Brainscape's Knowledge GenomeTM

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


See full index

STEP 1 Review > Renal > Flashcards

Renal Flashcards

1
Q

What happens to the pronephros

A

Degenerates at week 4

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

Mesonephros

A

Functions as the interim kidney for 1st trimester. Later contributes to male genital system.

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

Metanephros

A

Appears in 5th week of gestation, nephrogenesis continues through 32-36 weeks.

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

Ureteric bud

A

Derived from the caudal end of the mesonephric duct, develops into the collecting system of the kidney (collecting duct ->ureters).

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

Metanephric mesenchyme

A

Ureteric bud interacts with this tissue to induce differentiation and formation of glomerulus through DCT

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

Uretopelvic junction

A

Last site in kidney to canalize, most common site of obstruction in fetus (causes hydronephrosis).

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

Potter sequence

A

Renal agenesis/ARPKD/posterior urethral valves
lead to oligohydramnios. This causes compression of the developing fetus, especially pulmonary hypoplasia. Also twisted face/skin, micrognathia, low set ears

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

Horseshoe kidney

A

Inferior poles of both kidneys fuse. As they ascend they get caught on the inferior mesenteric artery and remain low in the abdomen. They function normally but increased risk of uretopelvic obstruction, hydronephrosis, renal stones, and rarely wilms tumor.

Associated with turner syndrome

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

Level of the kidneys

A

T12-L3

1,2,3 is where you find the kidneys

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

Multicystic dysplastic kidney

A

Abnormal interaction of the ureteric bud and the metanephric mesenchyme. Nonfunctional kidney with cysts and connective tissue. Bilateral is incompatible with life. Unilateral is asymptomatic.

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

Duplex collecting system

A

Kidney has 2 ureters due to bifurcation of the ureteric bud before interaction with metanephric mesenchyme. Predisposes to UTIs and vesicoureteric reflex (where valve doesnt close when bladder is full. Reflux of urine into ureter.

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

Which kidney is taken during donor transplantation?

A

Left kidney because it has a longer renal vein

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

Course of ureters?

A

Pass under uterine artery and under ductus deferens.

Can be cut during surgeries with ligation of uterine arteries and ovarian arteries.

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

Fluid compartments

A

40 non water

60% water -> 40 intracellular/20extracellular -> 5 plasma/15 interstitium

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

Extracellular fluid measured with?

Plasma volume measured with?

A

Inulin

Albumin

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

Glomerular filtration barrier?

A

Negatively charged due to presence of heparan sulfate. Fenestrated capillary endothelium form size barrier

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

GFR using inulin

A

Calculate using inulin clearance
(UV)/P = clearance of inulin

Normal GFR is 100.

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

Effective renal plasma flow?

A

Calculated using PAH.

RBF can be calculated from RPF using

RPF/(1-HCT)

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

Filtration fraction

A

GFR/RPF

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

Filtered load

A

GFR*plasma concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Prostaglandin effect on renal vasculature

A

Dilate the afferent arteriole. Increase RPF and GFR, so FF remains constant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Calculation of resorption or excretion

A

Use filtered load and excretion rate
GFRP and UxV

If filtered-secreted is positive, then there is net resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Glucose clearance

A

Glucosuria begins at 200 mg/dl. Transporters are fully saturated at ~375.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hartnup disease

A

No absorption and high excretion of amino acids (tryptophan), so decreased niacin causing pellagra (dermatitis, dementia, diarrhea).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

PCT

A

Reabsorbs sodium, nearly all glucose and amino acids, and most bicarb, chloride, phosphate, K and H2O. Isotonic absorption. Generates and secretes NH3 to buffer the H that is secreted during Na H antiport.

Ang II acts to increase Na H antiporter

PTH acts to inhibit Na PO4 costransport.

Carbonic anhydrase causes H2CO3 to become Co2 and H2O. Co2 enters cell and becomes H2Co3 and allows acid to be regenerated in the lumen.

Blocking carbonic anhydrase causes metabolic acidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

TAL

A

Location of the Na K 2Cl cotransporter, K backleak and paracellular transport of Mg and Ca due to positive lumen potential.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Distal tubule

A

Has Na Cl cotransporter, with Ca channel.

PTH increases Na Ca exchanger at the basal membrane. To increase Ca reabsorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Collecting tubule

A

Principal cell Na in K out and H2o via aquaporins.

Alpha intercalated cell has H pump

Aldosterone and ADH act on these two cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Fanconi syndrome

A

Defective proximal tubule resorption. Associated with excretion of amino acids and glucose. May result in a metabolic acidosis because bicarb can’t be resorbed.

Caused by wilson disease, ischemia, nephrotoxins, multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Bartter Syndrome

A

Resorptive defect in thick ascending limb due to an autosomal recessive defect at the na k 2cl transporter. Causes hypokalemia and metabolic alkalosis (because more Na to distal tubule leads to increased H out). Also hypercalciuria (no positive driving force from K backleak).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Gitelman Syndrome

A

Resorptive defect of Na Cl in DCT. Autosomal recessive, less severe than Bartter syndrome. Leads to hypokalemia, hypocalciuria. Also causes metabolic alkalosis. More Na delivery to collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Liddle Syndrome

A

Increased activity of ENac causes hypokalemia, metabolic alkalosis, hypertension. Autosomal dominant disease. Treat with amiloride.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Syndrome of apparent mineralocorticoid excess

A

Decrease in 11BHSD means much more cortisol around to activate mineralocorticoid receptors. Hypokalemia, hypertension, metabolic alkalosis. Can be caused by licorice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

TF/P graph

A

look this up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Things that increase renin

A

Decreased BP sensed in JG cells.

Less Na delivery to macula densa

Increased sympathetic tone (b1 receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

ANP

A

Released from atria in states of volume overload. Stimulates cGMP to relax vasculature causing increased GFR and decreased renin. With increased GFR there is no net increase in Na reabsorption so more is lost, decreasing BP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What shifts K into cells

A

B agonism (albuterol), insulin, hypoosmolarity. Alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What shifts K out of cells

A

Digitalis, acidosis, b blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Low Mg can cause…

A

Torsades, tetany.

40
Q

Things that cause respiratory acidosis

A

Hypoventilation: airway obstruction, acute lung disease, chronic lung disease, opioids, weakening of respiratory muscles (ALS).

41
Q

Things that cause anion gap metabolic acidosis

A

MUDPILES

Methanol
Uremia
DKA
Propylene glycol
INH or iron
Lactic acidosis
Ethylene Glycol
Salicylates
42
Q

Things that causes non gap metabolic acidosis

A 
Hyperalimentation 
addison disease
RTA
Diarrhea (loss of bicarb and na)
Acetazolamide
spironolactone
saline infusion
43
Q

Things that cause respiratory alkalosis

A

Hyperventilation (hysteria, hypoxemia, salicylates at first, tumor, PE

44
Q

Things that cause metabolic alkalosis

A

Loop diuretics, vomiting (loss of HCl), antacid use, hyperaldosteronism

45
Q

Renal tubular acidosis type 1

A

Distal. Defect in the ability of alpha intercalated cells to secrete hydrogen. No HCO3 generated, causes metabolic acidosis with no gap. Associated with hypokalemia (more K out into tubules) and increased risk for calcium phosphate kidneys stones.

Caused by ampho B and congenital abnormalities

46
Q

Renal tubular acidosis type 2

A

Proximal. Defect in the proximal tubule to resorb HCO3 causes excretion of HCO3 in urine and subsequent metabolic acidosis. Associated with hypokalemia and increased risk for hypophosphatemic rickets. Caused by fanconi syndrome, lead, aminoglycosides, carbonic anhydrase inhibitors.

47
Q

Renal tubular acidosis type 4

A

Hypoaldosteronism, aldosterone resistance, or K sparing diuretics. More Na in tubules leads to hyperkalemia, impairs ammoniagenesis in the proximal tubule. Decreases the buffering capacity and decreases H excretion into urine.

48
Q

RBC casts

A

Glomerulonephritis, ischemia, malignany hypertension

49
Q

WBC casts

A

Interstitial nephritis

50
Q

Fatty casts

A

oval fat bodies caused by nephrotic syndrome

51
Q

Muddy brown casts

A

Associated with acute tubular necrosis

52
Q

Waxy casts

A

Seen in advanced renal disease

53
Q

Hyaline casts

A

Nonspecific– can be a normal finding.

54
Q

Nephotic syndrome

A

> 3.5 protein in urine, hypoalbuminemia, hyperlipidemia. Loss of ATIII in urine, loss of immunoglobulin

55
Q

FSGS

A

Most commonly seen in african americans.

56
Q

Minimal change disease

A

Happens most commonly in kids. Normal glomeruli but effacement of foot processes on LM. Happens after a viral infection or if Hodgkins lymphoma (due to cytokine production). Responds very well to steroids.

57
Q

Membranous nephropathy

A

Thickening of capillar and basement membrane. IF granular deposits subepithelial with spike and dome appearance on EM. This is common in SLE. Also most common form in caucasian adults. Can be idiopathic or due to an antibody against phospholipase A2. May progress to chronic renal failure

58
Q

Amyloidosis

A

Most common site of amyloid deposition. Associated with MM, RA, TB.

59
Q

Diabetic glomerulonephropathy

A

Mesangial expansion with GBM thickening and kimmelsteilwilson nodules.

Caused by the nonenzymatic glycosylation of the basement membranes. This increases GFR and causes mesangial expansion. Add ace or ARb to protect

60
Q

Membranoproliferative glomerulonephritis

A

Can present as a nephritic or nephrotic picture.

Type I has subendothelial deposits and tramtrack appearance. Caused by HCV or HBV

Type II is associated with intramembranous immune complex deposits. Caused by C3 nephritic factor that stabilizes C3 convertase, increases complement activation and causes decrease in serum C3 levels.

61
Q

Nephritic syndrome

A

Inflammatory process that is characterized by RBC casts in urine, azotemia (uremia), oliguria

Caused by Rapidly progressive GN, Alport syndrome, PSGN, IgA, Diffuse proliferative, Membranoproliferative.

62
Q

Rapidly Progressive GN

A

Seen as a crescent on Light microscopy. Can be caused by a number of things including goodpastures syndrome, GPA, MPA. Crescent is macrophages and fibrin.

Poor prognosis, rapidly deteriorating renal function

63
Q

PSGN

A

2 or 3 weeks after pharyngitis or skin infection. Type III HSR. Causes enlarged glomeruli and lumby bumpy appearance of immune complex deposition in the subepithelial region.

64
Q

Diffuse proliferative glomerulonephritis

A

Full house staining on immune staining. Due to SLE. Wire lopping of capillaries. Subendothelial deposits. Most common cause of death.

65
Q

IgA nephropathy

A

Mesangial expansion with IgA. Seen with henoch schonlein purpura

66
Q

Alport syndrome

A

Defective type IV collagen synthesis. Glomerulonephritis, deafness, eye problems. X-linked splitting of the basement membrane.

67
Q

Calcium kidney stones

A

Calcium phosphate if ph high, calcium oxalate if ph low. Radioopaque stones that are envelope or dumbell shaped. Both promoted by hypercalciuria (idiopathic or from increased PTH or cancer). Oxalate crystals can happen from ethalene glycol, vitamin C abuse or crohn’s disease. Treat with thiazides and citrate.

Patients frequently are normocalcemic

68
Q

Ammonia Magnesium phosphate stones

A

15% of stones seen when urine ph is high from ureasepositive bugs like proteus, staph, kleb. Create ammonia. They are coffin lid in shape and are radioopaque.

69
Q

Uric acid stones

A

When ph decreases. Radiolucent rhomboid stones. Seen when urine volume is down or when uric acid is high (gout, tumor lysis syndrome). Treat by alkalinizing the urine

70
Q

Cystine stones

A

Radioopaque, hexagonal. Mostly seen in children secondary to cystinuria.

Hydrate and alkalinize the urine.

71
Q

Hydronephrosis

A

Distention dilation orf the renal pelvis and calices. Usually cause by urinary tract obstruction. Other casues can include retroperitoneal fibrosis and vesicoureteral reflux.

72
Q

Renal cell carcinoma

A

Carcinoma of the proximal tubule cells. Clear cells with lipids/carbohydrates. Most common in 50-70 year old men.
Presents with hematuria, flank pain, and a palpable mass.

Can spread to renal vein and spread hematogenously after invasion of IVC. Will spread to lung and bone.

Associated with gene on chromosome 3. Associated with VHL. Causes a wide number of paraneoplastic syndromes like ACTH, epo, renin, pthrp. Treat with resection or immunotherapy.

Generally resistant to chemo and radiation.

73
Q

Angiomyolipoma

A

Fatty kidney tumor seen in tuberous sclerosis.

74
Q

Renal oncocytoma

A

Tumor of the epithelial lining of the collecting system. Well circumscribed benign mass that is composed of eosinophilic cells wihtout a perinuclearclearing. Painless hematuria, flank pain, and abdominal mass. Treat with nephrectomy.

75
Q

Wilms tumor

A

most common renal malignancyof early childhood. Contains early glomerular like structures. Presents with a huge palpable flank mass +/- hematuria. Loss of function mutations inthe tumor suppresor genes WT1 or WT2 on chromosome 11. Can be part of beckwith wiederman syndrome (large tongue, organomegaly, muscular hemihypertrophy) or WAGR syndrome (wilms, aniridia, genitourinary malformation and mental retardation).

76
Q

Transitional cell carcinoma

A

Often multifactorial and recur. Smoking is a big risk factor. Most common tumor of the urinarytract system. Can occur in calices pelvis ureters and bladder. Painless hematoria without casts. Can be caused by phenacetin, smoking, aniline dyes and cyclophosphamide.

Can be papillary or flat
Papillary starts as low, then high, then invades
Flat starts high, then invades. and is associated with early P53 mutations.

77
Q

Squamous cell caricinoma of the bladder

A

Going to be seen in middle eastern young man with a schistosoma infection.

78
Q

Adenocarcinoma of the bladder

A

Associated with urachal remnant at the doma of the bladder or glandular metaplasia.

79
Q

Acute infectious cystitis

A

Inflammation of the urinary bladder that presents with pain nd dysturia. Systemic signs aregenerally absent (no fever, or chills) Risk factors include female gender, sex, and catheters.

Caused by e coli, staph sap, kleb, proteus, adenovirus

Positive for leuk esterase. Positive for nitrates if infection is with a gram negative organism.

Sterile pyuria suggests urethritis by n.gonorrheae or chlamydia.

80
Q

Treat UTIs?

A

With fluoroquinolones or nitrofurantoin if pregnant.

81
Q

Acute pyelonephritis

A

Affects cortex with relative sparing of glomeruli. Presents with dysuria fever and CVA tenderness. Most common cause is ascending UTI. Can also be caused by vesicoureteral reflux. Risk factors include Cath, obstruction, pregnancy, or diabetes.

82
Q

Chronci pyelonephritis

A

Scarring with blunted calices and THYROIDIZATION OF KIDNEY (with eosinophilic casts). Caused by a malformation (like vesicoureteral reflux) or chronic kidney stones.

83
Q

Drug induced interstitial nephritis

A

Acute interstitial renal inflammation. Pyria and azotemia especially with drugs like diuredics penicillins, sulfonamides, and rifampin. Can occur MONTHS after nsaids. Fever rash hematuria and CVA tenderness.

84
Q

Diffuse cortical necrosis

A

Acute generalized cortical infarction of both kidneys usually due to a combination of vasospasm and DIC. Associated with abrutio placentae and septic shock.

85
Q

ATN

A

Most common cause of intrinsic renal failure. Can be fatal. Death usuallyoccurs during oliguric phase. Key finding is granular casts in urine.

Caused by ischemia (hypotension, shock, sepsis, hemorrhage) or drugs (aminoglycosides, radioconstrast agents, lead, MYOGLOBINURIA, hemoglobinuria). Proximal tubule is most susceptible

86
Q

Renal papillary necrosis

A

Sloughing of renal papillae can be associated with DM, sickle cell and chronic phenacitin use.

87
Q

Acute kidney injury

A

Rapid decline in renal function with increases in creatinine and BUN over several days

88
Q

Prerenal AKI

A

Due to hypotension usually. FENa 20. Urine osmolality is >500. Na and H2O and urea retained to save volume so BUN:CR goes up.

89
Q

Renal AKI

A

Usually due to ATN. Backflow decreases GFR. Decrease in BUN:Cr due to less urea absorption. Urine NA/fena are both elevated.

90
Q

Postrenal AKI

A

Caused by obstruction.

91
Q

Symptoms of uremia

A

Increased bun and creatinine. Nausea and anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction (prevents aggregation and adhesion).

92
Q

Renal osteodystrophy

A

Failure of vitamin D hydroxylation, hypocalcemia hyperphosphatemia, increase in pTH.

93
Q

ADPKD

A

Cysts in enlarged kidneys, flank pain hematureia hTN chromosome 16. Or PKD2 on chromosome 4. Can cause berry aneurysms liver cysts

94
Q

ARPKD

A

In kids, autosomal recessive, associated with hepatic fibrosis and portal hypertension. Significant renal failure.

95
Q

Medullary cystic disease

A

Inherited disease causing tubulointerstitial fibrosis. Shrunken kidneys on ultrasound. can’t concentrate urine

96
Q

Simple vs complex cysts

A

Simple cysts are found in the outer cortex and are filled with ultrafilrate. Common. Complex cysts are septated require follow up. May predispose to renal cell carcinoma.

STEP 1 Review (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions