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NPLEX I (2022) > Renal > Flashcards

Renal Flashcards

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
Q

metabolic acidosis clinical

A

headache, hypotension, hyperkalemia, muscle twitching, warm flushed skin, N/V, dec muscle tone. dec reflexes, kussmaul respirations,

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26
Q

respiratory alkalosis cause

A

anxiety, hypoxemia, salicylates, tumor, PE, pregnancy

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27
Q

metabolic alkalosis clinical

A 
restlessness followed by lethargy 
dysrhythmias 
compensatory hypoventilation 
confusion 
N/V 
diarrhea 
tremors
muscle cramps
hypokalemia 
paresthesia
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28
Q

Nephritic syndrome path

A

glomerular inflammation leads to basement membrane damage > loss of RBC in urine > hematuria

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29
Q

Nephritic syndrome clinical

A

hematuria, RBC cats, oliguria, azotemia, HTN, proteinuria (mild), increased renin release

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30
Q

thin descending loop of henle

A

passive reabsorption of water
impermeable to sodium
makes urine hyeprtonic (concentrated)

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31
Q

ACE function

A

catalyzes conversion of angiotensin I to II

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32
Q

aldosterone function and mechanism

A

regulates extracellular volume and sodium content by targeting kidneys in response to hypovolemic and hyperkalemic (inc potassium excretion) states

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33
Q

low bicarb =

A

metabolic acidosis

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34
Q

high bicarb =

A

metabolic alkalosis (check urine chloride)

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35
Q

with low bicarb you suspect ___ and should check ___

A

metabolic acidosis, anion gap

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36
Q

with high bicarb you suspect ___ and should check ___

A

metabolic alkalosis, urine chloride

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37
Q

nephritic syndrome ex

A 
infxn-associated glomerulonephritis
goodpasture syndrome
igA nephropathy (berger dz)
alport syndrome
membranoproliferative glomeulonephritis
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38
Q

infxn associated glomerulonephritis etiology

A

type II hypersensitivity rxn
kids: group A strep
Adults: straph or strep

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39
Q

IgA nephropathy (berger disease)

A

episodic hematuria occuring concurrently with respi or GI infxn

igA secreted by mucosal linings

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40
Q

alport syndrome

A

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

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41
Q

nephrotic syndrome etiology

A

podocyte damage > impaired charge barrier > MASSIVE proteinuria

associated with hypercoagulable state d/t antithrombin III loss in urine

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42
Q

nephrotic syndrome clinical characteristics

A

edema, hypoalbuminemia, HLD, frothy urine with fatty casts

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43
Q

nephrotic syndrome ex

A

primary
secondary - amyloidosis, diabetic glomerulonephropathy, lupus nephritis, fabry dz

both - focal segmental glomerulosclerosis, minimal change dz, membranous glomerulopathy, membranoproliferatie glomerulonephritis

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44
Q

glomerulosclerosis etiology

A

idiopathic, or due to other conditions:

HIV, sickle cell, heroin use, obesity, congenital malformations, drug induced

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45
Q

glomerulosclerosis complication

A

CKD

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46
Q

erythryopoietin:

released from where
in response to what
function

A

released from interstitial cells in peritubular capillary bed in response to hypoxia

stimulate RBC proliferation in BM

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47
Q

calciferol (VitD) conversion process, and stimulation

A

PCT converts OH > OH calcitrol active form via 1a hydroxylase
^ by PTH

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48
Q

prostaglandins are secreted from where to do what

A

secreted by paracrine to vasodilate afferent arterioles to increase RBF

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49
Q

dopamine is secreted by what cells to do what

A

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

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50
Q

PTH:
secreted from where
in response to what
function

A

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

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51
Q

what is the primary fuel source for the kidneys

A

glutamine

nitrogen is used to help with acid-base balance, but not a fuel source

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52
Q

clinical characteristics of low Na

A

N, malaise, stupor, coma, serizures

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53
Q

clinical characteristics of high Na

A

irritability, stupor, coma

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54
Q

causes of hyponatremia

A

hypovolemic: renal loss/GI loss
euvolemic: SIADH, hypothyroid, adrenal insufficiency, primary polydipsia
hypervolemic: HF, cirrhosis, nephrotic syndrome

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55
Q

clinical characteristics of low K

A

U waves and flat T waves on ECG, arrhythmias, cramps, spasm, weakness

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56
Q

clinical characteristics of high K

A

wide QRS, peaked T wave, arrthmyias, muscle weakness

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57
Q

clinical characteristics of low Ca2+

A

tetany, seizures, QT prolongation, twitching chovsteks and spasm trousseau

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58
Q

clinical characteristics of high Ca2+

A

stones, bones, groans, thrones, psychiatric overtones

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59
Q

clinical characteristics of low Mg

A

tetany torsades de pointes, hypokalemia, hypocalcmia

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60
Q

clinical characteristics of high Mg

A

hyporeflexia, lethargy, bradycardia, hypotension, cardiac arrest, hypoCa

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61
Q

what electrolyte is used to treat vasospasm

A

Mg

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62
Q

clinical characteristics of low phosphate

A

bone loss, osteomalacia, rickets

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63
Q

clinical characteristics of high phosphate

A

renal stones, metastatic calcification, hypoCA

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64
Q

defining/differentiating clinical characteristics for acute cystitis

A

pyuria, no casts

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65
Q

defining/differentiating clinical characteristics for bladder CA and kidney stones

A

hematuria, no casts

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66
Q

what do urine casts indicate when present with hematuria or pyuria

A

hematuria and pyuria is from glomerulus or renal tubules

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67
Q

what dx do RBC casts suggest

A

GN, malignant HTN

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68
Q

what dx do WBC casts suggest

A

acute PN, tubulointerstitial inflammation, transplant rejection

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69
Q

what dx do fatty casts suggest

A

nephrotic syndrome

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70
Q

what dx do granular casts suggest

A

ATN

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71
Q

what dx do waxy casts suggest

A

ESRD, CRF

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72
Q

what dx do hyaline casts suggest

A

nonspecific, often seen in concentrated urine

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73
Q

membranous glomerulopathy etiology

A

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)

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74
Q

what cells are damaged in membranous glomerulopathy

A

podocytes an mesangial cells

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75
Q

RF membranous glomerulopathy

A

white

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76
Q

membranous glomerulopathy complications

A

RVT (renal vein thrombosis)

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77
Q

membranous glomerulopathy clinical characteristics

A

HTN

nephrotic sx

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78
Q

what are general sx of all nephrotic syndromes

A 
HIGH proteinuria
edema (pitting, periorbital)
hypoalbuminemia
hyperlipidemia
lipiduria
proteinuria
frothy urine
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79
Q

focal segmental glomerulosclerosis etiology

A

primary: idiotpathic, podocyte foot processes damaged
secondary: heroin drug use, HIV, sickle cell, interferon tx, congenital malformations

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80
Q

focal segmental glomerulosclerosis RF

A

african american pts

young adults

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81
Q

what nephrotic syndrome makes up 1/6 of all

A

focal segmental glomerulosclerosis

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82
Q

focal segmental glomerulosclerosis prognosis

A

poor

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83
Q

minimal change disease etiology

A

primary: unclear; can occur afer URI or immunization
secondary: drugs (NSAIDS, antibiotics, lithium), hodgkins, syphilis, TB, allergy

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84
Q

minimal change disease clinical characteristics

A

none to mild
nephrotic sx

LM: mild mesangial prolif and few deposits
EM: epithelial foot process flattened

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85
Q

membranoproliferative glomerulonephritis (MPGN) etiology

A

immune complexes and complement

primary: idiopathic
secondary: RA, HCV, HBC
variant: C3 GN-C3 deposits: hematuria after URI

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86
Q

membranoproliferative glomerulonephritis (MPGN) complication

A

RPGN

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87
Q

membranoproliferative glomerulonephritis (MPGN) clinical characteristics

A

nephrotic sx
insidious

histology: difuse thickening (hypercellularity) of glomerular capillary wall with Ig deposits

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88
Q

diabetic glomerulonephropathy etiology

A

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

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89
Q

diabetic glomerulonephropathy complication

A

renal failure

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90
Q

diabetic glomerulonephropathy clinical

A

no overt sx

histology:
glomerulosclerosis - nodular (kimmelsteil wilson disease), diffuse, or nodular diffuse

microalbuminuria
macroalbuminuria
dec GFR

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91
Q

lupus nephritis etiology

A

anti DNA and anti dsDNA immune complexes deposit on glomerular mesangium

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92
Q

lupus nephritis RF

A

african amerians (APO1 gene variants common)

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93
Q

lupus nephritis clincal

A

renal involvement + skin, joint sx, anemia, photosensitivty, pericardial or pleural effusion

hematuria
proteinuria
casts

low C3, C4

wire loop lesions on biopsy

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94
Q

fabry disease etiology

A

x linked deficiency of alpha galactosidase A leading to an accumulation of glycolipids

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95
Q

fabry disease clinical characteristics

A

proteinuria, renal failure

lipids in:
joints
skin
eyes
heart
GI
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96
Q

pre-renal acute renal failure pathophys

A

dec renal flow inc Na + H2O retention, baroceeptors activate > inc sympathetioc > afferert vasoconstriction > dec GFR renin/aldosterone > inc Na + H2O water resroption

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97
Q

pre-renal acute renal failure causes

A

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)

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98
Q

pre-renal acute renal failure RF

A

DM, hypertensives, geriatrics

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99
Q

pre-renal acute renal failure complications

A

death

fluid accumulation

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100
Q

acute renal failure general sx for all types

A 
N/V
malaise
ecchymosis
pallor
arrhythmias 
edema
fasiculation
seizure
blood volume abnormalities 
dehydration
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101
Q

3 types of acute renal failure differentiating clinical characteristics

A

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

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102
Q

intrinsic acute renal failure etiology

A

damage to tubules, interstitium, vasculature, glomeruli > loss of function

ATN: cannot resorb Na, water, electrolytes, urea

AIN: loss of concentation ability

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103
Q

intrinsic acute renal failure causes

A

ATN, AIN

PSGN, RPGN, acute pyelonephritis, vasculitis, nephrotic syndromes

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104
Q

intrinsic acute renal failure RF

A

DM, hypertensives, geriatrics, IV drugs, URI

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105
Q

post-renal acute renal failure etiology

A

abrupt obstruction of urine from both kidneys > inc nephron intraluminal back pressure > inc bowmans capsule hydrostatic pressure > dec GFR

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106
Q

post-renal acute renal failure causes

A

prostatic enlargement, tumors, urolithiasis, renal vein stenosis, neurogenic bladder, meds, trauma, post-surgical

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107
Q

post-renal acute renal failure RF

A

DM, hypertensives, geriatrics

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108
Q

chronic renal failure etiology

A

loss of functioning nephron leads to buildup of urea, cant regulate fluids and electrolytes

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109
Q

chronic renal failure causes

A

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
Q

chronic renal failure sx

A 
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
Q

what is the most common cause of ARF

A

acute tubular necrosis (ATN)

112
Q

acute tubular necrosis (ATN) etiology/pathophys

A

patchy focal nerosis of tubule, lumens fill with casts, cellular debris; due to drugs, contrast, lithium

113
Q

ATN - contrast induced nephropathy etiology

A

iodinated radiocontrast agent

48 hrs causing renal hypoxia and tubular obstruction

114
Q

ATN - contrast induced nephropathy RF

A

elderly, DM, CHF, liver dz

115
Q

ATN general sx

A 
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
Q

ATN - cisplatin induced nephropathy etiology

A

chemotherapeutic agent causes both vascular damage and tubular inflammation

117
Q

ATN - lithium induced nephropathy etiology

A

one month onset of lithium

118
Q

ATN - lithium induced nephropathy differentiating sx

A 
cardiotoxicity
polydipsa
obtundation
polyuria
ortho hypo
119
Q

ischemia/hypotension ATN causes

A

shock, trauma, surgery, DIC, vasoconstrictive drugs (ACE, ARBs)

120
Q

ischemic ATN etiology

A

partchy PCT and DCT due to hypovolemia, shock, renal artery stenosis, embolism in renal artery, etc. causes skin lesions through tubules

121
Q

ischemia/hypotension ATN clinical characteristics

A 
pericardial friction rub
uremic pruritis
HTN
edema
oliguria
122
Q

hydronephrosis etiology

A

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
Q

hydronephrosis clinical characteristics

A 
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
Q

what are two main inflammatory urinary tract diseases?

A

AIN, chronic pyelonephritis

125
Q

acute interstitial nephritis (AIN)

A

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
Q

AIN sx

A 
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
Q

chronic pyelonephritis etiology/path

A

often bilateral pyogenic kidney infxn or congenital reflux nephropathy > renal parenchymal scarring and atrophy of calyces

128
Q

chronic pyelonephritis RF

A

elderly, DM, chronic urolithiasis, low water intake, infrequent urination, urine reflux, sedentary lifestyle, BPH with obstruction, chornic analgesic use, recurrent bacterial UTI

129
Q

chronic pyelonephritis sx

A

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
Q

what are some common congenital urinary diseases?

A

alport syndrome
ADPKD
renal agenesis
vesicouretal reflux (VUR)

131
Q

alport syndrome etiology

A

hereditary or familial nephritis

inherited collagen synthesis defect leading to GBM thinness and dysfunction

132
Q

alport syndrome RF

A

males

133
Q

alport syndrome complication

A

progression > ESKD

134
Q

alport syndrome sx

A 
sensorineural hearing loss
ocular lesions
HTN
edema
hematuria aftre URI
proteinuria
oliguria
135
Q

autosomal dominant polycystic kidney disease (ADPKD) etiology

A

mutation in PKD 1 or PKD 2
mutation in renal tubule cell causes cellular divison until cysts develop

major cause of CKD

136
Q

autosomal dominant polycystic kidney disease (ADPKD) complications

A

CKD, ESRD, rupture, UTI, nephrolithiasis, HTN, ESRF, cerebral aneurysm, MVP, aortic aneurysm, colonic diverticula, cyst in liver, pancreas, spleen, CNS

137
Q

autosomal dominant polycystic kidney disease (ADPKD) sx

A 
hematuria
flank pain
HTN
kidney stones
pain over both kidneys
nocturia
HA
N/V
wt loss
progressive uremia
bacteruria
pyuria
proteinuria
anemia
138
Q

autosomal dominant polycystic kidney disease (ADPKD) diagnostic criteria

A

15-39 - 3 cysts in both k
40-59 - 2 cysts in both k
pos fam hx

CT diagnostic

139
Q

vesicouretal reflux (VUR) etiology

A

malposition or incompetent closure of UVJ allows for urine to reflux from bladder

congenital or acquired (scarring, obstruction)

140
Q

vesicouretal reflux (VUR) sx

A

asym
present as recurrent UTI (esp pyelonephritis)

HTN

141
Q

common urinary vascular diseases

A 
hemolytic uremic syndrome (HUS)
hyperensive nephrosclerosis
renal artery stenosis
renal infarction
sickle cell nephropathy
142
Q

hypertensive nephrosclerosis etiology

A

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
Q

hypertensive nephrosclerosis RF

A

aging, poorly controlled HTN, DM, black individuals, genetics (APOL1)

144
Q

hypertensive nephrosclerosis complications

A

second most common cause of ESRD

145
Q

hypertensive nephrosclerosis clinical

A

inc BUN, cr
hyperuricemia
kidneys may look small from scarring
no sediments/proteinuria

146
Q

renal artery stenosis etiology

A

from atherosclerotic plaque or fibromuscular dysplasia (intractable HTN from renin release)

147
Q

renal artery stenosis causes

A

HTN

148
Q

renal artery stenosis RF

A

older males, atherosclerotic plaques, HTN

in younger pts, from fibromuscular dysplasia of renal arteries (more in F)

149
Q

renal artery stenosis clinical

A

bruit
inc BP
hypokalemia

stenotic kidney inc renin
contralateral kidney responds to HTN by dec renin

150
Q

renal infarction etiology/causes

A

reduction of blood flow to one or both kidneys

caused by thromboemboli (from heart or aorta) and in situ thrombosis

151
Q

renal cell carcinoma (RCC) etiology

A

malignant

originates from PCT cells, polygonal clear cells filled with accumulated lipids and carbs

most common primary renal malignancy

152
Q

renal cell carcinoma (RCC) RF

A

smoking, analgesics, toxin exposure, high coffee consumption, chemo, hysterectomy, obesity, cystic kidney dz, contrast, HTN, dialysis, von hippel landau dz

males 50-70

153
Q

renal cell carcinoma (RCC) complications

A

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
Q

renal cell carcinoma (RCC) sx

A 
hematuria
palpable mass
polycythemia
flank pain
fever
wt loss
155
Q

nephroblastoma (wilms tumor) etiology

A

malignant

most from defects on chromosome 11

most comnmon primary renal tumor of childhood

156
Q

nephroblastoma (wilms tumor) RF

A

black pts
fhx
children 2-5

157
Q

nephroblastoma (wilms tumor) complications

A

mets to lungs

158
Q

nephroblastoma (wilms tumor) sx

A 
abdominal enlargment
flank mass
abd pain
N/V
constipation
loss of appetite
SOB
hematuria
HTN
anemia
159
Q

acute pyelonephritis etiology

A

common

inflammation affecting the tubules, interstitium, and renal pelvis

ascending infxn most common

85-90% from gram neg bacilli (usually e coli)

160
Q

acute pyelonephritis causes

A

urinary tract obstruction/stasis (organisms multiply)
vesicouretal reflux
intrarenal reflux

161
Q

acute pyelonephritis complications

A

renal abcess
recurrent infxns
papillary necrosis (worse prognosis)

162
Q

acute pyelonephritis sx

A 
fever
N/V
chills
unilateral flank pain
abd pain
myalgia
fatigue
weakness
CVA tenderness
WBC in urine
WBC cats
leukocytosis
pyuria
bacteruria
hematuria
163
Q

bacterial cystitis etiology

A

e coli, proteus, klebsiella, enterbacteria

164
Q

cystitis RF

A

females

165
Q

cystitis sx

A 
urgency, frequency, dysuria, nocturia
hematuria
pain with filling/emptying
suprapubic pain
burning
pressure
chronic pelvic pain
166
Q

interstitial cystisis sx

A 
cystitis sx
pain with bladder fullness
severe frequency
hunners ulcers
bladder distention

sx > 6 weeks, absences of other sx

167
Q

gonoccocal urethritis etiology

A

STI
common
men
neisseria gonorrhoeae

168
Q

gonoccocal urethritis complications

A

epididymitis, prostatic involvement, infertility, prostatitis, recurrent infxns

169
Q

gonoccocal urethritis sx

A

copious, purulent urethral discharge (yellow, brown)

dysuria
urethral itching
meatal edema
urethral tenderness
pyuria
bacteriuria
hematuria

gram neg diplococci

170
Q

non-gonoccocal urethritis etiology

A

chlamydia

incubation 2-35 days (less acute onset)

171
Q

non-gonoccocal urethritis complications

A

epididymitis, prostatitis, proctitis, reactive arthritis, lymphogranuloma venereum

172
Q

non-gonoccocal urethritis sx

A

scant, white to clear watery urethral discharge

dysuria
urethral itching
meatal edema and erythema

cant culture chlamydia

173
Q

acute urethritis in women etiology

A

gonorrheal or chlamydial

174
Q

acute urethritis in women sx

A 
asx
frequency
urgnecy
lower abdominal pain
cervicitis
175
Q

maple syrup urine disease (AR) etiology

A

blocked degradation of branch chain amino acids (isoleucine, leucine, valine)

dec branched chain a ketoacid dehydrogenase

inc a keto acids in blood

176
Q

maple syrup urine disease (AR) sx

A 
vomiting
poor feeding
urine smells like syrup
severe CNS defects
intellectual disability
death
177
Q

embryologic origin of bladder

A

endoderm: epithelial lining

178
Q

embryologic origin of kidneys

A

mesoderm

179
Q

bladder circulatory supply

A

internal iliac arteries

180
Q

ureters plug into bladder at the

A

bottom

181
Q

Ureters pass where in relation to the uterine artery or vas deferens

A

under (retroperitoneal)

182
Q

renal artery and vein enter and exit at the

A

hilium

183
Q

the glomerulus is surrounded by the

A

bowmans capsule

184
Q

the nephron includes

A 
afferent + efferent arterioles
glomerulus/bowmans capsule
PCT
loop of henle
DCT
collecting duct
185
Q

two types of nephrons

A

cortical (only have asc and desc loops)

juxtamedullary (thin loop of henle)

186
Q

afferent arteriole brings blood

A

into glomerulus

187
Q

efferent arteriole brings blood

A

out of glomerulus

188
Q

where does the peritubular capillary system/vasa recta come off of?

afferent or efferent

A

efferent arteriole

peritubular capillary sys keeps you from reabsorping bad stuff, keeps good stuff going back into blood.

189
Q

glomerulus is made up of

A

type 2 capillaries; mildly leaky, can filter

190
Q

afferent arterioles are sensitive to

A

epinephrine (constriction/dec GFR)

191
Q

efferent arterioles are sensitive to

A

angiotensin-2 (constriction/inc GFR)

192
Q

epinephrine effect on GFR

A

decreases

193
Q

angiotensin 2 effect on GFR

A

increases

194
Q

glomerulus filtration type + components

A

pure filtration;
pressure, fluid, pore size

> urinary filtrate

195
Q

peritubular capillaries function

A

resorb good stuff

secrete bad stuff

196
Q

macula dense function and location

A

sensory apparatus at end of tubular system and wound up near afferent/efferent arterioles

197
Q

renal blood flow (RBF) values compared to renal plasma flow (RPF) values

A

RBF is about double RPF

198
Q

why is normal filtration fraction high?

A

FF = GFR / RPF

type II glomerular capillaries ONLY filter plasma, and RPF is half of RBF

199
Q

interpretation of clearance > GFR

A

filtration + net secretion

200
Q

interpretation of clearance = GFR

A

filtration only (or secretion = resorption)

201
Q

interpretation of clearance < GFR

A

filtration and net resorption

202
Q

most common cause of hyperosmolality

A

dehydration

203
Q

hyperosmolality results in:

A

thirst
ADH release

trying to thin blood out

204
Q

where are receptors for osmoregulation located

A

hypothalamus

205
Q

what are the receptors for volume regulation

A

baroreceptors

macula densa

206
Q

blood volume loss results in:

A

sympathetic activation

renin release from JGA

207
Q

proximal tubule reabsorption/activity

A

67% Na reabsorption via Cotransporter + countertransporter in Na/H exhange

67% K reabsorption along with Na + H2O

all glucose, PCO3, and amino acids

208
Q

thick asc loop of henle reabsorption/activity

A

25% Na resorption

20% K resorption

Na-K-2Cl transporter

209
Q

distal tubule/collecting duct reabsorption/activity

A

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
Q

carbonic anhydrase inhibitiors site of action

A

proximal tubule

211
Q

loop diuretic site of action

A

henle loop

212
Q

thiazide diuretics site of action

A

distal tubule

213
Q

where is H+ secreted and as what

A

proximal and distal tubule

NH4, phosphate, uric acid, H+

214
Q

recovery of bicarbonate takes place mostly where

A

proximal tubule

215
Q

juxtoglomerular apparatus function

A

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
Q

low GFR =

ion levels

A

= inc Na/Cl reabsorption in loop of henle

= low Na/Cl at macula densa

217
Q

angiotensinogen produced by the

A

liver

218
Q

activation of aldosterone-renin-angiotensin system

A

dec GFR (low blood vol/high blodo osmolarity) > juxtoglomerular cells release renin which converts angiotensin to angiotensin I

219
Q

conversion of angiotensin I-angiontensin II

A

conversion by ACE enzyme from lungs

220
Q

activities of angiotensin II

A
  1. GFR inc by efferent arteriole constriction

2. zona glomerulosa (adrenal cortex) activation of aldosterone

221
Q

aldosterone action

A

> distal tubule, causes Na reabsorption, K excretion

inc H2O resorption, inc blood vol, dec osmolarity

222
Q

renin produced by the

A

kidney (JGA)

223
Q

ANP produced by the

A

heart

224
Q

aldosterone-renin-angiotensin system function

A

regulation of blood volume

activated by dec in renal blood flow

225
Q

less ADH effect on osmolarity and urine volume

A

inc urine vol
dec urine osmolarity
inc plasma osmolarity

226
Q

more ADH effect on osmolarity and urine volume

A

dec urine volume
inc urine osmolarity
dec plasma osmolarity

227
Q

ADH response to dehydration

A

increases

228
Q

transamination and amine transfer occur in the

A

liver (most)

kidneys

229
Q

oxidative deamination

A

taking amine off of amino acid > alpha keto acid

230
Q

reductive amination

A

taking alpha keto acid > amino acid

231
Q

transamination rxns consist of

A

oxidative deamination

reductive amination

232
Q

transamination rxns purpose

A

removing nitrogen

233
Q

transaminases require

A

vit B6

234
Q

where does urea cycle occur

A

liver cell

235
Q

main purpose of urea cycle

A

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
Q

why is urea safer to excrete than CO2 and ammonia?

A

because CO2 and NH4 (ammonia( are directly toxic to every cell, urea is mildly inert unless it builds up a LOT

237
Q

what part of the urea cycle happens in the mitochondria?

A

CO2 + NH4 > carbamyl phosphate (CP) via CP synthase

CP + ornithine > citrulline via ornithine transcarbamoylase

238
Q

what part of the urea cycle happens in the cytosol?

A

citrulline > arginosuccinate > arginine

argninase cleaves urea molecule off of arginine to leave to liver + kidney

residue ortnithine goes back into mitochondria

239
Q

backup for N excretion

A

glutamate shuttle (glutamate is multi-N carrier)

240
Q

glutamate shuttle

A

glutamate > deaminated > NH3 to urine

NH3 meet H+ > NH4 > excreted into urine

NH4 excreted DIRECTLY into urine

241
Q

acute post-strep glomerulonephritis clinical characteristics

A

RBC casts, 1-2 wks after sore throat

kids 6-10, mod proteinuria

242
Q

IgA nephropathy/bergers dz patho

A

inc IgA in response to viruses, bacteria, food proteins

antibodies injure glomerulus

243
Q

IgA nephropathy/Bergers dz clinical characteristics

A

hematuria comes and goes, chronic GN

244
Q

goodpastures syndrome patho/etiology

A

rapid GN with type II autoantibodies to basement membrane

245
Q

goodpastures RF

A

young men who smoke

246
Q

goodpastures complications

A

death due to renal failure or lung hemorrhage

247
Q

henoch schonlein purpura patho/etiology

A

purpuric skin lesions on extensor surface of extremities and buttock

igA precipitation after respiratory infxn, kids 3-8

hematuria recurres for years

248
Q

pyelo- indicates

A

renal pelvis

249
Q

most common cause of nephrotic syndrome in kids

A

primary kidney dz

250
Q

most common causes of nephrotic syndrome in adults

A

membranous GN, SLE, DM, amyloidosis

251
Q

pyelonephritis affects which locations

A

tubules and interstitium

252
Q

common causes of pyelonephritis

A

ascending fecal flora, females, pregnancy, BPH (secondary to stasis of urine)

253
Q

what is hydronephrosis

A

dialtion of renal pelvis and calyces asso. with progressive atophy of kidney due to obstruction of urine outflow

254
Q

ways pyelonephritis can kill you

A

kidney failure

bacteria > blood > sepsis

255
Q

most common kidney stone substance

A

Ca Oxalate

256
Q

intrinsic causes of obstruction

A

renal calculi, strictures, blood clots, tumors

257
Q

extrinsic causes of obstruction

A

pregnancy, periureteral inflammation/salpingitis/peritonitis, tumors of rectum/bladder/prostate/ovaries

258
Q

uric acid calculi are secondary to

A

gout

259
Q

causes of obstruction of bladder neck

A

prostate enlargement
chronic cystitis
tumors, foreign body, calculi

260
Q

what is the number one RF for renal cancer

A

smoking

261
Q

what is a common sx of renal cancer

A

painless hematuria

262
Q

most common bladder tumor

A

transitional cell carcinoma

263
Q

wilms tumor (nephroblastoma) occurs in what age group

A

2-5

264
Q

what would you suspect in a child 2-5 with abdominal mass

A

nephroblastoma (renal)

neuroblastoma (adrenal medulla)

265
Q

kidneys role in maintaning acid-base balance of the blood

A

reabsorb bicarbonate HCO3- from urine > blood

secrete H+ ions > urine

266
Q

which kidney has a longer renal vein

A

left

267
Q

describe renal blood flow

A

renal a > segmental a > interlobar a > arcuate a > interlobular a > afferent art > glomerulus > efferent art > vasa recta/peritubular cap > venous outflow

268
Q

what part of the kidney is more susceptible to ischemia and hypoxia? why?

A

renal medulla (less blood flow than cortex)

269
Q

the visceral layer of bowmans capsule is made up of

A

podocytes

270
Q

3 common points of uretal obstruction

A

uretopelvic junction
pelvic inlet
ureterovesical junction

NPLEX I (2022) (20 decks)

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