Renal Disorders Flashcards

1
Q

Pyelonephritis: Upper UTI, Kidney Infection

A

– Inflammation of the kidneys

– Etiology: Ascending infection or bloodstream infection
– Risk factors: pregnancy, recurrent lower UTIs, antibiotic resistant strain
– Inflammatory response → kidney tissue DAMAGE
– Abscesses and necrosis can develop impairing renal
function

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2
Q

Pyelonephritis: Clinical Manifestations

A

Sudden onset:
* Fever
* Chills
* CVA tenderness

Lower UTI symptoms (dysuria)

Hematuria may occur

Accompanying symptoms:
* N/V
* Anorexia

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3
Q

Pyelonephritis: Treatment

A

Antibiotics: trimethoprim/sulfamethoxazole [Bactrim], ciprofloxacin, nitrofurantoin [Macrobid]

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4
Q

Pyelonephritis: Complications

A

Complication: urosepsis
– More likely in elderly
– Severe systemic response
– High mortality rates

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5
Q

Nephrolithiasis/renal obstruction Locations

A

– Renal Pelvis
– Ureter
– Bladder or Pelvis

– Blockages in any point of the
‘plumbing’ system prevents the flow
of the liquid causing the system to
back up

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6
Q

Obstruction Causes

A

Renal Pelvis: Renal calculi (stones)

Ureter: Renal calculi, preganancy, tumors

Bladder and Urethra: Bladder cancer, nerogenic bladder, prostatic hyperplasia, prostate cancer, urethral strictures

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7
Q

Complication of obstruction

A

Stasis of urine flow

Back-up presssure
-Hydroureter
-Hydronephrosis
-Postrenal acute kidney injury

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8
Q

Manifestations of Acute Obstruction

A

Depend on the
* Site
* Cause (ex., kidney stones, prostate problems)
* Speed of onset

Which factor primarily
determines severity of pain?

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9
Q

Nephrolithiasis
Definition, size, shape

A

Definition: Renal calculi or “kidney stones”
-clumps of crystals in the urinary tract
-most common cause of renal obstruction

Size: small as a grain of sand

Shape: may be smooth or jagged

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10
Q

Nephrolithiasis: Pathogenesis

A

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

Problem: Super-saturation with a solute
– Crystals begin forming in the NEPHRON

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11
Q

Crystal formation is enhanced by:

A

– PH changes: example: UTI
– Excessive concentration of insoluble salts in the urine (dehydration, bone disease, gout, renal disease)
– Urinary Stasis - immobility/sedentary lifestyle

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12
Q

Nephrolithiasis: Risk Factors

A

– Sex: Men (for now)
– Age: 20s – 30s
– Race: white
– Family history
– Congenital defect
– Weather?
– Obesity

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13
Q

Types of kidney stones

A

-Calcium oxalate
-Calcium phosphate
-Struvite (staghorns)
-Uric acid

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14
Q

Calcium oxalates/Calcium phosphate kidney stone
-Incidence and specific risks

A

Incidence: 70-80%

Specific risks: family history, idiopathic
-High calcemia
-High oxaluria

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15
Q

Struvite kidney stone
-Incidence and specific risks

A

Incidence: 15%

Specific risks: Urinanry tract infection

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16
Q

Uric acid kidney stone
-Incidence and specific risks

A

Incidence: 7%

Specific risks: gout

17
Q

Nephrolithiasis: Clinical Manifestations (Pain)

A

Pain of Acute Renal Colic:
– location – “flank”
– radiation – “lower abd and groin”
– spasms – “colicky” last 20-60 minutes
– intermittent - ”ureter spasms”
– sharp - “calculi scrape the ureter wall”

18
Q

Nephrolithiasis: Pharmacotherapy

A

Acute Pain:
-Morphine
-IV fluids

Preventive meds:
* Calcium = thiazide diuretics
* Struvite = antibiotics
* Urate = allopurinol (covered in gout lecture)

19
Q

Nephrolithiasis: Clinical Manifestations (symptoms)

A

Accompanying symptoms:
– N/V
– Dysuria
– Chills, Fever (ONLY if infection is present)
– Hematuria
– Foul smelling urine
– Diaphoresis

20
Q

Urologic Cancers: Kidney
-Risk factors

A

Risk factors:
– Smoking
– Obesity
– Age
– Male
– Genetics

– Prognosis depends on metastasis
-Renal Cell Carcinoma (85%)

21
Q

Renal Cell Carcinoma: Clinical manifestations &
Treatment

A

Early manifestations: none

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

Metastasis usually occurs to bone or lung

Usually resistant to chemo but surgery to remove kidney likely

22
Q

Urologic Cancers: Bladder

A

– Risk factors:
– Smoking*
– Male
– Occupations with exposure to toxins
– Low fluid intake

Fourth most common cancer in men
Urothelial carcinoma (>90%)

23
Q

Bladder Cancer: Clinical Manifestations & Treatment

A

Early symptoms:
– Hematuria

Later symptoms:
– Frequency
– Urgency
– Dysuria

Chemotherapy (depends on the stage!)
– Stage 1 = Intravesical chemo
– Advanced stages = Systemic chemo

24
Q

BCG Vaccine: Intravesical Therapy
Indication and MOA

A

For early stage bladder cancer
– Given weekly for 6-12 weeks
– MOA: stimulates inflammatory response in the bladder
(goal is for immune system to recognize cancerous cells
and attack)

25
Q

BCG Vaccine: Intravesical Therapy
Adverse Effects and Patient Education

A

Adverse effects: bladder irritation, systemic infection

– Patient instructions:
1. Empty bladder
2. Instill BCG vaccine into the bladder [dwell time 2
hours]
3. Change position q 15 minutes
– Disinfect urine for 6 hours post treatment; watch for
infection

26
Q

Glomerulonephritis: Definition

A

Definition: A variety of conditions that cause inflammation of glomeruli

Can be focal or diffuse

3rd leading cause of kidney failure in the U.S.

Primarily an IMMUNE process

27
Q

Glomerulonephritis: Where does the damage occur?

A

Glomerulus
– Delicate network of arterioles within the Bowman’s capsule

Tubules
– Massive consumer of oxygen

28
Q

3 capillary membrane layers of the glomerulus

A
  1. Endothelium
  2. Basement membrane
  3. Podocytes (special epithelial cells)
29
Q

Type II vs. Type III

A

Type II and Type III both have immune complexes, but they are different because:

– Type II- reactions occur on the cell surface and result in direct cell death or malfunction

– Type III- immune complexes are deposited into tissues and the resulting inflammation destroys the tissue

30
Q

Etiology of Glomerulonephritis

A

Two types of injury:
1. Antibodies attach to antigens of the glomerular basement membrane (“anti-GBM antibodies”) - 5%
2. Antibodies react with circulating antigens and are deposited as immune complexes in the GBM – 90%

BOTH forms have this in common:
– Accumulation of antigens, antibodies, and complement
– Complement activation results in tissue injury

31
Q

Acute Glomerulonephritis
-Manifestations

A

Abrupt sudden onset
Manifestations: HARP
–(H)ematuria
-(A)zotemia
–(R)etention: sodium & water [oliguria] (hypertension, edema)
– (P)roteinuria

32
Q

Acute Glomerulonephritis: Triggers

A

Post-Infectious
– Poststreptococcal infection
– Nonstreptococcal infection
– Bacterial, viral, parasitic

Primary Disease
– Berger disease

Multisystem Disease
– Goodpasture syndrome, systemic lupus
erythematosus (SLE), vasculitis

33
Q

Chronic Glomerulonephritis

A

– Long term inflammation of the glomerulus –> scar tissue

– Clinical Manifestations like presentation of acute
glomerulonephritis

Prognosis
– Slow progressive destruction –> ESRD

34
Q

Nephrotic Syndrome

A

Definition:
– The glomerulus is too permeable to plasma proteins
– Elimination of >3 grams of protein per day

Etiology:
– Glomerulonephritis
– Diabetes mellitus

35
Q

Nephrotic Syndrome: Pathogenesis

A
  1. Increased glomerular permeability
  2. Proteinuria
  3. Hypo-albuminemia
36
Q

Nephrotic Syndrome: Clinical Manifestations

A

Edema
Hypertension
Liver Problems
–Hyperlipidemia
–Hypercoagulation
–Loss of antithrombin III and plasminogen

37
Q

Glomerulopathy: Diabetes & Hypertension Complications

A

Diabetic Nephropathy
– Major complication
– Gross thickening of the GBM
– Ultimately leading to –> ESRD

Hypertensive Glomerular Disease
– Decreased renal perfusion –> sclerotic glomerular changes

38
Q

Glomerulopathy: Manifestations

A

Hematuria
Oliguria
Fluid retention
Increased BUN/Cr ratio
Proteinuria
Low albumin [hypoproteinemia]