Elimination

glomerular filtration Rate- the firltration of plasma per unit of time which is directly related to renal blood flow

the blood tests that you use to determine renal functions are serum creatinine. 

creatinine clearance clearance is how fast tocompltely remove creatinine. 

renin is released--> turns to angio 1--> turns to angio 2---> causes vasoconstriiton and stimulates aldosterone release

aldosterone is produces by adrenal cortex.  regulates water reabsorption by distal tubules.

low plasma aldosterone promotes sodium and water excretion

high aldosterone incr excretion of K+

EGFR- tells how well urine is working

produced in kidneys

stored in bladder

exreted thru urethra

altered neuro muscular funct, conseq: incont

altered perfusion- inadequate blood supply - conseq- pain, ischemia

altered patency: obsturction, consqe: dilation of structure proximal to obstrition

altered motility- not pushing urine out well (problelm with renal tubules or ureters)

consequence: altered reabsorption an secretion and risk of obstrction

leads to acute renal failure

occurs mostly bc of drugs

blockage of urin flow w/in urinary tract

can be a block in ureter or in the urethra

things that can cause blockage: cancer, kidney stones, urinary stones

obstruction can be caused by an anatomic or functional defect that leads to urinary stasis, dilates the urinary syst, incr the risk for infections and compromises urinary functions

obstrction in the upper tract: depends on location , complteness, involvement of one or both upper urinary tracts, duration, cause

if its only one side the body can counteract w/ compensatory hypertrophy of the other kidney

careful of postobstructive dieresis- after blockage removed body will become dehydrated from removing sodium so much

abnormal dilaton of the renal pelvis and calyces of one or both kidneys

caused by an obstruction of urine flow in the GI tract

total obsturction causes atrophy of the cortex

• masses of crystal protein, or other substances that form w/in and may obstruct the urinary tract
• Risk factors: M, not black, in the south, more in the summer, more fluids less chance, high sodium, calcium diet, and occupation

 super saturation of one or more salts/ substances

presence of salt/substance in high [c] than the volume able to dissolve the salt.

precipitation of the salt from liquid to solid state 

growth thru crystallization or aggregation

causes 4 types of stones

salt growth leads to stones-PAINFUL!

DEHYDRATION- INCR [C] of substances

infection- infected scarred tissue provides site for calculus development

pH- acidic or basic urine provides favorable medium

ostruction: urinary stasis allows calculus to collect and adhere

immobilization- allows calcium to be released into circ and eventually filtered by kidneys

diet: high Ca

metabolic factors: excessive intake of vit D

70% of stones

made of magnesium ammonium phosphate

w/ infections. makes staghorn

ppl who are gouty (arthritus) and also ppl who have acidic urine

genetic disorder of AA metabolism

use ultrasound to shock to break up stones

pass the stone if its smaller than 5mm

need to work on diet and hydration in the long run- get fluids!!

removed by surgery if too large

low Ca diet

pain, hematuria (stones abrade ureter), abd distension, oliguira (low output of urine), dysuria (painful urination)

• Flank pain
• hydration often makes pain worse

pain can travel to lower back to sides then to pubic region

urinalysis, kidney ureter, bladder x ray

adb CT

hydronephrons- water in kidneys

pyelonephritis- UTI that reached pelvis of kidney

acute renal failure

inflammation of the urinary epithelium following the invasion and colonization of some pathogen w/in urinary tract

risk much higher in women

• escherichia Coli- 80%
• usually form the intestines and in women

staph sapro and enterobacter

• an inflammation of bladder
• causes freq of urinaton, dyuria, urgency, and lower abd pain

prolonged infection could lead to slophing of bladder mucosa w/ ulcer formation

complitated UTI develops when there is an abmormality in the urinary sys

treathment: antimicrobial therapy, incr fluid intake, avoidance of bladder irritants, and urinary analgesics

UTI not treated soon enough it will move to the bladder then the kidneys and can lead to sepsis 

infeection of ureter, renal pelvis


becomes very severe when it gets into the kidneyscan cause shockalways treat it in children!

rapid onset of fever, chills, malaise and flank pain

sympt may be diff in elderly

treated: antibiotics

over a long time i can lead to death of tubules

persistent or recurring epidoes of acute pylinephritis

risk of chroinic pyel.. in indiv's w/ renal infections and some type of obstrution

this leads to scarring of the kidney and can lead to end stage renal disease

occurs when the kidney is no longer able to effectively maintain homeostasis and removes wastes

chronic renal disease, is a progressive loss in renal function over a period of months or years. The symptoms of worsening kidney function are non-specific, and might include feeling generally unwell and experiencing a reduced appetite.

cause: ARF, DM, HTN, glomerulonephritis


HTN: kidney: chronic damage in AfAm  higher rates

HTN and edema- due to soium/water imbalance, can lead to CHF, pulm edema, or periipherla edema

hyperkalemia- can lead to cardiac arrest, arrythmias,

uremia-high serum urea- can lead to bleeding easier

anemia- due to reduced erythropoitin production- which produce RBC

hypocalcemia- due to vit d not being activated--> cant absorb calcium 

hyperphosphatemia- high levels of phsophorus

encephalitis- confusing- like delirium- but diff bc has specific cause

• hemodialysis
• transplant
• med's

multiple types

inability to voluntarily prevent the discharge of urine

• causes: impaired muscl contraction
• alt neural transmission
• mech factors

Stress Incontin-exertional stim- cough/laugh- weak pelvic fore muscles

Urge incontin- over activy of detrusor musc- elderly!

overflow incont- exceeding bladder capacity

function incont- inability to indep toilet!- dementia or neuro disorder

• bladder training
• pelvic floor strengthening

anticholinergic meds

surgical

growth of fluid filled cysts bilaterally (both) in kidneys

• - funcitonal tissue replaced
• - reduced perfusion
• - tubule obstrution

autosomal dominant

only treat complications and attempt to prevent further disease by treating underlying conditions DM, HTN

• Stage 4- severe- start dietary restrictons on water, K+, protein, Mg
• Stage 5- end stage renal disease- req dialysis

• UTI- bladder
• liver, pancreatic cysts

• cardiac valvular disease
• cerebral aneurysms

• genetic
• imaging studies
• extrarenal cysts

symptomatic care: pain, infection, BP control

Promote renal function: dialysis, renal transplant

suportive care

• Elimination patterns
• characteristics: color, consistency, volume, shape, odor

Altered Motility:

• altered water/vitamin absorption
• altered storage time
• risk for obstruction

coneq: diahhrea/constipation

• Altered Perfusion:
• conseq: ischemia/pain

patench: tumor, impaction, conseq distention--> which mens pressure on diaphargm, from there decr respiration volume, which causes atelectasis and then causes pneumonia

• bleeding
• melena=tarry stool

• Diag- stool charact
• treatment- underlying cause

simple: obstructions due to mechanical blockage: tumor, inguinal hernia, 

hyperkalemia can be extreme and helps promot acidosis.  distention may cause ischemia which incr acidosis bc of lactic acid buildup

• functional: lack of motility (mvmt)
• common after abd surgery, NPO until pas gas (bc of anasthesia- paralytic illeus)

peritonitis- inflammation of the perioteneal cavity, if perforation happens

inflammation of the vermiform appendix

• possible causes
• obstruction, ischemia, incr intraluminal pressure, infection, ulceration

• epigastric and RLQ pain and rebound tenderness
• the most serious complication is peritonitis

gurny test to se if they have appendicitis

obstructed appendix means secretions cant flow out...incr pressure--> leads to hypoxic and mucosa ulcerates that allows microbial invasion and inflammation. Performation

too much pressure on the colon causes puches, you want to treat it with a high fiber diet so that no fecal matter goes into the pouches

most common in left sigmoid colon

diverticula- herniations of mucosa throught eh musc layers of colon wall

sympt: cramping pain, diarrhea, distention, if puch inflammed: get fever incr WBC and tenderness in LLQ

• dysfunction w/ swallowing
• a neural disorder causes this suck as stroke, dementia, muscular dystropy

esophageal: pushing down food

achalasia: loss of esophageal peristalsis and failure of hte lower esophageal sphincter to relax

functional neural or muscular disorder

• if you put in feeding tube then they will still aspirate
• primary risk is for aspiration which can lead to aspiration pneumonia and eventually impaired gas exchange, for ppl with DM- poor nutrition low blood sugar

oropharyngeal dysphagia- dysfucntion of the mouth, can be due to both neuro dis and radiaiton, parkingosns

sometimes correction w/ speech therapy

• heartburn
• reflux of chyme from stomach to esophagus
• chronic inflamm

• bc of:
• when sphincter isnt as high pressure as food in stomach then stuff flows up
• symptoms: heart burn, stress gas

• causes: alcohol, cigs, caffeine, acidic foods,
• abd pressure- preggers, obesidty
• NG tube for for than 4 days

• treatment: diet therapy w/ small meals
• antacids

can lead to barretts esophagus: metaplasia, cells look more like GI tract cells

protrusion of upper part of stomach thru diaphragm and into thorax

• due to age usually and muscle weakness of sphincter which allows prt of stomach to go up
• can cause GERD

a break or ulceration in the protective mucosal lining of the lower esophagus, stomach or duodenum (most common)

emergency if GI is bleeding

• duodenal ulcers usually develop from an H pylori infection
• can be caused by a hypersecretion of stomach acids
• use of NSAIDS
• or acid production by cig smoking

bleeding- black and tarry stools, perforation, obstruciton

freank blood stool if its in the lower sigmoid

if H pylori- acid will complicate ulcer--> penetration may happen and will go into nearby organs such as pancreas/liveer

• endocospy, barium swallow, h pylori test
• administer antacids]]

look for: recent wt loss/appetite, pain, heartburn, fullness, pain triggered while eating

hematemesis- throw up blood/melena- tarry dark stools, hematochezia- severe cases that have stool that are bright red

occult bleeding, slow, must test stool using a guic test

greater chance in men 

chronic, relapsing inflammatory bowel disorder of unknown disorder

stem from genetics, alt in epitherlia barrier funct, immune reactions , abn t cell *autoimmune: believed!

has period of remission and exacerbations

• chronic imfalmm disease that cause ulceration of colonic mucosa
• USUALLY in the SIGMOID COLON and RECTUM
• 20-40 yrs olds

• caues: infecitons, immunologive, dietary, generics,  jewish decent and white
• lupus might accompany, starts w/ small erosions

symptoms: diarrhea 10-20 times a day with bloody stool snad cramping, CARDINAL SYMPTOM: RECURRENT BLOODY DIARRHEA THAT CONTAIN MUCUS AND PUS.  usually dont throw up blood bc its in lower intestine

• Treatment: broad spectrum antibiotics w/ steroids- could also cause c diff
• use imunnosuppressive agents, or surgery,  HIGH RISK of developing colon cancer

• AKA granulomatou colitis
• idiopathic
• affect lg and small intestines

• anemia may result due to malabsportion of b12 and folic acid
• cobblestone like appearance

lymph nodes enlarge and lymph flow in submucosa is blocked

this obstruciton causes edema, mucosal ulceration, fissures

these are the skip intestings

oval patches called peyer patches (elevated lymph follicles) develop on the small intestine

fibrosis occurs on the bowel walls, causes smaller lumen (narrowing is called stenosis) and malabsorption

• neutrophils and macrophages are activated and cause inflammation that attacks the intestines
• these attacks create skip lesions (alternates every other segment of colon)
• ulcerations create longitudinal and transverse inflam fiddues that extend to lymphatics
• asceding and transverse colon

complicaitons: most common are anal fisutals from severe diarrhea

hepatitis a b c d e g

viral hep is a systemic viral disease that primarly affects liver

• can be found in feces, bile, nd sera of infected indiv
• transmitted by fecal/oral route

risk factors: crowded unsanitary conditions, food and water contamination, is the only non chornic type of hep

- Day care centers, homo's-HIV

mild sympt- good prognosis

vaccine!

transmitted thru contact w infected blood, body fluids, or contaminated needles

maternal transmission can occur if affected during tri mester

hep b vaccine prevents transmision and develop

symtp: jaundice, liver fail, cancer, liver cirrohsis

• blood borne, parenteral route, sexual, maternal-neonatal
• virus is shed in all bdoy fluids

worse w/ age-debility, chronic

• same risk factors as B
• mainly found in IV drug users and blood-blood

hep c is responsible for most cases of post transfsion hep

resulsts in chronic hep

some ppl are able to fight of primary acute phase

moderate sympt/ moderate prognosis

depends on Hep B for replicaiton

confined mostly to ppl who are exposed to blood and blood products

• parenteral route, most ppl infected w/ hep D also have hep B
• can be severe and lead to fulminant hep

prognosis is fair but worsens in chronic case

• fecal oral route
• in developing countries

highly viulent w/ common progression to fulimant hep and hepatic failure

good prognosis unless you are preggers

recently discovered

parentally and sexually transmitted

• Prodromal phase- begins 2 weeks after exposure w/ non specific sympt
• general sympt: fatigues, wt loss, temp, dark colors urine and clay colored stools

• Icteric phase- lasts 2-6 wks
• 1-2 wks after prodromal phase
• phase of actual illness
• may have symptoms of itching, abdominal pain or tenderness, indigestion, appetite loss
• jaundice lasts for 1-2 wks and indicates that damaged liver cant remove bilirubin from blood
• liver enlarged

recovery phase: improv of sympt- beings w/ resolution of jaundice and lasts 2-6 wks.  608 wks after exposure

three primary liver enymes are: AST, ALT, Alkaline phosphate

• irreversible inflamm disease
• disrupts liver function/struct

decr hep funct due to nodular and fibrotic tissues snth (fibrosis)

• cause portal HTN
• due to the HTN, clood can be shunted away from the liver, and a hypocix necrosis develops 
• acites- fluid in peritoneal cavity.  causes incr pressure in mesenteric tributaries of the portal vein.  hydrostatic pressure forces water out of these vessels and into the peritoneal cavity

end stage liver disease: reduced clotting

impaired ammonia metabolism- pts get nutty and liver cannot process ammonia, this causes delirium, allows toxins from GI tract to circulate freely in the blood.  Ammonia that reaches brain may alter the cerebral energy metabolism

impaired bilirubin metabolism- itching, jaundice

abn High BP in portal venous sust

• disorder that obstruct impede the blood flow thru andy component of the portal venous syst
• most common cause is obstruction caused by cirrhosis of the liver

• varices- distended tortuous collateral veins, particularly in lower esophagus and stomach
• rupture of one can be life threaenint hemorrhage

splenmeagaly- enlargement of spleen caused by incr in pressure in spenic vein which branches into the portal vein

usually caused by ostruciton or inflamm

risks for cholelithias are middle age, F (use of hormonal contraceptives), native america ancestry, and gallbladder, pancreas

Cholelithiasis: gallstone formation- leads to jaundice

it is an inflamm of the pancrease that is usually seen with alcoholics

it is associated w/ several other clinical disorders- caused by an injury or damage to pancreatic cells and ducts, caussing a leakage of pancr enzymes into pancr tissue

cause autodigestion of pancr tiss and leaks into blood stream and cause injury to blood vessels and organs