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163 Cards in this Set
- Front
- Back
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What organs are retroparitoneal?
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Duodenum
Descending colon Ascending colon Kidney and ureters Pancreas Aorta IVC |
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What is the course of the ureter?
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Ureters pass under uterine artery and under ductus deferens
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What is the role of the Proximal convoluted tubule?
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Resorption of all glucose, amino acids, and filtered proteins and 80% of Na and H2O
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What percentage of body weight is water?
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60%
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What percentage of the water in our body is extracellular?
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1/3rd
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What percentage of the fluid is plasma?
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1/4th
plasma proteins- albumin and globulins |
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Breakdown the fluid calculations of the body?
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TBW-ECF=ICF
ECF-PV (Plasma volume) =Interstitial volume TBW is highest in men and babies and fat people 60-40-20 rule 60% water 40% ICF 20% ECF Plasma volume measured by albumin |
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What are the cations and anions of ICF and ECF
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ICF
Anions- protein and organic phosphates Cations- K and Mg ECF anions- Cl HCO3 Cation- Na |
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What measures TBW?
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D2O
titrated H2O |
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What measures ECF?
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sulfate
inulin mannitol |
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WHat measures plasma?
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RISA- radiolabeled albumin
Evans blue |
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How does ECF and ICF change in OSMs and Liters in the following:
Diarrhea Lost in desert adrenal insufficiency |
Diarrhea- decreased ECF volume, no Osm change
Lost in a desert- loss of volume on both sides, increase in osms (sweat is hypoosmotic) Adrenals- loss of ECF volume, gain of ICF volume; loss of Osm |
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How does ECF and ICF change in OSMs and Liters in the following:
infusion of isotonic NaCl Excessive NaCL SIADH |
Infusion of Isotonic NaCL- increase in ECF
Excessive NaCl- increase in ECF volume, decrease in ICF; increased Osm SIADH- increase in volume all around, decreased Osms. |
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What is the formula for calculating clearance?
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C=UV/P
Volume of plasma from which the substance is cleared per unit time. If C<GFR reabsorbtion If C>GFR secretion If C=GFR no net secreation or reabsorption |
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What is the Renal blood flow?
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25% of the CO
directly proportional to pressure difference Inversely proportional to resistance. Flow and GFR are indirectly proportional |
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How does the kidney autoregulate blood flow?
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Myogenic- renal arteries contract in response to stretch.
Tubuloglomerular feedback- increased pressure increases delivery to the macula densa. RBF is constance over arterial pressures from 80 to 200 because of this. |
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How do you measure calculate Renal plasma flow?
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measure clearance of paraaminohippuric acid.
- filtered and secreted by the renal tubuels. clearance measures RBF |
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How is RBF calculated?
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RBF=RPF/(1-Hct)
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How does the kidney filter work?
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1. Fenestrated capillary- size barrier
2. Fused Basement membrane w/ heparan sulfate- negative charge barrier 3. Epithelial layer of podocyte foot processes |
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What makes up the charge barrier of the kidney filter?
When is it lost? |
Heparan sulfate
lost in: nephrotic syndrome-> albuminuria, hypoproteinemia, generalized edema, hyperlipidemia |
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How is GFR calculated?
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clearance of inulin/creatinine
GFR=UixV/Pi=Ci GFR=Kf[(Pgc-Pbs)-(PIgc-PIbs)] GFR decreases w/ age |
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What is the filtraction fraction
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fractio nof RPF that's filtered
FF=GFR/RPF normal=.2 increased filtration-> increased protein concentration of peritubular capillary blood. |
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What is the relationship between starling forces and GFR?
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GFR=Kf[(Pgc-Pbs)-(PIgc-PIbs)]
Kf changes in glomerular disease Pgc increases w/ dilation of afferent arteriole, or constriction of effecrent Pbs increased w/ ureter constriction or stone Pigc- increased along the length of the capilarry; increased by increases in protein concentration |
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What are teh changes in the GFR, RPF and FF in the following:
constriction of the afferent arteriole Constriction of the efferent arteriole increased plasma protein ureteral stone |
GFR, RPF, FF
afferent- down, down, none efferent- up, down, up protein- down, none, down stone- down, none, down |
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What constricts the afferent arteriole?
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NSAID
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What dilates the afferent arteriole?
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Prostas
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What constricts the efferent arteriole?
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Ang II
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What dilates the efferent arteriole?
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ARB, ACE
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How is Glucose reabsorbed?
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filtered load increased w/ increased plasma glucose
reabsorption from na-gcose cotransport in proximal tubuel. At less than 200 mg/dl all can be reabsorbed. above-> glucosuria at > 350, carriers are saturated and no more can be reabsorbed-> Threshold, Tm |
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What is the relative clearance of common proteins?
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PAH>K>inulin>urea>Na>glucose, AA, HCO3
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What is the role of the Early proxmial convoluted tubule?
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workhorse- all the gcose, AAs adn most of the bicarb, Na, water.
Na,glucose; Na,AA co-transporters Na,H countertransporter Secretes ammonia as buffur for secreted H. |
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What is the role of the thin descending loop of Henle?
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passively reabsorbs water via medullary hypertonicity (impermeable to Na)
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What is the role of the thick ascending loop of henle?
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actively reabsorbs Na, K, and Cl and indirectly reabsorbs Mg, Ca, Impermeable to H2O
Diluting segment has the Na, K, 2Cl pump that's blocked by furosemide. Like Barters |
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What is the role of the early distal convoluted tuble?
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actively reabsorbs Na, Cl.
Ca absorb regulated by PTH Thiazides work here. on the Na, Cl- pump |
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What is the role of the collecting tubule?
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reabsorb Na in exchange for K or H- aldosterone
all channels. ADH works on the principal cell on V2 receptor Intercalated cell secretes H |
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Wha tis the relationship of Na in the tubular fluid to that of it in the plasma?
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TF/P = 1
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What is the role of carbonic anhydrase?
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catalizes HCO3 reaction.
acetazolamide inhibs this reaction -> inhibition of HCO3 reabsorption |
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What happens in the late proximal convoluted tubule?
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HCO3, AA, and Gcose is filtered.
Na reabsorbed with Cl. |
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What factors affect K secretion?
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Dietary K
- high K-> k secretion Aldosterone - increases K secretion Acid-base - acidosis- decreases K secretion - alkalosis- increases K secretion Thiazides and loop diuretics- increase secretion |
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How do you calculate the clearance of free water?
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Ch2o=V-Cosm
V=urinary flow rate |
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What are the actions of Angiotensin II?
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Vasoconstriction
release of aldosterone from adrenal cortex release of ADH from posterior pituitary Stimulates hypothalamus-> thirst overall increase in BP and intravasc volume ANP is a check on the system. |
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What is the role of the juxtaglomerular apparatus?
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JG cells are modified smooth muscle of afferent arteriole and the macula densa, an Na sensor secrete reinin leading to increased angiotensin II and aldosterone in reponse to decreased bp, na and increased symp tone.
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What is the role of ANF on the tubules?
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secretes w/ increased atrial pressure
causes increased GFR and Na secretion |
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What is the role of PTH on the tubules?
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acts to:
increase Ca reabsorption in DCT decrease P reabsorp in the PCT |
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What is the role of Aldosterone on the tubuels?
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Increased Na reabsorption and increases K secretion at Collecting tubules
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What cells secrete epo?
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endothelial cells of peritubular capillaries
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What is the kidney's role in Vit D?
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1alpha-hydroxylade converst 25-> 1,25
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How can NSAIDs cause acute renal failure?
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in high vasocnstrictive states, prostas help dilate the afferent arteriole.
NSAIDs inhib. |
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What serves as extracellular and intracellular buffers?
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extra-
HCO3 Phosphate- minor Intra AMP, ADP, ATP, DPG Proteins- imidazole, alpha amino groups, Hemoglobin |
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What are some fixed acids made that can be overproduced in disease?
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ketoacids
lactic acid salicylic acid |
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What is teh compensation for Metabolic acidosis?
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Pco2=1.5 HCO3 + 8 +/- 2
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What is the converstion for metabolic alkalosis?
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Pco2 up .7; up 1 HCO3
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What is the conversion for Acute resp acidosis?
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up 1 HCO3 for 10 Pco2
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What is the conversion for chronic resp acidosis?
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up 3.5 HCO3 for every 10
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what is the conversion for acute resp alkalosis?
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down 2 HCO3 for every 10
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What is the conversion for chronic resp alkalosis?
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down 5 HCO3 for every 10
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How do you calculate the anion gap?
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Na - (Cl + HCO3)
normal is 12 |
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What is Potter's syndrome?
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bilateral renal agenesis-> oligohydramnios-> limb deformities, facial deformities, pulm hypoplasia. Malformation of ureteric bud
Potter can't Pee |
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How does a horseshoe kidney develop?
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inferior poles fo both kidneys fuse. As they ascend from the pelvis during fetal development, horse shoe kidneys get trapped under inferior mesenteric artery and remain low in the abdomen
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What does an RBC case indicate?
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glom inflammation (nephritic), ischemia, or malig HTN
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What do WBC casts indicate?
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tubulointerstitial disease, acute pyelonephritis, glom disorder
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What do granular casts indicate?
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acute tubular necrosis
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What do Waxy Casts indicate?
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advanced renal disease/CRF
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what do hyaline cases indicate
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they are not specific
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What do casts indicate?
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hematuria/pyuria is of renal origin.
WBCs-> acute cystitis RBCs-> bladder cancer |
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What are the symps of Nephritic syndrome?
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hematuria, HTN, oliguria, azotemia
Inflamation |
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What are the Sx of Nephrotic syndrome?
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proteinuria (massive)- >4 gm
hypoalbuminemia peripheral and periorbital edema hyperlipidemia, hypercholesterolemia- increased hepatic synth hypercoag |
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Minimal Change Disease
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most commmon nephrotic in kids.
lipoid nephroiss lipid-laden renal cortices normal glomeruli- light microscopy fused foot processes- electron microscope Rx- steroids |
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Focal Segmental Glomerulosclerosis
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nephrotic
clinically similar to minimal change disease older pts sclerosis w/in capillary tufts of deep juxtamedullary glomeruli w/ focal or segmental distribution - Focal some, but not all glomeruli - segmental- only part of the glomerulus |
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Membranous glomerulonephritis
what is the cause? Who does it affect? What are some things that can help Dx? What is a complication? |
commonest cause of nephrotic in adults
immune complex high incidence in teenagers and yougn adults when nephrotic has azotemia thickened capillary walls. electron-dense immune complexes in intramembranous and epimembranous locations - spike and dome appearance granular flourescense can cause renal vein thrombosis |
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What diseases can occur with membranous glomerulonephritis?
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SLE
HBV Syphilis malaria gold salts penicillamine maligs |
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What is seen in membrounous glomerulonephritis w/ light microscopy?
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diffuce cap and BM thinckening
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what is seen w/ immunoflourecense w/ membranous glomerulonephritis?
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granular pattern
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What is seen on EM w/ membranous glomerulonephritis?
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spike and dome
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Diabetic nephropathy
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often manifests as nephrotic syndrome
increased thickness of glomerular BM. increased mesangial matric - diffuse glomerulosclerosis - nodular glomerulosclerosis nodular accumulations of mesangial matrix (Kimmelstiel-Wilson lesions) |
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Renal amyloidosis
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nephrotic
subendo and mesangial amyloid deposits associated w/ RA and multiple myeloma |
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SLE and nephropathy
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nephrotic syndrome w/ nephritic features
Type I- none observable type II- mesangial form. FSGS, w/ increased mesangial cells and quantitative increase in mesangial matrix. Type III- focal proliferative, less than half the glomeruli. Type IV- prototype most severe all glomeruli nephrotic and nephritic thrombosis and proliferation endothelial prolif subendothelial deposits Type V- indistinguisable from membranous golmerulonephritis |
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What are the characteristics of nephritic syndrome?
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inflamm rupture of glomerular capillaries w/ resultant bleeding into the urinary space; proteinuria and edema may be present but are usually mild.
Oliguira Azotemia HTN Hematuria- casts; smokey brown urine |
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Poststrep golmerulonephritis
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most frequently seen in kids. Peripheral and periorbital edema. Recovers on its own.
follows an infection- nephritogenic strains of group A B-hemolytic strep Immune complexes Decreased C3 |
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What are the gross, light microscopy and EM findings of poststrep glomerulonephritis?
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punctate hemorrhages
enlarged, hypercellular, swollen, bloodless glomeruli w/ prolif of mesangial and endothelial cells. glom BM of normal thickness and uniformity despite inflam changes electron-dense "humps" on the epithelial side of the BM (supepithelial localization) Lumpy-bumpy immunofluorescense |
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Rapidly progressive glomerulonephritis (RPGN)
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nephritic syndrome; rapid renal failure in wks.
50% post strep 10 % goodpastures Pauci-immune- no immune complexes. ANCA type I- anca - type II- anti-BM type III- anca + Histo is the crescent of bowman's space. |
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Goodpastures
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anti basement membrane disease
linear immunoflourescence - Nephritic - pneumonitis w/ hemoptysis - men in mid-20s - crescents |
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What is focal glomerulonephritis?
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focal and segmental but not FSGS.
prolipheraltive, not nephrotic immune complex disease, occurs as a manifestation of various disorders, SLE, subacute bacterial endocarditis, polyarteritis nodosa, goodpastures, wegener granulomatosis and IgA nephropahty |
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what is alport syndrome?
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hereitary nephritis w/ nerve deafness and ocular disorders- lens dilocation and cataracts
nephritic syndrome- end-stage renal disease by 30 mutation in the alpha chain type IV collagen irregular glomerular basement membrane thickening w/ foci of splittin of the lamina densa |
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What is IgA nephropathy?
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Berger disease
common. after a URI deposition of IgA in the mesangium. benign recurrent hematuria in kids following an infection glomerulonephtritis henoch-Schonlein disease |
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what is membranoproliferative glomerulonephritis?
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slow progression to chronic renal disease
BM thickened, cell prolif reduplication of glomerular BM into two layers from mesangial matrix expansion into glomerular capillary loops. tram-track appearance Type I - immune complex type II- Dense deposit disease C3 is reduced. dense deposits on membrane caused by an IgG antibody |
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What is the cause of calcium stones?
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most common
calcium oxalate, calcium phosphate, or both cancer, PTH, vit D, milk -alkali recur radiopaque |
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What is a renal colic?
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excruciating pain caused by acute distention of the ureter from transit of a small stone.
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What is hydronephrosis?
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progressive dilation of the renal pelvis and calyces
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What are th characteristics of UTIs?
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increasesd in women- shorter urethra, increased in preggers
hematogenous spread to kidney or external entry E. Coli |
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What predisposes one to UTI?
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obstruction
surgery catheters gyne abnlties |
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What are the clinical symps of UTIs?
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Urinary frequency
Dysuria Pyuria- neutrophils Hematuria Bacteriuria |
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what is the cause of ammonium magnesium phosphate stones (Struvite)?
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2nd most common from urease-+ bugs- Proteus vulgaris, staph, klebsiella
staghorn calculi radioopaque |
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What is the cause of Uric acid stones
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hyperuricemia- gout
icnreased cell turnover- leukemia MPDisoders radiolucent |
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What is the cause of cystine stones?
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Radiolucent cystinuria
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Drug induced interstitial nephritis
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penicillin derivatives, nsaids, diuretics
immune acute interstitial renal inflam |
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Renal papillary necrosis
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ischemic necrosis of the tips of the renal papillae
most often associated w/ DM sometimes acute pyelonephritis long-term persistent about of phenacetin |
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Acute tubular necrosis
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most common cause of acute failure
reversible 2 wks hyperkalemia in initial oliguric phase-> hyperkalemia. ATN must be distinguished from oliguria from prerenal causes like reduced blood volume renal ischemia from htn or shcok from spepsis, trauma, or hemorrhage crush injury w/ myoglobinuria Ethylene glycol |
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What is Fanconi syndrome?
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manifestation of generalized dysfunction of the proximal renla tubules
may be hereditary or aquired characterized by impaired reabsorption of glucose, AAs, phosphate, and bicarb glycosuria hyperphosphaturia hypophosphatemia aminoacidura acidosis |
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Cystinuria?
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genetically determined impaired tubulaar reabsorption of cystine
manifest clinically by cystine stones |
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Hartnup
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genetically determined impaired tubular reabsorption of tryptophan
pellagra |
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Chronic pyelonephritis
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coarse asymmetric corticomedullary scarring and deformity of the renal pelfvis and calyces
inflam infiltrate, interstitial fibrosis and atrophy |
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What can cause diffuse cortical necrosis?
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ischemic infarction of the cortices
obstetric catastrophes septic schok end-organ vasospasm and DIC |
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what is the milk-alkali syndrome?
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hypercalemia from self medication of peptic ulcer w/ milk and absorbable antacids.
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Adult polycystic kidney disease
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15-30, genetic defect at birth
AD inheritance and is the most common inherited disorder of the kidney bilateral, greatly enlarged partial replacement of renal parenchyma associated with: berry aneurysm cystic disease of liver and other |
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How does adult polycystic kidney disease manifest clinically?
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HTN
hematuria palpable renal masses progression to renal failure |
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Infant polycystic kidney disease
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cysts present at birth
AR disorder. closed cysts that are not in continuity w/ collecting system |
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simple renal cyst
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solitary
common asymptomatic lesion |
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uremic medullary cystic disease
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nephronophthisis
serious, uncommon form of cystic disease |
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medullary sponge kidney
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multiple small medullary cysts and impaired tubular function, usually w/o renal failure; renal stones may form in the dilated ducts
may be complicated by infection |
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Acquired cystic disease
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long-term dialysis therapy
multiple cysts, glomerular and tubular atrophy and scarring increased incidence of renal cell carcinoma |
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What are the major clinical characteristics of uremia?
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Azotemia
Acidosis- sulfates, phophates, organic acids hyperkalemia abnl control of fluid volume-> CHF Hypocalcemia Anemia HTN- renin Neuro- diminished mental function to convulsions and coma Uremic encephalopathy - anorexia, nausea, vomiting - bleeding - skin urochrome - fibrinous pericarditis |
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What are the major causes of acute and chronic renal failure?
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acute- hypoxia
chronic- HTN or DM |
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Acute renal failure
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1. Prerenal azotemia- decreased RBF-> down GFR.
2. intrinsic- acute tubular necrosis or ischemia. Patchy necrosis -> debris -> obstruction -> down GFR. (Granular casts) Postrenal- obstruction (stones, BPH, neoplasia) Only if bilateral |
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In acute renal failure, what are the measurements of urine osms, urine Na, FeNa, BUN/Cr for Prerenal, intrinsic and Postrenal disease?
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Urine osms, urine Na, FeNa, BUN/Cr
Prerenal- high osm, low urine Na, FeNa, BUN/Cr>20 Renal- under 350, >20, >2%, <15 PostRenal- under 350, >40, >4%, >15 |
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Renal adenoma
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small and asymptomatic
derived from renal tubules precursor to carcinoma |
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renal angiomyolipoma
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hamartoma of fat, smooth muscle, blood vessels
tuberous sclerosis |
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Renal cell carcinoma
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most common malig
more in men, 50-70 higher in cigarette smokers chromosome 3 deletion (von Hippel-Lindau) originates in Renal tubules invades renal veins or the vena cava and can extend up the vena cava early hematogenous dissemination polygonal clear cells flank pain, palpable mass, and hematuria - Fever, 2ry polycythemia, ectopic ACTH, PRL, Gonados, renin, PTH |
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Wilms tumor
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nephroblastoma
most common renal malig in kids WT1 on chrom 11 WAGR- Wilms, ANiridia, Genitourinary malform, mental motor retard. palpable flank mass primitive emetanephric tissue immature stroma, primitive tubules, and glomeruli, and mesencymal elements- ct, cartilage, bone, striated muscle |
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What is teh denys-drash syndrome
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abnlties of WT1 gene, intersex disorder, nephropathy and wilms
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What is Beckwith-Wiedemann syndrome
|
WT-2 deletion -imprinting from Moms
hemihypertrophy, macroglossia, organomegaly, neonatal hypoglycemia, various embryonal tumors |
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Transtitional cell carcinoma
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most common tumor of collecting system
renal calyces, pelvis, ureter, or bladder multifocal renal pelvis- phenacetin can recur hematuria local extension - benzidine or B-naphthylamine - cigs - long-term cyclophosphamide use |
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Squamous cell carcinoma of the kidney
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minority
Schistosoma haematobium infection renal calculi |
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What happens w/ low serum Na?
|
disorientation
stupor coma |
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What happens with high serum Na?
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neurolgic: irritability, delirium, coma
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when do you see low serum Cl?
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2ry to met alk
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when do you see high serum Cl?
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2ry to non-anion gap acidosis
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what are the effects of low serum K?
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U waves on ECG, flattened Ts, arrhythmias, paralysis
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What are the effects of high serum K?
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peaked Ts, arrhythmias
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What are the effects of low Ca?
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tetany, neuromusc irritability
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What are the effects of high Ca?
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delirium, renal stones, ab pain
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What are the effects of low Mg?
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neuromusc irritability
arrhythmias |
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What are the effects of high Mg?
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Delirium
down DTRs, cardiopulm arrest |
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What are the effects of high P?
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High-mineral ion product -> mets calcification, renal stones
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What are the effects of low P?
|
low mineral ion product-> bone loss
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What is the mechanism of Mannitol?
|
osmotic diuretic
increased tube fluid osm increased urin |
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What is the clinical use of mannitol?
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Shock, drug OD, decrease intracranial/intraoc pressure
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What are the SEs of mannitol?
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pulm edema, dehydration
contraindicated in anuria, CHF |
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What is the mechanism of Acetazolamide?
|
blocks carbonic anhydrase
self-limited NaHCO3 diuresis and reduction in HCO3 stores. Acts at the proximal convoluted tubule. |
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What is the clinical use of Acetazolamides?
|
Glaucoma, urinary alkalinization, met alk, altitude sickness
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What are the SEs of Acetazolamide?
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Hyperchoremic met acidosis, neuropathy, NH3 tox, sulfa alergy
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What is the mechanism of Furosemide?
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blocks Na, Cl, K channel
abolishes hypertonicity of medulla, prevents concentration of urine increase Ca excretion |
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What is the clinical use of furosemide?
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Edematous states
CHF, cirrhosis, nephrotic syndrome, pulm edema, HTN, HyperCa |
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What are the SEs of Furosemide?
|
OH DANG!
Ototox Hypokalemia Dehydration Allergy Nephritis Gout |
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What is the mechanism of Ethacrynic acid?
|
Phenoxyacetic acid derivative (not sulfonamide)
like furosemide |
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What is the clinical use of Ethacrynic acid?
|
diuresis in pts w/ sulfa allergy
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What are the SEs of Ethacrynic acid?
|
same as furosemide (OH DANG) w/o the G
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What is the mechanism of HZT?
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thiazide diuretic. Inhibs NaCl reabsorp in early distal. decreases Ca excretion
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What is the clinical use of HZT?
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HTN, CHF, idiopathic hyperCa, nephrogenic DI
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What are the SEs of HZT?
|
hyperGLUC
hyperGlycemia hyperLipidemia hyperUricemia hyperCalcemia sulfa allergy |
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What is the mechanism of spironolactone?
|
competitive aldosterone receptor antag in corticla collecting tubule
K sparing |
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What is the clincal use of spironolactone?
|
hyperaldosteronism, K depletion, CHF
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What are the SEs of spironolactione?
|
hyperkalemia
gynecomastia antiandrogen effects |
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What is the mechanism of Triamterine, Amiloride?
|
block Na channel of the CCT
K sparing |
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What is the clincal use of Triamterine, Amiloride
|
hyperaldosteronism
K depletion CHF |
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What are the SEs of triamterine, amiloride
|
hyperK
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What is the mechanism of Ace inhibitors?
|
inhibit ACE
decrease angiotensin II adn prevent inactivation of bradykinin- a botent vaso dilator renin release is increased from decreased inhibition |
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What is the clincal use of ACE inhibitors?
|
HTN, CHF, diabetic renal disease
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What are the SEs of ACE inhibitors?
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CAPTOPRIL
Cough Angioedema Proteinuria Tast changes hypOtension Preg problems Rash Increased Renin Lower angiot II and hyperkalemia |
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What diuretics cause an increase in urine NaCl
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all of them
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What diuretics cause an increas in urine K
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all but thos that make it STAy
Spironolactone Triamterene Amiloride |
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What diuretics cause an increase in pH in blood?
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loop, thiazides
carbonics, K casue lower blood pH |
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What diuretics cause an increase in urine Ca?
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loop
thiazides decrease |
