Renal Flashcards
Atrial Natriuretic peptide (ANP) and BNP function on the kidney?
constricts EFFerent arterioles
DILATES AFFerent arterioles
thus inc GFR, Diuresis (natriuresis)
MOA: ANP/BNP stimulated to inc volume –> relaxes vascular smooth muscle via cGMP–> inc GFR and Dec renin.
Vasopressin (ADH) effect on kidney
water reabsorption
urine concentration
prostaglandins are secreted from? and whtas its affect on kidney
paracrine secretion from kidney leading to vasodilation of the AFFerent arterioles to inc RBF. and GFR
no change to FF
what does dopamine secreted from the PCT at high doses due ?
acts as a vasoconstrictor
what does dopamine secreted from the PCT in low doses do>
promotes natriuresis.
dilates interlobular arteries, AFFerent adn Efferent arterioles –> inc RBF little to no change in GFR.
what is diagnosis
LOW serum Osmolality
Low serum Na
associated with (small cell lung cancer, pulm pathology, head trauma, stroke, cns infections, drugs “cyclophosphamide”)
SIADH
in SIADH
you would expect BP, Plasma renin, aldosterone,
to inc, dec, or no change?
BP: no change or inc
Plasma RENIN; dec
aldosterone Dec
diagnosis ?
inc urine Volume
dilute urine
HIGH serum osmolarity
LOW urine specific gravity
diabetes insipidus
what drug can cause diabetes insipidius by blocking the insertion of Aquaporins into the lumen side stimulated by ADH for water reabsorption.
and how would you treat this?
lithium causes it by entering the principle cell.
amiloride (blocks the na channels lithium uses to enter the principle cell)
drugs and other causes that can cause nephrogenic diabetes insipidus by making the kidneys unresponsive to ADH are?
lithium
demeclocyline (can treat SIADH)
hypercalcemia
mutation of ADH receptor gene
central DI treatment
Intranasal Desmopressin and hydration
Nephrogenic DI
tx
1st line = hydrochlorothiazide
causes the pt to become a little dehydrated. thus the PCT will now reabsorb more water
2nd line = indomethacin (it inhibits prostaglandin synthesis decreases RBF –> dec urine output)
the promixal tubue and loop of henle due what to urine
the distal tubule does _____
the collecting tubule____ does what
PCT and loop henle concentrate the urine
the DT = dilutes
collecting tubule = concentrates it again
what two electrolyte inbalances can lead to
prolongation of QT interval (widened QRS)
V-Tach, torsades de pointe.
HYPOkalemia
HYPOmagnesium
note hyperkalemia can lead to Vtach
what is the Classic ECG finding for
hyperkalemia
hypokalemia?
remember: the T waves mirror the K+ levels
HYPOkalemia –> Flattened T waves
really low –> U wave.
Hyperkalemia –> Tall and peaked T waves
____________________ causes K shift OUT of cells–> HYPERKALEMIA
“DO LABSS”
lOW insulin ( DKA)
B-blockers
Acidosis
(cells are tryign to correct the acidosis by moving the excess H ions out of the blood by exchanging K ions for H ions
Digoxin (blocks Na/K/ATPase)
Cell lysis (leukemia, _crush injur_y, rhabdomyolysis)
maybe Succinylcholine (inc risk in burns/muscle trauma)
what caues K shift into cells –> HYPOkalemia
Insulin
B-agonists
Alkalosis
Cell creation/proliferation
what intervention would correct this finding?
1st treatment! IV Caclium to prevent arrhythmias
(does not correct the hyperkalmeia, just stablize)
we need to shift K back into the cells!!!
acute treatment B-agonist (albuterol)
IV bicarb to cause Alkalosis
Dextrose 1st + IV insulin.
you see tall peaked T waves (hyperkalemia)
low serum concentrarton of Mg2+
you would expect?
tetany, torsades de points (vtach)
HYPOkalemia,
HYPO calcemia (when [Mg2+] < 1.2 mg/dL)
high Mg2+ (hypermag) you would expect?
dec DTRs
llethargy, bradycardia,
hypotension
cardiac arrect
hypocalcemia.
low PO43- (hypophos)
you would expect
bone loss,
osteomalacia (adults)
rickets (children)
high serum concentration of PO43- (HYPERphosphatemia) you would expect what findings/ labs
renal stones
metastatic calcifcations
hypocalcemia
pt with
polyuria
dilute urine (low specific gravity and osmolality)
water deprivation test –> urine osmolarity does not inc.
whats the diagnosis.
Diabetes insipidus
then give desmopression
central = urine osmolarity inc
nephrogenic = no change
what causes anion gap acidosis
MUDPILES
Methanol (formic acid
Uremia
Diabetic ketoacidosis
Proylene glycol
Iron tablets or INH
Lactic acidosis (think pt thats in shock not perfusing)
Ethulene glycol (–> oxalic acid)
Salicylates (late)
causes of norma lanion gap metabolic acidosis
HARDASS
Hyperalimentation
.Addison Disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion.
causes of respiriatory alkalosis
(hyperventilation)
- psychogenic
- high altitude
- PE
- aspirin toxicity (only acutely)
causes of metabolic alkalosis?
excessive vomiting
diuretic
- (loss chloirde and the hypocloremia causes alkalosis) or thiazides –> K excretion
hyperaldosteronism
- triad: hypokalemia, htn, metabolic alkalosis
a
what type of renal Tubular acidosis
urine pH > 5.5
HYPOkalemia
metabolic acidosis (all RTA have normal anion gap metabolic acidosis)
type 1 distal
defect in alpha intercalated cells in collecting tubule unable to secrete H+
what type of renal tubular acidosis?
urine ph < 5.5
HYPERkalemia
type 4 hyperkalemic RTA
hypoaldosteronism –> hyperkalemia –> dec NH3 synthesis in PCT –> dec NH4+ (ammonium) excretion
what type of renal tubular acidosis
phypokalemia
hypophosphatemia
inc bicarb in urine
urine ph < 5.5
type 2 proximal renal tubular acidosis
defect in PCT HCO3- reabsorption –> inc excretion of bicarb in urine –> metabolic acidosis.
what nerve runs with anterior interoseesous artery?
ant interousseous nerve
what nerve runs with posterioro interosseous artery
deep branch of the radial nerve
what nerve runs with the posterior circumflex artery
axillary nerve
suprascapular artery runs with what nerve?
suprascapular nerve
deep brachial artery runs with?
radial nerve
dorsal scapular artery runs with
lateral thoracic artery runs with?
dorsal scaqpular nerve.
long thoracic nerve
ulnar artery runs with
brachial artery runs with
ulnar nerve
median nerve
linear pattern of IgG deposition on IF
Goodpasture disease
type II HSR
lumpy-bumpy deposits of IgM, IgM, and C3 in the Mesangium
poststreptococcal glomerulonephritis
deposits of IgA in the mesangium
IgA nephropathy
Anti-GBM antibodies
Hematuria,
hemoptysis
Good pasture disease
crescent formation in the glomeruli
rapidly progressive glomerulonephritis
wire loop appearance on LM
lupus nephritis
(diffuse proliferative glomerulonephritis)
describe what labs and symptoms that are associated with Nephrotic syndrome
proteinuria > 3.5 g/day
hypoalbuminemia
edema
inc risk of infection
inc risk of thrombosis
hyperlipidemiab (bc when oncotic pres falls it stimulates the liver to make more lipoprotiens)
child presenting with proteinuria > 3.5 g/day
edema w.out inciting event
pitting edema.
on labs 3+ proteinuria, hypoalbuminemia, hyperlipidemia.
what would you expect to see on LM and EM
minimal change disesase (Lipoid nephrosis)
LM- normal glomeruli (lipid may be seen in PCT cells
EM- effacement (flattening) of FOOT PROCESSES
if you see HIV + or sickle cell disease, or heroin abuse.
that is African american or hispanic and nephrotic syndrome.
you expect to see what on LM, IF, EM
LM - segmental focal sclerosis and hyalinosis
- affects less than half of glomeruli, certain regions affected
IF - often negative, but may be + for nonspecific focal deposits of IgM, C3,C1
EM- effacement/dearrangement of foot process similar to minimal change disease
biospy: mesangial collapse w/ sclerosis of some glomeruli
if you see this image what renal syndrome is it
membranous nephropathy
you see spike and dome appearance with subepithelial dposits
on LM you see diffuse capillary and GBM thickening
all the following can cause/
hep B
hep C
Lupus
Subacute bacterial endocarditis
(MPGN)
membrano-proliferative glomerulonephritis
subepithelial humps
decreased C3 levels
coca colal urine
+ anti-DNAse B titer
Post streptococcal GN
mesangial deposits of IgA
Henoch-Schonlein purpura
may occur after URI
AKA berger disease
Iga nephropathy
protein deposits in heart, liver, and kidney
apple green birefrinigence
associated with multiple myeloma
amyloidosis
defect in type IV collagen
Cataracts
Nephritis
High freequency HEARing loss
Alport syndrome
cant see can pee cant hear high C
diffuse proliferative GN
“wire loop” basement membranes
Anti-dsDNA ab
Lupus nephritis
Microscopic hematuria
Pulmonary infiltrates
type II HSR
anti-GBM ab
Goodpastures syndrome
hematuria and proteinuria
Pulmonary infiltrates
Nasopharyngeal granulomas
C-ANCA
Granuomatosis w/ polyangiitis (Wegener’s)
proteinuria and edema
podocyte foot process effacement
most common causes of nephrotic syndrome in children
TX corticosteriods
Minimal change disease
most common cause of nephrotic syndrome in
us adults
hiv pts
blacks and latinos
Focal segmental glomerulosclerosis
what is the most common tumor of urinary tract system (renal calyces, renal pelvis, ureters and bladder)
transitional cell carcinoma (urethelial carcinoma_)
NOT: RCC which is the most common tumor of the kidney itself
how does transitional cell carcinoma present
painless hematuria
what are the risk factors for transitional cell carcinoma?
know these
pnemonic
“Pee SAC:
Phenacetin
***Smoking
Aniline dyes
Cyclophosphamide
you have a pt that presents with painless hematuria. upon further workup he tells you that hes from the middle east and travels to africa to visit his family. you further work him up and diagnosis him with squamous cell carcinoma of the bladder
what is the most likely strongest risk factor for this patient and how would you treat the cause?
Schistosoma haematobium infection
treat with praziquantel
most common renal malignancy in early childhood (2-4)
wilms tumor
most common type of renal stone
calcium oxalate
type of renal stone associated with proteus vulgaris
struvite stones
most common primiary renal tumor in adults
RCC
pt complains of not being able to reach the bathroom in time.
you diagnosis her with urgency incontinence
what is the pathogensis behind this and the tx
overactive bladders (detrusor instability*) –> leak with urge to void immediately.
antimuscarinics (oxybutynin.
also (combank) says you can use
antispasmodics (tolterodine)
effects smooth m –> inc bladder capacity, dec uninhibited contraction, ,dec desire to void.
outflow incontinence is caused by?
incomplete empyting secondary to (detrusor underactivity or outlet obstruction) –>
increased POST VOID RESIDUAL on ultrasound and catheterization!!!!!1
in fanconi syndrome. what part of the nephron is defective. and electrolyte disturbances do you expect to see
PCT
thus no absorption of glucose, amino acids, bicarbg, phosphate.
Bartter syndrome is a reabsorption defect in what part of the nephron?
bartter syndrome is an autosomal_________ mutation of what transporter
thick ascending loop of henle
autosomal Recessive mutation iin the NA/K/2Cl cotransporter
Bartter syndrome results in what electrolyte abnormalities
hypokalemia
metabolic ALKALOSIS .
Giltelman syndrome is an autosomal Recessive mut of what part of the nephron and what cotransporter
distal convoluted tubule
and
Na/Cl cotransporter
note similiar to thiazides
and less severe than bartter syndrome bc most of the Na reabsorption occurs in early nephron
Liddle syndrome results in ________ in the distal collecting tubules due to iinc activity of the epithelial Na channel
inc Na reabsorption in the distal collecting tubules
liddle syndrome is autosomal____
and causes?
htn,
hypokalemia
metabolic Alkalosis
dec Aldosterone.
it presents like hyperaldosteronismb but aldosterone is nearly undetectable.
treatment for liddle syndrome?
Amiloride which blocks Na reabsorption channels (Enac)
Syndrome of Apparent Mineralcorticoid Excess
cortisol tries to be the SAME as aldosterone
is a hereditary def of ____ enzyme
11B-hydroxysteroid dehydrogenase
that normally converts
cortisol (active) —> cortisone (nonactive)
Syndrome of apparent mineralocorticoid
will present with
htn
Hypokalemia
metabolic Alkalosis
low serum aldosterone levels.
if a child presents with symptoms characteristic of Syndrome of apparent mineralocorticoid excess (11B hydroxysteroid dedhydrogenase) and you ruled out the inherited cause. what is another possible acquired cause?
Glycrrhetinic acid (present in licorice) which blocks the actibity of 11B hydroxysteroid dehydrogenase
treatment of Syndrome of apparent mineralocorticoid excess
corticosteroids (exogenous corticosteroids dec endogenous cortisol prodcution–> dec mineralocorticoid receptor activation.
which renal tubular defect has
hypokalemia and metabolicalkalosis with HYPERCALCIURIA
bartter syndrome
