Renal Disorders Flashcards

(38 cards)

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
BCG Vaccine: Intravesical Therapy Adverse Effects and Patient Education
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
Glomerulonephritis: Definition
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
Glomerulonephritis: Where does the damage occur?
Glomerulus – Delicate network of arterioles within the Bowman’s capsule Tubules – Massive consumer of oxygen
28
3 capillary membrane layers of the glomerulus
1. Endothelium 2. Basement membrane 3. Podocytes (special epithelial cells)
29
Type II vs. Type III
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
Etiology of Glomerulonephritis
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
Acute Glomerulonephritis -Manifestations
Abrupt sudden onset Manifestations: HARP –(H)ematuria -(A)zotemia –(R)etention: sodium & water [oliguria] (hypertension, edema) – (P)roteinuria
32
Acute Glomerulonephritis: Triggers
Post-Infectious – Poststreptococcal infection – Nonstreptococcal infection – Bacterial, viral, parasitic Primary Disease – Berger disease Multisystem Disease – Goodpasture syndrome, systemic lupus erythematosus (SLE), vasculitis
33
Chronic Glomerulonephritis
– Long term inflammation of the glomerulus --> scar tissue – Clinical Manifestations like presentation of acute glomerulonephritis Prognosis – Slow progressive destruction --> ESRD
34
Nephrotic Syndrome
Definition: – The glomerulus is too permeable to plasma proteins – Elimination of >3 grams of protein per day Etiology: – Glomerulonephritis – Diabetes mellitus
35
Nephrotic Syndrome: Pathogenesis
1. Increased glomerular permeability 2. Proteinuria 3. Hypo-albuminemia
36
Nephrotic Syndrome: Clinical Manifestations
Edema Hypertension Liver Problems –Hyperlipidemia –Hypercoagulation –Loss of antithrombin III and plasminogen
37
Glomerulopathy: Diabetes & Hypertension Complications
Diabetic Nephropathy – Major complication – Gross thickening of the GBM – Ultimately leading to --> ESRD Hypertensive Glomerular Disease – Decreased renal perfusion --> sclerotic glomerular changes
38
Glomerulopathy: Manifestations
Hematuria Oliguria Fluid retention Increased BUN/Cr ratio Proteinuria Low albumin [hypoproteinemia]