Quiz 2 Flashcards
1
Q
Where is Tamm-Horstfall protein made?
A
Thick ascending limb
2
Q
Role of virulence determinants
- fimbriae
- flagellum
- siderophore
- cytotoxic necrotizing factor I
- hemolysin
- Lipopolysaccharide
A
- fimbriae -> bind to bladder epithelial cell receptors via glycosphinolipid ix
- flagellum -> movement
- siderophore -> assist in acquiring iron
- cytotoxic necrotizing factor I -> tissue damage
- hemolysin -> tissue damage
- Lipopolysaccharide -> antiphagocytic
3
Q
List the inhibitors of bacterial adherence
A
– Tamm-Horstfall protein – Mucopolysaccharide – Oligosaccharides – sIgA – Lactoferrin
4
Q
Dx for cystitis
A
Pyuria
- > 5 WBCs per HPF
- leukocyte esterase positive
- nitrite positive - not all
- gm + NOT nitrite positive - urine culture
5
Q
Sxs used to distinguish cystitis from pyelonephritis
A
Fevers, chills, flank pain
6
Q
Only oral antibiotic approved for tx of pyelonephritis?
A
Fluoroquinolones
7
Q
How to distinguish b/w relapse and reinfection recurrent infections?
A
– Relapse
• Same organism-may mean uneradicated focus
• Symptoms return < 2 weeks; one has to consider antibiotic resistant organism
– Reinfection
• Same organism but > 2 weeks after last infection
• Most recurrences are reinfection
• Original risk factors still exist
8
Q
Young men getting UTIs think?
A
– Strictures
– Neurogenic bladder
– Incomplete voiding for any reason
– Vesicoureteral reflux
9
Q
Old man w/ UTI?
A
prostatic hypertrophy
10
Q
Sexually active male w/ prostatitis -> evaluate for?
A
Neisseria gonorrohoeae and Chlamydia trachamotis
11
Q
Chronic prostatitis
- time frame
- organism
- presentation
- tx
A
• Infection persisting for > 3 months
• E. coli is the most common, but also Pseudomonas aeruginosa, Proteus, and Klebsiella
• Enterococcus is in fact the second most commonly isolated organism
• Often present with recurrent UTI symptoms
• Or perineal or back pain
-tender boggy prostate
TX w/ fluoroquinolones
12
Q
Define primary vs 2ndary TIN
A
Primary
-glomeruli and vasculature normal
2ndary
-consequence of primary changes in glomeruli or vasculature
13
Q
Out of the 3, which one correlates best w/ renal fx?
- Tubulointerstitial changes
- glomerular changes
- vascular changes
A
TI changes
14
Q
Hallmark of analgesic nephropathy is
A
Papillary necrosis
15
Q
Acute TIN + MCGN is the classic lesion associated with?
A
ARF due to NSAIDs
16
Q
What effect does NSAID use have in patients w/ CRF or hemodynamic instability
A
Dec GFR: prerenal azotemia -> dec prostaglandins -> dec RBF/GFR
17
Q
Mech for hyperkalemia with NSAID use
Hyponatremia?
A
Hyperkalemia: dec in PGE -> dec in renin -> inc in K
Hyponatremia: removal of inhibitory effect of PGE on ADH
18
Q
Mech for Na retention with TIN due to NSAIDs
A
dec RBF and GFR
-if HTN -> gets worse
19
Q
Where in the kidney does lithium accumulate?
Mechanism of toxicity
A
Accumulates in collecting duct
Enters cells via ENaC
Down regulates APQ-2: dec regulation of cAMP -> Nephrogenic DI (can tx w/ HCTZ)
Dec activity of H+-ATPase pump -> RTA
20
Q
3 major renal conditions due to lithium
-also describe recovery from each
A
RTA -> resolves if d/c’d
Nephrogenic DI -> resolves if d/c’d EARLY
Chronic TIN -> may continue to progress even w/ d/c
-creeping Cr
21
Q
Which type of RTA can cause nephrocalcinosis?
A
Distal RTA - problem w/ maintaining proton gradient
- needed to excrete proton and reabsorb bicarb
- also get hypokalemia
NOT proximal RTA
22
Q
Define nephrocalcinosis
- where does it occur?
- associated w/ conditions causing?
A
Calcium deposition (commonly oxalate) in renal parenchyma -mostly in medulla
Associated w/ conditions causing:
- hypercalcemia
- hypercalciuria
- hyperphosphaturia
- hyperoxalosis
23
Q
Causes of nephrocalcinosis (6)
A
Distal RTA Primary HyperPTH Milk Alkali syndrome -> Calcium carbonate -CKD and on Ca supplements Sarcoidosis Vit D intoxication Vit C abuse -> contains oxalate
24
Q
Renal effects of hypercalcemia
MUST KNOW SLIDE
A
- DI – down regulation of AQP-2 ARF
- Pre-renal
- Dehydration & renal vasoconstriction - TIN/Nephrocalcinosis – if sustained
- Nephrolithiasis – if sustained
- Hypertension (vasoconstriction)
25
Exception to the following rule - Na and Ca excretion go in the same direction
HCTZ use
26
Tx for hypercalcemia
MUST KNOW SLIDE
1. Normal saline
- To repair volume
- Na and Ca excretions go in same direction (exception – HCTZ)
2. Furosemide
- To increase calcium excretion (via NKCC blockade)
- Replace K, Mg as needed
3. Bisphosphonates – Pamidronate, Alendronate
- To reduce osteoclastic activity
- Alendronate IV a good choice
4. Steroids
- To decrease intestinal absorption
27
Tubulo-interstitial disease
- Urinalysis
- Quantitative proteinuria
MUST KNOW SLIDE
Urinalysis
- minimal proteinuria
- benign sediment
Quantitative proteinuira
-typically =/< 500mg/day
28
2 ways to get pylo
1. Ascending UTI
- E. coli
- MOST COMMON
2. Hematogenous
- Staphylococcal
- minority
29
Light chain cast nephropathy
- associated with?
- leads to?
- clues to ID on histopath (3)
Multiple myeloma
ARF w/ proteinuria
-Bence jones proteins = Ig light chains (kappa or lambda)
Histopath
-tubule filled w/ protein cast
-inflammatory rxn w/ giant cells (macrophages) -> unique quality in light chain gammopathies
-another clue -> light chain doesn't react with PAS
last clue -> cracks seen in the protein cast
30
MCC of nephropathy
Diabetic nephropathy in T2DM
31
Microalbuminemia in HTN w/out diabetes is a sign of?
Inc CV risk
- endothelial association w/ GBM
- start tx
32
90% of essential HTN onset occurs in which age group? Which race does it occur earlier in?
35-55 - Caucasians
-earlier in A.A.
If earlier age -> 2ndary cause
33
1st? MCC of ESRD
| 2nd MCC of ESRD?
```
1 = diabetes
2 = HTN nephrosclerosis
```
34
Classical lesion for onset of essential HTN in kidney is?
Glomerular ischemia
- due to chronic afferent arteriole constriction -> neointimal hyperplasia
- wrinkling of GBM
- eventually get global sclerosis
35
Which mutation associated w/ earlier onset and more rapid progression of diabetic nephropathy, HTN nephrosclerosis, HIV nephropathy, and focal glomerulosclerosis
- which race?
- where expressed?
- evolutionary advantage?
- Apol 1
- AA
- podocytes and renal arterioles
- protective against trypanosomes -> sleeping sickness
36
List the proven tx for slowing progression of diabetic nephropathy (5)
```
diabetic control
BP control
Smoking cessation
weight loss in obesity
reducing proteinuria to <1g/24 hrs
```
37
In what instances is kidney bx in diabetic nephropathy indicated?
Rapid decline in renal fx
active urine sediment
other findings suggestive of alternative disease
38
Classic sign on EM in diabetic nephropathy w/ regards to GBM
Uniform thickening of the lamina densa
-abnormally glycosylated proteins accumulate
Also see mesangial sclerosis
39
At what stage of pathological classification of diabetic kidney disease is nodular sclerosis seen?
Global glomerular sclerosis?
Stage III
Stage IV (last stage)
40
List stage of CKD
Stage 1
>90
Stage 2
60-89
Stage 3
30-59
Stage 4
15-29
Stage 5
<15 or dialysis
Most people fall under stages 1-3
-more likely to die due to CV events in these stages rather than progress to IV and V
41
What 2 prognostic tests are good for CV and renal disease?
eGFR + albuminuria
42
Proteinuria followed by HTN suggestive of?
Primary renal disease
43
Final common pathway pathogenesis
loss of nephrons -> hypertrophy of remaining nephrons to maintain GFR -> glomerular hypertrophy -> inc capillary radius and increased hydrostatic pressure -> HYPERFILTRATION DAMAGE
-2ndary glomerular sclerosis = component adaptive nephron
44
Examples of disease that lead to final common pathway
HTN nephrosclerosis
Reflux nephropathy
Lupus nephritis
nephrectomy -> single kidney in patient w/ renal disease (RCC)
-all these cause SCATTERED LESIONS (not all glomeruli are involved)
45
Final common pathway accompanied by? (5)
| -which stage?
STAGE 3
```
HTN
Anemia
Metabolic acidosis
phosphate retention
renal osteodystrophy
```
46
If not HTN by stage IV or V of CRF think?
diminished EF or renal salt wasting
47
```
Renal diet
CRF stages 3-5
-protein
-Na
-K
```
Protein
-0.8g/kg -> reduces H+, PO4 intake; avoids protein malnutrition and delays uremia
Na
-2-2.5 gNa = 5G NaCl = 100mEq Na
K
- avoid high K food especially if tendency (e.g. diabetes)
- dec renin release w/ diabetes -> inc risk of hyperkalemia due to dec aldo
- also insulin pushes K into cells
48
Metabolic acidosis in CRF due to?
contributes to?
how much NaHCO3 needed?
Diminished NH4 production
-contributes to CRF progression and catabolism of protein and bone; bone is a buffer system for protons
-shift hyperkalemia
- 20-30mEq of NaHCO3 adequate to restore HCO3 > 22 mEq/L
- CaCO3 also useful
49
Describe the osteoid to mineralized bone ratio in osteomalacia
Too much osteoid and not enough mineralized bone -> weak bones
-due to inc Ca resorption
50
Cholesterol clefts seen with?
atheroembolic renal disease
51
What is the gene involved with ARPKD? what does it code for?
PKHD1 - fibrocystin
52
What is the proposed pathogenesis for PKD?
Improper connection b/w nephron and collecting system OR squeezing of the connection -> cysts = swollen nephrons that can't drain
53
What does the cloaca form
Rectum
Primitive UG sinus -> bladder + pelvic urethra + definitive UG sinus
54
Tourneux vs Rathke folds
Tourneux fold -> superior portion of urorectal septum
- b/w rectum and bladder
- T = top
Rathke -> inferior portion of urorectal septum
- b/w rectum and urethra
- right and left
55
What happens when both Tourneux and Rathke folds fail to form
Rectovesical fistula - connection b/w rectum and bladder
56
ureteric buds (urethra) become directly attached to?
Mesonephric ducts become attached to
Bladder
urethra (prostatic)
57
Ectopic ureter occurs when
Describe the drainage
consideration for females
consideration for males
2 ureteric buds sprout from same mesonephric duct
- gets pulled down inferiorly w/ mesonephric duct
- ectopic ureter drains inferior to the bladder
URETERS CROSS
Ectopic ureter -> drains the superior pole
Normal ureter -> drains inferior pole
In females -> ectopic ureter may drain into vestibule, vagina or uterus
- all are BELOW the sphincter urethrae muscle -> incontinence
- urinate normal w/ dribbling in b/w
- apparent during potty training
In males -> drains into prostatic urethra, ejaculatory duct, vas def, or seminal vesicles
- all are ABOVE the sphincter urethrae muscle -> NO incontinence
- but inc risk for infection
58
most common inherited autosomal dominant kidney disease
ADPKD
59
Characteristics of Frasier Syndrome
```
46, XY w/ female phenotype
kidney disease
pubic hair
mullerian structures
mutation in WT1
```
60
PKD1
- codes for?
- linked to?
polycystin -> large membrane bound protein
linked to TSC2 -> tuberous sclerosis
61
PKD1 vs PKD2
- chromsome
- avg age for renal failure
PKD1 - 53
-chromosome 16
PKD2 - 69
-chromosome 4
62
Mutation in ARPKD
- chromosome?
- death from
- which part of nephron gets the cysts?
PKHD1
- chromosome 6
- pulmonary hypoplasia -> respiratory insufficiency
- Cysts = DILATED COLLECTING DUCTS
63
We have no reliable testing for mutations in
regulatory elements
64
MCC of palpable mass in newborn is
cystic kidney disease
65
90% of multicystic dysplastic kidney disease associated with? (renal dysplasia)
Path?
obstruction (urinary tract malformations)
Path
- disruption of pre-renal mesenchyme coming together w/ ureteral bud
- ureteric bud and metanephric blastema
66
Wilms tumor
- sporadic and unilateral vs congenital syndrome/family hx percentages
- genes
- sporadic and unilateral = 90%
- congenital syndrome/family hx = 10%
- chromosome 11 - deletion of short arm
- WT1 gene
- WT2 gene
Loss of heterozygosity
67
WAGR
- wilms tumor
- aniridia
- genitourinary anomalies
- mental retardation
68
Denys-Drash
- wilms
- dysgenetic disorders
- glomerular disease
69
Beckwith-Wiedemann syndrome
-Wilms
-hemihypertrophy visceromegaly
macroglossia
70
Nephrogenic rests
- define
- precursor for
- risk of
small foci of persistent primitive blastemal cells
precursor lesion for wilms tumor
risk of bilateral wilms
71
MC renal tumor in neonate?
- presents as
- uni or bilateral
- risk of mets
- tx
- histology
- gross comparison to wilms
Mesoblastic nephroma
- less than 3 months of age
- 1/3 to 1/2 noted w/in 1st week of life
- abdominal mass
- ALWAYS unilateral
- low risk of mets
- nephrectomy
histo -> spindles cell tumor
-no primitive appearance
Unlike Wilms -> no sharp distinction b/w normal kidney and tumor
72
Subgroups w/ HTN at inc risk
```
African american
hispanic
elderly
metabolic syndrome
DM2
CKD
```
73
ACEI don't work well in which population?
African Americans
74
Minimum eval of HTN patient
```
urinalysis, microalbumin test
Hct
renal profile
fasting glucose
lipid profile
EKG
```
75
Describe the rule of tens with regards to HTN tx
1 additional drug for every additional 10-mmHg reduction in BP
76
JNC-8 guidelines for HTN drugs
- General population
- AA
- CKD
1. general (including diabetics) -> initiate tx w/ a thiazide, Ca channel blocker, ACE inhibitor or ARB
2. Black population -> include a thiazide or a CCB
3. In patients w/ CKD -> include ACE-I or ARB until age 75
- use clinical judgement to tx > 75
77
Chronic proteinuria is predictive of
CRF
78
Why is proteinuria harmful to kidney?
1. Podocyte damage
2. fibrosis and tubulointerstitial disease
AGII, endothelin and TGF-beta play role
79
What is an acceptable inc in Cr following ACEI tx?
25-30%
80
What occurs in adynamic bone disease?
Bone doesn't respond normally to PTH
81
Cinacalcet
- class
- action
- indication
- side effects
- other
1. class -> calcimimetic agent
2. Action
- reduces PTH production at same Ca level -> sensitizes Ca-sensitive receptor to serum Ca
3. Indication -> 2ndary hyperPTH
4. Side effects -> hypocalcemia
82
Sevelamer Carbonate
- class
- action
- indication
- side effects
- other
Sevelamer Carbonate
Class
-Phosphate - Blocker
Action
-Chelates PO4 in gut
Indication
-CRF with elevated serum PO4
Side effects
(a) hypophosphatemia ((a) = action of drug)
(b) constipation – may interfere with absorption of other drugs * ((b) = other side effects)
Other
-Reduces serum LDL also
* Take other drugs at least 1 hour before Sevelamer
83
Calcitriol
- class
- action
- indication
- side effects
- other
Class
-Calcitriol (1-25 (OH)2Vit D)
Action
- Most active effect on vitamin D receptors (VDR)
- stimulates bone Ca++ mobilization and gut Ca++ reabsorption
- directly lowers PTH levels
Indication
-Hypocalcemia due to low levels of 1-25(OH)2VitD in presence of normal levels of 25(OH)VitD
Side effects
(a) Hypercalcemia
Other
(a) Beneficial effects in CV disease, immune function, cancer?
(b) Paricalcitol in CRF may have reduced effects on absorption of calcium and phosphate in the gut and thus cause less hypercalcemia while reducing PTH levels
84
Starting drug tx for HTN vs renal disease
HTN -> amlodipine + ACE
renal disease -> ACE or ARB
85
Malignant HTN
- hallmark
- characterized by
- papilledema
| - fibrinoid and necrotizing arteriolitis
86
3 toxic effects of aldosterone
- fibrosis
- hyperplasia
- inflammation
87
Typical presentation for unilateral renal artery stenosis txed with ACEI
Dec in BP and slight dec in GFR (inc Cr)
88
When should a loop be used over thiazide for HTN management?
If filtered low is too low (i.e. low GFR)
| <30??
89
If K is high in urine with high serum K ->
If K low in urine with high serum K ->
If K is high in urine with high serum K -> diet problem
If K low in urine with high serum K -> renal problem
90
Simplified henderson-hasselbalch eq
log (P/U) = pKa - pH
91
Weakly basic drugs are concentrated/trapped in?
-can be eliminated more quickly by?
How about weak acids
1. Acidic fluid; acidify urine
| 2. Opposite for weak acids
92
Given a fixed pH, the higher the pKa of a weak acid, the more will be in the (charged/uncharged) form?
UNCHARGED
93
Relationship b/w elimination rate constant and half life of drug
INVERSELY PROPORTIONAL
94
Vol distribution =
Vd = dose/[drug in plasma] at t=0
95
Cl=
kVd
96
Css (steady state) =
Css = k0/Cl
| steady state plasma [drug] = influx (infusion rate)/efflux (CI
97
Inc risk for getting what with glyburide or metformin in patients with DM and renal insufficiency
LACTIC ACIDOSIS
98
Dose levels in CRF
- Stage 3
- Stages 4 and 5
3 -> 50% decrease
4+5 -> 75%
99
DOC for txing volume overload in AKI or low GFR
LOOPS
100
Drugs that can cause pre-renal AKI
ACEI and ARB -> inhibit efferent arteriole vasoconstriction
NSAIDs -> inhibit afferent arteriole vasodilation
Cyclosporin + Tacrolimus
-calcineurin inhibitors and potent renal vasoconstrictors
101
Intra-renal injury by drugs
- ATN -> 3
- AIN -> 8
Acute tubular necrosis
- Aminoglycoside antibiotics (e.g., Gentamicin) – bind to and uptake by proximal tubule cells in renal cortex---cell death
- Amphotericin B (anti-fungal) – renal arterial vasoconstriction and distal renal tubule cell toxicity (minimize with liposomal drug formulations)
- Cisplatin (and to a lesser degree, carboplatin - antineoplastics)
Acute interstitial nephritis (only main drug examples listed)
- Beta-lactam antibiotics (penicillins and cephalosporins) Fluoroquinolones (e.g., ciprofloxacin)
- Thiazide diuretics (HCTZ, chlorthalidone) – rare, but heavily used
- Loop diuretics (furosemide) – rare, but heavily used
- Allopurinol (xanthine oxidase inhibitor used to treat gout)
- Sulfonamides (including sulfonylureas for diabetes (e.g., glipizide))
- Rifampin (anti-mycobacterial used to treat tuberculosis, CYP450 inducer)
- NSAIDS
102
Post-renal AKI
| -drugs
1. Acyclovir (a nucleoside analogue HSV antiviral drug used for genital herpes, cold sores, shingles)
2. Methotrexate (anti-folate anti-metabolite used for cancer and autoimmune diseases)
3. Indinavir (antiviral protease inhibitor used to treat AIDS)
4. diuretics -> excess Ca in urine -> inc risk of stones
103
Probenecid competes w/ which 2 drugs
- for what?
- transporter?
- effect?
- penicillins and MTX
- secretion via organic anion transporter
- dec secretion -> inc plasma concentration of penicillins or MTX
104
Half life of Li+?
| what happens when give thiazide to chronic Li patient
24 hours
inc concentration of Li
105
What metabolizing enzyme is found in kidney?
CYP450
UDP-glucuronyltransferase (Phase II) -> furosemide metabolized here
-inc half life in AKI patients
106
Which drug can make inc risk of euvolemic hyponatremia with thiazides? how?
NSAIDS
- PGE2 is an ADH antagonist
- blocking PGE2 with NSAIDs will lead to inc water reabsorption
- combine that with Na loss -> euvolemic hyponatremia
MCC of of EH in old people is thiazides
107
Match up the drugs associated w/ the following:
-from luke 2-24 lecture
ATN
AIN
HUS
RTA
ATN -> gentamycin (aminoglycosides)
AIN -> amoxicillin
HUS -> clopidogrel
RTA -> amphotericin B
108
Which type of RTA does amphotericin B cause? What's the mech?
Type ! RTA
- alpha intercalated cells can't secrete H+ -> new HCO3- can't be generated -> met acid with hypokalemia
- also inc risk of of CaPO4 kidney stones due to inc urine pH and inc bone turnover
Amphotericin B pokes holes in walls of collecting duct
-also vasoconstricts kidneys
109
Should a patient stop taking ACEI, ARB and/or diuretics d/c if GI loss or high fever? If so why?
YES!!!
Inc risk of Pre-renal AKI
110
ATN risk factors for aminoglycosides (like gentamycin) are (list 4)
- high trough levels
- prolonged administration
- older age
- concomitant use of loops (also for 8th nerve damage)
111
Which endogenous chemical is both naturetic (salt wasting) and aquaretic? What is an inhibitor of this chemical? What effect does the inhibitor have on response to antiHTNs and diuretics
PGE2; inhibited by NSAIDs
-dec response; always ask about NSAID use!
112
NSAIDs
- effect on Na
- effect on K
- effect on kidneys
Hyponatremia: inhibit PGE2 = an ADH antagonist
Hyperkalemia: less renin release -> diminished aldosterone production
Renal: AIN; nephrotic syndrome and ATN by inhibiting autoregulation of GFR
113
Signs/sxs of AIN
| -difference with NSAID?
Rash
fevers
eosinophiluria
hematuria
W/ NSAIDs -> no rash or fever!!!
114
Rxing in ARF and CRF
-which adjustment to the drug dose is better if patient needs high blood levels quickly? (e.g. sepsis)
-what about for ppl in stage 3 CRF? Stage 4 and 5?
reduce dosing interval for 1st question
If stage 3 CRF -> reduce dose level by 50%
If stage 4 and 5 -> reduce dose level by 75%
115
Give 2 reasons why there is an inc risk of hypoglycemia w/ glyburide in diabetics w/ renal failure
1. Renally excreted
- Drug will be higher in blood
2. Half life of insulin is longer in patients w/ chronic renal failure
- Insulin will stay around longer
3. Use glipizide instead -> handled by liver
116
Salicylate poisoning
- toxicity at what level?
- signs and sxs (list 4)
- how to promote excretion
- tx for severe poisoning
- kids vs adults w/ regard to acid-base presentation
- can mimic?
Toxicity when >40 mg/dL
- hyperventilation and respiratory alkalosis
- tinnitus
- fever
- vomiting and GI bleeding
- mental status change
- lactic acidosis - anion gap, mixed acid base disturbance
alkalinizing urine increase renal excretion
- target = 6.5 - 7
- don't go too high
Hemodialysis effective tx for severe poisoning
adults - alkalotic side
kids - acidemic side
can mimic sepsis
117
how to calc ratio of charged over uncharged salicylate
pH - 3 = Log SALc/SALus
118
Acids responsible for causing inc anion gap acidemia for the following poisons:
- methanol
- ethylene glycol
- what effects can they cause?
methanol -> formic acid
-blindness
ethylene glycol -> oxalic acid
-renal failure -> death
119
How to calc osmolar gap
| -MCC of osmolar gap?
osmolar gap = MEASURED serum
Osm - calculated Osm
Calculated Osm = (Na x 2) + [glucose] + [urea] = 280 + 18 mOsm + 2.8 mOsm
If > 10 mOsm then osmolar gap
MCC = ethyl alcohol
(mg/dL) / 5 = mOsm due to alcohol
120
Fomipezole
- MoA
- indications
MoA -> competitive antagonist of alcohol dehydrogenase which converts toxic alcohols to their anionic metabolites
For methanol and ethylene glycol toxicity
121
Which toxic alcohol cause osmolar gap and CNS toxicity but NOT metabolic acidosis?
Isopropyl alcohol
122
Alcoholic ketoacidosis
- main ketonacid
- is it detected by acetest (nitroprusside) tabs?
- tx w?
- watch out for?
Beta hydroxybutyrate
NOT DETECTED
tx w/ glucose and saline and refeeding
watch out for refeeding syndrome
-K, phosphate and Mg replacement requirements
123
Lithium
- CNS side effects in acute vs chronic toxicity
- Renal effect?
- tx?
- watch out for what with tx?
- CNS side effects come on later with acute
- nephrogenic DI: Li = ADH antagononist
- tx by restoring ECF volume and produce natriuresis by saline infusion
- hemodialysis w/ severe toxicity and renal impairment
-avoid hypernatremia in those w/ polyuria especially if isotonic saline being infused
124
3 major criteria for a single simple cyst on US?
- mass is round and sharply demarcated w/ smooth walls
- no echoes w/in mass
- strong posterior wall echo indicating good sound transmission through the cyst
Can't be seen on plain film radiography
125
RCC imaging
- dxic procedure of choice
- screening test to dx renal cyst
- vascular invasion
1. CT
- peri-renal extension
- vascular invasion
- liver involvement
2. US
3. MR
126
Nephrogenic phase of CT
- time?
- good for?
90-100 sec after contrast injection
Renal masses
127
What can mimic RCC on CT?
renal abscess
128
Is MRI good for renal calculi
NO
129
Clear cell RCC on T1 vs T2 MR
T1 - low signal
T2 - high signal
130
Rxns to contrast
Minor
Moderate
Major
Minor
-hives/flushing
Moderate
-bronchospasm
Major
- laryngeal edema
- hypoTN ->aggressive IV fluids
- arrhythmia -> atropine for brady if no response to fluid
131
Risk factors for rxn to contrast
- dose and rate
- elderly patients
- allergy hx
- hx of previous rxn
- not predictive
- higher risk of arrythmias and MI
- doubles risk
- high risk -> pretreat
drugs -> can give steroids and benadryl
132
Indications for RRT?
1. ARF or CRF
-uremic syndrome
-pericarditis
Failed conservative management for
-hyperkalemia
-acidosis
-fluid overload
2. Drug overdose:
- lithium
- ethylene glycol
- methanol
- salicylate
3. Electrolyte disorders
- hypercalcemia
- hyperkalemia
4. Metabolic disorders
- severe hyperuricemia - tumor lysis
133
CRRT vs IHD -> when is CRRT preferred
CRRT only used in ICU
- high fluid removal needed (4L+)
- hemodynamically unstable
134
Absolute indications for RRT w/ acute or chronic renal failure
MUST KNOW SLIDE
```
ARF or CRF
-uremic syndrome
-pericarditis
Failed conservative management for
-hyperkalemia
-acidosis
-fluid overload
```
135
2 key fxs of dialysis
-how are they accomplished
MUST KNOW SLIDE
1. Solute removal
a) diffusion -> 85% (size dependent)
b) convective transport -> 15%
- solvent drag effect
- for middle molecules
2. Fluid removal
- by hydrostatic pressure (ultrafiltration) -> HD
- by osmotic pressure -> PD
136
Best vascular access for hemodialysis
-why?
MUST KNOW SLIDE
AV fistula
- long life
- effective
- least prone to infection
Catheter is worst
137
PD vs HD - which one is better?
PD - better for 1st 3 years
HD - takes over after that
138
What are 2 fxs of the kidney that dialysis can't replace?
MUST KNOW SLIDE
endocrine and erythropoiesis
139
Complete sentence:
After 1 year, 50% of grafts are lost due to?
NON-ADHERENCE
140
What are the top 2 reasons for exclusion from transplant eligibility?
1 -> medical CI = ~50%
2 -> patient declined = 25%
141
CI for kidney donation w/ regards to:
- age
- BP
- proteinuria
- GFR
AGE
- 65-70
BP
> 140/90
PROTEINURIA
>250 mg/24 hrs
GFR
<80 ml/min
142
3 factors involved in tissue matching and Ab production
1. HLA
2. Crossmatch
3. Panel-reactive Ab
143
drugs used for induction immunosuppression
Corticosteroids
- high dose and then tapered off
- efficacy due to immunosuppressive and anit-inflammatory effects
Anti-lymphocyte Abs
-poly and monoclonal
144
Adverse effects of corticosteroids include
```
METABOLIC
l Obesity
l Hyperlipidemia
l Diabetes mellitus
l Osteopenia/Osteoporosis
l Growth retardation (children)
```
COSMETIC
```
OTHER
l HTN
l Poor wound healing
l Mood changes
l Proximal myopathy
```
145
UC induction prototype for immunosuppression (3 drugs)
thymoglobulin
MMF
Solumedrol
146
List 4 lymphocyte proliferation inhibitors
azathioprine
mycophenolate mofetil
Mycophenolate sodium
Sirolimus
147
List 2 calcineurin inhibitor
cyclosporine
tacrolimus
148
List a CNI sparing T-cell inhibitor
Belatacept
149
Adverse effects of azathioprine
Myelosuppression - dose dependent
Hepatotoxicity
acute pancreatitis
skin cancer
150
MMF adverse effects
diarrhea
leukopenia
anemia
tissue invasive CMV disease
151
Cyclosporine adverse effects
| -include cosmetic effects
```
l Nephrotoxicity
l Hypertension
l Cosmetic side effects – gingival
hyperplasia, hirsutism
l Hyperlipidemia
l Neurotoxicity – headache, tremor,
seizures
l Hepatoxicity – transaminitis
```
152
Tacrolimus adverse effects
| -include race dependent effects
l Nephrotoxicity
l Neurotoxicity – tremor, paraesthesias
l Diabetes mellitus – more common in African-Americans & Hispanics
l Alopecia
l Hypertension
l Hyperlipidemia
153
Cyclosporine and tacrolimus are metabolized by?
| implication?
CYP-450 3A4
LOTS OF DRUG-DRUG IX
154
Belatacept
- MoA
- black box warning
MoA -> selective T-cell costimulation blocker
BLACK BOX
- Inc risk of post-transplant lymphproliferative disorder
- mostly in the CNS
- esp in patients who are EBV seronegative
155
Sirolimus
- class
- indications
- adverse effects
class -> macrolide anitbiotics
indication -> CNI sparing tx
```
Adverse effects
l Thrombocytopenia
l Hyperlipidemia – predominantly hypertriglyceridemia
l Oral ulceration
l Impaired wound healing
l Proteinuria
```
156
CER
-proportion of people not exposed who experienced the event
c/(c+d)
157
EER
-proportion of people exposed who experience the event
a/(a+b)
158
RR
-relative risk
EER/CER
159
RRR
-relative risk reduction
(CER - EER) / CER
160
ARR
CER - EER
161
Best interest Standard
- acting to promote maximally the good of the individual
- legal standard
- medical standard
Parents ALWAYS need to make decision most favorable to the child
162
Medical reasoning in kids parallels
Piaget Stages
Age 2-6 -> preoperational stage
Age 7-10 -> concrete operational stage
Age 11-16+ -> formal operation stages
- developmental milestone
- can start making their own decision
163
Acutely sick vs chronically sick kids with regards to maturity of explanation
Acutely sick -> less mature
Chronically sick -> more mature
164
3 exceptions when minors can CONSENT for themselves
- emancipated minor laws
- mature minor laws
- public health/awkward topic laws
165
What are the NEWEST guidelines for when to start tx for HTN (JNC-8)
-break down by age
60+ -> tx to goal BP less that 150 over 90
less than 60 -> tx to goal BP less than 140 over 90
Over 18 w/ CKD and/or diabetes -> tx to goal less than 140 over 90
166
Compare unilateral stenosis w/ bilateral RAS
Unilateral
- sensitive to ACE inhibition:
1. drop in BP
2. can cause drop in GFR
Bilateral
- more severe hypertension
- small effect of ACEI
- drop in BP ONLY after volume depletion
167
List foods high in K
1. Fruits – bananas, oranges, melons, etc.
2. Vegetables – potatoes, tomatoes, greens, mushrooms, vegetable juices, pumpkin, etc.
3. Dried beans, nuts, seeds
4. Salt substitutes
5. Milk
6. Chewing tobacco
168
List foods high in phosphate
1. Dairy products
2. Dried beans, peas, nuts, seeds
3. Bran and whole grain breads
4. Beer and dark sodas
5. Processed meats
169
Renal multivitamins contain?
i. Renal multivitamin contains B vitamins (B6, B12, etc.), folate, vitamin C, zinc (sometimes)
170
IDWG should be (blank %) of dry body weight
4%
171
Fluid MNT for AKI
For CKD on HD?
AKI
-replace output from previous session + 500ml
CKD
-1000 + urine out
