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OME > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Patient presentation of kidney stone

A

o Colicky flank pain
o Radiates to groin
o Nausia / vomiting

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2
Q

• How to tell pyelonephritis from a kidney stone and Renal cell carcinoma

A

o Pyelonephritis will have fever and WBC casts*
o RCC will have palpable mass
o All could have hematuria

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3
Q

Tests to order if kidney stone is suspected

A

o UA
o Noncon CT is gold standard. IF PREG: use US
o NO KUB

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4
Q

• UA of kidney stone

A 
o	Blood (even microscopic hematuria) (Note: in the absence of blood,  probability of symptomatic stone is low) 
o	Absence of casts
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5
Q

• Treatment of stone and Difinitive Management based on size of kidney stone

A

o IVF and analgesia
o < 0.5mm : Pass spontaniously: Hydration and pain control
o 0.7 – 1.5 mm : Medical Exulsive therapy: CCB (amlodipine) and/or Alpha blockers (terazosin
o > 1.5mm : Resection (laproscopic (proximal) / lithotripsy (distal)
o Strain and analyze stone, 24 hr urinalysis in 6 weeks

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6
Q

Radio opaque vs radio leucent stones with causes

A

o Opaque: Calcium oxalate / Magnesium Ammonium Phosphate

o Leucent: Uric acid / cystine

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7
Q

• What happens in hyponatremia and hyper

A

o Hyponatrimia – less in blood, fluid extravisates into body
o Hypernatrimia – more in blood, fluid extravisates into blood

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8
Q
  • Hypernatrimia
  • What is it
  • How do you fix it
A

o Always a deficiency of water
o Fix is with PO water if possible. Consider hypotonic sulutions such as D5W or 1/2ns.
Before replacing the free water deficite, fix volume with NS

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9
Q

• Hyponatrimia AND hypernatremia –sxs in Mild vs Moderate vs Severe state

A

o Mild – asymptomatic
o Moderate – Nausia, vomiting, headache
o Acute / Severe – Coma, Seizure

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10
Q

• Tx for severe state hyponatremia

A

o Coma / Seizure

o Hypertonic Saline (3%)

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11
Q

• How fast can you correct hyponatremia?

A

o No faster than 0.25 mmol / hr OR 6 in a day
o Usually symptoms will go away after a day of treatment
o Correction Too fast will lead to osmotic demyelination syndrome

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12
Q

• General rules of thumb when looking at Urine osms and Na in a patient with hyponatremia

A

o If urine Na is low – kidneys are working, low perfusion is cause
o If urine has high osms [ ] then ADH is high.

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13
Q

• Euvolemic Hyponatremia

A 
o	RATS
o	Renal Tubular acidosis  (UA) 
o	Addisions ( urine cortisol) 
o	Thyroid disease (TSH) 
o	SIADH (dx of exclusion)
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14
Q

SXS of volume up

A

o JVD
o Edema
o CHF
o Anasarca

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15
Q

• Sxs of volume down

A

o Dry mucous membranes
o Tachypnia, Hypotension
o Fevers
o Burns

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16
Q

• SIADH tx

A

o Volume restriction
o Possible gentle diuresis
o If refractory – demeclocycline

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17
Q

• Steps to make DX of cause with Na <135

A

1) Determine serum osmoles – for every 100 glucose over 100, subtract 1.6 Na

2) Volume status?
Overload (hypervolemic)
— Determine cause and diurese

Normal (Euvolemic)
—- RATS – UA, Cortisol, TSH

Down
IVF – see if it corrects
Urine Na
Intrarenal – High urine Na: ATN AIN

Extranrenal - low urine Na

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18
Q

• Calculation fo Serum Osmoles

A

o 2xNa + gluc/18 + BUN/2.8

o Normal is 275-295

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19
Q

K normal

A

o 3.5-5.5

o >4 is normal in cardiac patatients

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20
Q
  • Sxs of hyperkalemia

* Exam Findings of hyperkalemia

A 
Usually its asymptomatic. If severe pt will report 
o	Decreased motor, dec sensation 
o	Flaccid paralysis
o	Parestheisea
o	Chest pain / palpitations 
EXAM may show
o	ECG changes 
o	Areflexia
o	Numbness 
`
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21
Q

• First thing to do when there is a high K level?

A

o Repeat lab

o ECG

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22
Q

• DDX of hyperkalemia

A 
o	Artifact
o	K-sparing diuretics (Ace, Arb, Spironilactone ) 
o	Hypoaldosterone 
o	CKD / RTA 
o	Ingestion
o	Hemolysis 
o	Iatrogenic (over administered)
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23
Q

• Findings of High K on ECG

A

o PR prolongs
o QRS widens
o T waves Peak

24
Q

• 3 stages of treatment of hyperkalemia

A

o I : Stabalize myocardium with calcium gluconate
o II: Dec serum K : Insulin + glucose or Bicarbonate
o III: Dec total body K with Kayexalate or diuretics
o If Renal failure or extreme ECG changes, dialysis
o NOTE: if stable – just give kayexelate

25
Q

• Causes of Hypokalemia

A

GI loss
♣ Vomiting
♣ Diarhea
♣ Laxatives

Renal Losses
♣ Hyperaldosterone (primary or secondary)
♣ Loop diuretics
♣ Thiazide Diuretics

26
Q

• Replacement of K

A

o Oral preferred

o IV: <10meq/hr peripheral or <20 central

27
Q

What are the regulators of calcium?

What is it bound to?

How to adjust for Alb?

A 
o	Clacitonin
o	PTH 
♣	Activates osteoclasts 
♣	Kidneys: Ca in, P out
♣	Inc Vit D 1,25absorb Ca and P from gut

o Mostly bound to albumin. Very little is ionized
♣ Alb adjust: every point below 4, add 0.8 Ca

28
Q

Symptoms of hypercalcemia

A

Bones – fracture, osteopenia

Psychic Moans – AMS only if severe – 13-15

Stones

Abdominal Groans – (Nausia, Vomiting, abdominal pain)

29
Q

TX of hypercalcemia

A

o IVF – always first line

o Furosimide – inc naturesis and Ca exc but ONLY when volume status is corrected

o Calcitonin – acts / fades fast

o Bisphosphonates – long term

30
Q

DDX of Hypercalcemia

A 
o	Primary, secondary, tertiary hyperparathyroid
o	Familial hypocalciuric hypercalcemia 
o	Malignancy 
o	Immobilization 
o	Vit D excess
31
Q 
Primary Hyperparathyroidism. 
Cause 
labs 
an interesting sequellae, 
dx
tx
FU
A

Cause: Single autonomous gland PTH
Labs: High Ca, Low P
Seq: Could get Brown tumor (fibrosa cystica) – osteoclast stimulation
DX – radionucliotide scan. (sestamibi)
TX – resection
FU – watch for hypocalcemia on FU (Hungry bone syndrome)

32
Q

Secondary hyperparathyroid

  • cause
  • labs
A

Cause: Erly renal failure – vit D not made – causes low Ca, so inc PTH and parathyroid hypertrophy

Labs: High Ca, Low P

33
Q 
Tertiary hyperparathyroid: 
Cause
labs
tx
a note
A

o Continued renal failure causes PTH glands to become autonomous (just like primary)
o Labs: High Ca, Low P
o TX –resction
o Note: no risk of cancer

34
Q

Familial Hypocacciuric Hypercalcemia:

Cause
Labs
Sxs
tx
sequellae
A

o Cause – abnormal calcium sensing receptor, so new set point.
o Labs: inc Ca, low P (inc PTH)
o SXS, Asymptomatic
o TX – none
o Sequellae: inc risk of stenotic aortic disease in old age

35
Q

Malignancy - two ways it can cause increased Ca

A

PTH-rp – looks like primary hyperPTH but low PTH
♣ High Ca, Low P

Mets – way high Ca
♣ High Ca, High P

36
Q

Immobilization as cause of inc in Ca.

Cause
labs
sxs
tx

A

o Cause – dec impact stress
o Labs- low PTH , Inc Ca, Inc P,
o Sxs – asx
o Tx – inc movement

37
Q

Vit D excess as a cause of inc Ca

Cause
labs
tx

A

o Cause: granulomatous dz: TB, sarcoid
o Labs –low PTH, Inc P, Inc Ca
o Tx – steroids to treat dz

38
Q

Hypocalcemia DDX – extensive

A

Hypoalbuminemia (adjuct fo alb and ca will normally correct)
♣ Cirrhosis, Nephrosis, poor nutrition

Hypoparathyridism
♣ Iatrogenic (postsurgical “hungry bone” which means atrphyied glands)

Vit D deficiency
♣ Renal failure
♣ Sunlight / diet deprivation
♣ These lead to secondary hyperparathyroidism – initially though there will be decreased Ca

CRF

Calcium Sequestration
♣ PANCREATITS

Pseudohypoprarthytroidism

39
Q

Sxs of Hypocalcemia

tx

A

SXS
Perioral tingling
Tetany (chovstek = chvozTAP , trassaue = arm)

TX
replace Ca:
PO Ca and Vit D If non emergent.
IV if emergent

40
Q

Pseudohypoprarthytroidism – what it is and why the name is bad, labs

A

o High PTH due to end organ resistance

o High Ca, high P but everything is functioning normally. ignore it.

41
Q

Hypoparathyridism, cause and labs

A 
o	Iatrogenic (postsurgical “hungry bone” which means atrphyied glands) 
o	Labs – dec PTH, Dec Ca, Dec P
42
Q

Presentation of AKI

A

o Elevate Cr
o Decreased urine output

Note: Kidneys are redundant, so electrolytes will not be out of wack until GFR is severely reduced. Patient will likely be asx and it will be noted on routine labs

43
Q

Prerenal AKI
Cause
Labs
TX.

Note on most common cause in outpatient

A

Cause: Low perfusion
Make sure to check volume status! (ask about this in the future)

Labs:
Low Urine Na, Low Fe Na (Make sure patient not on diuretic)
BUN/CR >20

TX
Volume Down - fluids (this is prerenal azotemia
(gentle diuresis if vol up?)

Note: prerenal azotemia is most common cause in outpatient setting.

44
Q 
Postrenal AKI: 
Cause, 
DDX, 
DX, 
TX depending on location
A

Cause: obstruction

DDX
Distal: BPH, Neurogenic bladder, Kinked cath
Proximal: stones and cancer

DX – US preferred, CT can be used.

TX –
Distal – cath.
Poximal – stent, nephrostomy tubes, surg

45
Q

• Intrarenal AKI ddx and qyick notes about each

A

ATN
♣ Ischemia
♣ Toxin exposure
♣ Muddy brown casts – phases of recovery

AIN
♣ Drugs, infection, deposition dz
♣ RBCS, WBCS , eosinophils

Glomerularnephritis
♣ RBC casts. TONS of causes. Lupus, IgA neph, goodpast, HSP, etc
♣ Rule out nephrotic synd with with UA spot test / 24 hr urine

46
Q

AEIOU

A 
reasons for dialysis
A - acidosis 
E -electrolytes (K) 
I - intoxicants / toxins (methanol ethylene glycol, Li, ASA)
O - overload 
U - uremia
47
Q

You have ARF, how do you work it up?

A

Order
U-Na, FEna
BMP for Bun / Cr levels (will rule out Pre renal)

US – R/o post renal

Then get a UA

48
Q

• Goals of CKD Treatment

A

Prevent progression
♣ If HTN or Protinuria – Ace / Arb
♣ If DM – Annual UA with goal A1C <7

Manage Complications
♣ Anemia – from dec EPO. Give Iron / EPO. Goal Hg >10. Transfusions w/ dialysis if refractory.
♣ Secondary hyperparathyroidism – A product of phosphate retention (inc PTH!) and Vit D def (no conversion to 1,25). Give binders (sevelamir – causes excretion of P in gut) and calcimimetics (Cinacalcet – acts like Ca, lowers PTH needs). Osteoporosis from long term high PTH – dexa >-2.5 – prev with Calcium and Vit D supplementation.
♣ Volume Overload – due to loss of urinary output. Stilulate nephroms that are working with Furosimide intially, can add metolazone. Ultimately dialysis
Acidosis – will cause bicarb between

49
Q

• General Pathology of CKD

A

o Over three months of reduced GFR (60ml/hr), this will cause the Cr to rise (above 2 generally)

50
Q

Stages of CKD

A 
♣	1   Above 90
♣	2   60-90 mild 
♣	3   30-59 Moderate 
♣	4   15-30 Severe kidney disease  - Prep dialysis / xplant
♣	5 <15    Kidney falure  - Dialysis
51
Q

How to determine if acid base disturbance is resp vs metabolic

A

♣ pH above or below 7.4?

♣ Is the Co2 above or below 40

52
Q

What would indicate metabolic acidosis, and what would you do next.

What would DDX be

A

Labs: pH < 7.4, CO2 < 40

Next: Calculate Anion Gap: Na – Cl – Bicarb
♣ Gap above 12: MUDPILES.

gap below 12: do urine anion gap Na + K – Cl
♣ If positive – RTA
♣ If negative – Diarhea

53
Q

MUDPILES

A 
Acronym for high anion gap metabolic acidosis 
M methanol
U uremia 
D KA 
P paradehyde - ignore 
I  iron  - izoniazid
L lactiac acidosis
E thalyne glycol (antifreeze)
S salicylates
54
Q

What labs indicate resp acidosis, and what is the DDX

A

Labs pH < 7.4, CO2 >40

DDX: Hypoventilation
•	Opiates
•	COPD
•	Asthma
•	OSA
55
Q

What labs would indicate Resp Alkalosis and what is the DDX

A

♣ pH > 7.4, CO2 < 40

♣ Hyperventialation
• Pain
• Anxiety
• Hypoxia

56
Q

What labs would indicate Metabolic Alkalosis

what do you do next

If it is volume responsive, general treatment for each.

A

♣ pH > 7.4, CO2 < 40

♣ Get a urine Cl to rule out weird stuff:
if >10 then consider Hyper aldosterone (RAS, Conns* will also have htn!) or genetics (Bartter, gitelman)

♣ If <10, then it is volume responsive:
DDX inc Diuretics, dehydration
emesis
NG suction

Diuretics - Red dose. Can add K sparing diuretics (spironilactone, amiloride, eplerinone, triamterine) / acetazolamide can be added

dehydration - Fluids

emesis - anti emet.

NG suction - if has to continue, use PPI or H2blockers to lower secretion

57
Q

• Triad for RCC, risk factors, workup, worried about

A

o Flank pain, flank manss, hematuria (almost garuntees cancer)
o RF – VHL gene, smoking, ESRD.
o Workup: UA, US or CT, then BX /resect
o Worry about renal vein thrombosis, anemia, polycythemia

OME (11 decks)

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