Renal Path- Bik Flashcards
Excretion rate=
Excretion rate= Filtration Rate-Reabsorption Rate+Secretion Rate
The urine entering bowman’s capsule has the______________ as the plamsa of the blood
The urine entering bowman’s capsule has the same composition of ions as the plamsa of the blood
Azotemia
Increased BUN(blood Urea nitrogen), creatinine
Increased BUN(blood Urea nitrogen), creatinine
Azotemia
Azotemia + more problems(GI, nervous, cardiac)
Uremia
Azotemia+ GI problems(Gastroenteritis, bleeding, acute pancreatitis)
Azotemia+ Peripheral neuropathy
Azotemia+ Fibrinous pericarditis
Glomerulopathies
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)
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…
Glomerularopathies(glomerular injury)
Two main classes of glomerulopathies:
Secondary classes of glmoerulopathies:
Two main classes of glomerulopathies: Nephrotic/ Nephrosis syndrome & Nephritic/nephritis syndrome
Secondary classes of glmoerulopathies: Lupus nephritis, diabetic nephropathy, DIC w/ thrombotic microangiopathy
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.
Nephrotic Syndrome/Nephrosis
Name the three types of Nephrosis
Minimal change disease
Focal segmental
Membranous
Clinical manifestations of Nephrosis/Nephrotic syndrome
Edema(especially in eyes and face)
Hypotension
Treatments for nephrosis/nephrotic syndrome
Anti-inflammatory steroids
Anti-immune drugs if antibody related
Treat condition(diabetes)
High protein diet
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
Type 1 Nephrosis
Children
Few discernable changes(podocyte foot loss)
Good prognosis
This type of nephrosisis characterized by scarring of the glomerulus, relates to the 3 H’s(HIV, Heroin, Hypertension), and has a poir prognosis
Type 2- Focal segmental glomerulus
This type of Nephrosis is autoimmune activated, has deposition of antibodies on basement membrane, and increased membrane permiability/thickening
Type 3- Membranous glomerulonephritis
Autoimmune
Deposition of antibodies
Permiability&thickening
Defining characteristics of each type of nephrosis
Type 1 minimal change:
Type 2 Focal segmental glomerulosclerosis:
Type 3 membranous:
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
Nephritis
Inflamation of glomerulus.
Symptoms: slight proteinuria, Hematuria, Azotemia, Hypertension
resulting from immunologic abnormalities
drugs/toxins
vascular disorders
systemic disease
viral causes.
Name the 4 types of Nephritis
1) acute postinfectious
2) IgA nephropathy
3) RPGN
4) Chronic
Type 1 Nephritis: Acute postifectious glomerulonephritis
Causes:
Treatment:
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
Type 2 Nephritis: IgA nephropathy(Berger disease)
Cause:
Treatments
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
Type 3 Nephritis: Rapidly progressive glomerulonephritis
Causes
Treatment
Type 3 Nephritis: Rapidly progressive glomerulonephritis
Goodpasture syndrome
Causes: antibodies against basement membrane formed
Treatment: anti inflammatory/ immune drugs if autoimmune, kidney transplant
Type 4 Nephritis: Chronic Glomerulonephritis
Defomotion:
Cause:
Manifestations:
Treatment:
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
_______ 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 _______
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
Fanconi syndrome
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
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
_______ _______ _______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.
Urolithiasis
Urolithiasis
Stone formation in urinary collection system.
M>F; genetic tendency.
Extremely painful
Hydronephrosis
Blockage leading to dilation of the renal pelvis and calyces.
_______ 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%.
Micturition syncope
Fainting after/during urination
three components of glomerular membrane
epithelial cells
basement membrane
podocytes
Concentration of “stuff” in serum
Osmolarity
_______ 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
Pt with fibrous pericarditis abd azotemia has
Uremia
Pt with peripheral neuropath, gastroenteritis, acute pancreatitis and azotemia has
uremia
What are glomerulopathies
(glomerular injury) disorder that directly affects the glomerulus and the most common cause of kidney failure.
Primary gomerulopathies
nephrosis/ Nephrotic syndrome
Nephritis/Nephritic syndrome
Secondary glomerulopathy disorders
Lupus Nephritis(immune complexes)
DIabetic Nephropathy(Disrupted Basal membrane and mesangial)
DIC with thrombotic microangiopathy
Damage to glomerular membrane resulting in elnargement of fenestrations between endothelial cells.
Nephrotic syndrome/Nephrosis
___________ 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.
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.
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
Nephrosis can be treated with
anti-inflammatory steroids, auto-immune drugs, treating underlying condition, and a high protein diet
Slight proteinuria(<3.5g/day), hematuria, azotemia, and hypertension are all indications of
Slight proteinuria(<3.5g/day), hematuria, azotemia, and hypertension are all indications of Nephritis
___________ 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
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
Hydronephrosis
Blockage leading to dilation of renal pelvis and calyces.
Potential causes: Congenital atresia of ureter, calculi, tumors, inflammation
Inflamation of the glomerulus resulting from Immunologica abnormalities
drugs/toxins
vascular disorders
systemic disease
viral causes
Nephritis/(ic)
GLomerulopathy with slight proteinuria(<3.5g/day)
Nephritis(ic)
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 glomerulonephritis.
2-3 WEEKS
Nephritis where capillary endothelial cell proliferation leads to thickening of membrane
Acute postinfectious glomerulonephritis
3 treatments for Acute postinfectious glomerulopathies
antibiotics
anti-inflammatory steroids
dialysus in not corrected
Seen 2-3 days after URT or GI viral infection.
antibody binds glomerular mesangial cells inducing proliferation
Berger disease-IgA nephropathy
2-3 DAYS
Treatments for IgA nephropathy(berger disease)
antibiotics
ant-inflammatory steroids
dialysis in not corrected
Antiglomerular basement membrane disease(goodpasture syndrome)
Antibodies form against basement membrane
Rapidly progressive glomerulonephritis (RPGN) (goodpasture)
Treatment for rapidly progressive glomerulonephritis
anti inflamatory steroids
anti-immune drugs if autoimmune
kidney transplant
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
Treatment for Chronic glomerulonephritis
autoimmune medication
(reversed card)
Acute postinfectious glomerulonephritis
Nephritis where capillary endothelial cell proliferation leads to thickening of membrane
(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
(reversed card)
Rapidly progressive glomerulonephritis (RPGN) (goodpasture)
Antiglomerular basement membrane disease(goodpasture syndrome)
Antibodies form against basement membrane
(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
