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NUR 326 (Patho 1) > Renal Exam 2 > Flashcards

Renal Exam 2 Flashcards

1
Q

Pyelonephritis

A

Upper UTI or Kidney Infection

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2
Q

Pyelonephritis is

A

Inflammation of one or both kidneys

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3
Q

Pyelonephritis Etology

A

Start as lower uti and goes up the tract. E Coli is most common pathogen

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4
Q

Pyelonephritis risk factors

A

Pregnancy

Recurrent lower utis

Antibiotic resistant strain

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5
Q

Pyelonephritis can lead to

A

permanent kidney damage with abscess and necrosis

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6
Q

Pyelonephritis: Clinical Manifestations

A

Sudden onset:
-Fever
-Chills
-CVA tenderness

Systemic infection = fevers and chills vs those with lower UTI

Hematuria may occur

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7
Q

Pyelonephritis: Treatment

A

Antibiotics

Bactrim - Ciprofloxacin - Nitrofurantoin

Review bactrim and ciprofloxacin for exam

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8
Q

Pyelonephritis complications

A

Urosepsis most likely in elderly and pregnant

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9
Q

Where can you have a urinary obstruction

A

Anywhere along the tract

-Renal pelvis
-Ureter
-Bladder or pelvis

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10
Q

Common Renal Obstruction: Renal Pelvis

A

Renal calculi

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11
Q

Common Renal Obstruction: Ureter

A

Renal calculi
Pregnancy
Tumors

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12
Q

Common Renal Obstruction: Bladder and Urethra

A

Bladder cancer
Neurogenic bladder
Prostatic hyperplasia
Prostate cancer
Urethral strictures

Kidney stones not as common

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13
Q

Complications of Obstruciton

A

Stasis of urine flow. Infections is much likely

Back up pressure
-Hydroureter
-Hydronephrosis
-Post Renal acute kidney injury

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14
Q

Hydronphrosis

A

Back of fluid into kidney

Surgical intervention

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15
Q

Hydroureter

A

Back of fluid in the ureter

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16
Q

Acute Obstruction: Clinical Manifestations

A

Depends on site

Obstruction in renal pelvis does not cause as much pain or difficulty urinating because there is room for the stone there.

Once the stone leave renal area and into the ureter the place is much small and the pain is going to be very severe

Pain comes in waves as the ureter tries to move the stone out

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17
Q

Nephrolithiasis

A

Renal calculi or kidney stones

Clumps of crystals in the urinary tract

Can be small or the size of gold ball

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18
Q

Nephrolithiasis: Pathogenesis

A

Urine is a solution of solvent (water) and solutes (particles)

Super saturation with a solute and crystals begin forming in the nephron of the kidney

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19
Q

Crystal Formation is enhanced by

A

Ph changes: UTI

Excessive concentration of insoluble salts in the urine. (Dehydration - Bone disease - Gout - Renal disease)

Urinary stasis - Immobility/sedentary lifestyle

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20
Q

Nephrolithiasis: Risk Factors

A

-Men

-Age 20-30’s

-White

-Family history

-Congenital defect (long urine in system)

-Weather? Hot weather = dehydration

-Obesity

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21
Q

Types of kidney stones

A

Calcium oxalate or calcium phosphate

Struvite (staghorn)

Uric acid

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22
Q

Types of stones: Calcium oxalate / calcium phosphate RF’s

A

Family history
Idiopathic

Diet
Increase Calcemia
Increase Oxaluria

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23
Q

Types of stones: Struvite Staghorn

A

Risk factor = UTI

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24
Q

Types of stones: Uric Acid

A

Risk factor = Gout

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25
Q

Nephrolithiasis: Clinical Manifestations

A

Renal Colic: Pain in the flank area that radiates from lower abd and groin. Spazzy. Sharp from stone scraping

26
Q

Accompanying symptoms of neprholithiasis

A

NV
Dysuria
Chills and fever with infection
Hematuria
Foul smelling urine
Diaphoresis

27
Q

Nephrolithiasis: Pharmacotherapy

A

Morphine or NSAIDS

IV fluids

28
Q

Preventive Med for Calcium Stones

A

thiazide diuretics

29
Q

Preventive meds for struite stones

A

antibiotics

30
Q

Preventive meds for urate stones

A

allopurinol

31
Q

Urologic Cancers

A

Kidney cancer

Bladder cancer

32
Q

Urologic Cancer: Kidney

A

Renal cell carcinoma 85% of kidney cancers

33
Q

Kidney cancer: Risk factors

A

Smoking #1

Obesity
Age - Older
Male - Men
Genetics

34
Q

Renal Cell Carcinoma: Clinical Manifestations

A

-No early manifestations

Late manifestations: CVA tenderness - Hematuria - Possible palpable abdominal mass

35
Q

Metastasis of Renal Cell Carcinoma

A

Occurs to the bone or lungs

36
Q

Renal cell carcinoma is often

A

Resistant to chemo so you have to have surgery

37
Q

Bladder Cancer

A

-Urotherlial carcinoma (>90)

38
Q

Bladder Cancer: Risk facotrs

A

Smoking #1

Male

Occupations with exposure to toxin RUBBER OR PAINT TOXINS

Low fluid intake toxins sit in the bladder

39
Q

Bladder Cancer: Clinical Manifestations and Treatment

Early and Late

A

Early = Hematuria

Later:
-Frequency
-Urgency
-Dysuria

40
Q

Bladder cancer: Treatment

A

Stage 1 = Intravesical chemo

Advanced stage = systemic chemo

41
Q

Glomerular Disease

A

Glomerulonephritis

Nephrotic Syndrome

42
Q

Glomerulonephritis

A

A variety of conditions that cause inflammation of the glomeruli

Primarily and IMMUNE process

43
Q

Glomerulitis: Where does the damage occur

A

In the glomerulus: Delicate network of arterioles within the bowman’s capsule

In the tubules: Massive consumers of oxygen

44
Q

The Glomerulus: 3 Capillary membranes

A
  1. Endothelium
  2. Basement membrane (a lot of issues occur here)
  3. Podocytes (special epithelia cells) (start of urine)
45
Q

Type II Hypersensitivity Reaction

A

Reactions occur on the cell surface and results in direct cell death or malfunction

Direct cell death

46
Q

Type III Hypersenstivity reaction

A

Immune complexes are deposited into tissues and the resulting inflammation destroys the tissues

Inflammation destroys the tissues by becoming deposited and becoming inflamed

47
Q

Glomerulonephritis: Etiology 2 types of injury

A
  1. Antibodies attach to antigens of the glomerular basement membrane (Anti-GBM antibodies) - 5% = Type II reaction
  2. Antibodies react with circulating antigens and are deposited as immune complexes in the GBM - 90% = Type III reaction
48
Q

Acute Glomerulonephritis: Onset and Symptoms

A

-Abrupt HARP

-Hematuria
-Azotemia (to much waste in blood)
-Retention (sodium and water) (Edema and In BP)
-Proteinuria

49
Q

Acute Glomerulonephritis Triggers

A

Post infections

Primary Disease

Multisystem Disease

50
Q

Acute Glomerulonephritis Triggers: Post infections

A

-Postreptococcal infections

-Nonstreptococcal infection (bacterial viral parasitic)

51
Q

Acute Glomerulonephritis Triggers: Primary disease

A

Berger disease

Antibodi IGA builds up in the kidney

52
Q

Acute Glomerulonephritis Triggers: Multisystem Disease

A

-Goodpasture’s syndrome, systemic lupus erythematosus (SLE), vasculitis

These can attack the kidneys

53
Q

Anti-GBM Antibodies

A

These are similar to the ones the lungs so patients typically have respiratory problems and cough up blood

Goodpasture syndrome

54
Q

Acute Glomerulonephritis: Pathogenesis

A
  1. Trigger
  2. Immune complexes form
  3. Complement activated
  4. Release of mediators
  5. Tissue injury
  6. HARP
55
Q

Chronic Glomerulonephritis

A

-Long term inflammation = scar tissue

Scar tissues can not filter correctly and as the build up scar tissue occurs the kidneys are able to maintain less

56
Q

Nephrotic Syndrome

A

The glomerulus is too permeable to plasma proteins

Eliminations of 3 grams of protein per day

57
Q

Nephrotic Syndrome: Etiology

A

-Glomerulonephritis

-Diabetes mellitus

58
Q

Nephrotic Syndrome: Pathogenesis

A

Increased glomerular permeability

Proteinuria

Hypoalbuminemia (start to 3rd space)

59
Q

Nephrotic Syndrome: Clinical Manifestations

A

-Edema

-Hyper tension

Liver problems:
-Hyperlipidemia
-Hypercoagulation
-Loss of antithrombin and plasminogen

60
Q

Glomerulopathy: Diabetes and HTN complications

A

DM:
-Major complications
-Gross thickening of the GBM
-Ultimately leading to –> ESRD

HTN:
-Decrease renal perfusion –> sclerotic glomerular changes

61
Q

Glomerulopathy: Manifestations

A

Hematuria

Oliguria

Fluid retention

Increase BUN/Cr ratios

Proteinuria

Low albumin (hypoproteinemia)

NUR 326 (Patho 1) (62 decks)

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