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renal disease Flashcards

1
Q

what is the Globmeruli

A

network of capillaries in the kidney between afferent (bringing) and efferent (taking away) arterioles

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2
Q

what does the capillary wall of the glomeruli consist of

A

Endothelium
basement membrane
epithelium (lines urinary space)

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3
Q

what comes from the epithelial cells of the clomeruli

A

Finger like projections from cell body to contact basement membrane

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4
Q

what connects the adjacent finger processes

A

slit diaphram membrane

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5
Q

what is the importance ofthe slit diaphram membrane

A

prevents proteinuria

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6
Q

what is the capilary wall permeable to of the glomeruli

A

water

small molcules

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7
Q

what is the capillary wall

of the glomeruli impermeable to

A

Albumin

larger proteins

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8
Q

what supports the capillaries of the glomeruli to hold them together

A

Connective tissue mesagium

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9
Q

what forms the interstitum

A

Collagen

Blood vessels between the tubules and glomeruli

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10
Q

what suppliest the capillary bed around some of the tubules

A

VAsa rector

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11
Q

what is Azotemia

A

Elevated BUN(blood urea nitrogen) and creatinine

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12
Q

what causes Azotmia

A

decreased Glomerular filtration rate (less filtration

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13
Q

what is Uremia

A

Azotemia plus other symptomes

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14
Q

what are the other symptoms associated with Uremia

A 
Gastroenteritis
Peripheral neuropathy
Dermatitis
Acidosis
Pericarditis
Hyperkalemia
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15
Q

what causes Acute Nephritic syndrome

A

Results from glomerular injury

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16
Q

what are the symptoms of acute nephritic syndrome

A

acute onset of hematuria
Mild to moderate proteinuria
Azotemia
Hypertneions

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17
Q

what are the signs of nephrotic syndrome

A
  • heavy proteinuria (greater 3.5 grams per day)
  • hypoalbuminemai
  • severe edema
  • hyperlipidemia
  • lipiduria
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18
Q

what is the sudden onset of Azotemia with Oliguria/anuria

A

Acute renal failure

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19
Q

what is proteinuria

A

loss of protein

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20
Q

what is Hematuria

A

broken capillaries lead to peeing blood

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21
Q

what does severe proteinuria lead to

A

severe edema

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22
Q

what is anuria

A

no pee is made

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23
Q

how common is Autosomal dominant (adult polycycstic kidney disease

A

1 in 500-1000 people

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24
Q

how does Autosomal dominant adult polycystic kdiney disease present itself

A
  • Multiple expanding cysts in both kidneys
  • gradual onset of renal failure in adults
  • urinary tract hemorrhage (hematuria)
  • pain
  • hypertension
  • UTI
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25
Q

what is the defective gene in autosomal dominant (adult) polycystic kidney disease

A

Defect PKD1 gene on chromsome 16

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26
Q

what does Autosomal dominant (adult) polycystic kidney disease code for

A

Polycystin-1

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27
Q

how does Autosomal dominant (adult) polycystic kidney disease affect other ogans

A

1/3 have cysts in liver

aneurysms develop in ciricle of willis

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28
Q

what happens to kidneys in autosomal domianny (adult) polycystic kidney disease

A

Very large (4kg) kidneys with many cysts in every part of the tubular system

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29
Q

where do cysts arise in autosomal dominant (adult) polycystic kidney disease

A

all levels of the nephron

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30
Q

what are the clinical signs of Autosomal dominant (Adult) polycystic kidney disease

A 
Flank pain around 4th decade
Hematuria
Hypertension
UTI
renal failure
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31
Q

how common is Autosomal recessive (childhood) polycystic kidney disease

A

1:20,000 births

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32
Q

what mutation causes Autsomal recessive (Chidlhood) polycystic Kidney disease

A

PKHD1 gene muttation

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33
Q

what is the defective protein in Autosomal recessive (childhood) Polycystic kidney disease

A

Fibrocystin

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34
Q

when does renal failure occur in autosomal recessive (childhood) Polycystic kidney disease

A

Shortly after birth to serveral years of age

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35
Q

what happens to the kidney in autosomal recessive (childhood) polycystic kidney disease

A

Numerous unifrom-sized cysts that arise from the collecting tubules

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36
Q

what other organs may be affected by autosomal recesissive(childhood) polycystic Kidney disease

A

Liver cysts

progressive liver fibrosis

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37
Q

what are the mechanisms of glomerular injury

A

Immune complex deposites in glomerular basement membrane or mesangium leading to epithelial and endothelial cell injury

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38
Q

where can immune complexes for loerular injury come from

A
  • circulating immune complexes that dposite in the glomerulus
  • circulating antibodies direct aginast glomerular compants
  • non-glomerular antigens “planted” in the gloerulus
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39
Q

what methods are used to evaluate Kidney biopsies

A

Light micrscopy
Immunofluorescence
Electron microscopy

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40
Q

what is used to do light micrscopy

A

H& E stains
PAS
trichrome (collagen)
Jones (PAS methenamine silver) - basement membrain eval

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41
Q

what is used in immunofluorescence

A

Immunoglobulins and complement

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42
Q

what is Immunofluorescence used for

A

Identification of immune complexes

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43
Q

what is electron micrscopy used for

A

ID immune complexes
Epithelial cell canges
Basement membarne morphology
others

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44
Q

how does it look when immune complex deposition occurs from ciluating growing between the endothelium and basement membrane

A

Bumps

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45
Q

how does it look when immune complexes grow under the foot processes

A

bumps

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46
Q

how does it look when immune complexes linearily aranged in the basement membrane

A

smooth line

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47
Q

what are the sings of Nephrotic syndrome

A 
Heavy proteinuria
Hypoalbuminemia
Sever edema (most obvious sign)
Hyperlipidemia
Lipidura
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48
Q

what causes Nephrotic syndrome

A

Increased glomerular capilary permeability to plasma proteins

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49
Q

what is the most common cuase of neprotic snydrome in children

A

Minimal change disease (2/3 of cases)

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50
Q

how does minimal change disease look in a bioposy of the glomeruli

A

LM: Normal appearing glomeruli
IF: no immune complex deposites
EM: foot process effacement

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51
Q

how is minimal chnage disease treated

A

Corticosteroids

- especially in children

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52
Q

what is the common cause of adult nephrotic syndrome

A

Focal segmental Glomerulosclerosis

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53
Q

does focal segmental glomerulosclerosis usually exist alone

A

Can be primary or secondary glomerular disease

- some is Familiary

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54
Q

what does focal segmental glomerulosclerosis show in microscopes

A

LM: focal (some glomeruli) and segmental (part of invovled glomerulus) sclerosis wth obliteration of capillary loops
IF and EM: no immune complex deposites in the primary (idopathic) form

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55
Q

how does focal segmental clomerulosclerosis respond to corticosteroid treatment

A

not well

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56
Q

how well does the kidney last in Focal and segmental flomerulosclerosis

A

renal failure in 50% after 10 years

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57
Q

who tends to get Membranous Nephropathy

A

Most common in adults

may affect children

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58
Q

what can cause membranous nephropathy

A

Primary

secondary to infection malignancy, SLE, drugs

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59
Q

how does Membranous nephropathy look in micrscop

A

LM: normal, thickned BM
IF: immune complex depostes
EM: deposties in subeitheilail side of GBM

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60
Q

how well does Membranous nephropathy respond to Corticosteroids

A

Poor response

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61
Q

how long does the kindey last in membranous nephropathy

A

40% develop renal failure in 2-20 years

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62
Q

what is the 2nd cause of death after MI for Diabetes Mellitus

A

Renal fialure

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63
Q

how does Diabetes Mellius show itself in a microscope

A

LM: nodular glomerulosclerosis
IF: no immune complex deposites
EM: Thick GBM

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64
Q

what are th other changes that occur in Diabetes mellitus to the kidney

A

Hyaline arteriolosclerosis
Atherosclerosis
Nephrosclerosis

65
Q

what characterizes Nephritic syndrome

A

Acute onset of

  • Hematuria
  • Oliguria and Azotemia
  • hypertension
66
Q

what happens to the cells of the flomeruli in Nephritic syndrome

A

Proliferation of cells within glomeruli and inflammatory cells

67
Q

what does inflammation do in Nephritic syndrome

A

Inflammation injures capillary walls

68
Q

injury to capillary walls leads to what in nephritic syndrome

A

Blood passing into urine

Reduce GFR

69
Q

what causes Nephritic Syndrome

A
  • Acute postinfection (poststreptococcal) glomerulonephritis

- IgA nephropathy

70
Q

when does Acute Postinfectious glomerulonephritis occur

A

follows (1-4 weeks) streptococcal pharyngitis

- other infections may also cause problem (bacterial and viral)

71
Q

who tends to get acute postinfectious glomerulonephritis

A

Children

72
Q

what does a microscope show in Acute postinfectious glomerulonephritis

A

LM: Proliferation of endo and mesangial cells, inflammatory cells, develop cellular crescents
IF: immune complex deposition, granular
EM: immune complexes in GBM and sometimes mesangium

73
Q

who tends to have acute postinfectious (poststreptococcal) glomerulonephritis progress to chronic renal disease

A

Adults

74
Q

who tends to be affected by IgA nephropathy

A

Children and young adults

75
Q

what are the signs of IgA nephropathy

A

Hematuria 1-2 days post-upper respiratory tract infection

- resolution and recurence

76
Q

what is Henoch-Schonlein Purpura

A

when renal disease associated with purpuric skin rash, GI pain, arthritis in IGA nephropathy

77
Q

what does IgA nephropathy look in a microscope

A

LM: variable mesangial cell proliferation

IF and EM: immune (IGA) complexes within the mesangium

78
Q

what type of Glomerulonephritis is Rapidly Progressive Glomerulonephritis

A

Acute clinical syndrome, not a form of glomerulonephritis

79
Q

what is Rapidly progressive Glomerulonephrits

A

PRogressive loss of renal function

80
Q

what does the lab show in Rapidly progressive glomerulonephritis

A

C/w nephritic syndrome

Severe oligouria

81
Q

what happens if Rapidly progressive glomerulonephritis is untreated

A

Death from renal fialure in weeks/months

82
Q

what is the characteristic finding of Rapidly progressive Glomerulonephritis

A

crescentic glomerulonephritis

83
Q

what causes Crescentic glomerulonephritis in Rapidly progressive glomerulonephritis

A

Proliferation of epithelial cells

Infiltration of histiocytes

84
Q

what are the dissorders associated with Rapdily progressive Glomerulonephritis

A

Anti-GBM antibody disease (12% of cases)
Immune complex disesase (44% of cases)
Pauci immune, lack of anti-GBM or immune complexes (44% of cases)

85
Q

what is pauci immune glomerulonephritsi

A

lack of immune complex deposition

86
Q

what does untreated glomerular disease lead to

A

Loss of glomeruli and tubules with fibrosis

87
Q

can you tell the OG renal disease by the time Chronic Glomerulonephritsi is diagnosed

A

No

88
Q

who may get chronic Renal disease

A

Young and middle aged adults

89
Q

when may chronic renal disease be detected

A

At a routine exam

90
Q

what is the signs of chronic renal disease from a routine exame

A

Proteinuria
Hypertension
Azotemia

91
Q

what is the prognosis of chronic renal disease

A

Poor prognosis

92
Q

what happens to surviving glomeruli after advanced loss of tubules in glomeruli in Chronic renal disease

A

develop adaptive changes

93
Q

what is the effectiveness of the adaptive changes in chronic renal disease

A

lead to further injury and progressive renal failure

94
Q

what is needed in chronic renal disease treatment

A

Renal dialysis and kidney transplant

95
Q

other name for acute Pyelonephritis

A

Tubulointerstitial nephritis

96
Q

what is acute pyelonephritis

A

Suppurative(bacterial) inflammation of kidney and renal pelvis caused by bacterial infection

97
Q

what all is affected by acute pyelonephritis

A

Tubules
Interstitium
renal pelvis

98
Q

how does Acute Pyelonephritis spread

A

Ascends from bladder (most common UTI)

and spreads to kidney through blood(hematogenous)

99
Q

how does the body respond to acute Pyelonephrits imunologically

A

Neutrophil infiltration of interstitium and tubules

cluster of neutrophils in the tubular lumens

100
Q

what are clusters of neutrophils in the tubular lumens

A

Neutrophil casts

101
Q

what are the predisposing conditions for acute pyelonephritis

A 
Urinary tract obstruction
Instrumentation
Ureteral reflux
Pregnancy
Females
Immunosuppression
Diabetes Mellitus
102
Q

why do females get more acute Pyelonephrtis

A

cuz their butthole is close to their peehole

103
Q

what is the clinical signs of Acute pyelonephritis

A

Sudden onset of pain at the costovertebral angle and systemic evidence of infection
- accompany dysuria, frequency and urgency

104
Q

what is the prognosis of Acute pyelonephritis

A

repeated bouts of acute inflammation of cont inflammtion leading to chronic pyelonephritis
- mononuclear inflammatory infiltration and irregular scarring

105
Q

what drugs tend to cause Drug-induced interstitial nephritis

A

Antibiotics
NSAIDS
Diretics

106
Q

what is the pathogenesis of Drug induced interstitial nephritis

A

Hypersensitivity

-drug binds to tubular or interstitial cells to cause immunogenic response

107
Q

what are the clinical signs of Drug induced interstitial nephritis

A

Rapid onset (2-40 days) of fever
eosinophilia
Renal dysfuctnion with hematuria
Little to no proteinuria

108
Q

what is the body’s response fo drug-induced interstitial nephritis

A

Interstitial mononuclear cell infiltration
edema
Eosinophilis with non-necrotizing granulomas

109
Q

how does one treat Drug-inducing interstitial nephritis

A

Withdrawal of offending drug

Corticosteroids

110
Q

PRognosis of Drug-induced interstitial nephritis

A

Good (recovering 6-8 weeks)

111
Q

what are the clinical signs of Acute tubular necrosis

A

rapid onset of renal failure
Reduced Urine output/decreased GFR
Electrolyte imbalance
ACUTE KIDNEY INJURY

112
Q

can you heal Acute tubular necrosis

A

Reversible overa period of weeks as damaged tubular epithelium regenerates

113
Q

what damage does acute tubular necrosis lead to

A

Injury to tubular epithlium cells from ischemia (shock) or toxin)

114
Q

what is the pathology of Acute tubular necrosis

A

Dilation of tubules
Interstitial edema
necrosis of epithelium

115
Q

how does Necrosis of epithlium in acute tubular necrosis look different for ischemia and toxin

A

Ischemia: focal and subtle
Toxin: diffuse

116
Q

treating Acute tubular necrosis

A

Supportive care

Dialysis

117
Q

prognosis of Acute tubular necrosis

A

with no preexisting kidney disease, most fully recover renal function

118
Q

Thickening and sclerosis of Renal arteries associated with benign hypertension

A

Arterionephrosclerosis

119
Q

what gene is associated with arterionephrosclerosis

A

Apolipoprotein L1 gene

120
Q

who tends to get arterionephrosclerosis

A

African Americans

121
Q

what linkage does Arterionephrosclerosis share

A

FSGS

122
Q

how does arterionephrosclerosis look grossly

A

Grossly small kidneys

Granular surface

123
Q

what happens to kidney in arterionephrosclerosis at a tissue and micrscopic level

A
  • Hyaline arteriolosclerosis/Fibroelastic hyperplasia
  • Tubular atrophy and fibrosis
  • Global sclerosis of glomeruli
124
Q

what disease of arterionephrosclerosis tend to associate with

A

Hypertension greater than 200/120 mmhg (malignant hypertenion

125
Q

How common is arterionephrosclerosis in essential hypertension

A

occurs in 5% of patients

126
Q

what are the clinical signs of arterionephrosclerosis from malignant hypertension

A

Relative rapid onset of renal failure with increased intracrnail pressure

  • headache
  • nausea
  • vomiting
  • visual impairment
127
Q

what is the pathology of arterionephrosclerosis with malignant hypertension

A

hyperplastic arteriolosclerosis

reduced blood flow causing necrosis of glomeruli

128
Q

what causes thrombotic thrombocytopenia purpura(TTP)

A

an aquired deffect in ADAMTS 13

129
Q

what is the action of ADAMTS 13

A

plasma protease that degrades vWF multimers

130
Q

what do the vWF components activate

A

Platelets under certain conditions

131
Q

what is hemolytic-uremic sndrome

A

endo cell injury leading to platelet activation

132
Q

what causes Hemolytic uremic syndrome

A

Shiga-toxin from E. Coli

- shigella

133
Q

what happens in thrombotic microangiopathies

A

Microthrombus formation in capillaries with RBC damage(schistocytes)

134
Q

what types of disease is Thrombotic thrombocytopenia purpura and Hemolytic-uremic sydnrome

A

Thrombotic microangiopathies

135
Q

what is the overal involvement in Hemolytic-uremic syndrome and thrombotic thrombocytopenia purpura

A

Hemolytic uremic syndrome is specific to Renal and involves children
thrombotic Thrombocytopenia purpura is more widespread in organs (due to antibodies

136
Q

what is urolithiasis

A

Kidney stones

137
Q

who is affected by Urolithiasis

A

by 70, 11% men 6% women

138
Q

what are the clinical signs of urolithiasis

A 
Asymptomatic
Obstruction
intense pain
Infection
hematuria
139
Q

types of stones

A

Calcium (80%(
magngesium ammonium phosphate
Uric acid

140
Q

what causes calcium kidney stones

A

Increased Ca in urine

141
Q

what causes magnesium ammonium phosphate kidney stones

A

Alkaline urine

Proteus or staph infection

142
Q

what causes uric acid kidney stones

A

Gout
acid urine
high cell turnover

143
Q

large kidney stones

A

Staghorn calculi

144
Q

what is hydronephrosis

A

Dilation of renal pelvis/calyces with parenchymal atrophy secondary to obstruction

145
Q

Causes of hydronephrosis

A 
Renal stones
Congenital urinary tract obstruction
enlarged prostate
neoplasms
neurogenic bladder
pregnancy
146
Q

do men or female get renal cell carcinoma

A

2:1 male:female

147
Q

clinical sings of renal cell carcinoma

A 
Hematuria
Mass 
Pain
Fever
Polycythemia
Paraneoplastic syndrome
148
Q

what are the risk factors of renal cell carcinoma

A 
Smoking
Hypertension
obesity
cadmium expsore
Von hippel-lindau syndrome
149
Q

where does renal cell carcinoma come from

A

Tubular epithelium

150
Q

where does renal cell carcinoma invade

A

Renal vein

151
Q

how does renal cell carcinoma look

A

Cells with very pale or clear cytoplasm

152
Q

how do you treat renal cell carcinoma

A

Surgery +/- radiation

153
Q

prognposis of 5 year survival of renal cell carcinoma

A

stage 1:81%

Stage4:8%

154
Q

what is a wilm’s tumor

A

abdominal mass

155
Q

what increases risk of Wilm’s tumor

A

Inherited syndromes

156
Q

who tends to get wilm’s tumor

A

2-5 year olds

157
Q

what is the patholgy of wilms tumor

A

Triphasic proliferation of cell

- epithelial, stromal, and blastemal compents

158
Q

how do we treat wilms tumor

A

Surgery and chemo

159
Q

prognosis of WIlms tumor

A

Very good

general path (16 decks)

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