minim pH to which the urine may be driven
24 Hour Urine Check:
5 to 10 grams NH4Cl is given by mouth to stimuluate maximum acidification. Analysis of the 24 hour specimen is
then undertaken. Failure to excrete a total of more than 100 mEq of titratable acid + NH3 constitutes reduce capacity
for acid secretion.
*** Know the test and the process to induce maximal acidification to get hydrogen levels where they belong and if they can’t
do it within 24 hours it will indicate the extent of the kidney problem ***
Metabolic Acidosis in Chronic Renal Failure
Whole nephrons are destroyed (parallel glomerular and tubular failure). Acidosis results from inadequate tubular mass. The
remaining nephronrs are leargely functionally intact and produce a very acid urine (pH 4.5).
At 75% loss of funcito, the system is clearly damaged.
The disproproriton between total acid output and acid load secondary to diminished tubular mass retuls in retention and tupical
metabolic acidosis of chronic renal failure.
Evaluation of urinary acidification affords an estimate of tubular mass and helps to diagnose specific defects in this area.
Renal Tubular Acidosis (RTA)
In contrast to chronic renal failure, the glomeruli are spared. RTA is characterieze by tubular failure (H+ secretion failure).
IN proximal RTA, reduced ability of the proximal tubule to “reabsorb” filerted HCO3 results in escape of increased amounts
of bicarbonate into the urine. A normal urine pH may be achieved by lowering the plasma HCO3 concentration.
In distal RTA, the distal nephron cannot secrete H+ against a high concentration gradient. The minimum pH which can be
achieved is restricted. The cutoff point to establish diagnosis is pH 5.5
Mixed RTA designates cases showing features of both types. A fourth type of RTA (frequently found in diabetics) is
characterized by acidosis and hyperkalemia out of proportion to the degree of glomerular failure.
PCT Problems
We see metabolic acidosis due to bicarbonate problem, not a hydrogen handling problem.
DCT Problems
The issue is not bicarbonate. We can assume 90% filitered and removed but we can assume accumulation of H+. It leaves
urine pH high. The issue is handling probem of hydrogen and not bicarb problem.
In the Filed
We see cortical diseae. Loss of PCt function coupled with DCT problems. Cortical problems do not segregate between areas
of the kidney. The patient gets sick quick because of 2 reasons: 1). Loses Buffer in PCT 2). Can’t get rid of H+ in DCT.
Typically, the patient just doesn’t feel right, energy is low. Reduction of nitrogenous loads by abstaining from proteins, and
other nitrogenous loads can help the kidney.
*** Know PRTA, DRTA, and the consequences of mixed ***
Hematuria Panels
The most common of the abnormal lab findings. Anywhere from the kidney to the urethral tip hematuria can occur.
*** Diagram on Overhead ***
Many disease end by blood in the urine (polycystic disease, march hematuria, tumor, trauma, nephrocalcinisosi, ureteritis,
calculus, infections, ureteritis, renal vein thrombosis, bleeding and clotting disorders, malignant hypertension, granulomatous
disease, glomerulonehrititis, collagen vascular disease, infarction, papillary necrosis, sicky cell disease, stricture, vesical
varicosisites, foreng body, BPH).
*** Appreciate the range of disease that causes blood in the urine ***
Hematuria 3+ -- Patient HIstory
This designation helps up separate thepatient who does and doesn’t need more work up. 3 or more red cells per high powered
field is worth further investigation.
An episode of painless gross hematuria has a 20% chance of indicating a kidney or bladder tumor. Gross hematuria has a 1/5th
chance of being a tumor and 80% does not have a chance of tumor.
Hematuria accompnanied by lower urinary tract symptoms and signs (such as frequency, dysuria, and pyuria) points to a
diagnosis of cystitis (particularly common in females).
Storing RBC’s in the bladder for a long time, can suck fluid out of RBC’s and crenate them.
A sexually active young woman with hematuria in all likelihood has intercourse related (“honey-moon”) cystitis. Also,
pregnancy and increased pressure of the uterus on the bladder can cause blood to enter into the urine. Mostley the painful
urination with blood in there in sexually active female, quiz them about recent sexual history asking about # of sexual
encounters. This is periurethral trauma due to swelling that leads to increased outlet pressure.
A history of sore throat, hypertension and facial and peripheral edema in adolescent suggests acute glomerular nephritis.
Hematuriar developin after trauma involving the flank probably indicates a contusion or other injury.
Hematuria associated with colicky pain radiating from loin to groin strongly suggests passage of a urethral stone.
Documentation of easy bruisability or prolonged bleeding after a simple cut should direct efforts toward seeking a bleeding or
coagulation disorder.
Triple and Double Catches
*** Overhead Article on Triple (Males) or Double Catch (Females) Urine Test ***
The test can help to determine the anatomy/source of the problem creating urine in blood. Males are tested to retract the
foreskin (if they have it) with a triple catch test. Begin urination (1st drop into the cup 25-50 mL). The sample is followed by
culture analysis. Males move to cup #2 and fill it. Step #3 for males is the digital rectal exam also called provocative prostate
exam (insert, sweep right and left to feel size and consistency of lobe, followed by checking the isthmus). Any product of the
DRE goes on a slide. Following the DRE, the patient finishes 25-50 mL of urine in Cup #3.
A). Bleeding throughout urination = Consider a bladder lesion (All 3 cups with blood) or kidney lesion.
B). Last few drops (terminal hematuria)? = Suggests the bladder neck or prostate as the site (last cup with blood…prostate
because of prostate provocation is the culprit or bladder neck squeezing out blood into the urine)…First think prostate disease
because it is the more serious of the two.
C). At the onset of urination only (initial hematuria) = Lesions below the bladder (especially the prostatic urethra in males)…
Women Double Catch
A). Cup 1 and Cup 2 Blood = Upper Tract or Bladder
B). Cup 2 Blood = Terminal Hematuria due to base of bladder and squeezing of Detrussor muscle squeezing blood into urine
Dipstikc is Done on the Cups
Spine for Casts: Hemoglobin casts show Upper tract problem (renal tubule)
Intravenous Pyelogram – Testing for Hematuria
The most important functional test. IVP constitutes the logical next step in the work-up. Any calcification in the collecting
system noted on the plain abdominal film is correlated with films taken after the injection o contrast medium. The contrast
films outline the renal parenchyma, the caliceal system, the Ureters, and the bladder. Iodine is used.
Fluroscopy is used to watch the kidneys work in real time. We watch the dye move from cortical regions to the interior. This
is a functional study. This study allows us to watch the kidney work. If 1 kidney is obstructed, it fails to enahcne because of
contrast agent can’t enter. Failure of blood to enter causes ischemia and death of kidney cells.
IVP is a contrast exam, where we take still or moving pictures to determine kidney function.
Cystourehtroscopy – Testing for Hematuria
A flexible fiberoptic exam. When IVP is normal, cystourethroscopy may reveal the source of the bleeding. This is a very
important tool to check the urethral lining, bladder interior and we can even introduce a catheter for inspection and
intervention. We routinely use this tool now-a-days.
Retrograde Ureteropyelography – Testing for Hematuria
Often couple with cystoscope. If pathology is not found in the bladder, prostatic urethra, or urethra – particularly if bloodtinged urine is noted at one of the ureteral orifices – a retrograde ureteropyeloram may delineate and upper tract lesion better
than the IVP does. Selective uretreal urine specimens can be obtained for cytologic studies at the same time.
The introduction of the ureterescope ushered in a new diagnostic eera by permitting direct visualization of the Ureter and renal
pelvis.
The same contrast agent is put in the urethra and we work backwards. This is combined with cystourethroscopy for added
effect of exam.
CT Scannign and Arteriography – Testing for HEmaturia
If the source of urinary tract bleeding remains an enigma, CT scanning and arteriorgraphy facilitate renal parenchymal
imaging. CT can disclose small masses; arteriograms may show neovascularity, pathognmomonic of tumors. Helical CT scan
is preferred because is it quicker and easier for the patient
MRI – Testing for Hematuria
MRI can be used as well for observation. Time for the image to be generated is an issue. WE also want to give them
medications to limit activity of the kidneys and other organs. MRI abdomen studies as part of a renal exam is not common.
Between CT and MRI, MRI can comment on tissue physiology better than CT scan. MRI can comment on a wide range of
physiology more so than CT. MRI is a possible tool on a given patient.
Renal Biopsy – Testing for Hematuria
In some cases, glomerular lesions (Fabry’s disease, amyloidosis, etc) may require renal biopsy for definitive diagnosis. There
are some things we can name only by biopsy.
Algorithm for Testing for HEmaturia
*** Know the Diagram for the exam ***
1. Urinarlysis (Red Blood Cells greater than 3 HPF) = Repeat Test
2. Urinalysis Red blood cells greater than 3 HPF on the Repeat Test---- No red blood cells casts; proteins greater than 2+
3. a) Urine Cultre + = Treat as Appropriate
b). Urine Culture – (consider IVP and sonography)
5. IVP or sonography (when urine culture is -)
a). + IVP or Sonography = Assess abnormality and treat as appropriate
b). – IVP or sonography (consider age)
6. – IVP sonography
a). Age greater than 40 ----- Cystoscopy ---- 1). + Test treat as appropriate 2). – Cystocopy = Periodic
Monitoring (every y 6 months); urinarlysis and culture
b). age less than 40 = Periodic monitoring (every 6 months); urinalysis and culture
Other side of the Chart
1. Urinalysis (RBC’s greater than 3 HPF) = Repeat Test
2. Urinalysis (Red Blod Cells Greater than 3 HPF) --- Present or protein greater than 2+
3. BUN Test: a). BUN Test normal (do a urine culture and head down the urine culture paradigm --- listed above)
B). BUN greater than 20 or CR greater than 2.0)
4). BUN GREater than 20 or CR greater than 2.0 = Perform ASO Titer
5). ASO Titer = a). + Test = Treat as post streptococcal glomerulonephritis b). Consider Renal Biopsy
*** Know the chart and the Paradigm ***
KUB – Search Pattern
1. Organ Size (kidney size is 3 vert. Heighs and 2 disc spaces, liver should stay under the ribs)
2. Organ Number (2 kidneys, 1 liver, etc.
3. Organ Location (kidney is pushed down and in, may be a suprarenal tumor. Kidney is pushed lateral and may be a
pyloric tumor)…R kidney is lower than L due to liver.
4. Calcification: Conduit…Look for aneurysm in the splenic, aorta, iliac arteries. The uretuers lie along with TP’s so
look for stones.
5. Gas pattern: (should be none in the small intestine. Gasslessness suggest SOL, including poop). Nogas in the RUQ
due to liver.
a. Is gas contained or uncontained. Uncotained under the diaphragm best seen between diaphragm and liver
b. 3 or more air/fluid levels = obstruction
(DP = diaphragm, T = transverse, D = descending)
L side is the Meganblaz and R side is the liver.
9/23/08
IVP with Contrast
Retrograde exam can help to determine if obstruction of blood flow or stone is present. Obstruction of blood flow will cause
death of cells.
Lab Definition of UTI
Microscopic analysis of urine showing 5 or more per high powered filed or 20 or more bacteria of same species in high
powered filed, we have met the laboratory definition for UTI. If we see 1,000 or more on culture of same species, that is the
culture definition of a UTI. Iedally all 3 the lab, the culture and the clinical picture should match up.
DCT Injury
The DCT is the last chance to introduce H+ waste into urine. Damage will cause acidosis of blood and alkalinization of urine.
H+ remains in the blood and does not pass to the urine.
Both DCT and PCT Injury
Both the PCT and DCT are cortical structures, but often the problem is both the PCT and DCT. The patient gets sick quick
because of overly buffered urine (very high due to lack of H+) and metabolic acidosis of the blood as H+ is dumped onto the
blood.
RENAL FAILURE
Disrupting 1 of the normal functions of the kidney is a cause of renal failure.
We subdivide renal failure into acute and chronic forms. We then assign key words to the categories.
Renal Failure
The 2 keywords: 1). Oliguria 2). Diuresis
Acute Renal Failure
1). Oliguria = Low urinary output (less than 500 mL/24 hours per day) …Anuria is 100 mL/day
The key things of the clinical picture is 1). Accumulation of waste in the blood 2). Blood Volume goes Up (Increases the
Work Load of the Heart) 3). Increase in BP (due to increase volume load and RAA system is activated) 4). Weight Gain 5).
Dependent Edema (Foot, Ankles, lumbosacral junction)…eventually fluid can be trapped in the airway (pleural effusion which
can be dangerous in these patients) 6). Anorexia, Nausea, Vommitting (accumulation of fluid especially around the small
intestine creates loss of function. Stretch stimulates satiety center in the brain that decreases apetitite).
Low urinary output will trigger swelling (puffiness) and weight gain. The descriptin is acute renal failure is Puffy, Wieght
Gainer. There is increases work load in multiple systems (heart and lungs). Urea elevation leads to azotemia (elevated
BUN levels). Anorexia can also present do to stretching of the small intestine and stretching of the receptors affecting the
brain.
The good news in the renal and post-renal forms of failure is that over 90% of the time the patient will recover without
measureable deficit. The acute renal failure usually does not progress into chronic because the populations who get the
conditions are different
Pre-Renal Causes
Hypotension
Medical Overdose
Occlusive Vascular Disease
Cardriogenic Problems
Post-REmal Acute Renal Failure
Stone
BPH
Obstructive Disease
Early Chronic Renal Failure
Diuresis is the key word.
Chronic Renal Failure
Keyword is diuresis. The are the opposite of acute renal failure: 1). Decrease in BP 2). Hypovolemia 3). Dehydration 4).
Thirsty 5). Sodim Loss in Urine 6). Creatinne Loss in Urine 7). DECREASES the BUN/CREATININE RAtion (High GFR and
High Tubular Flow reate leads to high urea levels in urine, and less urea in blood) 8). Long Process 9). Loss of glucose
(Diabetes is the #1 cause of chronic renal failure) 10). Osteopenia 11). HPT (Classification #3…Primary is tumor/secretory,
Secondary HPT is kidney failure…The sick kidney is the most likely cause of HPT….Tertiary HPT is due to dialysis…--Early
Late Chronic Renal Failure
Oliguria is the Key Word….
Causes of Chronic Renal Failure
Chronic renal failure
1. Diabetes
2. HTN heart disease
3. Glomerulonephritis – membranous form
4. Hereditary polycystic disease).
The typical acute renal failure does not usually become the typical chronic renal failure patient. If this does happen, is
progresses from acute renal failure to late chronic renal failure very rapidly and they skip the middle stage (early chronic renal
failure)
End Stage Renal Failure
DEfiend as 90% loss of function or more. Prior to that it is just renal failure
ACUTE NEPHRITIC SYNDROME (ANS) -- aka (Acute Glomerulonephritis --- AGN)
This is an autoimmune response to a common antigen. Strep is the organism. Most people have antibodes to the strain of
strept. The antibody mark the organism for Phagocytosis with enzymes. For these patients, the precipitant (antigen-antibody
complex) sets up an alarm response flooding the tissue with anti-inflammatory products (WBC’s). WE see edema.
The body mobilizes anti-inflammatory products to the membrane that causes swelling to the membrane. The Glomerulus is a
filter on the vascular system. In the Glomerulus under normal conditions to leak (it has holes in it). The membrane swells and
the holes become smaller in AGN. The filter now becomes a barrier and not a filter. The patient has oliguria.
The precipitant is a trigger (Antigen-Antibody complex). Size of the wound has n othing to deal with the condition. Severity
of illness has nothing to do with it (either you are sensitive or not). The response is always exaggerated. The condition may
even be described as an “allergy.”
Classically
Classic you deal with streptococcus. The case is that this is an autoimmune disease. The immune system saw the bugged,
tagged it for destruction, and the tagging for antibody and phagocytic destruction causes damage to the Glomerulus.
This is an exaggerated autoimmune response. This IS NOT AN INFECTION BUT AN AUTOIMMUNE REACTION! There
is a prior history of infection (URTI, Skin infection, etc.) that has led to the autoimmune reaction.
Adults and Kids can both get AGN, with slight bias to children. At the time of the 1st diagnosis, it tends to be a child. There is
also a gender bias with boys more likely to get AGN than girls. Dirty wounds is more likely a consequence of boys.
Pt Presentation
It presents as early on as the flu with aching, lethargy, malaise, etc. Once the oliguria becomes present, the condition is hard to
miss. Dependent edema is an observation that can help. Some other symptoms are bloating (due to edema). Swelling in the
ankles is either cardiogenic, nephrogenic or lymphogenic. The history will help to differentiate the cause of swollen ankles.
Ibuprofen toxicity can induce acute renal failure.
Patients often feel hungry. The stretch receptors are stimulated triggering the satiety centers of the brain.
Progression of the condition leads to other system involvement. Fluid overlead leads to congestive heart failure. Pleural
effusion can develop in the lungs and fluid can accumulate in the lungs. Fluid overlead can lead to RAA system activation.
Acmulation of key wastes ensues with azotemia. Elevated BUN and acidosis effect RBC membranes more fragile. Pateints
get thirsty and drink water leading to greater fluid accumulation. Casts develop. TAM-Horsefall proteins can lead to cast
development. The holes in the Glomerulus can enlarge and the patient can go into diuresing state (reversal of the process).
The patient needs to go to the hostpital. They will be prescribed corticosteroids. The body will go back to baseline on its own,
but corticosteroids helps rverse the trend quicker (5-7 days vs. 14-20 days). The sooner you get the patient away form the
hospital the better as they have a chance of nosocomial infection, so often they prescribe corticosteroids, wait and then watch
the patient. Nutritional recommendation is advised as supportive care.
ACUTE TUBULAR NECROSIS
The target tissue and function is the tubules. There are 2 major subcategories: 1). Ischemia – Loss of Blood Supply 2). Renal
Toxins.
Ischemia
The most common cause of Acute Tubular Necrosis and most serious of the causes of acute renal failure. The death occurs as
a consequence of ischemic disase and is followed by fibrotic repair leading to non-funcitonal renal tissue. 6-8% of
measureable deficit usually occur to ischemia leading to acute tubular necrosis.
Typically this is an embolic event. A small percentage also gets this via sickle cell anemia, atherosclerosis (leading to emboli)
and plugging of vessel. The test for following up a potential necrosis patient is an IVP. Spiral CT can be used as well as IVP.
IVP presenting with dots is called a “shower event.” The shower event is several small emboli leading to polka dot
appearance. Contrast is carried throughout the kidney and low attenuation tissue showing as black polka dots meaning
multiple small emboli.
Big chunks that break free are called wedge shaped or pyramidal area of ischemia. The vessels show arborization.
Arborization or tree-like branching of the vessels may not get contrast showing as a wedge shaped area of black. The other
areas light up with contrast. This is a quick way to show a large loss of functional anatomy. Pyramidal ischemia is a big chunk
of loss often 15-20% or more. If this happens enough (embolic events), they can transition to chronic renal failre.
Fat emboli can also be a cause. Breaking a long bone liberates fatty, yellow marrow which can enter the vascular tree.
Corticosteriods can mobilize lipids that occlude the vascular tree.
Renal Toxins
Sources can be occupational. In some cases, you can reverse the occupational, behavioral, or other advice. Some of the toxins
are drugs (aminoglycosides, NSAIDS, etc.). NSAIDs were first linked with tubular cell destruction and glomerular function
loss. You can see dependent edema, back pain, dose tolerane-response (as the patient thinks they must take more to get pain
relief). The NSAIDss can lead to acute renal failure.
Chemicals like mercury can cause ATN. Carbon Tetracholoride can cuase this. Carbon Tetrachloride is in spot removers,
carepet cleaners, etc. Ethylene Glycol toxicity can lead to ATN. Antifreeze (ethylene glycol) toxicity is treated with alcohol
drip. Often, people overdose on ethylene glycol to get an alcoholic drip (alcoholics).
Presentation
Oliguria with progression to anuria occurs with ATN patients. Casts formation more commonly occurs with ATN. Blood
profile shows increased WBC’s. Cleanup needs to be done with ATN. Waste accumulation, with elevation of BUN, and the
ratio goes up. Oliguric renal failure tend to elevate BUN. BUN goes up quicker as new urea is not eliminated and urea in the
system escapes back via the tubules. The low tubular flow rates activate the RAA system. We see patients with edema, thirsty
and low output. Dependent edema is present (either in ankles, lumbosacral junction, pulomary edema, pleural effusion, etc.)
Consequences of ATN and AGN
The consequences are similar ast they both lead to renal failure. The big difference is severity. Loss of cells due to ischemia
and toxicity is huge. The cells do not come back in ATN vs. AGN which can show return of cells (in some cases).
CHRONIC RENAL FAILURE
It is not a continuation of acute renal failure. Different patient populations is a big way to differentiate.
Early Chronic Failure = Diuresis
VS
Late Chronic Failure = Oliguria,
Patient Population who gets Chronic Renal Failure (#1 Diabetes, #2 Hypertension #3??? #4 Polycystic Diseae)
Diabetes: Polydipsia, Glucose Intolerance, Polyuria, Glucosuria, Hypoglucosemia, Diuresis…It is not true that the better
controlled the diabetes the better the prognosis. The research shows that kidney function is independent of controlled diabetes.
It doesn’t seem to matter if they have controlled diabetes regarding renal health. The patient is diuresing because water follows
solutes. They leak glucose and glucose leads to water loss.
Hypertension: 3 Pressures…Hydrostatic Pressure, Osmotic Pressure, Hydrostatic Pressure in Glomerulus???...Increased
hydrostatic pressure, increases GFR, and incrases urine. Late chronic failure shows oliguria and this is pathological. There is a
pressureized system where the walls can be burst. We lose surface area. Loss of surface area causes loss of leaking. We tend
to see protein in urine. The Glomerulus is elastic tissue and when blown up, the holes get bigger and protein that normally
doen’t pass, now do pass. We don’t have a way to recover albumin. The bigger proteins are hydrophilic and drain water from
the system. Frank damage makes the holes bigger which allows protein and water through.
Polycystic Disease is breaking of connective tissue making the holes bigger. We see retiention cysts that collect urine in the
renal parenchyma. The condition starts with diuresis as connective tissue and the process continues with retention cysts that
displace healthy tissue leading to transplantation.
Urinarlysis Result of Early Chronic Renal Failure
Output, we see 2L or more per day. The urine will dilute. Decreased SG (specific gravity). Urea will incrase in urine. BUN
will decrease. Other changes include loss of calcium, loss of sodium as we can’t recapture the “cherished” moleculres.
Urinarlysis REsutls of Late Chronic Renal Fialurei
Concentratd urine, dark in color. IN the blood side, elevated creatinine.
Early vs. Late
1. decreased GFR = Late
2. Increased BUN = Late
3. Hypoanatremia = Early (electrolyte loss)
4. Poluria = Early
5. Polydipsia = Both
6. Diarrhea = Late
7. Hemolysis = Late…because of acidosis and azotemia (red cell fragility)
Chronic Renal Failure patients do not get better. Between DM and Hypertension, we can affect the outcome in hypertension.
If we can control BP better, the less the consequence on nephrons and renal function. Diabetes becomes a management issue
mostly.
Calcium, Vitamin D becomes important with diuresis. You need to make the body believe it has enough calcium by
supplementation or else it will use Parathormone. Vitamin D couple with calcium helps more than either individually. The
kidney helps in the process of converting to active Vitamin D, so we need to supplement both active D and calcium.
There will be stress in the CV system, especially in the Late Phases (Oliguria). You may need to take BP regularly. The
patient may also demonstrate Uremic Frost. The frost is a fine white powder that develops in the axillary and popliteal surface
where fluid leaves uric acid/urea. The patient needs dialysis because of harmful levels of urea.
Oliguris phase patients require management of diet. Malabsorption occurs in the late phase (we don’t absorb) vs. the early
pahse where we lose nutritents. We may need vitamin megadoses.
A change in diet can occur. Proteins and nitrogenous wastes become an issue along with hydrogen load. Nirtogenous wastes
become detrimental.
9/29/08
URINARY TRACT INFECTIONS
*** Test #1 for UTI’s will include the background, gender bias, age bias, factors that tie into it. General questions with
specifics on Upper and Lower UTI’s for test #1. Test #2 will have urinary infections, prostatitis, urethritis, etc. Test #2 will
have more specifics than test #1 ***
Common Features
2nd most commcom infection in the USA
Infection Categorized by location of infection
Most don’t produce serious kidney disease
Lower UTI more common than upper
More common in females
Serious UTI complications most times involve Upper Urinary Tract Infection. Female to male ratio is about 10:1. Increased
incidence as the patient ages. 60-80 years old age group have the highest incidence of problems. About 4 people in 100 above
60 have a UTI. There is also an adolescent spike of UTI. Young females 2-4 have increased rate, and then the condition dies
down. Teenage females may then get it because of hygiene issues. The condition is mostly older population that get the
problem.
Female
Females get UTI’s more because of a short urethra. The spread of an organism may occur quickly because of E Coli coming
from the GI tract. Shortness of the urethra, wiping in the wrong direction (more risk if back to front wiping pattern), activity of
the organism (E. Coli thrives in the GI and in the Urinary Tract) – biofilm, allwows the bacteria to spread. The bacteria
conquers surface area.
The urinary tract is in close proximity to the anus and makes it easier to spread. Diabetes (both men and women) have higher
incidcdenc of UTI. Sugar in the tract and in the bladder allows the rapid growth of the organism. pH in irritated tissue can
increase the symptoms. Symptoms are more or less noticeable based on the pH, but the ability to destroy the organism doesn’t
change. The prostate (in males) has bacteriocidal properties. The lack of a prostate decreases women’s ability to resist the
invader.
The longer the urethra the less the chance for spread and attaining critical mass to lead to spread. The greater the length the
greater the attrition.
Urinary Obstruction
Bladder withheld in the urine, static urine is good for 2 things: 1). Stones 2). Bacterial Proliferation. As you empty the
bladder you get rid of some bacteria, as you don’t pee, you withhold bacteria and prolong the infection.
RisksFactos
Chemotherapeutic agents, Immunosuppressed, Diabetes, Chronic Disease…These all are risk factors that lead both men and
women to getting UTI’s.
Definition of UTI
A lab diagnosis, not a clinical diagnosis
100,000 colonies on culture
If greater than 2 colony types on culture – probably contaminated
Slie Exam: 20+ bacteria/HPF and 5+ WBC/HPF (pyuria)
White cell incrase in urine only, think sample contamination and redo the test emphasizing retraction of foreskin, cleaning of
area and keeping soft tissues retracted.
UTI Etiology
Endogenous: We don’t see a lot of them, but they can be serous
Instrumentation: Surgery, testing, catheterization all increase risk. Catheterization risk can be 5% per day or even up to 70%.
The active insertion of a catheter allows bugs to be escorted by the bodies defenses. Organisms spread by bile film using an
edge to anchor on. A Teflon edge helped resist E. coli spreading by attaching/anchoring. Catheters are also left in slightly
longer, because frequent changing actually increased risk. Other risk management techniques include weak antiobiotic
substances that are used to clean/sterilize the catheters prior to implant.
Urethral Trauma
Prostatitis
Bladder Distention: Urine (Static Urine makes the bladder very large and able to retain bugs)
Diabetes Mellitus: Immune suppression of the patient. Sugar in urine gives a breeding ground for growth.
Obstruction: Static Urine
Hypertension: Thinks that shound’t make it through bladder do make it through.
Neurogenic Bladder: (especially in cases of cord injury)
Congenital Anomalies: Seen mostly with pediatrics and pedicatric practices
Pre-exsiting renal disease:
Signs and symptoms of Upper UTI
Flank Pain: Usually lateralized to one side over the other. Bilateral Flank pain is another differential list. Unilateral flank
pain, always include Upper UTI in the differential list
Casts, bacteria and renal epithelium in UA sample: The infection respects nobody and no boundaries. By the time we see
casts, it represents a historical marker rather than a diagnosis. Mismanagement of the patient, and they’ll show casts.
Fever/Chills: Common to a Upper UTI and kidney, not a Lower UTI.
Malaise:
Prostration
Pt “looks” Ill
Endogenous Sourcing usually stpreads by blood to the kidney. This is the most rare and most serious problem. The second
type is pyelonephritis. The organism takes up space on the interior of the kidney (calyces). If the organism is in the periphery
that is hemotogenous spread and if the organism is in the interior it is hematogenous spread. Hematogenous spread is more
common of the two type sof URTI.
Lower UTI – Signs and Symptoms
Signs and symptoms with urine excretion: Especially burning pain with elimination are associated with Lower tract
infection. Signs in the form of discharge is a big indicator of problem
Burning: Comes with elmination
Suprapubic pian: Often linked with cystitis
RBC and WBC in UA, but no casts: White Cells and bacteria are typically present
Low fever: Mostly low to no fever are present in lower UTI.
Ureter, bladder, urthera, and prostate in men constitute the lower Urinary tract.
Kidney Infection – Upper UTI
Renal Medulla more sucesptible to infection (Pyelonephritis constitutes renal meduall infection)…
Coftical Involvement more severe: The osmotic environement is more like blood
Kidney Infection Etiology
Hematogenous Spread leads to cortical involvement (Cortical = Hematogenous)
Reflux
DX Methods
There are about 4x higher osmotic pressurein the medulla leading to crenation (water sucked out). Macrophages do their job
by Phagocytosis and eating the bug. There is less cytoplasm, less lytic activity, so the white cell is not allowed to do its job.
Typical Pathway –Ascending Infection from the Lower Tract
Order of infection:
Conditions associated with infection
Obstruction
Pregnancy
Preexisting Renal Diseaes
Diabetes/impaied immunity
Hypertension
Young children both have similar incidence of UTI’s. Children poop and pee in diapers. Poor diaper removal, child care, can
lead to a UTI. The next layer of sourcing, 2-4 years of age shows spikes with UTI’s.
Antibiotic course should be about 3-10 days. The rates of recidivism is virtually identical for 10 day course and 3 day course
of AB therapy. The risk of 3 days is no greater than 10 day therapy of AB’s. 1 day AB therapy for UTI is not recommended,
because of high relapse rate.
You may have to teach your kids to wipe front to back. Other home remedies include cranberry juice (10%), drinking more
water to flush the system.
Cystitis
Can be a painful, acute abdominal presentation that often leads your differential thinking to obstruction of GI and/or
appendicitis.
Therapies
Antiobiotic Therapy
Hydration: Superficial organisms, so increasing frequcney of urination removes part of the biofilm layer to remove bugs.
Cranberry Juice: A good agent, particularly cranberry extract. It needs to be at least 10% cranberry juice by volume. That
appears to be the minimum effectiveness. Extreme pH irritates the mucosal tissue. This is an organism that attahces to the
tissue, so etreme pH (high or low) are the irritants. The juice is not toxic to the bugs, but it does decrease the bugs ability to
attach. It does not affect the organism’s survival, but makes it difficult for the organism to attach. Water and cranberry juice
creates polyuria, where the patient sheds the biofilm. This allows the immune system to better to its job against smaller #’s of
invaders.
Acidification of the urine, has no effect on colonly counts only may help with symptom management.
Reinforce Wiping Front to Back
Ureteritis
A pass through organ, not a good hsot for bacteria.
Upper UTI
Greater risk to the patient for permanent loss of function to kidney proper. The patient needs antibiotic management and even
IV antibiotic management. That is how we get enough medication into the blood to treat the patient. Often the tendency is go
for 10 days with AB treatment. This can be based on the organism and organism sensitivity. We want the highest kill with the
lowest dose.
The least common form of UTI is hematogenous spread to the cortical area of the kidney. As far as the upper the ascension
and pyelonephritis is greater risk. Older men have a greater risk because of prostate hypertrophy (incomplete prostate voiding
and irritation of the system leading to growth of bacteria). Compressing a hydraulic system, and it’ll seek release valves. Now
urine latent with organism will go up the Ureter and into the renal pelvis. This is the model of Upper UTI infection.
Obstruction --- Infection --- Spread of Disease
9/30/08
Symptoms of UTI
Bladder Infection
Frequent urge to urinate, difficulty urinating
Burning or pain during urinating
Feeling pressure or fullness
Cloudy, milky or reddish urine
Generally feeling bad, itred and shaky
E. Coli is by far the most common bug for UTI’s (over 90%). Cranberry juice affects the pilli of E. Coli. Pilli attach the bug to
the lining of the system. E. Coli is a superificial cell. E. Coli grows along the surface and does not invade deep, rather it
invades thoroughly. Cranberry juice makes it difficult to attach to the walls. Cranberry juice knocks more cells off, but does
not destroy the bug. Cranberry juice and increased water intake are physical means to help the condition.
E. Coli is a “bug factory.” The pod has a big density of viable organism. The pod is called a biofilm and can rupture. The
rupture of the pod/biofillm ruprutre and then reinfects. The process of infection/reinfection continues. UTI’s just don’t go
away. If nothing is done, we are right back where we started from.
Honeymoon Cystitis
There is a 70% reduction in the incidence of UTI with post-coidal Micturition (going to the bathroom when you are done
with sex). Some other simple solutions are water, cranberry juice, and other things. There are some patient that are sensitive
to chlorine in city water.. So drinking water will actually bother them. So to help them, use steam distilled water, without
chlorine and have them drink it or mix it in solutions like tea to impact hydration status.
Conservative Care
See the patient the following day and if not, make sure you see them by the second day. If it doesn’t get better with
conservative care by the second day, refer them out to a medical doctor.
Aggressive Care
Typically about 3 days of antibiotics are recommended
______________________________________________END OF TEST #1 MATERIAL ____________________________