Renal Flashcards

(270 cards)

1
Q

Proximal convoluted Tubule

A

brush border reabsorbs ALL glucose and AA

reabsorbs most bicarb, sodium, chloride, potassium, water, uric acid, and PO4^3-

(PTH inhibits sodium/phosphorus cotransport)

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2
Q

Thick Ascending Loop of Henle

A

reabsorb Na (20%), K, Cl, Mg/Ca
Na/K ATPase, Cl/K pump
impermeable to water
urine less concentrated

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3
Q

Distal Convoluted tubule

A

reabsorb Na (5-10), Cl
can’t reabsorb water
Na/K ATPase
PTH: Na/Ca antiporter; inc ca reabsorption via Ca/Na exhange

makes urine fully dilute (hypotonic)

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4
Q

Collecting Tubule

A
reabsorbs Na (3-5) in exchange for K/H
aldosterone regulates impacting exchanger of Na/H20

ADH increases aquaporin on apical side of membrane (urine side) > inc urea reabsorption

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5
Q

Where is angiotensinogen made

A

liver

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6
Q

Where is renin secreted from

A

Juxtaglomerular cells in kidney

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7
Q

What stimulates renin

A

decrease in renal perfusion, b1 adrenergic effect

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8
Q

Where is angiotensin converting enzyme (ACE) made

A

lung and kidney

located in multiple tissues; conversino occurs most in the lung, provided by vascular endothelial cells in lung

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9
Q

What does angiotensin II do

A

increase sympathetic activity
increase aldosterone
tubular Na, Cl reabsorption and K excretion, H20 retention
arteriolar vasoconstriction, increase BP
increase ADH to increase H20 reabsorption
limit reflex bradycardia

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10
Q

renin function

A

decrease NaCl reabsorption

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11
Q

Inhibition of RAAS

A

normal renal profusion, ANP/BNP

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12
Q

ANP/BNP (atrial/brain natriuretic peptide)
released from…
due to..
functions

A

released from atria and ventricles d/t inc volume to inhibit RAA system

inhibit RAAS; relaxes vascular smooth muscle via cGMP leading to increased GFR and decreased renin, dilates afferent arteriole

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13
Q

ADH (vasopression)

functions

A

regulates serum osmolality
responds to low blood volume states
stimulates reabsorption of water and urea in collecting ducts

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14
Q

Respiratory acidosis

A

low pH, high CO, high bicarb

hypoventilation (obstruction, lung dz, opiods, sedatives, weak respiratory muscles) > hypoxia

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15
Q

respiratory acidosis clinical

A

rapid, shallow respirations, hypotension, dyspnea, headache, hyperkalemia, dysrhythmias, drowsiness, dizziness, disorientation, muscle weakness, hyperreflexia

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16
Q

metabolic acidosis w/ high anion gap

A

low ph, low bicarb, elevated anion gap
GOLDMARK
glycols, oxoproline, l-lactate, methanol, aspirin, renal failure, ketones

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17
Q

Anion gap

A

sodium- cl+bicarb

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18
Q

metabolic acidosis w/ normal gap cause

A

HARDASS

hyperchloremia, Addison dz, renal tubular acidosis, diarrhea, acetazolamide, spironolactone, saline infusion

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19
Q

Respiratory alkalosis

A

low CO2, high pH

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20
Q

Respiratory alkalosis clinical/cause

A

hyperventilation (anxiety, hypoxemia, salicylates, tumor, PE, pregnancy)

tachycardia, hypo or N BP, hypokalemia, numbness and tingling of extremities, hyper reflexes & muscle cramping, seizures, irritability

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21
Q

Saline-resistant metabolic alkalosis

A

high chloride
hyperaldosteronism
Bartter syndrome
Gitelman syndrome

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22
Q

saline-responsive metabolic alkalosis

A

low chloride
vomiting
recent loop/thiazide diuretics
antacids

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23
Q

respiratory acidosis causes

A
airway obstruction 
acute lung disease 
chronic lung disease 
opioids, sedatives 
weakening of respiratory  muscles
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24
Q

metabolic acidosis w/ high anion gap causes

A

diabetic ketoacidosis
hypoxia
carbonic anhydrase inhibitor
renal tubular acidosis

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25
metabolic acidosis clinical
headache, hypotension, hyperkalemia, muscle twitching, warm flushed skin, N/V, dec muscle tone. dec reflexes, kussmaul respirations,
26
respiratory alkalosis cause
anxiety, hypoxemia, salicylates, tumor, PE, pregnancy
27
metabolic alkalosis clinical
``` restlessness followed by lethargy dysrhythmias compensatory hypoventilation confusion N/V diarrhea tremors muscle cramps hypokalemia paresthesia ```
28
Nephritic syndrome path
glomerular inflammation leads to basement membrane damage > loss of RBC in urine > hematuria
29
Nephritic syndrome clinical
hematuria, RBC cats, oliguria, azotemia, HTN, proteinuria (mild), increased renin release
30
thin descending loop of henle
passive reabsorption of water impermeable to sodium makes urine hyeprtonic (concentrated)
31
ACE function
catalyzes conversion of angiotensin I to II
32
aldosterone function and mechanism
regulates extracellular volume and sodium content by targeting kidneys in response to hypovolemic and hyperkalemic (inc potassium excretion) states
33
low bicarb =
metabolic acidosis
34
high bicarb =
metabolic alkalosis (check urine chloride)
35
with low bicarb you suspect ___ and should check ___
metabolic acidosis, anion gap
36
with high bicarb you suspect ___ and should check ___
metabolic alkalosis, urine chloride
37
nephritic syndrome ex
``` infxn-associated glomerulonephritis goodpasture syndrome igA nephropathy (berger dz) alport syndrome membranoproliferative glomeulonephritis ```
38
infxn associated glomerulonephritis etiology
type II hypersensitivity rxn kids: group A strep Adults: straph or strep
39
IgA nephropathy (berger disease)
episodic hematuria occuring concurrently with respi or GI infxn igA secreted by mucosal linings
40
alport syndrome
mutation of type IV collagen irregular thinning and thickening and splitting of glomerular basement membrane x-linked dominant condition cant see, cant pee, cant hear a bee
41
nephrotic syndrome etiology
podocyte damage > impaired charge barrier > MASSIVE proteinuria associated with hypercoagulable state d/t antithrombin III loss in urine
42
nephrotic syndrome clinical characteristics
edema, hypoalbuminemia, HLD, frothy urine with fatty casts
43
nephrotic syndrome ex
primary secondary - amyloidosis, diabetic glomerulonephropathy, lupus nephritis, fabry dz both - focal segmental glomerulosclerosis, minimal change dz, membranous glomerulopathy, membranoproliferatie glomerulonephritis
44
glomerulosclerosis etiology
idiopathic, or due to other conditions: | HIV, sickle cell, heroin use, obesity, congenital malformations, drug induced
45
glomerulosclerosis complication
CKD
46
erythryopoietin: released from where in response to what function
released from interstitial cells in peritubular capillary bed in response to hypoxia stimulate RBC proliferation in BM
47
calciferol (VitD) conversion process, and stimulation
PCT converts OH > OH calcitrol active form via 1a hydroxylase ^ by PTH
48
prostaglandins are secreted from where to do what
secreted by paracrine to vasodilate afferent arterioles to increase RBF
49
dopamine is secreted by what cells to do what
secreted by PCT cells to promote natriuresis low doses: dilate interlobar arterise, aff arterioles, and eff arterioles to inc RBF with little to no change in GFR high doses: acts as a vasoconstrictor
50
PTH: secreted from where in response to what function
secreted by hypothalamus/pituitary in response to dec Ca, inc phosphate or dec vit D causes increase of Ca RA in DCT, dec phos RA in PCT, inc active D production increases both Ca and phos absorption from gut
51
what is the primary fuel source for the kidneys
glutamine | nitrogen is used to help with acid-base balance, but not a fuel source
52
clinical characteristics of low Na
N, malaise, stupor, coma, serizures
53
clinical characteristics of high Na
irritability, stupor, coma
54
causes of hyponatremia
hypovolemic: renal loss/GI loss euvolemic: SIADH, hypothyroid, adrenal insufficiency, primary polydipsia hypervolemic: HF, cirrhosis, nephrotic syndrome
55
clinical characteristics of low K
U waves and flat T waves on ECG, arrhythmias, cramps, spasm, weakness
56
clinical characteristics of high K
wide QRS, peaked T wave, arrthmyias, muscle weakness
57
clinical characteristics of low Ca2+
tetany, seizures, QT prolongation, twitching chovsteks and spasm trousseau
58
clinical characteristics of high Ca2+
stones, bones, groans, thrones, psychiatric overtones
59
clinical characteristics of low Mg
tetany torsades de pointes, hypokalemia, hypocalcmia
60
clinical characteristics of high Mg
hyporeflexia, lethargy, bradycardia, hypotension, cardiac arrest, hypoCa
61
what electrolyte is used to treat vasospasm
Mg
62
clinical characteristics of low phosphate
bone loss, osteomalacia, rickets
63
clinical characteristics of high phosphate
renal stones, metastatic calcification, hypoCA
64
defining/differentiating clinical characteristics for acute cystitis
pyuria, no casts
65
defining/differentiating clinical characteristics for bladder CA and kidney stones
hematuria, no casts
66
what do urine casts indicate when present with hematuria or pyuria
hematuria and pyuria is from glomerulus or renal tubules
67
what dx do RBC casts suggest
GN, malignant HTN
68
what dx do WBC casts suggest
acute PN, tubulointerstitial inflammation, transplant rejection
69
what dx do fatty casts suggest
nephrotic syndrome
70
what dx do granular casts suggest
ATN
71
what dx do waxy casts suggest
ESRD, CRF
72
what dx do hyaline casts suggest
nonspecific, often seen in concentrated urine
73
membranous glomerulopathy etiology
damage due to immune complexes activating complement which causes damage to podocytes and mesangial cells primary (idiopathic) 75% secondary: hodgkins, lupus, drugs (NSAIDs, gold, mercury, captopril, penicillamine), infxn (hep B/C, syphilis), solid tumors (colorectal carcinoma)
74
what cells are damaged in membranous glomerulopathy
podocytes an mesangial cells
75
RF membranous glomerulopathy
white
76
membranous glomerulopathy complications
RVT (renal vein thrombosis)
77
membranous glomerulopathy clinical characteristics
HTN | nephrotic sx
78
what are general sx of all nephrotic syndromes
``` HIGH proteinuria edema (pitting, periorbital) hypoalbuminemia hyperlipidemia lipiduria proteinuria frothy urine ```
79
focal segmental glomerulosclerosis etiology
primary: idiotpathic, podocyte foot processes damaged secondary: heroin drug use, HIV, sickle cell, interferon tx, congenital malformations
80
focal segmental glomerulosclerosis RF
african american pts | young adults
81
what nephrotic syndrome makes up 1/6 of all
focal segmental glomerulosclerosis
82
focal segmental glomerulosclerosis prognosis
poor
83
minimal change disease etiology
primary: unclear; can occur afer URI or immunization secondary: drugs (NSAIDS, antibiotics, lithium), hodgkins, syphilis, TB, allergy
84
minimal change disease clinical characteristics
none to mild nephrotic sx LM: mild mesangial prolif and few deposits EM: epithelial foot process flattened
85
membranoproliferative glomerulonephritis (MPGN) etiology
immune complexes and complement primary: idiopathic secondary: RA, HCV, HBC variant: C3 GN-C3 deposits: hematuria after URI
86
membranoproliferative glomerulonephritis (MPGN) complication
RPGN
87
membranoproliferative glomerulonephritis (MPGN) clinical characteristics
nephrotic sx insidious histology: difuse thickening (hypercellularity) of glomerular capillary wall with Ig deposits
88
diabetic glomerulonephropathy etiology
occurs several years after onset of DM (I and II) excess glucose causes BSM of efferent arteriole to thicken, creating obstruction and inc pressure > expansion of mesangial cells
89
diabetic glomerulonephropathy complication
renal failure
90
diabetic glomerulonephropathy clinical
no overt sx histology: glomerulosclerosis - nodular (kimmelsteil wilson disease), diffuse, or nodular diffuse microalbuminuria macroalbuminuria dec GFR
91
lupus nephritis etiology
anti DNA and anti dsDNA immune complexes deposit on glomerular mesangium
92
lupus nephritis RF
african amerians (APO1 gene variants common)
93
lupus nephritis clincal
renal involvement + skin, joint sx, anemia, photosensitivty, pericardial or pleural effusion hematuria proteinuria casts low C3, C4 wire loop lesions on biopsy
94
fabry disease etiology
x linked deficiency of alpha galactosidase A leading to an accumulation of glycolipids
95
fabry disease clinical characteristics
proteinuria, renal failure ``` lipids in: joints skin eyes heart GI ```
96
pre-renal acute renal failure pathophys
dec renal flow inc Na + H2O retention, baroceeptors activate > inc sympathetioc > afferert vasoconstriction > dec GFR renin/aldosterone > inc Na + H2O water resroption
97
pre-renal acute renal failure causes
dec intravascular volume (hemorrhage, dehydration, pancreatitis, burns, trauma) changes in vascualr resistance (sepsis, anaphylaxis, drugs [ACEi, NSAIDs], renal artery stenosis) low CO (CHF, PE, pericardial tamponade)
98
pre-renal acute renal failure RF
DM, hypertensives, geriatrics
99
pre-renal acute renal failure complications
death | fluid accumulation
100
acute renal failure general sx for all types
``` N/V malaise ecchymosis pallor arrhythmias edema fasiculation seizure blood volume abnormalities dehydration ```
101
3 types of acute renal failure differentiating clinical characteristics
pre-renal: osmol >500, FeNa <1, BUN/Cr >20 dehydration sx, orthostatic hypo, tachycardic intrinsic: osmol <350, FeNa >1, BUN/Cr N (10-15:1) WBC casts (PN, AIN), RBC casts (PSGN) hearing loss, ischemic toe, uveitis, scleroderma, bruit post-renal: osmol >500, BUN/Cr 10-20:1 renal pain, lower ab pain, post surgery urine leak, overhydration, abd disten Na <20 early, >40 late
102
intrinsic acute renal failure etiology
damage to tubules, interstitium, vasculature, glomeruli > loss of function ATN: cannot resorb Na, water, electrolytes, urea AIN: loss of concentation ability
103
intrinsic acute renal failure causes
ATN, AIN | PSGN, RPGN, acute pyelonephritis, vasculitis, nephrotic syndromes
104
intrinsic acute renal failure RF
DM, hypertensives, geriatrics, IV drugs, URI
105
post-renal acute renal failure etiology
abrupt obstruction of urine from both kidneys > inc nephron intraluminal back pressure > inc bowmans capsule hydrostatic pressure > dec GFR
106
post-renal acute renal failure causes
prostatic enlargement, tumors, urolithiasis, renal vein stenosis, neurogenic bladder, meds, trauma, post-surgical
107
post-renal acute renal failure RF
DM, hypertensives, geriatrics
108
chronic renal failure etiology
loss of functioning nephron leads to buildup of urea, cant regulate fluids and electrolytes
109
chronic renal failure causes
diabetes, HTN, PCKD, focal segmental glomerulosclerosis, membranous nephropathy, membranoproliferatie GN, IgA nephropathy, PIGN, RPGN, nephrolithiasis, tumor, prostate conditions, drugs/toxins, sickle cell, amyloidosis, SLE, renal artery stenosis
110
chronic renal failure sx
``` HTN edema fatigue weakness SOB N/V numbness low SG low osmol broad waxy casts dec GFR anemia azotemia low Bun:Cr microalbuminemia hyperkalemia, hyperphosphatemia hypocalcemia ```
111
what is the most common cause of ARF
acute tubular necrosis (ATN)
112
acute tubular necrosis (ATN) etiology/pathophys
patchy focal nerosis of tubule, lumens fill with casts, cellular debris; due to drugs, contrast, lithium
113
ATN - contrast induced nephropathy etiology
iodinated radiocontrast agent | 48 hrs causing renal hypoxia and tubular obstruction
114
ATN - contrast induced nephropathy RF
elderly, DM, CHF, liver dz
115
ATN general sx
``` Bun:Cr <15 dec GFR brown granular casts, hyaline casts dilute urnie inc K FeNa >2 RTE + RTE casts osmol <400 inc creatinine hematuria mild proteinuria ```
116
ATN - cisplatin induced nephropathy etiology
chemotherapeutic agent causes both vascular damage and tubular inflammation
117
ATN - lithium induced nephropathy etiology
one month onset of lithium
118
ATN - lithium induced nephropathy differentiating sx
``` cardiotoxicity polydipsa obtundation polyuria ortho hypo ```
119
ischemia/hypotension ATN causes
shock, trauma, surgery, DIC, vasoconstrictive drugs (ACE, ARBs)
120
ischemic ATN etiology
partchy PCT and DCT due to hypovolemia, shock, renal artery stenosis, embolism in renal artery, etc. causes skin lesions through tubules
121
ischemia/hypotension ATN clinical characteristics
``` pericardial friction rub uremic pruritis HTN edema oliguria ```
122
hydronephrosis etiology
congenital or acquired dilation of renal pelvis and calyces from obstruction/retained urine back pressure causes renal atrophy, compresses renal vasculature > dec ability to conc urine, damage to gloomeruli retained urine diffuses into interstitium and perineal spaces, returns to lympathic and venous system leads to scarring and atrophy of papillae > inability to conc urine, salt wasting, HTN if complete: anuria (>death)
123
hydronephrosis clinical characteristics
``` flank, lower abd, testes/labia pain pain in flank during urination abdominal mass N/V urgency, frequency polyuria/nocturia HTN anuria ``` BUN/Cr inc hypernatremia, hyperkalemia
124
what are two main inflammatory urinary tract diseases?
AIN, chronic pyelonephritis
125
acute interstitial nephritis (AIN)
inflammation of renal interstitium from cell mediated immune response binding to interstitial proteins, leading to dec in renal function 1-2 weeks after taking NSAIDS/ibuprofen, acetaminophen, penicillins, thiazides, sulfa, PDE5 in, acyclovir infxn: strep, s aureus, corynebacterium, brucella, pneumococcus, TB, HIV, EBV, lepto SLE, sarcoidosis, sjogrens
126
AIN sx
``` fever wt loss flank pain fatigue hadache polyuria rash hematuria oliguria N/V malaise ``` ``` inc eosinnophils, WBC, neutrophils WBC casts proteinuria, hematuria, no bacteria inc BUn and cr FeNa >1 dec urine conc, dec GFR ```
127
chronic pyelonephritis etiology/path
often bilateral pyogenic kidney infxn or congenital reflux nephropathy > renal parenchymal scarring and atrophy of calyces
128
chronic pyelonephritis RF
elderly, DM, chronic urolithiasis, low water intake, infrequent urination, urine reflux, sedentary lifestyle, BPH with obstruction, chornic analgesic use, recurrent bacterial UTI
129
chronic pyelonephritis sx
asx HTN olioguria late stage bactururia, pyuria if active infxn dec SG and osmol late: granular, waxy, broad casts small atophic kidney, irregular outline, poor exception of contrast
130
what are some common congenital urinary diseases?
alport syndrome ADPKD renal agenesis vesicouretal reflux (VUR)
131
alport syndrome etiology
hereditary or familial nephritis inherited collagen synthesis defect leading to GBM thinness and dysfunction
132
alport syndrome RF
males
133
alport syndrome complication
progression > ESKD
134
alport syndrome sx
``` sensorineural hearing loss ocular lesions HTN edema hematuria aftre URI proteinuria oliguria ```
135
autosomal dominant polycystic kidney disease (ADPKD) etiology
mutation in PKD 1 or PKD 2 mutation in renal tubule cell causes cellular divison until cysts develop major cause of CKD
136
autosomal dominant polycystic kidney disease (ADPKD) complications
CKD, ESRD, rupture, UTI, nephrolithiasis, HTN, ESRF, cerebral aneurysm, MVP, aortic aneurysm, colonic diverticula, cyst in liver, pancreas, spleen, CNS
137
autosomal dominant polycystic kidney disease (ADPKD) sx
``` hematuria flank pain HTN kidney stones pain over both kidneys nocturia HA N/V wt loss progressive uremia bacteruria pyuria proteinuria anemia ```
138
autosomal dominant polycystic kidney disease (ADPKD) diagnostic criteria
15-39 - 3 cysts in both k 40-59 - 2 cysts in both k pos fam hx CT diagnostic
139
vesicouretal reflux (VUR) etiology
malposition or incompetent closure of UVJ allows for urine to reflux from bladder congenital or acquired (scarring, obstruction)
140
vesicouretal reflux (VUR) sx
asym present as recurrent UTI (esp pyelonephritis) HTN
141
common urinary vascular diseases
``` hemolytic uremic syndrome (HUS) hyperensive nephrosclerosis renal artery stenosis renal infarction sickle cell nephropathy ```
142
hypertensive nephrosclerosis etiology
chronic HTN (>10 yrs) damages microvascualture, glomeruli, tubules, interstitial tissues > nephrosclerosis may progress to ESRD injuries include ischemic glomerular tuft collapse, glomerulosclerosis, interstitial fibrosis and tubular atophy
143
hypertensive nephrosclerosis RF
aging, poorly controlled HTN, DM, black individuals, genetics (APOL1)
144
hypertensive nephrosclerosis complications
second most common cause of ESRD
145
hypertensive nephrosclerosis clinical
inc BUN, cr hyperuricemia kidneys may look small from scarring no sediments/proteinuria
146
renal artery stenosis etiology
from atherosclerotic plaque or fibromuscular dysplasia (intractable HTN from renin release)
147
renal artery stenosis causes
HTN
148
renal artery stenosis RF
older males, atherosclerotic plaques, HTN in younger pts, from fibromuscular dysplasia of renal arteries (more in F)
149
renal artery stenosis clinical
bruit inc BP hypokalemia stenotic kidney inc renin contralateral kidney responds to HTN by dec renin
150
renal infarction etiology/causes
reduction of blood flow to one or both kidneys caused by thromboemboli (from heart or aorta) and in situ thrombosis
151
renal cell carcinoma (RCC) etiology
malignant originates from PCT cells, polygonal clear cells filled with accumulated lipids and carbs most common primary renal malignancy
152
renal cell carcinoma (RCC) RF
smoking, analgesics, toxin exposure, high coffee consumption, chemo, hysterectomy, obesity, cystic kidney dz, contrast, HTN, dialysis, von hippel landau dz males 50-70
153
renal cell carcinoma (RCC) complications
invades the renal vein and may develop a variocele if L sided can go into IVC and spread hematogeously, mets to bone and lung
154
renal cell carcinoma (RCC) sx
``` hematuria palpable mass polycythemia flank pain fever wt loss ```
155
nephroblastoma (wilms tumor) etiology
malignant most from defects on chromosome 11 most comnmon primary renal tumor of childhood
156
nephroblastoma (wilms tumor) RF
black pts fhx children 2-5
157
nephroblastoma (wilms tumor) complications
mets to lungs
158
nephroblastoma (wilms tumor) sx
``` abdominal enlargment flank mass abd pain N/V constipation loss of appetite SOB hematuria HTN anemia ```
159
acute pyelonephritis etiology
common inflammation affecting the tubules, interstitium, and renal pelvis ascending infxn most common 85-90% from gram neg bacilli (usually e coli)
160
acute pyelonephritis causes
urinary tract obstruction/stasis (organisms multiply) vesicouretal reflux intrarenal reflux
161
acute pyelonephritis complications
renal abcess recurrent infxns papillary necrosis (worse prognosis)
162
acute pyelonephritis sx
``` fever N/V chills unilateral flank pain abd pain myalgia fatigue weakness CVA tenderness ``` ``` WBC in urine WBC cats leukocytosis pyuria bacteruria hematuria ```
163
bacterial cystitis etiology
e coli, proteus, klebsiella, enterbacteria
164
cystitis RF
females
165
cystitis sx
``` urgency, frequency, dysuria, nocturia hematuria pain with filling/emptying suprapubic pain burning pressure chronic pelvic pain ```
166
interstitial cystisis sx
``` cystitis sx pain with bladder fullness severe frequency hunners ulcers bladder distention ``` sx > 6 weeks, absences of other sx
167
gonoccocal urethritis etiology
STI common men neisseria gonorrhoeae
168
gonoccocal urethritis complications
epididymitis, prostatic involvement, infertility, prostatitis, recurrent infxns
169
gonoccocal urethritis sx
copious, purulent urethral discharge (yellow, brown) ``` dysuria urethral itching meatal edema urethral tenderness pyuria bacteriuria hematuria ``` gram neg diplococci
170
non-gonoccocal urethritis etiology
chlamydia | incubation 2-35 days (less acute onset)
171
non-gonoccocal urethritis complications
epididymitis, prostatitis, proctitis, reactive arthritis, lymphogranuloma venereum
172
non-gonoccocal urethritis sx
scant, white to clear watery urethral discharge dysuria urethral itching meatal edema and erythema cant culture chlamydia
173
acute urethritis in women etiology
gonorrheal or chlamydial
174
acute urethritis in women sx
``` asx frequency urgnecy lower abdominal pain cervicitis ```
175
maple syrup urine disease (AR) etiology
blocked degradation of branch chain amino acids (isoleucine, leucine, valine) dec branched chain a ketoacid dehydrogenase inc a keto acids in blood
176
maple syrup urine disease (AR) sx
``` vomiting poor feeding urine smells like syrup severe CNS defects intellectual disability death ```
177
embryologic origin of bladder
endoderm: epithelial lining
178
embryologic origin of kidneys
mesoderm
179
bladder circulatory supply
internal iliac arteries
180
ureters plug into bladder at the
bottom
181
Ureters pass where in relation to the uterine artery or vas deferens
under (retroperitoneal)
182
renal artery and vein enter and exit at the
hilium
183
the glomerulus is surrounded by the
bowmans capsule
184
the nephron includes
``` afferent + efferent arterioles glomerulus/bowmans capsule PCT loop of henle DCT collecting duct ```
185
two types of nephrons
cortical (only have asc and desc loops) | juxtamedullary (thin loop of henle)
186
afferent arteriole brings blood
into glomerulus
187
efferent arteriole brings blood
out of glomerulus
188
where does the peritubular capillary system/vasa recta come off of? afferent or efferent
efferent arteriole peritubular capillary sys keeps you from reabsorping bad stuff, keeps good stuff going back into blood.
189
glomerulus is made up of
type 2 capillaries; mildly leaky, can filter
190
afferent arterioles are sensitive to
epinephrine (constriction/dec GFR)
191
efferent arterioles are sensitive to
angiotensin-2 (constriction/inc GFR)
192
epinephrine effect on GFR
decreases
193
angiotensin 2 effect on GFR
increases
194
glomerulus filtration type + components
pure filtration; pressure, fluid, pore size > urinary filtrate
195
peritubular capillaries function
resorb good stuff | secrete bad stuff
196
macula dense function and location
sensory apparatus at end of tubular system and wound up near afferent/efferent arterioles
197
renal blood flow (RBF) values compared to renal plasma flow (RPF) values
RBF is about double RPF
198
why is normal filtration fraction high?
FF = GFR / RPF type II glomerular capillaries ONLY filter plasma, and RPF is half of RBF
199
interpretation of clearance > GFR
filtration + net secretion
200
interpretation of clearance = GFR
filtration only (or secretion = resorption)
201
interpretation of clearance < GFR
filtration and net resorption
202
most common cause of hyperosmolality
dehydration
203
hyperosmolality results in:
thirst ADH release trying to thin blood out
204
where are receptors for osmoregulation located
hypothalamus
205
what are the receptors for volume regulation
baroreceptors | macula densa
206
blood volume loss results in:
sympathetic activation | renin release from JGA
207
proximal tubule reabsorption/activity
67% Na reabsorption via Cotransporter + countertransporter in Na/H exhange 67% K reabsorption along with Na + H2O all glucose, PCO3, and amino acids
208
thick asc loop of henle reabsorption/activity
25% Na resorption 20% K resorption Na-K-2Cl transporter
209
distal tubule/collecting duct reabsorption/activity
8% Na resorption via Na-Cl cotransporter site of thiazide diuretic action either reabsorbs (low blood potassium) or secretes K+ into urine (high blood potassium) based on dietary intake
210
carbonic anhydrase inhibitiors site of action
proximal tubule
211
loop diuretic site of action
henle loop
212
thiazide diuretics site of action
distal tubule
213
where is H+ secreted and as what
proximal and distal tubule | NH4, phosphate, uric acid, H+
214
recovery of bicarbonate takes place mostly where
proximal tubule
215
juxtoglomerular apparatus function
low Na/Cl at macula densa > low GFR > JGA releases renin in response to low GFR > forms ANG-II > constricts EFF art > inc GFR
216
low GFR = | ion levels
= inc Na/Cl reabsorption in loop of henle | = low Na/Cl at macula densa
217
angiotensinogen produced by the
liver
218
activation of aldosterone-renin-angiotensin system
dec GFR (low blood vol/high blodo osmolarity) > juxtoglomerular cells release renin which converts angiotensin to angiotensin I
219
conversion of angiotensin I-angiontensin II
conversion by ACE enzyme from lungs
220
activities of angiotensin II
1. GFR inc by efferent arteriole constriction | 2. zona glomerulosa (adrenal cortex) activation of aldosterone
221
aldosterone action
> distal tubule, causes Na reabsorption, K excretion | inc H2O resorption, inc blood vol, dec osmolarity
222
renin produced by the
kidney (JGA)
223
ANP produced by the
heart
224
aldosterone-renin-angiotensin system function
regulation of blood volume activated by dec in renal blood flow
225
less ADH effect on osmolarity and urine volume
inc urine vol dec urine osmolarity inc plasma osmolarity
226
more ADH effect on osmolarity and urine volume
dec urine volume inc urine osmolarity dec plasma osmolarity
227
ADH response to dehydration
increases
228
transamination and amine transfer occur in the
liver (most) | kidneys
229
oxidative deamination
taking amine off of amino acid > alpha keto acid
230
reductive amination
taking alpha keto acid > amino acid
231
transamination rxns consist of
oxidative deamination | reductive amination
232
transamination rxns purpose
removing nitrogen
233
transaminases require
vit B6
234
where does urea cycle occur
liver cell
235
main purpose of urea cycle
the way the liver takes two very dangerous metabolites (CO2 + NH4/ammonia) > combines them > converts them to urea > excrete into blood > filtered out via tubular system
236
why is urea safer to excrete than CO2 and ammonia?
because CO2 and NH4 (ammonia( are directly toxic to every cell, urea is mildly inert unless it builds up a LOT
237
what part of the urea cycle happens in the mitochondria?
CO2 + NH4 > carbamyl phosphate (CP) via CP synthase CP + ornithine > citrulline via ornithine transcarbamoylase
238
what part of the urea cycle happens in the cytosol?
citrulline > arginosuccinate > arginine argninase cleaves urea molecule off of arginine to leave to liver + kidney residue ortnithine goes back into mitochondria
239
backup for N excretion
glutamate shuttle (glutamate is multi-N carrier)
240
glutamate shuttle
glutamate > deaminated > NH3 to urine NH3 meet H+ > NH4 > excreted into urine NH4 excreted DIRECTLY into urine
241
acute post-strep glomerulonephritis clinical characteristics
RBC casts, 1-2 wks after sore throat | kids 6-10, mod proteinuria
242
IgA nephropathy/bergers dz patho
inc IgA in response to viruses, bacteria, food proteins antibodies injure glomerulus
243
IgA nephropathy/Bergers dz clinical characteristics
hematuria comes and goes, chronic GN
244
goodpastures syndrome patho/etiology
rapid GN with type II autoantibodies to basement membrane
245
goodpastures RF
young men who smoke
246
goodpastures complications
death due to renal failure or lung hemorrhage
247
henoch schonlein purpura patho/etiology
purpuric skin lesions on extensor surface of extremities and buttock igA precipitation after respiratory infxn, kids 3-8 hematuria recurres for years
248
pyelo- indicates
renal pelvis
249
most common cause of nephrotic syndrome in kids
primary kidney dz
250
most common causes of nephrotic syndrome in adults
membranous GN, SLE, DM, amyloidosis
251
pyelonephritis affects which locations
tubules and interstitium
252
common causes of pyelonephritis
ascending fecal flora, females, pregnancy, BPH (secondary to stasis of urine)
253
what is hydronephrosis
dialtion of renal pelvis and calyces asso. with progressive atophy of kidney due to obstruction of urine outflow
254
ways pyelonephritis can kill you
kidney failure | bacteria > blood > sepsis
255
most common kidney stone substance
Ca Oxalate
256
intrinsic causes of obstruction
renal calculi, strictures, blood clots, tumors
257
extrinsic causes of obstruction
pregnancy, periureteral inflammation/salpingitis/peritonitis, tumors of rectum/bladder/prostate/ovaries
258
uric acid calculi are secondary to
gout
259
causes of obstruction of bladder neck
prostate enlargement chronic cystitis tumors, foreign body, calculi
260
what is the number one RF for renal cancer
smoking
261
what is a common sx of renal cancer
painless hematuria
262
most common bladder tumor
transitional cell carcinoma
263
wilms tumor (nephroblastoma) occurs in what age group
2-5
264
what would you suspect in a child 2-5 with abdominal mass
nephroblastoma (renal) | neuroblastoma (adrenal medulla)
265
kidneys role in maintaning acid-base balance of the blood
reabsorb bicarbonate HCO3- from urine > blood secrete H+ ions > urine
266
which kidney has a longer renal vein
left
267
describe renal blood flow
renal a > segmental a > interlobar a > arcuate a > interlobular a > afferent art > glomerulus > efferent art > vasa recta/peritubular cap > venous outflow
268
what part of the kidney is more susceptible to ischemia and hypoxia? why?
renal medulla (less blood flow than cortex)
269
the visceral layer of bowmans capsule is made up of
podocytes
270
3 common points of uretal obstruction
uretopelvic junction pelvic inlet ureterovesical junction