Urinary System Flashcards
(125 cards)
1
Q
What does the kidney excrete?
A
- urea (end product of protein metabolism)
- uric acid (end product of purine and pyrimidine metabolism)
2
Q
What does the kidney regulate?
A
- electrolytes and minerals (Na, K, Ca, P)
- blood pressure
3
Q
What does the kidney secrete?
A
- erythropoietin
- active form of vitamin D
4
Q
The kidney eliminates ______, conserves _____, and maintains ______
A
- solutes
- protein
- pH
5
Q
What are the four main parts of the kidney affected by disease? What is each part most often affected by?
A
- Glomeruli: immunologic diseases
- Tubules: often affected by toxic/infectious agents
- Interstitium: often affected by toxic/infectious agents
- Blood vessels
6
Q
What are interdependent parts in relation to the kidney?
A
- effects on one often effect all the others.
- Chronic renal diseases eventually tend to damage all 4 parts which can lead to end stage kidney disease.
7
Q
What are important components of the glomerulus?
A
- Bowman’s space
- fenestrated endothelium (70-100nm space)
- glomerular basement membrane
- Podocytes
- mesangial cells support
8
Q
What is bowman’s space?
A
(urinary space)
lined by parietal epithelium on outside and visceral epithelium (podocytes) on the inside
9
Q
What is the Glomerular basement membrane (GBM) made of?
A
mostly made of Type IV collagen
10
Q
What are podocytes separated by?
A
20-30nm filtrations slits, bridged by a slit diaphragm made of nephrin
11
Q
In regards to kidney filtration, it is highly permeable to what? It is impermeable to what?
A
Highly permeable:
- water
- small
Impermeable
- large molecules/proteins
12
Q
What does the filtration slit diaphragm do?
A
- prevents backflow of water
- normally a diffusion barrier for proteins (loss leads to protein leakage = nephrotic syndrome)
13
Q
What are key clinical changes in renal disease?
A
- azotemia
- uremia
14
Q
What is azotemia?
A
↑ blood urea nitrogen (BUN) and creatinine, often due to ↓ glomerular filtration rate (GFR)
15
Q
What is uremia?
A
progression of azotemia to clinical level with failure of renal excretory function and systemic problems
16
Q
What are secondary effects of uremia?
A
► GI - gastroenteritis
► Neuromuscular - peripheral neuropathy
► Cardiovascular - pericarditis
► Oral - severe ulcers
17
Q
What is Glomerulonephritis
A
There is inflammation, mesangial and/or basement membrane thickening which causes barrier dysfunction.
18
Q
What are the 2 major clinical presentations of Glomerulonephritis
A
–nephrotic syndrome
–nephritic syndrome
19
Q
What is the pathogenesis of nephrotic syndrome?
A
Alteration of glomerular capillary walls causing permeability to plasma proteins
20
Q
What are some clinical results of nephrotic syndrome?
A
- Massive proteinuria (≥3.5gm/day)
- Hypoalbuminemia (plasma albumin <3gm/dL
- Generalized edema
- Hyperlipidemia and lipiduria
21
Q
In nephrotic syndrome, what happens when there is glomerular capillary leakage of albumin?
A
It leads to hypoalbuminemia → hyperlipidemia or anasacra
22
Q
In nephrotic syndrome, what happens when there is glomerular capillary leakage of water and sodium?
A
Leads to ADH and aldosterone production → water and Na retention → anasarca
23
Q
In nephrotic syndrome, what happens when there is glomerular capillary leakage of immunoglobulin or complement?
A
leads to staph infection and pneumonia
24
Q
In nephrotic syndrome, what happens when there is glomerular capillary leakage of anticoagulants?
A
Leads to hypercoagulability → thrombosis and thromboembolism
25
Understand what can happen after glomerular capillary leakage in nephrotic syndrome
(See chart on slide 17)
26
What is the pathogenesis of nephritic syndrome?
Inflammatory (leukocytic) reaction injures glomerular capillaries, allows escape of RBCs into urine and leads to ↓GFR
27
What are signs and symptoms of nephritic syndrome?
- Hematuria with dysmorphic RBCs
- ↓GFR, oliguria (↓urination), and azotemia (↑BUN)
- Hypertension- due to renin release
- Mild proteinuria/edema: not as severe as nephrotic syndrome
28
Glomerulonephritis causes are most often ________
- immune-mediated
(antibody or immunocomplex formation)
29
What causes primary glomerulonephritis?
(kidney is only or predominant organ): Many won’t discuss
- Post-streptococcal glomerulonephritis: nephritic syndrome
- Acute postinfectious glomerulonephritis
30
What causes secondary glomerulonephritis?
(systemic disease leads to glomerular damage)
- hypertension
- diabetes: nephrotic syn.
- amyloidosis: nephrotic syn.
- lupus erythematosus: nephrotic or nephritic syn.
- Goodpasture sx
- granulomatosis with polyangiitis (GPA)
31
What is Post-streptococcal GN
- antibody bound to strep. proteins (immune complexes) causes proliferation of glomerular cells and activates complement which leads to infiltration of leukocytes (especially neutrophils)
32
In Post-streptococcal GN, you may have nephritic syndrome with gross ______ (smoky brown)
hematuria (urine in blood)
33
In post-streptococcal GN, what is the outcome for kids? Adults?
-Most kids recover completely
-In adults, 15-50% develop end-stage renal disease over years to decades
34
What is the Glomerulonephritis Immune Injury mechanism
► Deposition of circulating antigen/antibody complexes deposited in the glomerulus (type III hypersensitivity)
► Antibodies binding to glomerular antigens or molecules planted in the glomerulus (type II hypersensitivity)
35
What are examples of the injury mechanism:
deposition of circulating antigen/antibody complexes deposited in the glomerulus (type III hypersensitivity)
- Lupus
- Poststreptococcal
36
What are examples of the injury mechanism:
Antibodies binding to glomerular antigens or molecules planted in the glomerulus (type II hypersensitivity)
- Goodpasture sx: kidney and lung lesions
37
In Glomerulonephritis immune injury mechanism, Antigen/Antibody complexes (circulating or in-situ) activate what?
- complement
38
What happens when complement is activated in the immune injury mechanism of GN?
- C5a → recruits neutrophils and MACs
- also stimulates TGF-β production by podocytes → increased synthesis of extracellular matrix → GBM thickening
39
What do the neutrophiles release in the immune injury mechanism of GN? What is the result of each?
- Proteases → GBM degradation
- Free radicals → cell damage
- Arachidonic acid metabolites → ↓GFR
40
What is the end result of immune injury mechanism of GN?
Glomerular damage (whether to the endothelium, basement membrane or podocytes) → loss of barrier function → proteinuria and sometimes ↓GFR
41
How do you diagnose Glomerulonephritis
► Urinalysis - nephrotic syn., nephritic syn. or other
► Serology (blooddraw) - circulating autoantibodies
► Renal Biopsies (light microscopy, (immuno)fluorescence microscopy (no deposits, linear or granular), electron microscopy rarely))
42
What is Direct immunofluorescence (DIF) testing?
tests patient tissue directly for presence of autoantibodies
43
What is Indirect immunofluorescence (IIF)
- tests patient’s blood for presence of autoantibodies in: HEp-2 cell lines, Specific tissues, & Granulocytes
44
What are HEp-2 cell lines in indirect immunofluorescence
useful for wide range of antinuclear antibodies (ANA) and cytoplasmic components
45
What are Specific tissues in indirect immunofluorescence?
(e.g. skin, oral epithelium)- use a similar animal epithelium (i.e. monkey/rat) as a substrate
46
What are granulocytes in indirect immunofluorescence?
ANCA = anti-neutrophil cytoplasmic antibodies.
47
What are the different Indirect Immunofluorescence ANA Staining Patterns
Negative, nuclear, cytoplasmic, mitotic
48
What are the different Indirect Immunofluorescence antineutrophil cytoplasmic antibodies (ANCA) Staining Patterns
ANCA primarily involves antibodies that display perinuclear (pANCA) or cytoplasmic (cANCA) staining
49
What is Glomerular Injury, Non-immune-mediated
- Mutations in slit diaphragm (e.g. nephrin)
- Nephron Loss (due to any disease)
50
How does nephron loss cause non immune mediated glomerular injury?
When GFR is reduced to 30-50% of normal function →
triggers remaining glomeruli to hypertrophy to compensate →
increases single nephron GFR and glomerular blood pressure →
causes endothelial and epithelial injury →
more proteinuria, matrix production →
progression to end stage renal disease usually occurs with proteinuria and global glomerulosclerosis
51
What is Tubulointerstitial Nephritis (TIN)
- Most forms of tubular injury also involve the interstitium
- Caused by either bacteria or non-bacterial etiologies
52
What are the bacteria/non-bacteria etiologies of Tubulointerstitial Nephritis (TIN)
- Bacteria (Pyelonephritis)
– Non-bacterial cause (Interstitial nephritis): due to drugs, metabolic disorders, physical injury, viral infections, immune reactions
53
What is acute pyelonephritis
Common manifestation of extension from a lower urinary tract infection (bladder usually involved)
54
What causes Acute Pyelonephritis?
- Gram Negative bacteria (most often E. Coli)
55
How does Acute Pyelonephritis spread?
- ascending infection (most common)
- hematogenous (e.g. septicemia)
56
Why is Acute Pyelonephritis more common in females?
- shorter urethra
- close proximity to anus
- pregnancy (20-40% develop UTI)
57
What are predisposing factors for Acute Pyelonephritis (5)
- Urinary obstruction (BPH in males or renal lesions) or bladder dysfunction leads to stasis favoring bacterial growth
- Instrumentation of urinary tract (catheterization)
- Vesicoureteral reflux
- Diabetes mellitus: ↑ susceptibility to infection and neurogenic bladder dysfunction
- Immunosuppression and immunodeficiency
58
What are clinical features of Acute Pyelonephritis (5)
► abrupt onset of costovertebral angle pain
► systemic signs of infection (fever, chills, malaise)
► nausea/vomiting
► pyuria, bacteriuria
► urethral irritation (dysuria, increased frequency and urgency)
59
In Acute Pyelonephritis, how long do symptoms usually last without tx?
Symptoms usually last 1 week without tx. It is usually unilateral so renal failure does not occur
60
Describe the histology of Acute Pyelonephritis
- Patchy neutrophilic infiltration of interstitium. Glomeruli intact; tubules spread apart and necrotic.
- Collecting tubules filled with pus, passes out in the urine.
61
Chronic Pyelonephritis (either related to obstruction or vesicoureteral reflux) damages what?
Damages tubules, calyces, and pelvis leading to scarring
62
Chronic Pyelonephritis may be asymptomatic until....
Polyuria (can't concentrate urine) and resulting hypertension and renal failure (if bilateral) occur and/or routine urinalysis shows WBC's
63
What does Interstitial Nephritis refer to?
► Refers to scarring, atrophy, inflammation around tubules. Typically refers to a non-bacterial cause
64
What is drug-induced interstitial nephritis
- IgE or T cell mediated immune reaction to a drug (methicillin, ampicillin, diuretics, NSAIDS)
- interstitial mononuclear inflammation with eosinophils
65
What is acute tubular injury (ATI)
Clinicopathologic entity - damaged tubular epithelial cells with acute decline of renal function (decreased GFR)
66
What is the most common cause of acute kidney injury (renal failure)
Acute Tubular Injury (ATI)
67
What are the two patterns of Acute Tubular Injury (ATI)
- ischemic
- Nephrotoxic
68
When does ischemic Acute Tubular Injury (ATI) occur
occurs when marked decrease in blood flow to kidney (trauma, acute pancreatitis, or septicemia leading to shock)
69
When does nephrotoxic Acute Tubular Injury (ATI) occur
- exposure to toxins: poison
- heavy metals
- drugs: antibiotics
70
What is the pathogenesis of Acute Tubular Injury (ATI)
- ischemia or toxic injury causes tubule cells to be shed (casts seen in urine). This blocks urine output, increases interstitial pressure and decreases GFR
- Oliguria leads to uremia
71
What is the outcome of Acute Tubular Injury (ATI)
- Reversible when caught early--death is circumvented thru dialysis and maintaining electrolytes
- Final complete recovery (>90%)
72
What is the onset of Acute Kidney Injury (Acute Renal Failure)
Abrupt onset (within 48 hrs) of renal dysfunction
73
What are signs and symptoms of Acute Kidney Injury (Acute Renal Failure)
- Increased serum creatinine
- Oligouria or anuria
- Azotemia
74
What are the causes of Acute Kidney Injury (Acute Renal Failure)
- Prerenal: decreased blood flow to kidneys (e.g. cardiac failure)
– Intrarenal: ATI is most common cause but also acute glomerular, interstitial or vascular disease
– Postrenal: obstruction of urinary tract distal to the kidney
75
What are signs and symptoms of Chronic Kidney Injury (Chronic Renal failure)
- Azotemia slowly progressing to uremia which causes oral ulcers, gastroenteritis, pericarditis, peripheral neuropathy
- hypertension
- some degree of proteinuria
76
What can Chronic Kidney Injury (Chronic Renal failure) cause?
All chronic kidney diseases can cause severe progressive scarring leading to end stage kidney disease (ESRD)
77
What are some examples of renal vascular diseases?
- Benign nephrosclerosis
- Malignant hypertension/malignant nephrosclerosis
- Thrombotic microangiopathies
78
What is another name for Arterionephrosclerosis
Benign Nephrosclerosis
79
What is Arterionephrosclerosis
Thickening, luminal obstruction of arteries and arterioles most often associated with benign hypertension and diabetes
80
What does Arterionephrosclerosis cause?
Causes parenchymal ischemia resulting in small foci of parenchymal loss and fibrosis
81
What is the kidney like in Arterionephrosclerosis? The small vessels?
- Kidney is small and contracted with a grain leather surface
- Small vessels show hyaline deposition (arteriolosclerosis), thickened wall with narrowed lumen
82
What is malignant hypertension? Is it common or not?
- Blood pressure usually > 200/120 mmHg
- Uncommon, 5% of patients with hypertension, or may also arise de novo
83
What are symptoms of malignant hypertension?
- Increased intracranial pressure→ headache, nausea, vomiting, visual impairment
- Proteinuria, hematuria
- Renal failure arises later
84
What is the outcome if someone has malignant hypertension?
- Medical emergency requiring aggressive antihypertensive therapy
- 50% survive 5 yrs
85
What is the pathogenesis of malignant hypertension?
Long-standing hypertension →
vascular damage →
narrows lumen of the afferent arteriole →
ischemia →
↑ renin →
angiotensin II →
vasoconstriction →
↑↑ renin →
↑↑ blood pressure
86
What are general traits of cystic diseases of the kidney?
- Common; may be inherited, developmental or acquired
- can be confused with malignant tumors
- Adult polycystic kidney disease: a major cause of renal failure
87
How are simple cysts found in the kidney?
- Single or multiple
- Variably sized (1-5 cm)
- Usually in cortex
- Features that are different from tumors (Smooth contours, avascular, fluid filled)
88
Describe Dialysis-associated acquired cysts
– In cortex and medulla
– May bleed leading to hematuria
– Tumors may arise in them
89
What is Adult Polycystic Kidney Disease
- A common autosomal dominant condition
- Normal at birth, both kidneys progressively develop multiple enlarging cysts that destroy parenchyma
90
When do signs and symptoms of Adult Polycystic Kidney Disease arise? What are they?
symptoms develop in the 4th decade:
- hematuria
- flank pain
- hypertension
- polyuria
- kidney enlargement
91
What is the outcome of Adult Polycystic Kidney Disease
- Eventual renal failure by age 50-70
- Ultimately fatal due to hypertension or uremia
92
Why are tubular precipitations bad?
Can obstruct/damage the tubules and hinder renal function
93
What are the different types/causes of tubular precipitations
1. Urolithiasis (Urinary tract stones): a variety of types (discuss next)
2. Multiple myeloma
- Bence-Jones casts in tubules
- Hypercalcemia
- Amyloidosis
- tumor deposits
94
What is Nephrocalcinosis
Increased calcium content in the tubules and interstitium due to hypercalcemia
95
When does Nephrocalcinosis cause dysfunction
Generally do not cause dysfunction unless massive
96
What are Urolithiasis/nephrolithiasis (Kidney Stones)
Precipitations of a variety of different compounds due to increased urinary concentration of the stone's components (supersaturation)
97
What are effects of Urolithiasis/nephrolithiasis (Kidney Stones)
– Large stones collect in the calyces. May remain silent or cause obstruction with hematuria
– Small stones lodge in ureters where they cause intense renal colic (excruciating flank pain), ulceration and hematuria
– Both large and small stones predispose to infection
98
What is treatment for Urolithiasis/nephrolithiasis (Kidney Stones)
- Surgery
- chemical dissolution
- ultrasound lithotripsy
99
What makes up Kidney Stones (urolithiasis)
Calcium Oxalate and/or Calcium Phosphate (80% of cases)
100
What is the cause of Kidney Stones (urolithiasis)
Cause is not always clear, usually high urine levels of components (Hypercalciuria & Hyperoxaluria)
101
What is Hypercalciuria in relation to kidney stones?
overabsorption from gut or renal reabsorption defect. Can also be caused by hypercalcemia due to:
- Hyperparathyroidism
- Myeloma, sarcoidosis, bone destroying tumors
- Overdose of calcium or vitamin D in diet
102
What is Hyperoxaluria in relation to kidney stones?
can lead to oxalosis (deposits in other tissues). From eating rhubarb leaves (and other plants), antifreeze or from general anesthesia
103
What is Obstructive Uropathy
If ureters, calyces or urethra are obstructed, urine backs up and causes infection of kidney (pyelonephritis) or pressure atrophy of renal parenchyma (hydronephrosis)
104
What are causes of Obstructive Uropathy
- Congenital or secondary strictures
- Kidney stones
- Prostate enlargement
- Tumors
- Bladder atony
105
What are symptoms of Obstructive Uropathy
- Bilateral hydronephrosis causes anuria and can be quickly corrected
- Unilateral hydronephrosis is asymptomatic and causes loss of renal function. This is unfortunate because if it caused symptoms it could be corrected.
106
What is a renal adenoma?
Benign tumor of tubular epithelium
107
How do renal adenomas appear?
Grossly appear as well demarcated yellow, lipid filled nodules in the upper pole of the cortex and measuring < 2.5 cm
108
How should renal adenomas be treated?
No reliable way to differentiate them from kidney cancers so all should be treated as if it could be cancer
109
What is renal cell carcinoma?
Malignant tumor of renal tubular cells resembling the adenoma grossly and histologically but are larger (> 3 cm)
110
What are signs and symptoms of Renal Cell Carcinoma
– Dull flank pain
– palpable abdominal mass
– Painless hematuria (most common symptom)
– Polycythemia
– tumor makes erythropoietin
111
What is the outcome of renal cell carcinoma?
- Spreads to lung, bone
- Unpredictable course; usually fatal
112
What is Wilms Tumor?
► One of the common childhood malignancies
► Unilateral or bilateral kidney tumor derived from embryonic rests
113
Wilms Tumor is associated with ______
syndromes
114
How does Wilms Tumor present?
Present as large, painful abdominal masses with lung metastasis
115
What is the outcome of Wilms Tumor
90% survival with nephrectomy and chemotherapy
116
What is Cystitis
inflammation of the bladder
117
What causes Cystitis
► Infection with coliforms (gram neg. rods):
- Women are predisposed because of short urethras and trauma from sex
- Diabetes
- Catheterization
- Urinary retention or obstruction from hypotonic bladder, prostate enlargement
► Radiation, chemotherapy, immunosuppression
118
What are symptoms of Cystitis
- Urinary frequency
- Suprapubic pain
- Dysuria (pain or burning on urination)
119
What does cystitis predispose you to
predisposes to ascending kidney infection
120
What are risk factors of Transitional Cell (Urothelial) Carcinoma (Bladder Cancer)
- Cigarette smoking: excreted carcinogens in cigarette smoke
- Industrial exposure to aniline dyes
- Long term use of analgesics (aspirin with phenacetin)
- Previous radiation or chemotherapy
121
What does Transitional Cell (Urothelial) Carcinoma (Bladder Cancer) start as?
Typically starts as a papillary non-invasive tumor that causes painless hematuria
122
What is the difference in low grade and high grade transitional cell (Urothelial) carcinoma (Bladder Cancer)
- Low grade examples are slow to invade; high grade tumors are already invasive on discovery in 80%
- Low grade tumors tend to recur but have a 98% survival
123
What is the prognosis for transitional cell (Urothelial) carcinoma (Bladder Cancer) when it invades the muscle?
Once they invade muscle, prognosis is 50%
124
What causes bladder obstruction
- Prostate cancer, prostatitis or BPH
- Urethral strictures
125
What is the pathology of bladder obstruction
– Bladder becomes distended in acute obstruction
– In partial chronic obstruction, muscular hypertrophy develops and causes a thickened, trabeculated muscular wall
– if left untreated can affect the kidney
