Brainscape's Knowledge GenomeTM

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


See full index

M2 > Renal > Flashcards

Renal Flashcards

0
Q

What is specific gravity and what is normal for urine?

A

Specific Gravity: ratio: weight of vol. of urine / weight of vol. of distilled water

Normal: 1.003-1.035

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

What does the appearance of hazy, smoky, or foamy urine implicate?

A

Hazy: presence of cells or crystals
Smoky: acute glomerulonepritis
Foamy: protein

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

Define osmolality

A

number of solute particle dissolved in 1kg of water

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

What effect does protein have on urine pH?

A

high protein diet -> acidic urine (lower pH)

Vegetarian diet -> alkaline urine

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

What infection should be considered w/ very high (>8) urine pH?

A

Urea splitting microbes (ex. Proteus)

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

What is the cutoff size for protein filtration at the glomerulus?

A

25,000 daltons

Albumin: 69,000 - will not normally be filtered

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

How much protein is usually excreted in urine /day and what level will register as positive on a dipstick test?

A

250mg /day -> positive dipstick test

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

What is Tamm-Horsfall protein?

A

Glycoprotein Secreted by TALH
Constitutes the majority of protein excreted in urine
Can gel in lumen and produce urinary casts

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

4 sources of protein in urine

A

Tubular disorder: most filtered protein is taken up and degraded by proximal tubule. If damaged -> increased urine protein
Glomerular disease: increased filtration
Overflow state: excessive systemic production (ex. Ig light chain in multiple myeloma)
Contamination: semen, vaginal secretion, pus, blood, mucus

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

In a chemical test for blood in urine, what substances are detected?

A

RBC, Hb, Myoglobin

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

What is renal glycosuria? Causes?

A

glucose in urine due to reduction in reabsorption at PCT (normal blood glucose level)
-Fanconi’s syndrome, interstitial nephritis, pregnancy

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

In urine, how many RBCs are normally visible /HPF?

A

1-2

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

What does the presence of dysmorphic RBCs on urinalysis indicate?

A

glomerulonephritis

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

What are oval fat bodies seen in urinalysis?

A

tubular epithelial cells with fat droplets in cytoplasm
indication of NEPHROTIC syndrome
maltese-cross pattern of cholesterol / cholesterol ester

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

7 types of urinary casts

A

hyaline: may be normal w/ exercise or dehydration (Tamm-Horsfall)
RBC: glomerulonephritis
WBC: inflammation of tubular interstitium (nephritis / pyelonephritis)
epithelial: tubular injury (acute tubular necrosis)
granular: fine - may be normal; coarse (muddy brown) - tubular necrosis
fatty: nephrotic
waxy: renal failure casts - advanced CKD

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

What is a renal lobule?

A

A group of nephrons draining into a common collecting duct

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

What type of collagen makes up the glomerular basement membrane?

A

Type IV

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

What is a filtration slit?

A

space between foot processes of podocyte (visceral epithelium of glomerulus)
Nephrin: filtration protein: allows small things through

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

What is Heymann Nephritis?

A

Experimental model demonstrating possible mechanism behind in situ immune complex formation
Rats immunized with PCT brush border Ag develop Ab that is cross reactive w/ podocyte

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

Primary membranous glomerulonephropathy

A

In situ immune complex formation

Ab against unknown Ag in glomerular basement membrane

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

What determines the location of Ag or immune complex deposition in the glomerulus?

A

Charge:

neutral: deposit in mesangium
anion: subendothelial (bet. endothelium and GBM
cation: subepithelial (bet. GBM and podocyte

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

What is focal segmental glomerulosclerosis?

A

damage to glomeruli increase stress on other glomeruli -> endothelial injury, podocyte injury, coagulatin, inflammation, messangial cell proliferation and increased ECM

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

What is tubulointerstitial fibrosis?

A

glomerulosclerosis -> proteinuria and tubular ischemia -> injury and activation of tubular cells -> cytokines and growth factors -> interstitial inflammation and fibrosis

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

global vs. segmental

A

level of the glomerulus

global: entire glomerulus
segmental: portion of glomerulus

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

What morphological feature is associated with rapidly progressive glomerulonephritis?

A

Crescent formation
-form of hypercellularity. severe glomerular damage -> leakage of cytokines, procoagulant into bowman’s space -> parieal epithelial proliferation and leukocyte infiltration

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

Calculation for plasma osmolality and normal values

A

Plasma osmolality = 2 * [Na+] + ([glucose]/18) + (BUN/2.8)

Normal = 288
Na = 140
glucose = 100
BUN = 10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe water distribution in terms of body weight, ECF and ICF

A 
TBW = 0.6 * lean body weight
ECF = 1/3 TBW
ICF = 2/3 TBW
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

2 causes of pseudohyponatremia

A

1: lab artifact: elevated plasma protein expands plasma volume -> appearance of decreased [Na] (hyperlipidemia and hypergammaglobulinemia)
2: hyperosmolal hyponatremia: elevated glucose -> increased osm -> fluid shift from icf to ecf -> lowered [Na]

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

In the setting of elevated blood glucose, how is the post-correction [Na] estimated?

A

Post glucose correction [Na] = add 1.6 mM for every100 mg/dL blood glucose is over 200mg/dL to plasma [Na]

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

what effect does elevated BUN have on distribution of water?

A

None. Urea even distributes between ICF and ECF

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

Thirst regulator and 2 stimulators of thirst

A

Subfornical organ (hypothalamus)

increased plasma osmolality (2-3% increase)
decrease in blood volume or pressure (via Angiotensin II)

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

Process of ADH secretion

A

increased plasma osmolality (osmoreceptors) sensed (OVLT via TRPV1) -> ADH secretion from posterior pituitary

Other triggers:
baroreceptors, chemoreceptors, nociceptors, ATII

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

Where is ADH synthesized and stored?

A

Synthesized in magnocellular neurons of supraoptic and paraventricular nuclei of hypothalamus

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

What nerves do baroreceptors send their signals along?

A

CN IX and X

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

Effect of ADH

A

TALH: stimulation of NaKCl transporter -> solute reabsorption
Collecting Duct: binds V2 receptor -> increased cAMP -> PKA -> insertion of AQP 2 in apical membrane
stimulates urea reabsorption at inner medullary CD

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

Components of countercurrent multiplier

A

Descending limb of Loop of Henley: high water permeability, low solute permeability
Ascending limb of Loop of Henley: water impermeable, active solute reabsorption
Medullary interstitium: solute from TALH -> high osmolality

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

From what tissue does renal cortical adenoma originate?

A

tubular epithelium

Found in cortex

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

How large are the lesions in renal papillary adenoma?

A

papillary / cortical adenoma

lesions are low grade, <5mm

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

Describe renal oncocytoma

A

Brown well-circumscribed tumors (large, up to 12cm) from intercalated cells of collecting ducts
eosinophilic cells have many mitochondria

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

Diseases with which Renal cell carcinoma may be associated with

A

vonHippel-Lindau
Tuberous Sclerosis
Acquired Cystic Kidney Disease
Adult Polycystic Kidney Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Renal cell carcinoma cell types and associated genetic abnormalities

A

Clear cell: del(3p) (VHL gene: 3p25)
Papillary: trisomy 7, 17
Chromophobe: monosomy 1,2,6,10,13,17
Collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Paraneoplastic syndromes associated w/ RCC

A 
polycythemia (EPO)
HTN
fem/masculinization
Cushing's
Eosinophilia
Amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe staging of Renal Cell Carcinoma

A

T1a: kidney only, tumor < 4cm
T1b: kidney only, tumor 4-7cm
T2: kidney only, tumor >7cm
T3: invasion of perinephric fat, but not Gerota’s fascia. Renal vein, not into ipsilateral adrenal gland
T4: invasion of Gerota’s fascia, may include ipsilateral adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pathological description of Wilm’s tumor

A

Triphasic:

  • blastemal
  • mesenchymal
  • epithelial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How frequent is recurrence of papillary uroepithelial tumors after resection?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Invasion of what muscle by papillary uroepithelial cancer is concerning?

A

Muscularis Propria of the bladder
20% of patients
Requires cystectomy (stage T2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is PUNLMT?

A

Papillary Urothelial Neoplasm of Low Malignant Potential

Papillary fronds w/ fairly normal epithelium - little atypia or disorganization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are grades of papillary uroepithelial tumors?

A

Uroepithelial papilloma: fronds w/ normal epithelium
PUNLMP: fronds w/ minimal epithelial abnormality
Papillary urothelial carcinoma - low grade: mild-moderate nuclear atypia, mitotic figures basally
Papillary urothelial carcinoma - high grade: bizzare cells, loss of normal architecture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How is carcinoma in situ of the bladder often diagnosed?

A

Urine cytology: bladder epithelium is discohesive, so malignant cells are often found in urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the most common bladder cancer in North America?

A

Papillary carcinoma (90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

With what other condition is squamous cell carcinoma of the bladder associated?

A

Schistosomiasis - transmitted by snails

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the most common childhood bladder cancer?

A

rhabdomyosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the most common prostate cancer and its precursor?

A

Adenoma is most common

Prostatic Intraepithelial Neoplasia precursor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Where does prostatic adenocarcinoma tend to spread?

A

Bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Where do most prostatic adenocarcinomas arise?

A

Peripheral zone (>80%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the Gleason System?

A

Grading system for prostate cancer
Addition of 2 most prominent patterns (grades) observed in tumor
50% of tumors have multiple grades present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the most common sarcoma of the prostate?

A

Rhabdomyosarcoma - most often in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

2 functions that maintain normal plasma potassium concentration

A

distribution between ICF and ECF

excretion of potassium added to ECF via dietary intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How do hyper- and hypokalemia affect resting membrane potential of cells?

A

hyperkalemia: hypopolarization -> suppression of Na channel activity (cardiac myocytes), shortened repolarization time
hypokalemia: hyperpolarization -> enhanced Na channel activity (cardiac myocytes), arrhythmia risk, prolonged repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

relationship of membrane potential to EC and IC [K+]

A

Em inversely proportional to -[K+]c/[K+]e

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the effect of catecholamines on [K+]?

A

Catecholamines directly enhance Na/K ATPase activity -> hyperpolarization
B2 activation: increases cellular K+ uptake (esp. sk. muscle and liver) -> lower serum [K+]
**non-specific B-blockers (propanolol) impair K+ uptake -> increased serum [K+]
Alpha activation: impairs K+ cellular uptake and blocks insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Effect of insulin in K+ balance

A

Reduces serum [K+]
Promotes skeletal muscle K+ uptake (via Na/K ATPase)
Liver: stimulation of Na/H exchanger -> elevated IC [Na+] -> increased activity of Na/K ATPase
Insulin + glucose used to treat hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How does aldosterone affect K+ levels?

A

Decreases serum [K+]
Principal cell of collecting duct: increased Na/K ATPase -> K+ excretion
aldosterone -> metabolic alkalosis -> cellular K+ uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the effect of exercise on serum [K+]?

A

Increases serum [K+]

increased ADP -> opening of ADP sensitive K+ channels -> local [K+] increase -> vasodilation and increased bf.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

3 pathologic factors influencing K+ balance

A

pH: metabolic acidosis caused by mineral acids -> increased serum [K+]. organic and respiratory acidosis to a lesser extent
osmolality: hyperosmolality -> cellular water loss and increased IC [K+] -> passive effux. also, osmotic drag -> decreased IC [K+]
cell breakdown/ proliferation: BD -> increased EC [K+]; prolif -> decreased EC [K+]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How much K+ is filtered by the glomerulus daily? How much is excreted?

A

600-700mEq filtered daily

10% of that is excreted, the rest reabsorbed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

ROMK

A

Renal Outer Medullary K+ channels

Found in TALH. Secrete K+ in exchange for NaCl reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Where is most K+ reabsorbed?

A

TALH by NaKCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Describe K+ handling in the collecting duct

A

Principal cell: ROMK: K+ secretion if high tubular [Na]
Intercalated cell: K+/H+ ATPase: activity increased when interstitial (systemic) K+ is low -> reabsorption. activity decreased w/ elevated systemic K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is a WNK and how does it affect K+ levels?

A

With No Lysine (K) Kinase
-> internalization of ROMK in distal nephron -> decreased K+ secretion.
activated in low K+ state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What defines hypokalemia?

A

serum [K+] <3.5mEq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What defines hyperkalemia?

A

serum [K+] >5.1mEq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

3 syndromes that can -> hypokalemia

A

Liddle: ENaC constitutively open
Barter: defective NKCC
Gitleman: defective NaCl cotransporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How can antibiotics (penicillin) -> hypokalemia?

A

excreted as anions that increase K+ excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How can one differentiate between renal / extra renal K+ losses in a hypokalemic patient via 24 hr. urine collection?

A

25mEq/day K+ excreted = renal cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is psuedohyperkalemia?

A

apparent hyperkalemia due to K+ efflux from cells during / after blood draw. Lab artifact.
due to mechanical trauma, hemolysis
elevated WBC or platelet count.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How can penicillin -> hyperkalemia

A

anion paired w/ K+ as cation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

EKG changes in hypokalemia

A

decreased T wave amplitude (serum [K+] <2, T may disappear)
increased U wave amplitude
ST depression
P wave amplification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What EKG changes are seen w/ hyperkalemia?

A 
elevated T wave
Short QT
QRS widening (severe)
low P
Vtach -> Vfib
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Interventions for hyperkalemia

A

Calcium Gluconate: stabilizes cardiomyocyte membrane - rapid effect (1-2 min)
Insulin + glucose: rapid: 5-10 min w/ peak 30-60 min
NaHCO3: increased cellular K+ uptake
Albuterol (B2 agonist): ~30 min for onset
Kayexalate: remove K+ from body: 60 min onset
Dialysis: remove K+ rom body: 25-30 mEq/hour romoval, most efficient in 1st hr.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what characterizes nephrotic syndrome?

A 
Proteinuria >3.5g / day
hypoalbuminemia
proteinuria
edema
hyperlipidemia
lipiduria
increased risk of infections and thromboembolic complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

3 causes of nephrotic syndrome

A

Membranous Glomerulonephropathy
Minimal Change Disease
Focal Segmental Glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the difference between primary and secondary membranous glomerulonephropathy?

A

Primary: idiopathic autoimmune disorder - Ab against normal renal Ag (PLP A2 receptor on foot processes)

Secondary: meds (captopril, lithium), chronic infection (HepB+C, syph), malignancy (lung, breast, colon ca), autoimmune (SLE, autoimmune thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Prognosis / treatment for primary / secondary membranous glomerulonephritis

A

Primary: usually unresponsive to corticosteroids - slowly progressive
Secondary: varies depending on inciting Ag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Characteristics of Minimal Change Disease

A

Nephrotic syndrome - selective proteinuria (albumin) - mostly children, may be post immunization or resp. infection.
Primary disease or secondary to NSAID, lymphoproliferation (Hodgkin’s Lymphoma)
Poorly understood immunologic connection - assoc. w/ hx of allergic rxn
Podocyte foot process effacement seen on TEM (LM and DIF normal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Minimal change disease prognosis

A

Excellent.

Good response to corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What conditions is Focal Segmental Glomerulosclerosis associated with?

A

HIV (esp black males)

Heroin use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

3 forms of FSGS

A

Primary: idopathic. extension of MCD?
Secondary: loss of functional renal tissue (w/ compensation by functional areas), IgA nephropathy. Assoc. w/ HIV and heroin
Inherited: usually mutation in gene coding for slit membrane related proteins (esp. podocin: anchors actin intracellularly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What FSGS variant is especially associated w/ HIV?

A

Collapsing
collapsed glomeruli, enlarged visceral epithelial cells, dilated tubules
Endothelial cell Tubuloreticular inclusions (IFN-a modified ER)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Nephritic symptoms

A 
hematuria
azotemia (high BUN due to low GFR)
oliguria
hypertension
mild-moderate proteinuria
edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

2 causes of nephritic syndrome

A 
postinfectious glomerulonephritis (post strep)
acute proliferative glomerulonephritis (SLE assoc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How do etiologies behind MPGN types I and II differ?

A

I: glomerular immune complex formation -> classical and alternative complement pathway activation
II: autoantibody (C3 nephritic factor - C3NeF) stabilizes C3bBb (alternative C3 convertase) and stabilizes -> constitutively active alternative pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are some secondary causes of MPGN type I?

A 
autoimmune disorders (SLE)
chronic infections (bacterial, viral, parasitic)
malignancy
a1-antitrypsin deficiency
dysregulation of complement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What deposits are seen in types I and II MPGN?

A

Type I: IgG, C3,1q, 4 deposited in capillary loops and mesangium
TEM: subendothelial deposits w/ mesangial interposition
Type II: C3 in GBM and mesangium
TEM: Very electron dense material w/in lamina densa of GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Is kidney transplant a cure for MPGN?

A

high frequency of recurrence post-transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What does the GBM look like in RPGN (TEM)?

A

“wrinkled” convoluted with focal discontinuities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are three groupings of RPGN?

A

Type I: anti-GBM (antibody to non-collagenous portion of type IV collagen) IgG deposits in GBM (linear staining by DIF)
Type II: immune complex mediated (postinfectious GN, SLE, IgA nephropathy) granular staining by DIF
Type II: pauci-immune. usually ANCA positive, may be associated w/ systemic vasculitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is the difference in treatments for the 3 subtypes of RPGN?

A

Type I: plasmapheresis (remove IgG) and immunosuppression
Type II: treat underlying disease
Type III: immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is the most common glomerular disease worldwide?

A

IgA nephropathy (Berger Disease) - esp. SE Asia

persistent microhematuria, intermittent macrohematuria
+/- proteinuria
Usually older children and young adults w/in days of mucosal infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is Berger Disease?

A

IgA nephropathy
Disease of the mucosal immune system
Susceptible individuals produce excess IgA in setting of resp. infection or celiac, or decreased IgA clearance
Increased serum polymerization -> deposit in mesangium and activation of alternative complement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is Alport Syndrome?

A

X-linked hereditary nephritis

Defect in a-chain of type IV collagen -> defective assembly and dysfunction of GBM, cochlea, and ocular structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

2 diseases involving type IV collagen

A

Rapidly Progressive Glomerulonephritis (Type I): anti GBM Ab

Alport Syndrome: a-chain abnormality -> defective collagen assembly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is Henoch-Schonlein Purpura?

A

Form of IgA nephropathy w/ systemic vasculitis
Most commonly in children post resp. infection
Purpuric rash, usually lower extremities, arthralgias, possible GI bleeding
good prognosis in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Classes of renal disease seen in SLE

A

Class I: no changes
Class II: mesangial expansion
Class III: focal proliferative glomerulonephritis
Class IV: Most Common: diffuse proliferative glomerulonephritis - most gloms involved.
Class V: Nephrotic: membranous glomerulonephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What are glomerular wire loops indicative of?

A

Glomerular capillary wall thickening seen in SLE glomerulonephritis (class V)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What deposits are present in SLE glomerulonephritis?

A

IgG deposits

subepithelial: class V
subendothelial: class III and IV

Immune complexes also may be present in tubulointerstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What characterizes acute renal failure?

A 
azotemia
oliguria
increased ECF
hyperkalemia
metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

3 categories of ARF

A

Pre-renal: inadequate perfusion of kidney
Post-renal: obstruction of urine flow, usually bilateral
Renal: process affecting any kidney compartment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

2 factors on which acute kidney injury is reliant

A

tubular injury: ischemia or drugs. ischemia -> low ATP, increased Ca2+, reactive O2, apoptotic enzyme activation (caspases), cytokine production

persistent, severe disturbance in blood flow: vasoconstriction -> reduced GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

role of cell polarity in AKI

A

ischemia -> loss of brush border and cell polarity (reversible cellular injury)
redistrubution of Na/K ATPase to apical membrane -> increased Na transport to lumen, reased tubuloglomerular feedback and activation of Renin-Angiotensin-Aldosterone system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

In the case of AKI (acute tubular necrosis) what determines potential for tubular regeneration?

A

Tubular basement membrane coherence

if membrane is intact, cells can regenerate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is acute pyelonephritis?

A

Infection of renal parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Organisms most commonly assoc. w/ UTI

A

E. coli, enterobacter, enterococcus, Proteus, Klebsiella

113
Q

Who is most susceptible to UTIs by age /sex?

A

50: men - BPH

114
Q

3 factors that contribute to vesico-ureteral reflux

A
  1. absence of intra-vesicular ureter (ureter enters perpendicular rather than at an angle -> decreased sphincter action w/ bladder contraction)
  2. congenital para-ureteral diverticulum
  3. inflammation of bladder wall
115
Q

What are 2 non-bacterial causes of pyelonephritis and who is at risk

A

fungus, esp. Candida albicans: immunosuppressed and diabetic
CMV: transplant recipients

116
Q

3 complications of acute pyelonephritis

A

Pyonephrosis: complete obstruction -> filling of renal pelvis, calyces and ureter with pus
Perinephric abscess: infection penetrates renal capsule
Necrotizing papillitis: renal papillae necrosis, may slough into pelvis -> additional obstruction. involves 1) infection 2) obstruction 3) compromised blood flow (DM, Sickle Cell)

117
Q

What is acute tubulo-interstitial nephritis?

A

Inflammation of interstitium of kidney affecting tubules
Immune basis
May -> ARF
-patients have hx of hypersensitivity
-immune complexes present in tubular basement membrane
-anti-tubular basement Ab have been found
-Tcell damage has been implicated

118
Q

What is the most common cause of Acute Tubulo-interstitial nephritis?

A

Drugs

  • Beta lactams (penicillin, methicillin, ampicillin)
  • Sulfonamide (bactrim)
  • NSAID
  • Diuretics
119
Q

What infections are associated with ATIN?

A

Strep A
Diptheria
Toxoplasmosis
Legionnaire’s disease

Not due to infectious organisms - deposition of Ag in interstitium -> response

120
Q

What is normal GFR in adult men and women?

A

Men: 120+-25
Women: 95+-20

121
Q

What is the Crockoft-Gault equation for estimation of creatinine clearance?

A

Creatinine clearance = [(140-age)(weight (kg))]/72* serum creatinine (mg/dL)
multiply by 0.85 if female

122
Q

What criteria does the MDRD GFR equation include?

A

Age, sex, race, plasma creatinine, BUN, albumin

123
Q

What is the advantage of the CKD-EPI compared to MDRD?

A

more accurate for GFR over 60 ml/min/1.73m2

124
Q

Clinical picture of acute glomerulonephritis

A

Rapid course: worsening renal function over hours - days
RBCs, RBC casts, HTN, oliguria, edema, CHF

Inflammatory process

Causes: post infect, multisystem disease, primary

125
Q

What tests should be ordered for a pt. with RPGN?

A 
ANA
ANCA
cryoglobulins
Hep C Ab
Anti-GBM Ab
Complement levels
126
Q

2 theories to explain edema in nephrotic syndrome

A

Underfill: hypoalbuminemia -> reduced oncotic pressure and fluid movement to interstitium (results in arterial underfilling)

Overfill: renal disease -> salt retention -> fluid retention (better explanation)

127
Q

what is the underlying cause of hyperlipidemia in nephrotic syndrome?

A

Low oncotic pressure stimulates hepatic production of lipoproteins containing apolipoprotein B100 (VLDL, IDL, LDL) and cholesterol

Diminished catabolism: VLDL -> IDL -> LDL process impaired

128
Q

4 substances readily reabsorbed in PCT

A

Na, PO4, HCO3, K

129
Q

What are osmotic diuretics used for?

A 
Acute renal failure
Cerebral Edema**
Severe hyperuricemia
Dialysis Disequilibrium Syndrome
Intoxications
130
Q

What effects do CA inhibitors have on urine and blood composition?

A

Urine: Alkaline: increased HCO3- excretion (25-30% increase)
Normal Anion gap metabolic acidosis
Increased K+ excretion

131
Q

How do loop diuretics reach their site of action?

A

Secreted at prox tubule via organic acid pathway and transported to site of action

**potency dependent on urinary concentration of diuretic, not plasma conc.

132
Q

What are the effects of loop diuretics on blood and urine compositions?

A

Increase excretion of : Na+, Cl-, K+, Ca++, Mg+
Decrease free H2O clearance
Uric acid: acute use, up; chronic use down

**impairment of concentration and dilution

133
Q

Loop diuretics are the diuretics of choice for treating what?

A

Pulmonary edema
Edema in renal failure
Nephrotic syndrome

134
Q

What is the mechanism of diuretic induced metabolic alkalosis?

A

Loop diuretics and Thiazides increase Na+ delivery to collecting duct -> increased ENaC activity (Na reabsorption) and resultant K+ secretion -> K+ deficit
K+ deficit in ICF -> increased activity of H+/K+ exchanger and increased H+ excretion and increased HCO3- absorption

135
Q

What effect does acetazolamide have on urine pH?

A

Alkalinizes urine
Carbonic anhydrase inhibition -> increased HCO3- in tubular fluid and decreased CO2 liberation
Intracellularly: decreased AC activity -> decreased H+ production and inhibition of Na/H+ exchanger -> more Na stays in urine

136
Q

What are the major uses of CA inhibitors?

A

Non-edematous states: Glaucoma
Urine alkalinization: cysteine and uric acid more soluble
Altitude sickness: correct respiratory alkalosis

137
Q

What is the effect of loop diuretics on vascular tone?

A

Arterial: no effect
Venous: dilation

138
Q

What diuretic class produces the highest peak urine flow?

A

Osmotic

139
Q

What part of the nephron is most effected by mannitol?

A

TDLH: decreased H2O absorption

140
Q

What is medullary washout?

A

Increased medullary blood flow (vasa recta) -> loss of concentration gradient -> impaired free water reabsorption

*key to diuresis w/ osmotic diuretics (mannitol)

141
Q

Aldosterone antagonizing drugs and action

A

Spironolactone and Eplerenone

Competitive inhibition of aldosterone at collecting tubule, cytoplasmic receptor -> decreased ENaC insertion
**only effective in presence of Aldosterone!

142
Q

Major side effects of Aldosterone antagonists

A

Hyperkalemia

Gynecomastia (drugs also bind progesterone and androgen receptors)

143
Q

What is the overall incidence and risk of death for prostate cancer?

A

Incidence: 164/1000
Death: 34/1000

144
Q

How does smoking influence risk of prostate cancer

A

Uncertain

145
Q

What are Hereditary and Familial prostate cancers?

A

Hereditary: 3 or more men in family or 2 brothers with prostate cancer (suspected dominant gene, but unidentified)
Familial: have a person in the family with prostate cancer

146
Q

What degrees of relationship are considered in hereditary prostate cancer and what is the risk assoc. with incidence?

A

Paternal: Grandfather, Father, Uncle, Brother
Maternal: Grandfather, Brother

1 relative: 2.5x greater risk (familial)
2 relatives: 5x greater risk

147
Q

What dietary components have been linked to prostate cancer?

A

Saturated fat, red meat, dairy
Dietary fat has been estimated to account for 10% of the difference in incidence between African American and Caucasian men

148
Q

What are the most common symptoms of prostate cancer?

A 
Hematuria
Dysuria
Frequency
Urgency
Weak urine stream
Bone pain
**Most prostate cancers are asymptomatic!!
149
Q

What are the recommendations for prostate screening?

A

50 yrs if 10 yrs of life expectancy remaining
45 yrs if black or 1st degree relative w/ PCa
40 if relative w/ early diagnosis or PSA bet 1.0 - 2.5 ng/mL. >2.5, need biopsy

150
Q

What is the risk of complications in prostate screening?

A

PSA blood test: 26/10,000 (0.26%): bruising, hematoma, dizziness, fainting

Diagnostics (biopsy): 68/10,000 (0.68%): bleeding, infection, clot formation, urinary difficulty

Treatment: no data

151
Q

What is the PLCO trial?

A

US study evaluating Digital Rectal Exam vs. DRE + PSA in detection of prostate cancer. Used as basis for US Preventive Services Task Force recommendation against PSA as screening tool.
Showed no difference between groups
Major contamination!! 51% of DRE control group also received PSA. Also, premature reporting -> bad study

152
Q

What is the PIVOT trial?

A

Prostate cancer Intervention Versus Observation Trial
Demonstrated 31% reduced risk of dying from prostate cancer w/ prostatectomy. at 13 years follow-up, expected 40% reduction.

153
Q

Staging of prostate cancer

A

T1: small tumor, non-palpable
T2: palpable tumor
T3: local invasion (ex. seminal vessicle)
T4: invasion of bladder, bone, rectum, etc.
T1 and 2 are curable, T4 is not.

154
Q

Indications for prostate biopsy

A
  1. abnormal DRE
  2. PSA >4.0 ng/mL
  3. PSA change of >0.75ng/mL/year with baseline 4.0ng/mL
  4. PSA >2.5 with multiple affected family members
155
Q

What patients w/ diagnosis of prostate cancer should proceed with watchful waiting vs. treatment?

A

patients having <10 yrs life expectancy and low grade, low volume tumors.

156
Q

What is active surveilance in prostate cancer care?

A

For pts with:
PSA <50% of any one core

PSA and DRE q 3mo x 2 yrs, then q 6mos. if no changes
10-12 core biopsy at 1 year then every 3-5 years until 80 yoa

157
Q

What are the pathophysiological components of BPH?

A
  1. increased prostate size (static)

2. increased smooth muscle tone (dynamic): primary cause of symptoms

158
Q

What is the cause of BPH?

A

increased sensitivity to 5a-DHT

159
Q

What is a pharmaceutical option in treatment of BPH?

A

Second line: Finasteride: inhibits formation of DHT

First line: a1-blockers (prazosin) -> inhibition of smooth muscle contraction

160
Q

What is metabolic acidosis?

A

Results from a primary defect in [HCO3-] or [H+]

161
Q

Henderson Hasselbac

A

pH=6.1 + log ([HCO3-]/0.3pCO2)

162
Q

How does the kidney maintain acid-base balance (2 things)

A
  1. excrete the exact amount of nonvolatile acid produced (~70mmol/day) and replace consumed bicarb
  2. reclaim filtered bicarb (~4500 mmol/day)
163
Q

Total H+ secretion and Net H+ excretion

A

Total H+ secretion = HCO3 + NH4 + titratable acids

Net H+ excretion = [(U(NH4)x V + U(TA)x V) - (U(HCO3)x V)]

164
Q

What is the job of a B-intercalated cell? Important protein?

A

Excretion of HCO3- in condition of metabolic alkalosis

Pendrin: apical transport protein: HCO3- out / Cl- in
V-ATPase: basal H+reabsorption

165
Q

2 main urinary non-bicarb buffer systems

A
  1. NH3 -> NH4+ (non-resorbable)

2. HPO4– -> H2PO4-

166
Q

What is the source of NH4+ in tubular fluid?

A

Proximal tubule: glutamine -> 2 NH4 (secreted) + 2 HCO3- (absorbed) + a-ketoglutarate
glutaminease and glutamine dehydrogenase
process stimulated by low pH

167
Q

Outline the path of NH4 excretion

A

proximal tubule: glutamine -> 2 NH4 (stim by low pH)
TALH: NH4+ reabsorbed, transport to interstitium (via NKCC)
Collecting duct: NH4+ enters cells via basolateral K+ channel or NH3+ enters via basolateral Rhcg and leaves via apical Rhcg, protonated -> NH4+ which is trapped in urine

168
Q

What is the effect of Aldosterone on urine H+ content?

A

In Collecting Duct:
a-intercalated cells: direct effect - stimulates H+ secretion via ATPase
Principal cells: indirect effect - enhanced Na+ reabsorption -> increased luminal (-) favors H+ secretion by intercalated cells

169
Q

What is the difference between acidosis / -emia?

A

Acidemia / Alkalemia: deviation of pH above or below 7.4

-osis: process that can lead to -emia

170
Q

How does the change in pCO2 relate to the change in [HCO3-] in metabolic acidosis?

A

fall in pCO2 = 1.0-1.3 x fall in [HCO3]

171
Q

What is the cause of increased anion gap acidosis? what about normal anion gap acidosis?

A

Increased anion gap: production / addition of H+

Normal: addition of HCL or equivalent or primary loss of HCO3-

172
Q

What is a normal anion gap?

A

10 +/-2

140 - (105+25)

173
Q

How does albumin level affect anion gap?

A

for 1 g/dL decrease in albumin add 2.5 to gap

174
Q

What is urinary anion gap and what is it used for?

A

-NH4+ = U(Na) + U(K) - U(Cl)
should be 0 or very slightly positive

Normal plasma anion gap acidosis: elevated NH4+ excretion -> more negative urinary anion gap.

If 0 or (+), issue w/ urinary acidification -> Distal Renal Tubular Acidification (type I)

175
Q

What are types I and II renal tubular acidosis?

A

Type I RTA: distal tubule H+ secretion defect (urinary pH > 5.5 w/ very low plasma [HCO3]
Type II RTA: proximal tubule H+ secretion defect and decrease in reclaiming filtered HCO3- (urinary pH <15)

176
Q

What are some causes of Types I and II RTA?

A

I: ampho B, tonfovir, medullary sponge kidney, obstruction, H+ ATPase mutation

II: cystinosis, Fanconi, carbonic anhydrase inhibitors

177
Q

4 causes of metabolic acidosis with increased anion gap

A

addition of ketoacids (DM, alcoholic ketosis (isopropyl), starvation)
lactic acid
renal failure (decreased net acid excretion)
ingestion (salicylate OD, MeOH, ethylene glycol, metformin)

178
Q

What is the cause of metabolic alkalosis?

A

loss of H+

loss of Cl- in gradient greater than ECF

179
Q

What is oliguria vs. anuria (volumes)

A

Oliguria < 50mL / 24hr

180
Q

RIFLE criteria for ARF

A

Risk: GFR reduced 25%, SCr elevated 1.5x, urine output 4wks
esrd: complete loss of function >3mos

181
Q

Is RIFLE criteria frequently used clinically?

A

No - complex urine calculations, baseline Creatinine needed

182
Q

Signs of acute kidney injury

A 
accumulation of nitrogenous waste (uremia)
increased serum creatinine
deranged ECF balance
acid-base disturbance
electrolyte/ mineral disorders
183
Q

What is the most prevalent etiology of Acute Kidney Injury (outpatient and in-hospital)?

A

Outpatient: Pre-renal (decreased renal perfusion)

In hospital: Acute Tubular Necrosis (renal)

184
Q

What drugs can produce pre-renal AKI?

A

NSAID, ACEi, ARB, direct renin inhibitor, Cyclosporine, Tacrolimus

185
Q

treatment of pre-renal AKI

A 
Volume expansion (normal saline)
Address underlying issue:  stop drugs, correct BP
186
Q

Drugs associated with Acute interstitial necrosis

A 
Penicillin
sulfonomide
cephalosporin
rifampin
ciprofloxacin
NSAID
Allopurinol
187
Q

What is Hansel stain?

A

used for eosionophils in urine

188
Q

What is hydronephrosis?

A

Dilation of the urinary tract

189
Q

What is FENa?

A

Fraction of excreted Na
Urine Na x plasma Cr / Plasma Na x Urine Cr

If <1%: classic for pre-renal ATN, though not always the case

190
Q

In a patient with pre-renal failure, what can produce an elevated FENa?

A

diuretics
mannitol
glucosuria

191
Q

What are non-pre-renal causes of low FENa

A 
Cocaine
hepatorenal syndrome
radiocontrast injury and rhabdomyolysis
sepsis
burn
acute GN
192
Q

Define Acute kidney injury

A

Decline in kidney function over 48 hrs as reflected by:
Increase in serum Cr by more than 0.3 mg/dL
Increase in Cr by more than 50% from baseline
Development of Oliguria

193
Q

What are the most common causes of death associated with acute renal failure?

A

sepsis
cardiac failure
respiratory failure

194
Q

Features of pre-renal kidney injury

A

decreased perfusion
Treat cause, return to normal function
Tubular function remains intact
may -> ATN

195
Q

General causes of renal AKI

A

Vascular
Glomerular
Tubular (Toxin, pigment, ischemic)
Interstitial

196
Q

What is the difference between TTP and HUS and what kind of kidney injury do they contribute to?

A

TTP: caused by defect in ADAMTS13 -> vWF multimers -> excessive platelet agggregation
HUS: usually caused by E.coli O157:H7 (shiga-like toxin) -> endothelial injury and platelet aggregatin. Also caused by excessive complement activation

Both are renal causes of AKI

197
Q

key indications of acute interstitial nephritis

A

often associated w/ antimicrobials
Allergic response (eosinophils in urine - hansel stain)
Often skin involvement

198
Q

Signs of post-renal injury

A

hyperkalemia
acidosis
hesitancy and frequency (including nocturnal) of urination
incomplete emptying

199
Q

What volume of blood is typically filtered by the kidneys daily? How much of that is excreted as urine?

A

150-180 L/day (~100 mL/minute)

Urine: 1-2% of filtered volume (usually 1-2L / day)

200
Q

3 drugs that alter tubular secretion of creatinine

A

Trimethoprim
Cimetidine
Fenofribate

All inhibit creatinine secretion -> falsely elevated GFR calculation

201
Q

What is Cystatin C?

A

Protease inhibitor produced by all nucleated cells (constant rate of production)
Freely filtered and not reabsorbed, but metabolized by tubules

Serum test for GFR calculation - not yet widely used

202
Q

What is normal GFR range?

A

120-130 mL/min

varies by age, gender, race

203
Q

What is the definition of Chronic Kidney Disease?

A
  1. Kidney damage for >/= 3 mos (structural or functional abnormality of kidney) w/ or w/o decreased GFR manifest by either
    - pathological abnormalities
    - markers of kidney damage
  2. GFR /= 3mos w/ or w/o kidney damage
204
Q

In the staging of kidney disease, what marks kidney failure?

A

GFR <15 (G5)

205
Q

At what point in kidney disease does all cause mortality and CV events begin to increase?

A

GFR 60

206
Q

What are the greatest causes of CKD?

A

Diabetes and HTN

207
Q

What is isothenuria?

A

Inability of kidney to concentrate and dilute urine (as in CKD)

208
Q

How is salt and water overload managed in CKD?

A 
Limit salt intake:  <2g/day
Limit fluid intake:  1-1.5 L/day
Diuretics:  Loop, high dose (40-120mg/day, dose 2-3x/day)
Add Metolazone (thiazide like)
209
Q

How much acid is normally produced by the body / day? How much excreted?

A

12,000 mEq/day w/ ~60 mEq excreted
Carbs and fats -> CO2 and H2O -> lung
Protein -> SO4, PhO4, nitric acid

210
Q

At what point in CKD is acidosis accompanied by increased anion gap?

A 
Advanced CKD (G5)
due to retention of anions
211
Q

What is the value of treating metabolic acidosis with oral bicarb in patients w/ CKD?

A

Slows progression of CKD (reduced NH4 production -> decreased inflammation)
Slows/ prevents bone disease
Prevents muscle breakdown (improved nutritional status and preserves lean mass)

212
Q

At what point of CKD does K+ level become problematic?

A

Late stage - GFR HYPERKALEMIA

213
Q

Are diabetics at risk for hyper or hypo kalemia?

A

Hyperkalemia
Diabetics have reduced renin secretion -> reduced aldosterone and potential for inadequate excretion, esp. w/ CKD (may manifest in early CKD)

214
Q

What drugs can produce hyperkalemia?

A

Aldosterone altering drugs: ACEi/ARB, spironolactone, heparin
Na+ channel altering drugs: triamterene, amiloride, pentamidine
drugs that directly alter K+ handling: Digoxin, non-selective B-blocker, NSAID

215
Q

How is hyperkalemia treated in CKD patients?

A

Limit K+ intake
Stop K+ elevating drugs
Use Loop diuretics
Kayexalate (resin picks up K+ in exchange for Na+)

216
Q

What is the effect of CKD on phosphorus, calcium, and PTH status?

A

CKD -> reduced GFR and increased PO4 levels and decreased Ca++ levels-> chronically elevated PTH to maintain balance

217
Q

What is renal osteodystrophy?

A

Bone disease resulting from chronically elevated PTH seen in CKD

218
Q

What is osteitis fibrosa cystica?

A

Disease of bone reabsorption due to excess PTH

May occur in CKD

219
Q

What hormones are decreased in CKD?

A

EPO -> anemia
Vit D3 -> osteomalacia, OFC
Somatomedin -> decreased growth in children
Testosterone

220
Q

What happens with insulin in CKD?

A

Filtered by glomerulus and absorbed / metabolized by PCT

In CKD this -> elevated insulin -> resistance

221
Q

What hormones are elevated in CKD?

A

Prolactin
Gastrin
Renin-Aldosterone
PTH

222
Q

What drugs have been shown to slow progression of kidney disease in Types I and II diabetics?

A

Type I: ACEi and intensive BS control

Type II: ARB

223
Q

When is dialysis a consideration in CKD?

A 
Diabetic:  GFR <10
Volume overload
Persistent Hyperkalemia
Severe acidosis
Hyperphosphatemia
224
Q

What is the most common early manifestation of Diabetic Nephropathy?

A

Proteinuria: Microalbuminuria with progressive loss of protein over time

225
Q

What is the pathogenesis of Diabetic Nephropathy?

A

AGEs -> disturbance of formation / degradation of ECM -> ECM excess -> mesangial expansion -> obliteration of capillary lumen surface area

TGF-B implicated: stimulates ECM formation and inhibits degradation

226
Q

When is biopsy warranted in DN?

A
  1. Early onset renal disease: w/in 10 years of becoming T1 Diabetic
  2. Development of proteinuria absent significant retinal changes
  3. Atypical features: hematuria, accelerated renal impairment
227
Q

What are Kimmelstiel-Wilson nodules?

A

Nodular mesantial expansion seen in diabetic nephropathy

pink, hyaline, hypocellular

228
Q

What is Bence-Jones proteinuria and what is it associated with?

A

Ig light chain (usually lambda) in urine
May be associated w/ Multiple Myeloma (plasma cell proliferation)
May deposit as amyloid (AL - primary amyloidosis)

229
Q

What conditions are associated with secondary amyloidosis?

A

RA, connective tissue disease, TB, osteomyelitis

AA (improperly processed SAA (acute phase)) amyloid

230
Q

Where does amyloid deposit w/in the kidney?

A

Anywhere
First (typically) in mesangium (looks like DN - distinguish by DIF)
Later on and w/in GBM -> dysfunction: protein loss, decreased filtration

231
Q

What is myeloma cast nephropathy and what does it look like?

A

May occur in Multiple Myeloma
Ig light chains interact w/ Tamm-Horsfall protein -> occlusive casts w/in tubules
Pink, expanded tubule lumen w/ cracked appearance

232
Q

What is involved in treatment of Myeloma Cast Nephropathy?

A

Treat underlying MM with chemo and steroids -> reduction in lt. chain production
Reduce lt. chain aggretation: increase free water intake, alkalinize urine, avoid additional nephrotoxic insult (radiocontrast)

233
Q

What is the most common cause of acute renal failure in infants and young children?

A

Hemolytic Uremic Syndrome

234
Q

What is the cause of TTP and how does it affect the kidney?

A

ADAMTS13 deficiency -> vWF multimer formation and platelet aggregation

Clot formation in renal vasculature -> hematuria, proteinuria, azotemia,

235
Q

What is mesangiolysis and with what is it associated?

A

Apparent focal dissolution of the mesangial matrix

Associated with Thrombotic Microangiopathies

236
Q

What genes are implicated in Adult Polycystic Kidney Disease?

A

PKD1 (90%)

PKD2 (10%)

237
Q

What is the pathogenesis of ADPCKD?

A

Defect in PKD1 or 2 -> same manifestation (products probably linked)
Altered mechanosensation, Ca++ flux, cell-cell and cell-matrix interactions -> abnormal ECM, cell proliferation, fluid secretin -> cyst formation -> inflammation, fibrosis, insufficiency and failure

238
Q

What gene is defective in autosomal recessive polycystic kidney disease?

A

PKHD1 on chromosome 6 (6p21.1)

239
Q

How does the recessive form of PKD differ from the dominant?

A

In dominant, cysts develop from any portion of nephron
In recessive, from collecting duct only -> dilated tubules and compressed normal structures
Dominant presents at ~35 yoa while recessive presents early in life, usually by 1 year and necessitates renal transplant.
Recessive usually also presents w/ congenital hepatic fibrosis

240
Q

What is Fanconi’s syndrome?

A

Transport dysfunction in proximal tubule (defective energy metabolism?)
Presents with: hypophosphatemia, polyuria polydipsia dehydration, rickets (children, vitamin D resistant), osteomalacia (adults), growth failure, hypokalemia
May be congenital or acquired

241
Q

What is hydronephrosis?

A

product of sustained urinary obstruction
-> dilation of renal pelvis and calyces with cortical atrophy

obstruction triggers interstitial inflammatory reaction -> fibrosis

242
Q

4 types of renal calculi and associated factors

A

Calcium Oxalate: Hypercalcemia/uria, hyper PTH, sarcoidosis - radio opaque
Magnesium ammonium sulfate: Post infection w/ urea splitting bacteria (Proteus, some staph). Alkaline urine -> precipitation of staghorm calculi
Uric Acid: Gout, leukemia -> hyperuricemia. pH UA precip - radiolucent
Cystine: Genetic deficiency of AA reabsorption. stones at low pH

243
Q

3 forms of Ca++ in the body and which is physiologically important

A 
Ionized (50%) - physiologically important
Albumin bound (40%)
Complexed w/ anions (10%)
244
Q

How does pH affect Ca++ balance?

A

Acidosis: excess H+ -> displacement of Ca++ from proteins and anions -> hypercalcemia
Alkalosis: H+ deficit -> increase in bound Ca++

245
Q

3 hormones that regulate Calcium and net effect of each

A

PTH: increase serum Ca++, increase phosphate excretion
Calcitriol: increase Ca++ and phosphate
Calcitonin: decrease plasma Ca++, little effect on phosphate

246
Q

How is calcium reabsorbed at different parts of the nephron?

A

PCT: 90% paracellular, passive. Increased Na+ reabsorption -> increased Ca++ reabsorption.
10% transcellularly: Ca++ permeable channels and basal transport by Ca ATPase and 3Na / Ca++ exchanger
TAL: 50% paracellular: secondary to activity of NaKCC. increased Na reabsorption -> increased K secretion -> drives Ca++ reabsorption
50% transcellularly: same as PCT
DCT/CT: 100% transcellularly: TRPV5 - regulated by PTH and VitD

247
Q

What are claudin 16 and 19?

A

Tight junction proteins in TALH that allow paracellular reabsorption of Ca++
Mutation -> increased Ca++ excretion

248
Q

Role of Ca++ sensing receptor in TALH

A

Increased serum Ca++ -> inhibition of apical K+ channel -> increased Ca++ excretion

249
Q

What is TRPV5?

A

Ca++ channel in DCT / CT

Under control of PTH, and Vit D3

250
Q

Hypercalcemia treatment

A

Saline (high salt) and loop diuretic
High salt inhibits PCT Na+ reabsorption and Ca++ reabsorption
Loop diuretic decreases K+ secretion and Ca++ reabsorption

251
Q

Why might HCTZ be used to treat calcium stones?

A

Inhibition of Na++ reabsorption at DCT / CT -> stimulated Ca++ reabsorption, decreased Ca++ in urine

252
Q

4 causes for increased Ca++ mobilization from bone

A
  1. hyperparathyroidism: adenoma, hyperplasia, carcinoma (rare)
  2. malignancy: a) local osteolytic hypercalcemia b) humoral hypercalcemia of malignancy (PTHrP)
  3. immobilization
  4. Vitamin D intoxication
253
Q

What is humoral hypercalcemia of malignancy?

A

Tumor secretes bone reabsorbing agent: PTHrP - not detected by PTH assay

Usually associated with sq. carcinoma of lung, head, neck, esophageal, renal, bladder, or ovary.

254
Q

What is familial hypocalciuric hypercalcemia?

A

Defect in Ca++ sensing receptor -> failure of elevated Ca++ to suppress PTH
Elevated PTH -> enhanced Ca++ reabsorption by TALH and DT -> hypocalciuria

255
Q

Acute management for hypercalcemia

A

Volume restoration: normal saline
loop (not thiazide) diuretics

chronic management: treat underlying cause

256
Q

What is pseudohypoparathyroidism?

A

Bone does not respond to PTH -> decreased remodelling -> short stature, short metacarpals, hypocalcemia

257
Q

Clinical signs of hypocalcemia

A

Neuromuscular irritability -> paraesthesias and tetany
Trousseau’s sign: carpal spasm w/ BP cuff inflated above systolic BP for 3 min
Chovstek’s sign: twitching of facial muscles when facial nerve tapped anterior to ear

258
Q

Indicators of drug induced nephrotoxicity

A
  1. SCr increase of 0.5 mg/dL if baseline 2

3. corellated with initiation of drug therapy

259
Q

What is KIM-1?

A

Kidney Injury Molecule 1

Elevated with Proximal Tubular injury

260
Q

3 symptoms of distal tubule injury

A

Polyuria: fail to maximally concentrate urine
Metabolic Acidosis: failure to acidify urine
Hyperkalemia: impaired K+ excretion

261
Q

3 transporters involved in renal drug metabolism

A

OAT-1: Organic anion transporter
OCT-1: Organic cation transporter
P-gp: P-glycoprotein

Proximal tubule: active transport concentrates drugs in urine may lead to cytotoxicity.

262
Q

By what mechanism can ACEi and ARB produced Drug Induced Nephrotoxicity and what patients are at risk?

A

blockade of Angiotensin II -> efferent arteriole dilation -> decreased GFR

Patients w/ bilateral renal artery stenosis, diabetic nephropathy, any condition producing low RBF

263
Q

How can Hemodynamic Drug Induced Nephropathy be identified clinically?

A 
following initiation of ACEi / ARB
SCr increase >30%
BUN/Scr ratio >20
FENa 500
proteinuria, hyaline casts
264
Q

In a patient with HF and suspected Hemodynamic DIN, what is an appropriate replacement therapy?

A

Caused by ACEi / ARB

Replace w/ hydralazine and nitrate

265
Q

How can NSAIDs -> hemodynamic DIN?

A

COX inhibition -> decreased prostaglandins -> inability to dilate afferent arteriole

266
Q

What NSAID is less likely to produce in DIN in high risk patients?

A

Sulindac - possibly due to renal P450 metabolism

except in patients w/ hepatic disease

267
Q

Risk factors for DIN w/ NSAID use

A 
elderly
renal insufficiency
high plasma renin conditions:  hepatic disease w/ ascites, SLE, volume depletion
atherosclerotic CVD
diuretic use / hypoperfusion
diabetes
268
Q

What drugs are known for producing ATN?

A

Aminoglycosides
Amphotercin B
Radiocontrast

269
Q

What is the mechanism of amphotericin nephrotoxicity?

A

Related to cationic charge
Transported into lysosomes, inhibits function/ synthesis of cathepsin B and L (protolytic enzymes)
Inceased formation of superoxide and H2O2 -> oxidative stress

270
Q

Proteinuria containing B2 microglobulin is a symptom of ATN caused by what drug?

A

Aminoglycosides

271
Q

What is the mechanism of Amphotericin B’s nephrotoxicity?

A

Direct toxicity to Distal tubule
Increased permeability and necrosis
Arterial vasoconstriction
Reduced perfusion and ischemic injury

272
Q

What can be done to prevent Amphotericin B nephrotoxicity?

A

Avoid other nephrotoxic drugs (cyclosporine)
High salt diet w/ 1L saline / day
liposomal formulation

273
Q

What is the most common drug induced nephrotoxicity?

A

ATN

274
Q

What drugs have been known to cause Acute Allergic Interstitial Nephritis?

A

B-lactams, rifampin, NSAIDs

275
Q

What is the mechanism of Acute Allergic Interstitial Nephritis?

A

Drug binds to tubular basement membrane, acts as a hapten inducing antibody reaction
Antibody response in circulation, complex deposition in tubular interstitium

276
Q

What drugs have been linked to chronic interstitial nephritis?

A

Lithium

Analgesics: leading cause of papillary necrosis

277
Q

Clinical presentation of lithium induced chronic interstitial nephritis

A

Insidious onset over the course of years. Mild reduction in CrCl (>50ml/min)
Proteinuria, RBC, WBC, and granular casts
HTN

278
Q

What is the mechanism of Lithium nephrotoxicity?

A

decline in intracellular cAMP

defect in H2O transport in cortical CD

279
Q

What preventive measures can be taken to prevent contrast induced nephrotoxicity?

A

Low osmolality ionic and non-ionic contrasts
Hydration w/ saline or NaHCO3 isotonic solution pre- and post-admin. (HCO3: alkaline environment -> decreased ROS formation)
N-acetylcysteine
Alt. procedure (MRI, US)

280
Q

What causes increased vs. normal anion gap acidoses?

A

Increased AG acidosis: addition/production of [H+][unmeasured anion-]

Normal AG acidosis: addition of HCl or equivalent or primary loss of HCO3-

M2 (19 decks)

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