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Mercy CLS 3: Urinalysis > 6. Renal Disease > Flashcards

6. Renal Disease Flashcards

1
Q

definition of GN

A

dysmorphic RBCs or RBC casts
protein > 3-3.5 g/day

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2
Q

definition of nephrotic syndrome (4)

A

protein > 3.5 g/day
hypoalbuminemia < 3.5 g/dL
edema
hyperlipidemia, lipiduria

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3
Q

4 categories of GN based on glomerular involvement

A

diffuse (all glomeruli)
focal (< 50% of glomeruli)

global (whole glomerular tuft)
segmental (part of glomerular tuft)

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4
Q

acute glomerulonephritis

etiology, onset, mechanism

A

post-streptococcal (S. pyogenes) infection
1-2 weeks post-strep
antibody complexes against M protein (Spyo) deposit in glomerular membrane

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5
Q

acute glomerulonephritis

s/s, lab findings

A

fever; edema; periorbital edema; fatigue

hematuria; RBC casts/dysphormics; mild proteinuria

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6
Q

acute glomerulonephritis

treatment, prognosis

A

supportive
self-limiting

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7
Q

goodpasture’s

etiology, onset, mechanism

A

viral respiratory infection → cytotoxic antibody attached to glomerular and alveolar basement membranes

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8
Q

goodpasture’s

s/s, lab findings

A

hemoptysis; dyspnea
hematuria (macroscopic); RBC casts; proteinuria

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9
Q

goodpasture’s

prognosis

A

leads to chronic GN and end-stage renal failure

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10
Q

Henoch-Schonlein purpura

etiology, onset, mechanism

A

viral URT infection in children
↓ platelets
renal involvement is an eventual serious complication

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11
Q

Henoch-Schonlein purpura

s/s, lab findings

A

purpura; blood in sputum and stools
macroscopic hematuria; proteinuria; RBC casts

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12
Q

Henoch-Schonlein purpura

treatment, prognosis

A

50% make complete recovery
50% → renal failure

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13
Q

Rapidly progressive crescentic glomerulonephritis

etiology, onset, mechanism

A

associated with SLE
complication of other forms of GN
macrophages damage capillary walls in glomerulus
cells, plasma released into Bowman’s space
crescentic forms: macrophages, fibroblasts, polymerized fibrin

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14
Q

Rapidly progressive crescentic glomerulonephritis

s/s, lab findings

A

↑ fibrin degradation products, cryoglobulins, IgA deposits

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15
Q

Rapidly progressive crescentic glomerulonephritis

treatment, prognosis

A

poor prognosis; often terminates in renal failure
most serious acute GN

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16
Q

Membranous glomerulonephritis

etiology, onset, mechanism

A

associated with autoimmune disorders (SLE, Sjogren’s syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, malignancy)
thickening of glomerular membrane
IgG immune complex deposition

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17
Q

Membranous glomerulonephritis

s/s, lab findings

A

microscopic hematuria; very high proteinuria

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18
Q

Membranous glomerulonephritis

prognosis

A

slow progression to nephrotic syndrome (50%)

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19
Q

Wegener’s Granulomatosis

etiology, onset, mechanism

A

antineutrophilic cytoplasmic antibody (ANCA)
antibody to neutrophils damages small vessels in lungs & glomerulus

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20
Q

Wegener’s Granulomatosis

s/s, lab findings

A

hemoptysis
macroscopic hematuria; proteinuria; RBC casts; azotemia
immunofixation test (p-ANCA/c-ANCA)

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21
Q

Wegener’s Granulomatosis

treatment, prognosis

A

possible progression to end-stage renal failure

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22
Q

Membranoproliferative Glomerulonephritis (MPGN)

etiology, onset, mechanism

A

Type 1—thickening of subendothelial & peripheral capillaries
Type 2—dense deposits in glomerular basement membrane

often in children

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23
Q

Membranoproliferative Glomerulonephritis (MPGN)

s/s, lab findings

A

variable lab results—hematuria; proteinuria; ↓ serum complement

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24
Q

Membranoproliferative Glomerulonephritis (MPGN)

treatment, prognosis

A

poor prognosis
Type 1—progress to nephrotic syndrome
Type 2—progress to chronic GN

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25
# IgA Nephropathy (Berger’s Disease) etiology, onset, mechanism
**IgA** complexes deposited on glomerular membrane maybe from mucosal infection children and young adults #1 cause of primary GN
26
# IgA Nephropathy (Berger’s Disease) s/s, lab findings
recurrent macroscopic hematuria following exercise **rust-colored urine**; proteinuria; glycosuria; casts (cellular, waxy, broad)
27
# IgA Nephropathy (Berger’s Disease) treatment, prognosis
anti-HTN drugs; **low salt, low protein diet** slow progression to chronic GN (50%)
28
# Nephrotic Syndrome etiology, onset, mechanism
damage to **shield of negativity and podocytes**; increased permeability systemic shock ↓ blood flow to kidneys
29
# Nephrotic Syndrome s/s, lab findings
proteinuria > 3.5g/day; hematuria; **hypoalbuminemia** (stimulates lipid production in liver); edema RTEs; **OFBs**; casts (fatty, waxy, RTE); cholesterol crystals; fat droplets
30
# Nephrotic Syndrome treatment, prognosis
medication, diet
31
# Minimal Change Disease etiology, onset, mechanism
1st cause of nephrotic syndrom in children disruption of **podocytes** associated with allergic rxn, immunizations, HLA-B12
32
# Minimal Change Disease s/s, lab findings
**heavy edema** other nephrotic syndrome findings
33
# Minimal Change Disease treatment, prognosis
corticosteroids (may lead to steroid dependence)
34
# Focal Segmental Glomerulonephritis etiology, onset, mechanism
disruption of podocytes associated with **heroin, analgesics, HIV** partial glomeruli involvement
35
# Focal Segmental Glomerulonephritis s/s, lab findings
resembles nephrotic syndrome & minimal change disease hematuria; proteinuria
36
# Alport’s Syndrome etiology, onset, mechanism
sex-linked or autosomal genetic disorder **collagen IV mutation** lamellated appearance of basement membrane (thinning) **males < 6 yo associated with respiratory infections**
37
# Alport’s Syndrome s/s, lab findings
macroscopic & microscopic hematuria **hearing/vision** abnormalities
38
# Alport’s Syndrome treatment, prognosis
supportive can progress to renal insufficiency, failure, nephrotic syndrome
39
# Chronic Glomerulonephritis etiology, onset, mechanism
“slow and silent” progression of other GN disorders
40
# Chronic Glomerulonephritis s/s, lab findings
hematuria; proteinuria; glycosuria; **casts (cellular, waxy, broad) ↓ GFR**; ↑ BUN/creatinine; ↑ phosphate; ↓ calcium
41
# Chronic Glomerulonephritis treatment, prognosis
dialysis renal transplant
42
# Diabetic Nephropathy etiology, onset, mechanism
glycosylated proteins damage glomerular membrane sclerosis of vascular structure
43
# Diabetic Nephropathy s/s, lab findings
microalbuminemia (earliest biomarker)
44
# Diabetic Nephropathy treatment, prognosis
1st cause of end-stage renal disease strict control of BG, HTN
45
# Acute Tubular Necrosis etiology, onset, mechanism
**ischemic damage to RTEs** or presence of toxic substances shock, trauma, surgery, myoglobin (strenuous exercise), nephrotoxic antibiotics
46
# Acute Tubular Necrosis s/s, lab findings
oliguria, nocturia, edema, nausea, vomiting, seizures, decreased consciousness, easy bruising, joint pain, flank pain **RTEs, RTE casts**; blood strip +; ↓ specific gravity
47
# Acute Tubular Necrosis treatment, prognosis
correct underlying cause
48
# Fanconi Syndrome etiology, onset, mechanism
inherited associated with **cystinosis** and **Hartnum** disease or acquired through **toxic** agents (ex. outdated tetracycline) general failure of reabsorption in PCT
49
# Fanconi Syndrome s/s, lab findings
glycosuria; proteinuria; low pH; **cystine** crystals
50
# Fanconi Syndrome treatment, prognosis
supportive
51
# Uromodulin Associated Kidney Diseases (UMKD) etiology, onset, mechanism
autosomal **mutation** in gene for uromodulin ↑ abnormal uromodulin builds up and damages tubular cells teenage years
52
# Uromodulin Associated Kidney Diseases (UMKD) s/s, lab findings
gout (teenage years) ↑ serum uric acid
53
# Uromodulin Associated Kidney Diseases (UMKD) treatment, prognosis
eventual renal transplant
54
# Diabetes Insipidus etiology, onset, mechanism
**nephrogenic** (failure to respond to ADH)—inherited sex-linked recessive or acquired (lithium, amphotericin B, PCKD, sickle cell) **neurogenic** (failure to produce ADH)
55
# Diabetes Insipidus s/s, lab findings
severe dehydration, polyuria ↓ SG; glucose = nephrogenic—**1:1 osmo** after ADH injection neurogenic— **3:1 osmo** after ADH injection
56
# Renal Glycosuria etiology, onset, mechanism
inherited autosomal recessive failure of glucose active transport
57
# Renal Glycosuria s/s, lab findings
glycosuria with normal BG
58
# Renal Glycosuria treatment, prognosis
benign
59
# Renal Tubular Acidosis etiology, onset, mechanism
**distal**—defects in distal H+ excretion **proximal**—defect that reduces the capacity to reclaim filtered bicarbonate in PCT **voltage-dependent**—defects in distal Na+ reabsorption
60
# Renal Tubular Acidosis s/s, lab findings
metabolic acidosis
61
# Acute Pyelonephritis etiology, onset, mechanism
ascending infection from lower UTI rapid onset
62
# Acute Pyelonephritis s/s, lab findings
urinary frequency, nocturia, burning, lower back pain, malaise, chills LE +; nitrite +; mild proteinuria; hematuria; **WBCs; WBC casts; bacteria;** bacterial casts
63
# Acute Pyelonephritis treatment, prognosis
antibiotics no permanent damage
64
# Chronic Pyelonephritis etiology, onset, mechanism
structural abnormalities affecting flow of urine → recurrent infections
65
# Chronic Pyelonephritis s/s, lab findings
polyuria, nocturia, HTN LE +; nitrite +; moderate proteinuria; hematuria; WBCs; WBC casts; **bacteria +/=**; bacterial casts; **waxy and broad casts**
66
# Chronic Pyelonephritis treatment, prognosis
permanent scarring of renal tissue correction of underlying defect
67
# Acute Interstitial Nephritis etiology, onset, mechanism
allergic reaction to certain medications onset 1-2 weeks of initial dose
68
# Acute Interstitial Nephritis s/s, lab findings
**skin rash**, oliguria, edema hematuria; proteinuria; urine **eosinophils** (Hansel stain); no bacteria; WBCs; WBC casts
69
# Acute Interstitial Nephritis treatment, prognosis
d/c medication corticosteroids
70
# Cystitis etiology, onset, mechanism
frequent in women & children #1: E. coli
71
# Cystitis s/s, lab findings
urinary frequency, burning LE +; nitrite +; ↑ pH; WBCs; bacteria
72
# Cystitis treatment, prognosis
antibiotics
73
# Urethritis etiology, onset, mechanism
bacterial or viral infection often STI
74
# Urethritis s/s, lab findings
dysuria, polyuria, urethral discharge hematuria; WBCs; bacteria
75
# Urethritis treatment, prognosis
antibiotics
76
# Acute Renal Failure etiology, onset, mechanism
sudden loss of renal function prerenal, renal, or postrenal
77
# Acute Renal Failure s/s, lab findings
↓ GFR; oliguria, edema, anuria, flank pain, ↓ sensation, ↓ appetite, metallic taste, hiccups, change in mental status, seizure, tremors, nausea, vomiting, bruising, fatigue urine sediment not distinctive
78
# Acute Renal Failure treatment, prognosis
often reversible
79
# Chronic Renal Failure etiology, onset, mechanism
progressive loss of renal function usually due to DM or HTN
80
# Chronic Renal Failure s/s, lab findings GFR
↑↑ BUN and creatinine levels, ↑ K, electrolyte imbalance, ↓ Ca, secondary hyperparathyroidism, ↓ creatinine clearance, metabolic acidosis, anemia **GFR < 25 mL/min**; isosthenuria; proteinuria; glycosuria
81
# Chronic Renal Failure treatment, prognosis
irreversible control sx
82
# Renal Lithiasis etiology, onset, mechanism
pH, concentration, **urine stasis** contribute increased in the **summer**, dehydration increased dietary oxalates and ascorbic acid, cytotoxic drugs, endocrine disorders, foreign body seed, chemical salts in urine ultrafiltrate
83
# Renal Lithiasis s/s, lab findings
intense pain beginning in flank and radiating forward and downward, vomiting, sweating, frequent urge to urinate hematuria; ↑ SG; crystals (75% calcium)
84
# Renal Lithiasis treatment, prognosis
lithotripsy surgical removal
85
# Polycystic kidney disease etiology, onset, mechanism
hereditary fluid-filled cysts form on kidneys
86
# Polycystic kidney disease s/s, lab findings
HTN, hematuria, back pain, frequent bladder or kidney infections, ↑ BUN & creatinine, anemia
87
# Polycystic kidney disease treatment, prognosis
4th cause of chronic kidney failure supportive care renal transplant
88
# Wilm’s Tumor etiology, onset, mechanism
develops in fetus genetic component
89
# Wilm’s Tumor s/s, lab findings
abdominal pain, swelling of abdomen, hematuria, fever, loss of appetite, n/v, malaise, ↑ BP, constipation, **increased growth only on one side of body**
90
# Wilm’s Tumor treatment, prognosis
90% cure rate if localized
91
bladder cancer prevalence
4th most common cancer in men, 9th in women
92
pt hx for bladder cancer
older smoking
93
most common type of kidney cancer
renal cell carcinoma clear cell type
94
hemoptysis
Goodpasture's Wegener's granulamatosis
95
kidney diseases triggered by/associated with infections (5)
acute GN (strep) Goodpastures (viral resp.) Henoch-Schonlein purpura (viral URT in children) IgA nephropathy (maybe mucosal infection) Alport's syndrome (males < 6 viral respiratory)

Mercy CLS 3: Urinalysis (10 decks)

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