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Patho - Exam 3 > Renal > Flashcards

Renal Flashcards

1
Q

UTI

A

Inflammation of the urinary epithelium following invasion and colonization by a pathogen

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2
Q

Cystitis

A

Inflammation of the bladder caused by infection by bacteria, virus, fungus, or parasites (UTI)

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3
Q

Non-Infectious Cystitis

A

Inflammation of the bladder caused by trauma, autoimmune disease, or certain medications

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4
Q

Pyelonephritis

A

Upper urinary tract infection

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5
Q

Acute Pyelonephritis

A

Acute infection of the ureter, renal pelvis, and or renal parenchyma

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6
Q

Chronic pyelonephritis

A

Persistent or recurring episodes of acute pyelonephritis

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7
Q

Common pathogens of UTI

A

E coli (80%)
Staphyloccus saprophyticus
Enterobacter
Pseudomonas, Klebsiella

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8
Q

Other factors that contribute to UTI

A 
Immobility
Urinary retention 
Taking meds that cause urinary retention (ex: Beta blockers)
Renal stones that lead to obstruction 
Catheters
Fistula
Constipation 
Sexual Intercourse
Immunocmpromised
Benign Prostatic Hyperplasia (BPH)
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9
Q

BPH (benign prostatic hyperplasia)

A

Prostate is obstructing the urethra prohibiting urine flow out of the bladder

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10
Q

Causes of Acute Pyelonephritis

A

A bacterial lower UTI (cystitis or prostatis) travels up the urinary tract from the urethra, or from bloodstream to the kidneys

  • E Coli
  • Other hospitalized infections due to: choliform, enterocci, pseudomonas, klebsiella
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11
Q

Cause of Chronic Pyelonephritis

A

High risk in patients with renal infections and some type of obstructive pathological condition

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12
Q

What is pyelonephritis the most common cause of in hospitalized patients?

A

Sepsis due to use of urinary catheters

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13
Q

Normal UTI Symptoms

A

LUTS = lower urinary tract symptoms

-Frequency, dysuria, urgency, and lower abdominal and or suprapubic pain

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14
Q

Elderly patients show what kind of manifestations with a UTI?

A

Delirium, acting out

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15
Q

Acute Pyelonephritis Clinical Manifestations

A

Rapid onset of a fever, chills, malaise, and flank pain (may be different in elderly)

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16
Q

Chronic Pyelonephritis Manifestations

A

Loss of tubular function and ability to concentrate urine which can lead to polyuria, nocturia, proteinuria, end stage renal failure in 10-20% of cases

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17
Q

UTI Treatment

A 
Antimicrobial therapy 
Increased fluid intake 
Avoidance of bladder irritants
Consistent hydration 
Cranberry capsules
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18
Q

Acute pyelonephrtis treatment

A

Antibiotics (generally resolves within 10-14 days)

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19
Q

Renal Calculi are aka

A

Kidney stones

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20
Q

What are stones?

A

Masses of crystals, protein, or other substances that form within and may obstruct the urinary tract

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21
Q

Types of Stones

A

High Urine Alkalinity Stones:
-Calcium Oxalate or Calcium Photosphate (majority)
-Struvite = magnesium stones with ammonium and phosphate (more common in women than men)
High Urine Acidity stones:
-Uric Acid stones (common in pts with gout)
-Cystinuric stones (genetic disorder)

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22
Q

Most common forms of stones

A

Calcium Oxalate and Calcium Phosphate

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23
Q

Which type of stone is a genetic disorder?

A

Cystinuric stones

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24
Q

Which type of stone is seen in patients with gout?

A

Struvite stones

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25
Q

Which stones contains lots of magnesium?

A

Sturvite stones

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26
Q

Risk Factors for Renal Calculi

A
  • Gender, race, geographic location, season, fluid intake, occupation
  • High dietary intake of protein, sodium, refined sugars, fructose (especially high fructose corn syrup), grapefruit, apple juice
  • Urinary stasis/retnetion
  • Dehydration
  • Immobility

-Crohn’s disease

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27
Q

What disease is Renal Calculi common in, and why?

A

Crohn’s Disease

-High levels of oxylate and malabsorption of magnesium leads to stones

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28
Q

Pathophysiology of Renal Calculi

A

Requires a supersaturated urine and an environment that allows the stone to grow

  • Precipitation of a salt from liquid to solid state
  • Growth through crystalization or aggregation
  • High urine acidity, alkalinity, drugs (ex: Triamteren, acetazolamide) all contribute to stone formation
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29
Q

Clinical Manifestations of Renal Calculi

A
  • Flank Pain
  • Stones that form in the kidney moves into the ureter and tend to lodge where the ureter bends or changes shape
  • Pain often worsened by hydration
  • Nausea, vomiting
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30
Q

What happens when a stone occludes a ureter?

A

Ureter dilates, creating a hydroureter which can also cause hydronephrosis (= fluid buildup in the kidney)

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31
Q

Renal Calculi is a risk for…

A

Hydronephrosis = fluid buildup into the kidney from the hydroureter
Pyelonephritis = kidney infection
Acute Renal Failure (ARF) = due to ostruction

32
Q

Diagnostics for Renal Calculi

A 
Urinalysis
Kidney, Ureter, Bladder (KUB) x ray 
-Intravenous Pyelogram (IVP) uses contrast to visualize an obstructions 
-Abdominal CT scan
-Stone analysis
33
Q

Treatment Goal for Renal Calculi

A

Remove stones and prevent formation of new stones

34
Q

Glomerulonephritis

A

Inflammation of glomeruli or small vessels of the kidney usually affecting both kidneys

35
Q

Glomeruli

A

Filtering unit of the kidney

36
Q

Conditions that can lead to Glomerulonephritis

A

Lupis (autoimmune)

Diabetic nephropathy

37
Q

Most forms of Glomerulonephritis appear with collection of what?

A

Most forms appear with collection of immune complexes in glomeruli made up of antigens and antibodies

  • Antigen can be a part of a normal kidney tissue or dissolved in a body fluid (blood)
  • Bacteria and viruses are also antigens
  • Presence of anti-streptococcal (ASO) antibodies indicate post-streptococcal GN
38
Q

What is Glomerulonephritis caused by?

A

Exposure to bacteria, viruses, drugs, and other toxins trigger glomerular injury

39
Q

How does the formation of antibody complex cause Glomerulonephritis?

A

Formation of antigen-antibody complex activate complement system which triggers inflammatory response in the glomeruli. This increases capillary permeability, causing leakage of some protein and large numbers of erythrocytes.

40
Q

Manifestations of Glomerulonephritis

A
  • Dark cloudy urine from protein molecules and RBC
  • Facial and preorbital edema initially (followed by general edema)
  • Elevated BP due to increased renin secretion and decreased GFR
  • Flank or back pain caused by the edema and stretching of renal capsule
  • General inflammation
  • Decreased urine output
41
Q

When does the onset of Glomerulonephritis begin?

A

10 days from time of the infection

42
Q

What is a common source of Glomerulonephirtis, particularly in men?

A

Common from upper respiratory strep infections

43
Q

Polycystic Kidney Disease

A

Growth of fluid filled cysts bilaterally in the kidneys

44
Q

Categories of PKD

A

Genetic Autosomal dominant
Genetic Autosomal recessive
Acquired

45
Q

Factors of PKD

A
  • Decreased renal blood flow - decreased GFR
  • Tubular damage increases sodium delivery to macula densa causing tubular obstruction and back lead of filtrate - decreased GFR
  • Glomerular damage - decreased GFR
46
Q

Clinical Manifestations of PKD

A
  • Enlarged kidneys
  • HTN
  • Flank pain
  • Altered fluid and electrolyte balance
  • Renal calculi (diverticular disease)
  • UTI
  • Functional tissue replaced
  • Reduced perfusion
  • Additional organ involvement (liver and pancreatic cysts, CVD, cerebral aneurysms)
47
Q

Diagnostics of PKD

A

Family history (it’s a genetic disorder!)

  • Genetic testing
  • HTN
  • Imaging to see presence of 3 or more kidney cysts on ultrasound
  • Lab confirmation of renal failure (GFR, BUN, creatinine)
48
Q

Treatment of PKD - Symptomatic Care

A

Pain control
Treat infection if present
BP control

49
Q

Treatment of PKD - Promotion of renal function through …

A

Dialysis needed for life until a kidney transplant is available

  • 3 to 4 hours sessions 3 times a week
  • Very life altering

Renal Transplant
Supportive care during end-stage renal disease

50
Q

(AKI) Acute Kidney Injury

A

Rapid decrease in kidney function leading to the collection of metabolic wastes in the body

51
Q

Types of AKI

A

Prerenal, intrarenal, postrenal

52
Q

Prerenal AKI

A

Reduced blood flow to the kidney

Ex) hypovolemic shock

53
Q

Intrarenal AKI

A

Damage to the glomeruli, interstitial tissue, tubules

-Can be caused by infections such as pyelonephritis, GN

54
Q

Postrenal AKI

A

Obstruction to renal flow

-Can be caused by stones, BPH

55
Q

Possible causes of AKI

A
  • Reduced renal blood flow (poor perfusion)
  • Toxins
  • Infections
  • Tubular Ischemia
  • UTI
56
Q

Phases of AKI

A

Onset
Oliguric
Diuretic
Recovery

57
Q

When is kidney dysfunction indicated?

A

When BUN and creatinine levels rise and the ratio between the two maintains constant

58
Q

What stops glomerular filtration in AKI?

A

When pressure in the kidney tubules or intrarenal pressure exceeds glomerular pressure, glomerular filtrations stops, allowing nitrogen based wastes to collect in the blood

59
Q

How do the kidneys compensate during shock/problems that cause acute reduction in blood flow?

A

Constricts renal blood vessels through activating RAAS and production of ADH

60
Q

How does urine volume change in AKI?

A

Urine volume is reduced to

61
Q

Azotemia

A

Buildup and retention of nitrogenous wastes in the blood

62
Q

Is AKI reversible?

A

Yes with prompt intervention

63
Q

Interventions/treatments for AKI

A

Correct blood volume
Increase BP
Improve cardiac output

64
Q

CKD

A

Progressive irreversible disorder of kidney function that occurs when the kidney is no longer able to effectively maintain homeostasis and remove wastes

GFR is effective until 3/4 of kidney function is lost

65
Q

When kidney function is too poor to sustain life, you’re at…

A

End stage kidney disease

66
Q

Primary causes of CKD

A
  • Acute renal failure that was not treated properly
  • DM
  • HTN
  • Systemic Lupus Erythematous Polycystic Kidney Disease
67
Q

Kidney changes in CKD

A

Abnormal urine production

Poor water excretion

68
Q

Metabolic changes in CKD

A

Urea and creatinine excretion are disrupted by kidney dysfunction

69
Q

Sodium changes in CKD

A

Early: Risk for hyponatremia due to fewer healthy nephrons to reabsorb sodium
Later: Risk for hypernatremia due to the reduced excretion of sodium as urine production decreases

70
Q

Potassium Changes in CKD

A

Hyperkalemia

71
Q

Acid-Base Imbalance in CKD

A

Early: blood pH changes little with the remaining nephrons increasing their acid secretion
Later: as more nephrons are lost, acid excretion reduces, resulting in metabolic acidosis

72
Q

Cardiac Changes in CKD

A
  • HTN from fluid and sodium overload, dysfunction of RAAS
  • Hyperlipidemia - changes in fat metabolism that increase triglycerides, total cholesterol, and LDL (increases risk for coronary artery disease)
  • Heart failure - Increased workload of heart due to anemia, HTN, fluid overload, and coronary artery disease
  • Pericarditis - inflammation of pericardial sac due to infection or uremic toxins
73
Q

What happens if pericarditis is not treated?

A

It can lead to percardial effusion and cardiac tamponade, which results in dysrhythmias, death.

74
Q

What is the leading cause of death with end stage kidney disease?

75
Q

Why does anemia occur with CKD?

A

Kidneys produce erythropoietin - but if there are decreased levels of erythropoietin, there will be decreased levels of rbc production an decrease rbc survival due to uremia, iron and folic acid deficiency, and increased bleeding due to impaired platelet function

76
Q

GI changes in CKD

A
  • Uremia
  • Uremic cardiomyopathy
  • Ammonia generated in CKD causes halitosis (bad breath) or stomatitis (stomach inflammation)
  • Anorexia, nausea, vomiting, hiccups
  • Peptic Ulcer disease
  • Uremic colitis
  • Stomach, small or large intestine erosions of blood vessels – can lead to hemorrhagic shock from sever GI bleeding

Patho - Exam 3 (4 decks)

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