Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

First aid > Renal > Flashcards

Renal Flashcards

1
Q

Kidney embryology

A

P S T

Pronephros: week 4, then degenerates
Mesonephros: functions as interim kidney for 1st trimester, later contributes to male genital system system
Metanephros: permanent, first appears in 5th week, nephrogenesis continues though weeks 32-36 of gestation

Ureteric bud (Metenephric diverticulum)- derived from caudal end of mesonephric duct, gives rise to ureter, pelvis, calyces, collecting ducts, fully canalized by 10th week

Metenephric mesenchyme (Metenephric blastema)- ureteric bud interacts with this tissue interaction induces differentiation and formation of glomerulus through to distal convoluted tubule
Aberrent interaction between these 2 tissues results in several kidney malformations-- renal agenensis, multicystic dysplastic kidney)

Ureteropelvic junction- last to canalize–> congenital obstruction. Most common cause of prenatal hydronephrosis (detected by prenatal ultrasound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Potter sequence/syndrom

A

Oligohydramnios–> compression of developing fetus–> limb deformities, facial anomalies (low set ears and retrognathia, flattened nose), compression of chest and lack of amniotic fluid aspiration into fetal lungs–>pulmonary hypoplasia (cause of death)

Causes include ARPKD, obstructive uropathy (posterior urethral valve), bilateral renal agenesis, chronic placental insufficiency

Babies who cant pee- Pulmonary hypoplasia, oligohydramnios, twisted face, twisted skin, extremity defects, renal failure (in utero)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Horseshoe kidney

A

Inferior poles of both kidneys fuse abnormally, as they ascend from pelivis during fetal development they get caught on the IMA and remain low in the abdomen, kidneys function normally, associated with hydronephrosis (ureteropelvic junction obstruction), renal stones, infection increased risk of renal cancer

Higher incidence in chromosomal aneuploidy (turner syndrome (turner, 13 18 21)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Congenital solitary functioning kidney

A

only one functional kidney, asymptomatic, with hypertrophy of functioning, can be seen in utero

Unilateral renal ageneisis- utereteric bud fails to develop and induce differentiation of metanephric mesenchyme–> complete absence of kidney and ureter

Multicystic dysplastic kidney- Ureteric bud fails to nduce differentiation of metanephric mesenchyme–> nonfunctional kidney consisiting of cysts and CT, usually nongenentic and unilateral–> biat will be potter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Duplex collecting system

A

Bifurcation of ureteric bud before it enters the metanephric blastema creates a Y shaped bifid ureter,
Can also be 2 ureteric buds reaching and interacting with metanephric blastema

vesicoureteral reflux and/or ureteral obstruction, increased risk of UTIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Posterior urethral valves

A

membrane remnant in posterior urethra in males

Urethral obstruction- bilat hydronephrosis, dilated/thickwalled bladder on US

oligohydramnios in severe obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Kidney structure

A

Left kidney gets cut out, longer renal vein (with left gonal vein, the arteries both com from the aorta)

Renal blood flow: renal artery-> segmental artery-> interlobar artery-> arcuate artery-> interlobular artery-> aferrent arteriole-> glomerulus-> efferent arteriole-> vasa recta/ peritubular capillaries-> venous outflow

Left renal vein receives left suprarenal and left gonadal vein

Despite high renal blood flow, renal medulla recieves less blood flow–> very sensitive to hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Glomerulus

A

Filtration barier- Endothelial cells, Basement membrane-Podocytes (touch urine)

The afferent has the Juxtaglomerular cells that are connected to the macula dena near the distal convoluted tubules

Juxtaglomerular cells secrete renin in response to B1 receptors, decreased perfusion pressure, decrease NaCL (aka water) sensed by macula densa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Course of ureters

A

Renal pelvis, travels under gonadal arteries-> over common iliac artery-> underuterine artery/vas deferens (reteroperitoneal

Gynecologic procedures (ligating the uterine or ovarian vessels can damage the ureterpp> ureteral obstruction or leak

Bladder contraction compresses the intravesical ureter, prevening urine reflux

Blood supply to ureter: Proximal (renal arteries), Middle (gonadal artery, aorta, common and internal iliacs) Distal (internal iliac and superior vesicle arteries)

3 common points of ureteral obstruction: ureteropelvic junction, pelvic inlet, ureterovesicle junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fluid compartments

A

60-40-20 rule (percents of body weight)

60% total body water
40% Intracellular fluid, mainly composed of K, Mg, organic phosphates (ATP)
20% Extracellular fluid, mainly Na, CL, HCO3, albumin

Plasma volume 25% of ECG, 75% is interstitial fluid

Plasma can be measured by radiolabeling albumin
ECF volume can be measured by inulin or mannitol

Serum osmolality= 285-295 mOsm/kg of H20
Plasma volume= total blood volume x (1-Hct)

Total blood volume 6L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Glomerular filtration barrier

A

filters plasma
Fenestrated capillary endothelium
Basement membrane with type 4 collagen chains and heparanated sulfte
Visceral epithelial layer consisting of podocyte foot processes

All 3 layers contain negative charged glycoproteins that prevent entry of negative charged molecules (AKA Albumin)

Size barrier- fenestrated capillary endothelium (prevents entry of >100 nm molecules/ blood cells
Podocytes interpose with glomerular basement membrane: slit diaphragm (prevents entry of molecules > 50-60 nm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Renal clearance

A 
Cx= clearance (mL/min)
Ux= Urine concentration of X (mg/mL)
Px= Plasma concentration of X (mg/mL)
V= urine flow (Vlow) rate (mL/Min)

Cx= (Ux *Vx)/ Px (volume of plasma that a substance is completely cleared in urine /time)

If Cx < GFR (net Reabsorption or not completely freely filtered)

if Cx> GFR (net tubular secretion of X
if Cx = GFR (no secretion or REAB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

GFR

A

Inulin can be used to estimate GFR cause not REAB or secreted

Cinulin= (Uinulin * V)/ Plamsa inulin

Normal GFR= 100 mL/min
Creatinine clearance is an approximate measure of GFR (overestimates cause creatinine is a litttle secreted in renal tubules)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Effective renal plasma flow

A

eRPF can be estimated using para Aminohippuric acid clearacen

it is filtered and secreated bu no REAB, so 100% of it goes in urine

eRPF = (Upah * V)/ Ppah

RBF= RPF/ (1-Hct)

usually 20-25% of Cardiac output

eRPF underestimates true renal plasma flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Filtration

A

Filtration fraction= GFR/RPF ( how good is the glomerulus at fitering out the plasma)
proportion to GFR
normal 20%
filtered load (mg/min) = GFR x Plasma conentration

Ureter constriction does not change renal plasma flow
Dehydration - decreases RPF by a lot comared to gfR decrease so elevated FF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

REabsorption and secretion rate calculation

A

Filtered load: GFR x Px
Excretion rate: V x Ux

Reabsorption = filtered - excreted
Secretion rate= excreted - filtered

FeNA = fractional excretion of sodium

amount excreted/amount filtered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Glucose Clearance

A

Glucose is normally completely reabsorbed in proximal convoluted tubule (PCT) by Na/glucose co transport

In adults 200 mg/dl glucosuria starts, at 375 all na glucose co transportes are fully saturated

pregants is associated with increased GFR (glucose gets in urine at normal leverls

SGLT 2 inhibitors (Flozins –> glucosuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Proximal convoluted tubule

A

Early PCT contains brush border. reabsorbs all glucose and Amino acids and most HCO3-, Na, Cl, PO4-, K, H20 and uric acid

Isotonic absorption, generates and secretes ammonia (NH3) which enables the kidney to secrete more H+

SGLT2 inhibitors prevent Na/Glut co transporters

Angiotensin 2 increases the action of NA/H+ transporter

CO2 +H20 –> H2CO3 via carbonic anhydrase which then spontaneously turns into H+ and HcO3- (HCO3- gets reabsorbed and H+ gets secreted with Na being reabsorbed

Carbonic anhydrase ALSO can convert H2CO3 into CO2 and H2O from HCO3 and H+

Acetazolamide inhibits carbonic anhydrase

PTH inhibits Na/PO4 cotranssport–> PO4 excretion

Angiotensin 2 stimulates Na/H exchange–> increased Na and H20 and HCO3- reabsorption (permitting contraction alkalosis)
65-80% Na and H20 reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Thin descending loop of henly

A

Its thin because theres no water in it

passively reabsorbes H20, via medullary hypertonicity impermeable to Na, concentrating segment makes urine hypertonic

The medullary interstitium (extremely hypertonic) is highly permeable to water but not ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Thick ascending limb of henle

A

REABs NA, K 2 CL symporter
indirectly induces paracellular reabsorption of Mg2, Ca2 through + lumen generated by K+ in the urine, impermeable to H2O, makes urine less concentrated as it ascends

10-20% of Na reabsorption

Loop diuretics inhibit the Na K 2CL symporter

21
Q

Early distal convoluted tubules

A

Reabsorbs Na CL, impermeable to H20 Makes urine fully dilute

PTH increases Ca and/Na exchange–> increased Ca reabsorption

5-10 % of NA reabsorbed

Contains Na/Cl symporter,

Ca sucker

Na/Caswitcher on basal side, CL diffusion

Thiazides inhibit the NA,CL cotransporter

22
Q

collecting tubules

A

reabsorbs Na + in exchange for secreting K and H (regulated by aldosterone)

Aldosterone- acts on mineralocorticoid receptor–> mRNA–> protein synthesis

In principal cells increase in K conductance, Na/K pump, increase epithelial Na channels (ENaC) acitivity–> Lumen negativity–> K secretion

In alpHa intercalated cells- lumen negativity –>H + ATPase activity –> increased H secretion–> HCO3-/CL- exchanger activity

ADH acts at V2 receptors–> insertion of aquaporin H20 channels on apical side

3-5% Na reabsorbed

23
Q

Renal tubular defects

A

Fanconis BaGeLS

Fanconi syndrome- PCT
Barter syndrom- ascending loop of henle
Giltelman syndrome- distal convoluted tubule
Liddle syndrome
Syndrome of Apperent mineralocorticoid excess

24
Q

Fanconi Syndrome

A

Generalized reabsorption defect in PCT

Exctra excretion of amino acids, glucose, HCO3-, PO$- and all substances

May lead to metabolic acidosis (proximal RTA)
Hypophosphatemia, osteopenia

Hereditary defcts causes it, Wilson disease, tyrosinemia, glycogen storage disease, ischemia, multiple myeloma, nephrotoxins/ drugs (ifosfamide, cisplatin) lead poisoning

25
Q

Barter syndrome

A

Reab defect in thick ascending loop of henle (affects NaK2CL)

Metabolic alkalosis, hypokalemia, hypercalciuria

Autosomal recessive, presents similarly yo chronic loop diuretic use

26
Q

Gitelman syndrome

A

Reabsorption defect of NaCL in distal convoluted tubule

metabolic alkalosis, hypomagnesemis, hypokalemua, hypocalciuria

Autosoma recessive
Presents like lifelong thiazide diuretics, less severe than barterr syndrome

27
Q

Liddle syndrome

A

Gain of function mutation–> decreased Na channel degradation –> Na reabsorption increased in convoluted tubules

Metabolic alkalosis, hypokalemia, hypertension, decreased aldosterone

Autosomal dominant

Presents similarly to hyperaldosteronism but NO aldosterone

Treat with amiloride

28
Q

SAME (syndome of apparent mineralocorticoid excess

A

Cortisol activates mineralocorticoid receptors
11BHSD converts cortisol to cortisone (inactive on these receptors)

Hereditary 11B HSD deficiency-> increased cortisol –> increased cortisol leads to increased mineralocorticoid receptor activity

Metabolic alkalosis, hypokalemia, hypertension, decreased serum aldosterone level, cortisol tries to be the SAME as aldosterone

Autosomal recessive

Glycyrrhetinic acid (present in licorice) blocks 11BHSD

Treatment K-sparing diuretics (decreased mineralocorticoid effects) or Corticosteroids (exogenous corticosteroids decrease endogenous cortisol production–> decreased mineralocorticoid receptor activation

29
Q

Relative concentrations along proximal convoluted tubules

A

Tubular fluid / Plasma ratio > 1 when solute is not as reabsorbed

PAH, Creatinine, inulin, urea, CL K, OSM/NA (=1), HCO#,AA, Glucose

30
Q

RAAS Activators

A

Decreased BP (renal baroreceptors), decreased NaCl delivery (macula densa cells), increased sympathetic tone (B1 recptors)

Liver makes angiotensinogen, Renin Converts to Angiotensin 1 (aCe from lung converts Angiotensin 2) (bradykinin breakdown to increase pressure)

Ang2 –> hypothalamus ADH (renal cells) H20 reabsorption via aquaporins

Aldosterone secretion principle cells (Na REAB, K secretion, increased K conductance, Na/K ATPase, and Enac activity)

Alpha intercalated cells( H secretion increased H ATPase activity

Na/H activity PCT –> Alkalosis

Constricts effereent arteriole

Angiotensin 2 receptor type1 Vasoconstriction

31
Q

Juxtaglomerular apparatus

A

mesangial cells, modified smooth muscle of afferent arterioles and the macula densa (NaCL sensor located at distal end of loop of Henle

JG cells secrete renin in response to decreased renal blood pressure and increased sympathetic tone (B1 in the heart cardiovascular)

B blockers can decrease BP by inhibiting B1 receptors of the JGA- decrease renin release

32
Q

Kidney endocrine functions

A

EPO- Released by interstitial cells in peritubular capillary ben in response to hypoxia, Stimulates RBc proliferatoin in bone marrow, administered for anemia secondary to chronic kidney disease, increased risk of HTN

Calciferol (vitamin D)- PCT cells convert 25OH vit D3 to 1,25-Oh2D3 (calcitriol, active form)Calcidiol (250H D3–> 125OH2 D3 Calcitriol

via 1 alpha hydroxylase

PTH activates this 1 a hydroxylase ( stimulates Ca and Pho4 absorption

Prostaglandins: Paracrine secretion vasodilates the afferent arterioles to increase RBF

NSAIDs block renal- protective prostaglandins–> constriction of afferent artieriole and decreased GFR, leads to AKI in low renal blood flow states

Dopamine- secreted by PCT cells , promotes natriuresis, at low doses dilates interlobular arteries, afferent arterioles, efferent artiole–> increased RBF , at high doses is a vasoconstrictor

33
Q

Acidosis

A

if due to High PCO2
Respiratory: Hypoventilation, Airway obstruction, Acute lung disease, chronic lung disease, Opioids, Sedatives, Weakening of Resp muscles

elevated bicarb causes the anion gap
if due to Low Bicarb: Check anion gap (Na- ( CL+HCO3)
if elevated anion gap- MUDPILES (methanol, uremia, DKA, Propylene glycol (antifreeze), Iron tablets, INH, Lactic acidosis, Ethylene glycol (oxalate), Salicylates Late)

If Normal (ie 8-12) HARDASS: Hyperchloremia, hyperalimentation, Addisons disease, Renl tubular acidosis, Diarrheam Acetazolamide, Spironolactone, Saline - you wouldnt give drugs that cause anion gap elevation

34
Q

Alkalosis

A

If due to low PCO2
Respiratory: Hyperventilation, Anxiety, panic attack, hypoxia (high altitidue), Salicylates early on, Tumors, PE

If due to high bicarb
H+ Loss/ HCO3- excess: Loop diuretics, Vomiting, Antacid use, Hyperaldosteronism

35
Q

Renal tubular Acidosis

A

Disorder of the renal Tubules that causes normal anion gap (hyperchloremic metabolic acidosis)

Distal renal tubular acidosis (type 1): inability of alpHa intercalated cells to secrete H+ –> no new HCO3- is generated metabolic acidosis (urine ph is high >5 decreased serum K, amphoteric, increased risk for calcium phosphate kidney stONEs due to increased urine pH and increased bone turnover related to buffereing

36
Q

Casts in urine

A

Presence of casts indicates that hematuria/pyruia is of glomerular or renal tubular origin

Bladder cancer, kidney stones–> hematuria but no casts
Acute cystitis-> pyria, no casts

RBC casts- glomerulonephritis, hypertensive emergency
WBC casts- Tubulointerstitial infalmmation, acute pyelonephritis, transplant rejection
Granular casts: Acute Tubular necrosis (ATN, Can be muddy brown in appearance
Fatty casts, Oval fat bodies- Nephrotic syndrome, associated with maltese cross sign
Waxy casts- end stage renal disease, chronic kidney disease
Hyaline casts: non specific, can be a normal finding, form via solidification of Tamm-Horsfall mucoprotein (secreted by renal tubular cells)

37
Q

Nomenclature of glomerular disorders

A

Focal<50% of glomeruli are involved
Diffuse >50% of glomeruli are involved
Proliferative: hypercellular glomeruli
Membranous: thickening of GBM

NephrOtic syndrome- proteins
Nephritic syndrome- blood

38
Q

Nephritic syndrome

A

Glomerular inflammation-> GBM damage–> loss of RBC in urine–> hematuria

Hematuria, RBC casts in urine, decreased GFR–> oliguria azotemia, increased renin release, HTN, Proteinuria often in subnephrotic range but in severe can be in nephrotic range

Think inflammatory process–> hypercellularity and bleeding in glomerulus–> RBC casts in the little urine that is mage

Acute poststrep glomerulonephritis, Rapidly progressive glomerulonephritis, IgA nephropathy (Berger disease), Alport syndrome, Membranoproliferative glomerulonephritis

39
Q

Nephrotic syndrome

A

Podocyte damage–> impaired charge barrier–> proteinuria

Massive proteinuria (>3.5) with hypoalbuminemia, edema
Frothy urine with fatty casts (the liver senses the thin blood (from hypoalbumin) so tries to beef it up with throwing some fat in the blood-- then ends up in the glomerulus

Associates with hypercoagulable state (Antithrombin 3 is preferentially lost in urine) losing your anticoag

increased risk of infection (loss of IgG in urine and soft tissue compromise by edema)

May be 1’ (direct podocyte damage) 2’ (podocyte damage from systemic process) (focal segmental glomerulosclerosis, minimal change disease, membranous nephropathy, amyloidosis, Diabetic glomerulonephropathy

40
Q

Nephritic-nephrotic syndrome

A

Severe glomerulobasment membrane–> loss of RBCs into urine, impaired charge barrier–> hematuria and proteinuria

Nephrotic- range proteinuria and nephrotic syndormes

Most common with diffuse proliferatice glomerulonephritis, membranouproliferatic glomerulonephritis

41
Q

Acute poststreptococcal glomerulonephritis

A

Kids, a few weeks after strep pharyngitis or skin

Resolves spontaneosly but can progress to renal insuffiiciency in adults

type 3 HS (immune complex on EM). Cola colored ueine, HTN Periorpital edema

M protein in bacteria similar to basement membrane

Positive strep titers/ serologies

low complement leves (C3 due to consumptive

LM- glomeruli are enlarged and Hypercellular, Immunoflorescence is granular due to immune complex groups (lumpy bumpy), due to IgG, IgM and C3 deposition along GBM and mesangium

42
Q

Rapidly progressive (crescentic) glomerulonephritis

A

nephritic syndrome that progresses to renal failure in weeks to months

Poor prognosis, rapid- crescents form in glomeruli formed by fibrin and macrophages (plasma proteins) C3b) with glomerular parietal cel monocytes and macrophages

LM crescentic moon shape

you look at immuno floresence to delineate

goodpasture- Linear (anti-basement membrane Ab)- Ab against type 4 collagen in glomerular and alveolar basememnt membrane, Hematuria, Hemoptysis, young adult men (type 2 HS)- Treat with plamapheresis

PSGN (advanced), diffuse proliferative– granular immunoflorescnece- diffuse proliferative glomerulonephritis due to diffuse Ag-Ab complex deposition (subendothelial) most common in SLE

Wegners (gpa), - cANCA. Eosinophilic granulomatosis with polyangiitis (Churg stause or Microscopic polyangiitis (MPO or p ANCA)

43
Q

IgA nephropathy (berger disease)

A

Episodic hematuria that happens with resp or GIT infections

Think if a IgA is a cause it goes to kidney (HSP)

IgA deposits in mesangium, EM mesangial IC deposition

44
Q

Alport syndrome

A

Mutation in type 4 collagen–> thinning and splitting of GBM, Most commonly X linked, Eye problems, Retinopathy, anterior lenticonus, glomerulonephritis
sensorineural deafness

Can see can pee cant heer a bee

Alfoort syndrome

45
Q

Membranoproliferatic glomerulonephritis

A

Nephritic syndrome that often co-presents with nephrotic syndrome

Type 1 may be 2’ to Hep B or C infection, Subendothelial IC deposits with granular IF

Type 2 is associated with C3 nephritic factor (IgG autoantibody that stabilizes C3 convertase–> persistent complement activation –> decreased C 3 levels

Intramembranous deposits, dense depsotis

GBM spilts–> tram track on HE and PAS staits

Really thick GBM that splits (immune complexwith Hep B C, type 2- C3 nephritic factor)

46
Q

Nephrotic syndrome

A

Protein urua >3.5 g a day

47
Q

Minimal change disease

A

Lipoid nephrosis. Most common cause of nephrotic syndrome in kids

Often 1’ (idiopathic) may be trigered by recent infection, immunization, immune stimulus

Rarely may be 2’ to lymphoma (cytokine mediated damage)

1’ disease has response to corticosteroids
Normal glomeruli, lipid may be seen, negative immunoflorescences, effacement of podocyte foot processes

48
Q

Focal segmental glomerulosclerosis

A

Most common cause of nephrotic syndrome in AF AM and hispanics,

Can be 1’ (idiopathic) or 2’ to other conditions (HIV infection, SCD, heroin, massive obesity, IFN treatment, or congenital malfomation)

LM- segment sclerosis and hyalinosis

difference between it and diffuse glomerulonephritis is blood

49
Q

Membranous nephropathy

A

Thickineng GBM
Antibodies to PLA2, 2 drugs
NSAIDs

First aid (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions