Brainscape's Knowledge GenomeTM

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


See full index

CVPR > Renal Week 3 > Flashcards

Renal Week 3 Flashcards

1
Q

Chronic kidney disease: definition

A

Permanent reduction in GFR for at least 3 months

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

Stages of CKD

A

1: >90 GFR w/ evidence of kidney damage
2: 60-89 GFR w/ evidence of kidney damage
3: 30-59 GFR - mild CKD
4: 15-29 GFR - moderate CKD
5:

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

Common causes of CKD

A 
Diabetic nephropathy
HTN nephrosclerosis
GN
PKD
Interstitial dz
Obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical signs of CKD

A

Anemia (stage 2)
HTN (tx ASAP, stage 1)
Bone/mineral disorders

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

4 components of anemia in CKD

A

Decreased EPO
Decreased RBC survival
Increased bleeding risk
Bone marrow space fibrosis

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

3 reasons for HTN in CKD

A

Expansion of ECF volume
Increased RAS activation
Autonomic dysfunction

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

Water/sodium balance in CKD

A

Can concentrate/dilute urine
200-300 mOsm
Increase in intake = edema
Decrease in intake = volume depletion

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

Potassium balance in CKD

A

Decreased kidney excretion -> increased fecal excretion

Therefore hard to clear K+ quickly

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

How much acid is normally generated every day?

A

1 meq/day

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

3 forms acid is excreted

A

NaPO4 (titratable acids)
H+ (via Aldosterone)
NH4+ trapping

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

Which forms of acid excretion change with CKD?

A

H+

NH4+ -> less nephrons making NH3, acidosis seen with >25% decrease from normal (stage 3 ish)

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

Ca2+ and Pi

A

High Pi triggers FGF-23 -> inhibit 1,25 vit D
Low Ca triggers PTH release
Chronically elevating levels of PTH
Low Vit D (stage 2 ish)

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

Intact Nephron Hypothesis

A

Functioning nephrons maintain glomerulotubular balance

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

Magnification Phenomenon

A

Remaining nephrons magnify their excretion of a given solute

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

Trade-off Hypothesis

A

Increased PTH for normal Ca2+ levels

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

Creatinine balance in CKD

A

Excretion must remain constant

With decreasing GFR, elevation in serum Cr

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

Progressive disease characteristics in CKD

A

Glomeruli hypertrophy
Blood flow per nephron increases
Intra-glomerular pressure increases
Solute flow per tubule increases

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

Treatments for CKD

A

Eval cause/eval CVD risk
Control BP and reduce risk factors (stage 1)
Restrict diet phos, phos binders, Vit D (stage 2)
Select site for dialysis and preserve veins (stage 3)
Place AVF (stage 4)
Dialysis/transplant (stage 5)

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

Indications for dialysis

A

Volume overload while on diuretics
Hyperkalemia
Uremic pericarditis
Uremic symptoms

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

Uremic symptoms

A

Lethargy, difficultly concentrating (early)
Coma/seizures (late)
Nausea, decreased appetite
Uremic bleeding

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

Types of dialysis

A

Hemodialysis
Frequent/nocturnal dialysis (night, at home)
Peritoneal dialysis

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

Types of access for hemodialysis

A

AV fistula
AV graft
Double lumen catheter (tunnel cath in IJ to SVC)

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

Types of peritoneal dialysis

A

Continuous ambulatory PD - drain manually
Continuous cycling PD - machine at night, leave dialysate
Nocturnal intermittent PD - same, don’t leave dialysate

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

Complications of peritoneal dialysis

A

Infection, scarring, cath dysfunction
Hernias
Metabolic: hyperG, hyperL, hypokalemia

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

Warm vs. cold ischemia

A

Warm: death/clamp to cold perfusion (60 min)
Cold: Cold perfusion to @ (24-36 hours)

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

Direct vs indirect rejection

A

Direct: R Tcells to intact D HLA antigens (transplant only)
Indirect: R Tcells to fragments D HLA (normal)

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

Immune signals

A

Tcell CD3 R w/ MHC complex -> PLC -> Ca2+ release -> Calcineurin activity -> dephos NFAT -> enters nuc -> IL-2
(Co-stimulatory CD28 binding)
IL-2 proliferation of CD4 (Th1 and B cells) and CD8 (attack)

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

T and B cell rejection

A

T cell: tubulitis (Banff I) or vasculitis (Banff II)

B cell: antibody mediated, complement

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

Immunosuppression regimen in transplant

A

1st: calcineurin inhibitor (cyclosporine, tacrolimus) - SE nephrotox, HTN, diabetes
2nd: proliferation inhibitor (MMF, sirolimus)
3rd: prednisone

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

AKI eval in transplant

A

Pre-renal (volume down, renal artery thrombosis, calcineurin tox)
Renal (delayed graft/function, acute rejection, recurrent primary dz, infection)
Post-renal (obstruction)

31
Q

Routes of infection for UTI

A

Ascending (more common, ex fecal flora E.coli)

Bloodborne (less common, often ureteral obstruction/immunosuppression)

32
Q

Virulence factors in UTI

A 
Bacterial adhesion
O Antigens (hard to tx)
Endotoxin (decrease ureteric peristalsis)
33
Q

Host defense mechanisms against UTI

A

Mechanical (peristalsis, flow)
Chemical (prostatic secretions, pH, ammonia, P1 BG Ag)
Immune (IgA, complement)
Cellular (PMNs)

34
Q

Complications of UTI

A 
Acute pyelonephritis
Perinephric abscesses
Scarring
Recurrence
Stones
35
Q

Vesico-ureteral reflux

A

No valve, but oblique course in wall
Reflux with perpendicular entry - backflow of urine
Primary (congenital) vs. secondary (neurogenic bladder)

36
Q

Factors for stones

A 
HyperCa
Increased uric acid
low pH
low volume
Bacteria
37
Q

Acute pyelonephritis and consequences

A

PMNs in interstitium
WBC, WBC casts
microabcesses, perinephric abscess
Can lead to pap nec, urosepsis

38
Q

Chronic pyelonephritis and consequences

A

ESKD
Irregularly scarred, atrophy, periglomerular bifrosis
+ reflux = secondary FSGS, poor prognosis

39
Q

Renal papillary necrosis

A

Gross hematuria and proteinuria

Sickle cell, Acute pyelonephritis, Analgesics, DM

40
Q

Benign tumors of the kidney

A

Renal papillary adenoma(small, well circumscribed in cortex)
Angiomyolipoma (vessels, SM, fat, often w/ TS)
Oncocytoma (eosinophilic epithelial cells, lots of mito)

41
Q

Malignant tumors of kidney

A 
Renal cell carcinomas:
Clear cell
Papillary (chromophillic)
Chromophobic
Collecting (Bellini) duct
Familial RCC
42
Q

RCC Clear Cell

A 
Most common (80%)
Hematuria, ball like mass
Can extend renal cortex -> vein -> heart
Often single (unless familial)
Spherical, focal hemorrhage
Types on micro: clear, granular, spindle
43
Q

Papillary Carcinoma

A

Often multifocal
Papillary growth pattern
Better prognosis than clear cell

44
Q

Chromophobic Carcinoma

A

Prominent cell membranes
Halo around nucleus
Similar to oncocytoma (from intercalated cells)
Excellent prognosis

45
Q

Familial RCC

A

VHL: often bilateral and multifocal, hemangioblastomas of cerebellum and retina
Hereditary CCC: confined to kidney, same genes as VHL
Hereditary papillary carcinoma: AD, multiple bilateral with papillary histology (MET mutation)

46
Q

Familial vs. sporadic

A 
Hereditary = multifocal
Sporadic = single
47
Q

Urothelial carcinomas

A

Renal pelvis to urethra
M>F, >50yrs
Schistosomiasis

48
Q

Two functions of bladder and dysfunction symptoms

A 
Storage phase (frequency, uregency, incontinence)
Emptying phase (hesitancy, weak stream, incomplete emptying)
49
Q

LUT Innervation

A 
T10-L2 = sympathetic, hypogastric nerves
S2-S4 = parasympathetic, pelvic nerves
S2-S4 = somatic, pudendal nerves
50
Q

Micturition cycle

A
  1. Increase in wall tension
  2. Afferent input to pontine micturition center/cortical egress
  3. Pudendal nerve activity ceases, relaxation and detrusor neurons freed
  4. Proximal urethra opens
    Bladder immediately contracts
51
Q

Types of incontinence

A

Stress: F (post child), alpha-agonists
Urgency: frequency/nocturia, anti-chol drugs

52
Q

LUT obstruction in men

A

Most common: BPH
80% or 80 y/o have, 50% with symptoms
Tx: alpha-blocker
Younger men: urethral stricture (trauma)

53
Q

3 parts of embryonic kidney and destiny

A

Nephrogenic cord (in urogenital ridge) gives rise to:
Pronephros - degenerates by 4 weeks
Mesonephros - uteric bud, ureters -> collecting tubules
Metanephros - blastemia, SVT to capillary

54
Q

Two ducts and destiny

A

Mesonephric duct - Wolffian duct

Paramesonephric duct - Mullerian duct

55
Q

Urogenital sinus

A

From caudal portion of endoderm = cloaca
Allantosis (part of sinus) becomes urachus
Sinus becomes bladder and urethra

56
Q

Renal agenesis and hypoplasia

A

Failure of metanephric to develop or early degeneration

Unilateral more common (associated with 1 umbilical artery)

57
Q

Renal dysplasia

A

Abnormal differentiation of metanephric tissue

Presents w/in first decade

58
Q

Renal ectopia

A

Failure of kidney to rise or rotate

Can lead to uteral obstruction or discoid kidney

59
Q

Horseshoe kidney

A

Failure to separate along midline (90% lower pole)

Ureters exit anterior, stones likely

60
Q

3 classifications of pediatric cystic kidney disease

A

Acquired
Genetic (AD or AR PKD)
Developmental (MCDK)

61
Q

ADPKD

A 
PKD1 (16p13) - 90%: manifests earlier (Adult)
PKD2 (4q21) - 10% (Adult)
Cystic dilations in ALL parts of nephron
Can be spontaneous, 100% penetrant
HTN, CRF, ESKD (50%)
62
Q

ARPKD

A

PKHD1 (6p21) - Infantile
Early onset HTN, can’t concentrate urine
Cysts are dilations in collecting tubules

63
Q

ADPKD organs vs. ARPKD organs

A

ADPKD: Liver/pancreas cysts, cerebral aneurysms
ARPKD: Fibrous expansion of portal tracts, bile duct prolif

64
Q

MCDK

A

Abnormal induction of metanephros
Ureteral or uteropelvic atresia
Non-function and involuted over time kidney

65
Q

Congenital mesonephric blastoma

A 
Prenatal sonogram = ring sign
Fibrotic, firm mass
Non-cellular = bengin
Cellular = ETV6-NTRK3 fusion (kinda aggressive)
Often with trisomy 11
66
Q

Wilms tumor

A

Claw sign
Triphasic: blastemal, epithelial, stromal
Anaplasia present = unfavorable
Rarely bilateral - instant stage 5

67
Q

Wilms genetics

A

WT-1 11p13: intralobar rests (WAGR)

WT-2 11p15: perilobar rests (BW syndrome)

68
Q

Ureteral duplication

A

Both enter ipsilaterally
Reflux into lower pole
Obstruction in upper pole (ureterocele)

69
Q

Megalocystis

A

Chronic abnormal distention of bladder due to obstruction

70
Q

Posterior urethral valves

A

Obstruction of posterior male urethral valves (ab insertion of mesonephric duct on cloaca)

71
Q

Epispadias and hypospadias

A

Meatus on dorsal or ventral side of penis

72
Q

Chordee

A

Fibrous band causing curve of penis

73
Q

Potter sequence (consequences of obstruction/agenesis)

A

Large flattened ears/nose
Infraorbital skin folds
Amnion nodosum (skin cells on placenta)
Pulmonary hypoplasia (less fluid in lungs to expand)

74
Q

Prune belly (Eagle-Barrett)

A

Mostly males, atrophy of anterior abdominal muscles
Undescended testes
Develop megalocystis

CVPR (5 decks)

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