Renal Path- Bik Flashcards

(62 cards)

1
Q

Excretion rate=

A

Excretion rate= Filtration Rate-Reabsorption Rate+Secretion Rate

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2
Q

The urine entering bowman’s capsule has the______________ as the plamsa of the blood

A

The urine entering bowman’s capsule has the same composition of ions as the plamsa of the blood

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3
Q

Azotemia

A

Increased BUN(blood Urea nitrogen), creatinine

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4
Q

Increased BUN(blood Urea nitrogen), creatinine

A

Azotemia

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5
Q

Azotemia + more problems(GI, nervous, cardiac)

A

Uremia

Azotemia+ GI problems(Gastroenteritis, bleeding, acute pancreatitis)

Azotemia+ Peripheral neuropathy

Azotemia+ Fibrinous pericarditis

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6
Q

Glomerulopathies

A

Disorders that directly affect the glomerulus and are the most common cause of kidney failure.

Symptoms include decreased GFR(decreased urine output, elevated plasma creatinine,urea)

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7
Q

A pt. has decreased urine output and elevated plasma creatinine, urea. After performing a renal biopsy/clearance data/urine analysis you determine that the pt has…

A

Glomerularopathies(glomerular injury)

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8
Q

Two main classes of glomerulopathies:

Secondary classes of glmoerulopathies:

A

Two main classes of glomerulopathies: Nephrotic/ Nephrosis syndrome & Nephritic/nephritis syndrome

Secondary classes of glmoerulopathies: Lupus nephritis, diabetic nephropathy, DIC w/ thrombotic microangiopathy

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9
Q

Damage to glomerular membrane resulting in enlargement of fenestrations between endothelial cells and/or slit pores of epithelial cells.

Leads t excretion of 3.5g+ protein in urine/day.

Caused by hypertension, diabetes mellitus destruction of capillary beds, Lupus /rheumatoid arthritis immune disorders.

A

Nephrotic Syndrome/Nephrosis

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10
Q

Name the three types of Nephrosis

A

Minimal change disease

Focal segmental

Membranous

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11
Q

Clinical manifestations of Nephrosis/Nephrotic syndrome

A

Edema(especially in eyes and face)

Hypotension

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12
Q

Treatments for nephrosis/nephrotic syndrome

A

Anti-inflammatory steroids

Anti-immune drugs if antibody related

Treat condition(diabetes)

High protein diet

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13
Q

This type of nephrosis is most common in children. Few changes are discernable with microscope, but loss of foot processes of podocytes. Has a good prognosis

A

Type 1 Nephrosis

Children

Few discernable changes(podocyte foot loss)

Good prognosis

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14
Q

This type of nephrosisis characterized by scarring of the glomerulus, relates to the 3 H’s(HIV, Heroin, Hypertension), and has a poir prognosis

A

Type 2- Focal segmental glomerulus

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15
Q

This type of Nephrosis is autoimmune activated, has deposition of antibodies on basement membrane, and increased membrane permiability/thickening

A

Type 3- Membranous glomerulonephritis

Autoimmune

Deposition of antibodies

Permiability&thickening

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16
Q

Defining characteristics of each type of nephrosis

Type 1 minimal change:

Type 2 Focal segmental glomerulosclerosis:

Type 3 membranous:

A

Defining characteristics of each type of nephrosis

Type 1 minimal change: most common in children

Type 2 Focal segmental glomerulosclerosis: Scarring of glomerulosclerosis

Poor prognosis

3H’s

Type 3 Membranous glomerulonephritis: Autoimmune, antibodies, thickening/loss of permiability

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17
Q

Nephritis

A

Inflamation of glomerulus.

Symptoms: slight proteinuria, Hematuria, Azotemia, Hypertension

resulting from immunologic abnormalities

drugs/toxins

vascular disorders

systemic disease

viral causes.

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18
Q

Name the 4 types of Nephritis

A

1) acute postinfectious
2) IgA nephropathy
3) RPGN
4) Chronic

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19
Q

Type 1 Nephritis: Acute postifectious glomerulonephritis

Causes:

Treatment:

A

Type 1 Nephritis: Acute postifectious glomerulonephritis

2-3 weeks after strep

antigen-antibody complexes collect on glomerular membrane slowing GFR and cauing inflammation

Treatment: Antibiotics, antiinflammatory steroids, dialysis in noncorrected

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20
Q

Type 2 Nephritis: IgA nephropathy(Berger disease)

Cause:

Treatments

A

Type 2 Nephritis: IgA nephropathy(Berger disease)

Form of acute glomerulonephritis

2-3 days after URT or GI viral infection

IgA binds glomerular mesangial cells= proliferation

Treatment: Anti inflam, biotics, dialysis

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21
Q

Type 3 Nephritis: Rapidly progressive glomerulonephritis

Causes

Treatment

A

Type 3 Nephritis: Rapidly progressive glomerulonephritis

Goodpasture syndrome

Causes: antibodies against basement membrane formed

Treatment: anti inflammatory/ immune drugs if autoimmune, kidney transplant

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22
Q

Type 4 Nephritis: Chronic Glomerulonephritis

Defomotion:

Cause:

Manifestations:

Treatment:

A

Type 4 Nephritis: Chronic Glomerulonephritis

Slow progressive loss of renal fxn. From diabetes mellitis, hypertension, autoimmunity

Manifestations: Tubular atrophy, slight proteinuria, waxy RBC casts in urine

Treatment: Autoimmune meds

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23
Q

_______ is an inflammatory lesion caused by invasive kidney infection, usually ascends from UTI e.coli/ proteus, and causes fever/flank pain. There are two types: complicated and uncomplicated. E.coli is high in _______

A

Pyelonephritis is an inflammatory lesion caused by invasive kidney infection, usually ascends from UTI e.coli/ proteus, and causes fever/flank pain. There are two types: complicated and uncomplicated. E.coli is high in uncomplicated

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24
Q

Fanconi syndrome

A

Disease of proximal tubule associated with loss of reabsorption of glucose, AAs, phosphate.

May be inherited or aquired

Urine has more extretion molecules, blood has less

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25
There are two types of Nephrosclerosis. Both cause their type of hypertension \_\_\_\_\_\_\_ is characterized by hyaline thickening of arterial walls leading to mild functional impairment. Rarely fatal \_\_\_\_\_\_\_ is characterized by hyperplastic vessels, renal ischemia, and is an emergency. Cause their type of hypertension
There are two types of Nephrosclerosis. Both cause their type of hypertension **Benign** is characterized by hyaline thickening of arterial walls leading to mild functional impairment. Rarely fatal **Malignant** is characterized by hyperplastic vessels, renal ischemia, and is an emergency. High blood pressure 180+/120+, headaches scotomas, reduced renal blood flow leading to necrosis. Cause their type of hypertension
26
\_\_\_\_\_\_\_ _______ \_\_\_\_\_\_\_disease is an autosomal dominant, usually manifests after age 30, has many large cysts, and is associated with brain aneurysms. \_\_\_\_\_\_\_ _______ \_\_\_\_\_\_\_ disease is autosomal recessive, has many small cysts often accomponied by liver cysts, and is often lethan in infancy.
**Adulthood Polycistic Kidney Disease** is an autosomal dominant, usually manifests after age 30, has many large cysts, and is associated with brain aneurysms. **Childhood polycistic kidney disease** is autosomal recessive, has many small cysts often accomponied by liver cysts, and is often lethan in infancy.
27
**Urolithiasis**
**Urolithiasis** Stone formation in urinary collection system. M\>F; genetic tendency. Extremely painful
28
Hydronephrosis
Blockage leading to dilation of the renal pelvis and calyces.
29
\_\_\_\_\_\_\_ carcinoma is derived from tansitional epithelium and has a 5y survival `50% while _______ Carcinoma is dervived from tubular epithelium and has a 5y survival rate of `5%.
**Bladder** carcinoma is derived from tansitional epithelium and has a 5y survival `50% while **Renal Cell** Carcinoma is dervived from tubular epithelium and has a 5y survival rate of `5%.
30
Micturition syncope
Fainting after/during urination
31
three components of glomerular membrane
epithelial cells basement membrane podocytes
32
Concentration of "stuff" in serum
Osmolarity
33
\_\_\_\_\_\_\_ inserts aquaporins into the wall of the collecting duct which leads to water reabsorption without _______ reabsorption
**ADH** inserts **aquaporins** into the wall of the collecting duct which leads to water reabsorption without **ion** reabsorption
34
Pt with fibrous pericarditis abd azotemia has
Uremia
35
Pt with peripheral neuropath, gastroenteritis, acute pancreatitis and azotemia has
uremia
36
What are glomerulopathies
(glomerular injury) disorder that directly affects the glomerulus and _the most common cause of kidney failure._
37
Primary gomerulopathies
nephrosis/ Nephrotic syndrome Nephritis/Nephritic syndrome
38
Secondary glomerulopathy disorders
Lupus Nephritis(immune complexes) DIabetic Nephropathy(Disrupted Basal membrane and mesangial) DIC with thrombotic microangiopathy
39
Damage to glomerular membrane resulting in elnargement of fenestrations between endothelial cells.
Nephrotic syndrome/Nephrosis
40
\_\_\_\_\_\_\_\_\_\_\_ can be caused by Hypertension, diabetes mellitis destruction of capillary beds with glomerulus,and type 3 immune dissorders.
**Nephrosis** can be caused by Hypertension, diabetes mellitis destruction of capillary beds with glomerulus,and type 3 immune dissorders.
41
Nephrosis can be caused by \_\_\_\_\_\_\_\_\_, _______ \_\_\_\_\_\_\_\_ destruction of capillary beds with glomerulus,and ____ \_ ________ dissorders.
Nephrosis can be caused by **Hypertension**, **diabetes mellitis** destruction of capillary beds with glomerulus,and **type 3 immune** dissorders.
42
Edema(anasarca) especailly in the face and eyes along with hypotension are clinical manifestations of
Edema(anasarca) especailly in the face and eyes along with hypotension are clinical manifestations of **Nephrosis**
43
Nephrosis can be treated with
anti-inflammatory steroids, auto-immune drugs, treating underlying condition, and a high protein diet
44
Slight proteinuria(\<3.5g/day), hematuria, azotemia, and **_hyper_**tension are all indications of
Slight proteinuria(\<3.5g/day), hematuria, azotemia, and _hypertension_ are all indications of **Nephritis**
45
\_\_\_\_\_\_\_\_\_\_\_ polynephritis cases have a low ratio of E.coli while ____________ had a high ratio of E.coli to other bacteria
**Complicated** polynephritis cases have a low ratio of E.coli while **uncomplicated** had a high ratio of E.coli to other bacteria
46
Pt has loss or reabsorption in proximal tubule. (glucose, AAs, phosphate). Disease leads to urine having more excreted molecules and the blood less
**Fancoli Syndrome** Pt has loss or reabsorption in proximal tubule. (glucose, AAs, phosphate). Disease leads to urine having more excreted molecules and the blood less
47
Hydronephrosis
Blockage leading to dilation of renal pelvis and calyces. Potential causes: Congenital atresia of ureter, calculi, tumors, inflammation
48
Inflamation of the glomerulus resulting from Immunologica abnormalities drugs/toxins vascular disorders systemic disease viral causes
Nephritis/(ic)
49
GLomerulopathy with slight proteinuria(\<3.5g/day)
Nephritis(ic)
50
2-3 weeks after strep infection causes antigen-antibodies to precipitate on glomerular membrane resulting in inflammation leading to reduced GFR and Urine flow with high WBC recruitment
Acute postinfectious glomerulo**_nephritis._** 2-3 **_WEEKS_**
51
Nephritis where capillary endothelial cell proliferation leads to thickening of membrane
Acute postinfectious glomerulonephritis
52
3 treatments for Acute postinfectious glomerulopathies
antibiotics anti-inflammatory steroids dialysus in not corrected
53
Seen 2-3 days after URT or GI viral infection. antibody binds glomerular mesangial cells inducing proliferation
Berger disease-IgA nephropathy 2-3 **_DAYS_**
54
Treatments for IgA nephropathy(berger disease)
antibiotics ant-inflammatory steroids dialysis in not corrected
55
Antiglomerular basement membrane disease(goodpasture syndrome) Antibodies form against basement membrane
Rapidly progressive glomerulo**nephritis** (RPGN) (goodpasture)
56
Treatment for rapidly progressive glomerulonephritis
anti inflamatory steroids anti-immune drugs if autoimmune kidney transplant
57
Disease is a result of various diseases that cause slow progressive loss of renal fxn. Such as diabetes mellitus, hypertension, autoimmunity. Clinical manifestations may be: tubular atrophy slight proteinuria waxy and RBC casts in urine
Chromic glomerulonephritis
58
Treatment for Chronic glomerulonephritis
autoimmune medication
59
# (reversed card) Acute postinfectious glomerulonephritis
Nephritis where capillary endothelial cell proliferation leads to thickening of membrane
60
# (reversed card) Berger disease-IgA nephropathy 2-3 **_DAYS_**
Seen 2-3 days after URT or GI viral infection. antibody binds glomerular mesangial cells inducing proliferation
61
# (reversed card) Rapidly progressive glomerulo**nephritis** (RPGN) (goodpasture)
Antiglomerular basement membrane disease(goodpasture syndrome) Antibodies form against basement membrane
62
# (reversed card) Chromic glomerulonephritis
Disease is a result of various diseases that cause slow progressive loss of renal fxn. Such as diabetes mellitus, hypertension, autoimmunity. Clinical manifestations may be: tubular atrophy slight proteinuria waxy and RBC casts in urine