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2012-11-14 18:23:48

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  1. Renal- GFR
    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. 
  2. renal blood flow
    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
  3. urine elimination
    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
  4. alt urinary elimination
    altered motility- not pushing urine out well (problelm with renal tubules or ureters)

    consequence: altered reabsorption an secretion and risk of obstrction
  5. acute tubular necrosis
    leads to acute renal failure

    occurs mostly bc of drugs
  6. urinary tract obstruction
    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
  7. UTO: 
    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
  8. UTO: upper obstruction
    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
  9. hydronephrosis
    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
  10. Urinaty tract obstruction- Calculi aka urinary stones
    • 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
  11. Calculi- urinary stones: patho
     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
  12. urinary 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
  13. Calculi- Type 1 stone: Calcium oxalate/ calcium phosphate
    70% of stones
  14. struvite stones
    made of magnesium ammonium phosphate

    w/ infections. makes staghorn
  15. uric acid stones
    ppl who are gouty (arthritus) and also ppl who have acidic urine
  16. cystinuric stones
    genetic disorder of AA metabolism
  17. treating UTO
    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
  18. UTO: clin manif
    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
  19. UTO: Diag crit
    urinalysis, kidney ureter, bladder x ray

    adb CT
  20. Risk factors of Renal Calculi
    hydronephrons- water in kidneys

    pyelonephritis- UTI that reached pelvis of kidney

    acute renal failure
  21. UTI
    inflammation of the urinary epithelium following the invasion and colonization of some pathogen w/in urinary tract

    risk much higher in women
  22. UTI How it happens
    • escherichia Coli- 80%
    • usually form the intestines and in women

    staph sapro and enterobacter
  23. cystitis
    • 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
  24. pyelonepritis
    UTI not treated soon enough it will move to the bladder then the kidneys and can lead to sepsis 
  25. Acute pyelonephritis
    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
  26. Chronic pyelonphitis
    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
  27. Chronic Renal Failure
    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
  28. potential clinical complications
    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
  29. end stage renal disease treatment
    • hemodialysis
    • transplant
    • med's
  30. Urinary Incontinence
    multiple types

    inability to voluntarily prevent the discharge of urine

    • causes: impaired muscl contraction
    • alt neural transmission
    • mech factors
  31. Urinary Incont: classification (4)
    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
  32. Urinary Treatment
    • bladder training
    • pelvic floor strengthening

    anticholinergic meds

  33. Polycystic Kidney disease
    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
  34. PKD- adults- Clin Man
    • UTI- bladder
    • liver, pancreatic cysts

    • cardiac valvular disease
    • cerebral aneurysms
  35. PKD- Diag Crit
    • genetic
    • imaging studies
    • extrarenal cysts
  36. PKD- treatment
    symptomatic care: pain, infection, BP control

    Promote renal function: dialysis, renal transplant

    suportive care
  37. Stool Analysis
    • Elimination patterns
    • characteristics: color, consistency, volume, shape, odor
  38. Altered Stool Elimiation
    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
  39. Altered Bowel elimination manif
    • bleeding
    • melena=tarry stool
  40. Alt Elim Diag/Treat
    • Diag- stool charact
    • treatment- underlying cause
  41. Intestinal obstruction
    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
  42. Appendicitis
    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
  43. Diverticular disease
    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
  44. Dysphagia
    • 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
  45. GERD
    • 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
  46. Hiatial Hernia
    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
  47. peptic ulcers
    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
  48. peptic ulcers complications
    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
  49. peptic ulcers: treatment
    • endocospy, barium swallow, h pylori test
    • administer antacids]]

    look for: recent wt loss/appetite, pain, heartburn, fullness, pain triggered while eating
  50. Acute peptic upcers
    hematemesis- throw up blood/melena- tarry dark stools, hematochezia- severe cases that have stool that are bright red
  51. Chronic peptic ulcers
    occult bleeding, slow, must test stool using a guic test

    greater chance in men 
  52. inflammatory bowel syndrome
    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
  53. ulcerative colitis
    • chronic imfalmm disease that cause ulceration of colonic mucosa
    • 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
  54. Crohn's Disease
    • AKA granulomatou colitis
    • idiopathic
    • affect lg and small intestines

    • anemia may result due to malabsportion of b12 and folic acid
    • cobblestone like appearance
  55. Crohn's- patho
    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
  56. Liver Disorders
    hepatitis a b c d e g

    viral hep is a systemic viral disease that primarly affects liver
  57. Hep A
    • 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

  58. Hep B
    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
  59. Hep C
    • 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
  60. Hep D
    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
  61. Hep E
    • fecal oral route
    • in developing countries

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

    good prognosis unless you are preggers
  62. Hep G
    recently discovered

    parentally and sexually transmitted
  63. Acute Hep
    • 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
  64. Liver Cirrhosis
    • 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
  65. portal HTN
    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
  66. Disorders of Gallbladder
    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
  67. Disorders of Pancreas
    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