Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
116 Cards in this Set
- Front
- Back
Hypertonic Soln leads to both
|
Increased water intake (thirst) and Renal Water Retention (incr. ADH)
|
|
What stimulates ADH release?
|
Osmoreceptors and Baroreceptors
|
|
Small cell lung carcinoma
|
SIADH-inappropriate secretion of ADH-->hyponatremia and hypoosmolarity
|
|
Primary determinant of ECF osmolarity
|
Serum Na
|
|
Large hyperechoic kidneys, oligohydramnios, Cuboidal epithelium
|
ARPKD
|
|
Hepatic cysts and Intracranial aneurysms
|
ADPKD
|
|
Increased incidence of papillary renal cell carcinoma
|
Acquired cystic disease
|
|
Develop in patients on dialysis
|
Acquired cystic disease
|
|
Characteristics of Nephrotic Syndrome
|
Proteinuria, Hyperlipidemia, lipiduria, hypercoagulability, Edema
|
|
Characteristics of Nephritis
|
Mild proteinuria, Hematuria-RBC casts, dysmorphic RBC's, Edema
|
|
Diffuse
|
All of the glomeruli
|
|
Focal
|
Some of the glomeruli
|
|
Global
|
All of each individual glomerulus
|
|
Hematuria in conjunction with upper respiratory infection (synpharyngitic)
|
IgA nephropathy-Most most common; nephritis
|
|
IgA deposition in multiple organs
|
Henoch-Schonlein Purpura
|
|
EM-->Mesangial and large subepithelial "hump-like" deposits
|
Post infectious GN, Group A strep; nephritis; cola colored urine
|
|
Linear IgG and C3 on IF
|
Rapidly progressive GN (Goodpasture's Anti-GBM); Classic Nephritic syndrome with RAPID progression to renal failure
|
|
EM-->Podocyte foot processes effacement/fucion
can be d/t NSAIDS |
Minimal Change Disease; Nephrotic syndrome
|
|
HBV infection
|
Membranous nephropathy-most common cause of nephrotic syndrome in caucasian adults
|
|
Carcinoma of lung, colon, stomach, breast, non-hodgkins lymphoma
|
Membranous nephropathy-most common cause of nephrotic syndrome in caucasian adults
|
|
LM-->diffues thickening of GBM-Spikes; and Subepithelial deposits on EM
|
Membranous nephropathy-most common cause of nephrotic syndrome in caucasian adults
|
|
African americans
|
Focal segmental glomerulosclerosis-nephrotic syndrome; LM-->focal and segmental glomerular sclerosis
|
|
HIV
|
Focal segmental glomerulosclerosis-nephrotic syndrome-LM-->focal and segmental glomerular sclerosis
|
|
Hepatitis C
|
Membranoproliferative Glomerulo-Nephritis; both Nephrotic and Nephritic Features; Subendothelial deposits on EM
|
|
Increases number of capillary loop and mesangial cells (also expansion)
|
Diabetic Nephropathy
|
|
Widening of GBM d/t proteinuria; increased width of foot processes (also apoptosis, and reduced migration)
|
Diabetic Nephropathy
|
|
Lambda light chains
|
Amyloidosis-Enlarged kidney; NO HTN
|
|
Purpura around eyes, splenomegaly, joint pain
|
Amyloidosis-Enlarged kidney; NO HTN
|
|
Kappa chains
|
Light chain deposition disease
|
|
EM-->Granular deposits along GBM; LM-->Nodular Glomerulosclerosis
|
Light chain deposition disease
|
|
Defect in Basement Membrane (Type IV collagen)
|
Alport syndrome-HTN, ESRD, X-linked, Hematuria, COL4A5 gene
|
|
Cochlear and ocular defects
|
Alport syndrome-HTN, ESRD, X-linked, Hematuria, COL4A5 gene
|
|
Dominant; microhematuria, NO proteinuria, HTN or ESRD!
|
Thin Basement Membrane Disease; EM-->THIN GBM (usually <200 nm)
|
|
Medulla+surrounding cortex
|
Lobe
|
|
Medullary Ray+Surrounding cortex
|
Lobule
|
|
Heparan sulfate proteoglycan is on...
|
GBM
|
|
attach podocytes to BM
|
A3B1 integrin
|
|
Location: passive reabsorbion of Na+, Cl- & water; facilitated reabsorbtion of glucose, amino acids & proteins
|
Proximal Tubule
|
|
Fewer mitochondria and intedigitations-location
|
Convoluted distal tubule
|
|
Produce Renin
|
Juxtaglomerular Cells
|
|
Produce Erythropoietin
|
Cortical interstitial cells-transported by bone marrow
|
|
ADH sites of action
|
Kidney's collecting duct and distal convoluted tubule-absorbs urine
|
|
Aldosterone sites of action
|
Distal tubules and collecting ducts of nephron
|
|
Filled bladder cell type
|
Squamous (flattened)
|
|
Smooth muscle cells that lie between the capillaries and regulate blood flow
|
Mesangial Cells
|
|
Visceral layer of Bowmans' Capsule
|
Simple squamous epithelium lined by podocytes
|
|
Precursor tissue of Kidney
|
Intermediate Mesoderm
|
|
Solid cell cord that fuses with Cloaca
|
Mesonephric Duct
|
|
Immature Nephrons; Gets signals from Mesophrinc Duct
|
Mesonephric Tubules
|
|
Result in Nephron formation
|
Branching of Metanephrogenic Mesenchyme
|
|
Distal to 6th generation of metanephrogenic mesenchyme
|
Collecting ducts
|
|
prevent MM cell apoptosis and induce MM to aggregate around ampulla
|
MD signals FgF2 and Bmp7
|
|
Proximal S-shaped tubule-->
|
Distal tubule and loop of henle
|
|
Middle S-shaped tubule-->
|
Proximal tubule
|
|
Distal S-shaped tubule-->
|
Renal Corpuscle
|
|
Primary UG sinus is located-->
|
Ventrally
|
|
The mesonephric ducts in males connect to?
|
Gonads
|
|
Interactions between metanephrogenic Mesenchyme and metanephirc diverticulum are altered in?
|
Renal Agenesis
|
|
Failure of medial mesenchymal migration
|
Bladder Extrophy
|
|
Mucosal folds which obstruct the lumen of the urethra in boys
|
Posterior Urethral Valves
|
|
Functions of Amniotic Fluid
|
Physical (shock absorber); Nutritive, Excretory
|
|
Diarrhea leads to?
|
Metabolic Acidosis
|
|
Diuretics or excess aldosterone cause? (acidosis or alkalosis?)
|
Metabolic alkalosis
|
|
Metabolic Acidosis: What is the compensatory change for CO2?
|
1.3 x the change in HCO3 (will be a decrease)
|
|
Metabolic Alkalosis: What is the compensatory change for CO2?
|
0.6 X the change in HCO3 (will be an increase)
|
|
Respiratory Acidosis: What is the compensatory change for HCO3 ( Acute and Chronic)?
|
Acute: increase CO2 10-->increase HCO3 by 1
Chronic: Increase CO2 10-->increase HCO3 by 4 |
|
Respiratory Alkalosis: What is the compensatory change for HCO3 ( Acute and Chronic)?
|
Acute: decrease CO2 10-->decrease HCO3 by 2
Chronic: decrease CO2 10-->decrease HCO3 by 5 |
|
Anion Gap calculation
|
[Na+] − ([Cl-] + [HCO3−]); >12 is metabolic acidosis
|
|
Angiotensin Change in GFR
|
No change (typically prevents change); Decrease at high concentrations
|
|
When Arterial pressure increases...
|
RBF and GFR remain the same; URINE output increases
|
|
Decreased NaCl to macula densa affects arterioles how?
|
Constrict Efferent arteriole and dilate afferent arteriole
|
|
Thick ascending loop transporter
|
Reabsorbs 25% of filtered Na+ by the Na/K/2Cl transport
|
|
Where does Ag-II increase NaCl reabsorption?
|
Proximal tubule, thick ascending loop of Henle/distal tubule, collecting tubule
|
|
Where does PTH increase Ca+2 reabsorption?
|
Proximal tubule, thick ascending loop of henle/distal tubule
|
|
GBM in proteinuria
|
Thicker!
|
|
defective 11beta-HSD2 enzyme
|
Apparent Mineralocorticoid Excess; low aldosterone levels; HIGH cortisol levels
|
|
Directly increase ENaC channels; Dominant mutation
|
Liddle Syndrome; Low plasma aldosterone
|
|
Hyperaldosteronism; mimic thiazide diuretic (problem with NaCl transport); Adolescence/adulthood
|
Gitelman syndrome
|
|
Hyperaldosteronism; Mimic loop diuretic (ascending loop of Henle); Childhood
|
Barter Syndrome
|
|
Renal clearance (equation)
|
Cx = (Ux) x (UF) / Px
|
|
Fractional excretion of sodium=
|
(urinary concentration of sodium x urine flow rate)/(GFR x plasma concentration of sodium)
|
|
Excretion rate of X =
|
Ux x UF
|
|
Hypertonic soln cause high?
|
Cosm
|
|
Hypotonic soln cause high?
|
CH20
|
|
Acetazolamide makes the urine...
|
Basic
|
|
Elevation of nitrogen waste products
|
Azotemia
|
|
AKI d/t Volume Depletion
|
Pre-renal: Elevated BUN:Creatinine; FENa <1%
|
|
Post renal AKI results in-->
|
Hydronephrosis
|
|
AKI with brown muddy casts
|
Renal
|
|
Eosinophils/hypersensitivity reaction; NO positive urine culture
|
Acute Interstitial Nephritis
|
|
Yellowish raised abscesses-->Neutrophils; Bacterial infection
|
Acute Pyelonephritis
|
|
History of bone pain; Hypercalcemia, volume depletion, nephrotoxins
|
Multiple Myeloma; LM-->Crystalline, fractured casts
|
|
Finely cortical surface; Arteriolar hyaline nephrosclerosis
|
Hypertensive Nephrosclerosis
|
|
Nephrocalcinosis what part of nephron is spared?
|
Proximal tubules
|
|
Renal artery stenosis d/t
|
Atherosclerosis or FMD; Clinicall presents as resistant HTN or kidney dysfunction
|
|
Most common cause of CKD and ESRD
|
Diabetes
|
|
Triad of renal cell cardinoma
|
Painless hematuria, palpable abdominal mass, dull flank pain, Polycythemia (EPO producing tumor)
|
|
Type I papillary carcinoma
|
Cuboidal cells with Small amount of cytoplasm
|
|
RCC in African americans; sickle cell disease
|
Medullary carcinoma
|
|
RCC where cytoplasm is clear and nuclei is toward the apex of the cells
|
Clear cell(tubulo) Papillary
|
|
Mahogeny brown yellow mass w/ central scarring
|
Oncocytoma
|
|
Contains premelanosomes; consists of blood vessels, smooth muscle and fat
|
Angiomyolipoma
|
|
Mesoderm derived tissue
|
Wilms Tumor
|
|
Reactive cells; bladder wall irregularity
|
VonBrunn Nests/ Cystitis Cystica/ Glandularis
|
|
Blunt projections; arise from catheter, stone, etc
|
Polypoid Cystitis
|
|
Following GU surgery associated with chronic cystitis
|
Nephrogenic Adenoma (nephrogenic metaplasia)
|
|
SE: Nephrotoxicity, Cardiovascular effects (HTN & Hyperlipidemia), Hirsutism
|
Cyclosporine
|
|
SE: Diabetes/glucose intolerance, Nephrotoxicity, Neurotoxicity
|
Tacrolimus
|
|
SE: Cytopenias (BMS), Hyperlipidemia (more than Cyclosporin), Mouth Sores & Poor Wound Healing, Pneumonitis
|
Sirolimus
|
|
SE: Cushingoid facial appearance
|
Prednisolone
|
|
Maintenance agent that inhibits signal 1 (inhibit NFAT activation)
|
Cyclosporine and Tacrolimus
|
|
Maintenance agent that inhibits signal 3 at mTOR
|
Sirolimus
|
|
Induction agent that inhibit signal 3 at IL-2R
|
Basdiliximab and Daclizumab
|
|
Induction agent that inhibit signal 1 at TCR/CD3
|
Muromonab
|
|
What drug decreases PTH w/o an increase in Ca or PO4?
|
Calcimimetics
|
|
Calcitonin mechanism
|
Inhibs Ca resorption from bone, & incr PO4 excretion in urine
|