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Patho - Exam 3 > Renal > Flashcards

Renal Flashcards

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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
Which stones contains lots of magnesium?
Sturvite stones
26
Risk Factors for Renal Calculi
- 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
27
What disease is Renal Calculi common in, and why?
Crohn's Disease | -High levels of oxylate and malabsorption of magnesium leads to stones
28
Pathophysiology of Renal Calculi
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
29
Clinical Manifestations of Renal Calculi
- 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
30
What happens when a stone occludes a ureter?
Ureter dilates, creating a hydroureter which can also cause hydronephrosis (= fluid buildup in the kidney)
31
Renal Calculi is a risk for...
Hydronephrosis = fluid buildup into the kidney from the hydroureter Pyelonephritis = kidney infection Acute Renal Failure (ARF) = due to ostruction
32
Diagnostics for Renal Calculi
``` Urinalysis Kidney, Ureter, Bladder (KUB) x ray -Intravenous Pyelogram (IVP) uses contrast to visualize an obstructions -Abdominal CT scan -Stone analysis ```
33
Treatment Goal for Renal Calculi
Remove stones and prevent formation of new stones
34
Glomerulonephritis
Inflammation of glomeruli or small vessels of the kidney usually affecting both kidneys
35
Glomeruli
Filtering unit of the kidney
36
Conditions that can lead to Glomerulonephritis
Lupis (autoimmune) | Diabetic nephropathy
37
Most forms of Glomerulonephritis appear with collection of what?
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
What is Glomerulonephritis caused by?
Exposure to bacteria, viruses, drugs, and other toxins trigger glomerular injury
39
How does the formation of antibody complex cause Glomerulonephritis?
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
Manifestations of Glomerulonephritis
- 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
When does the onset of Glomerulonephritis begin?
10 days from time of the infection
42
What is a common source of Glomerulonephirtis, particularly in men?
Common from upper respiratory strep infections
43
Polycystic Kidney Disease
Growth of fluid filled cysts bilaterally in the kidneys
44
Categories of PKD
Genetic Autosomal dominant Genetic Autosomal recessive Acquired
45
Factors of PKD
- 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
Clinical Manifestations of PKD
- 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
Diagnostics of PKD
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
Treatment of PKD - Symptomatic Care
Pain control Treat infection if present BP control
49
Treatment of PKD - Promotion of renal function through ...
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
(AKI) Acute Kidney Injury
Rapid decrease in kidney function leading to the collection of metabolic wastes in the body
51
Types of AKI
Prerenal, intrarenal, postrenal
52
Prerenal AKI
Reduced blood flow to the kidney | Ex) hypovolemic shock
53
Intrarenal AKI
Damage to the glomeruli, interstitial tissue, tubules | -Can be caused by infections such as pyelonephritis, GN
54
Postrenal AKI
Obstruction to renal flow | -Can be caused by stones, BPH
55
Possible causes of AKI
- Reduced renal blood flow (poor perfusion) - Toxins - Infections - Tubular Ischemia - UTI
56
Phases of AKI
Onset Oliguric Diuretic Recovery
57
When is kidney dysfunction indicated?
When BUN and creatinine levels rise and the ratio between the two maintains constant
58
What stops glomerular filtration in AKI?
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
How do the kidneys compensate during shock/problems that cause acute reduction in blood flow?
Constricts renal blood vessels through activating RAAS and production of ADH
60
How does urine volume change in AKI?
Urine volume is reduced to
61
Azotemia
Buildup and retention of nitrogenous wastes in the blood
62
Is AKI reversible?
Yes with prompt intervention
63
Interventions/treatments for AKI
Correct blood volume Increase BP Improve cardiac output
64
CKD
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
When kidney function is too poor to sustain life, you're at...
End stage kidney disease
66
Primary causes of CKD
- Acute renal failure that was not treated properly - DM - HTN - Systemic Lupus Erythematous Polycystic Kidney Disease
67
Kidney changes in CKD
Abnormal urine production | Poor water excretion
68
Metabolic changes in CKD
Urea and creatinine excretion are disrupted by kidney dysfunction
69
Sodium changes in CKD
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
Potassium Changes in CKD
Hyperkalemia
71
Acid-Base Imbalance in CKD
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
Cardiac Changes in CKD
- 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
What happens if pericarditis is not treated?
It can lead to percardial effusion and cardiac tamponade, which results in dysrhythmias, death.
74
What is the leading cause of death with end stage kidney disease?
CAD
75
Why does anemia occur with CKD?
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
GI changes in CKD
- 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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