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Rotation 2: IM Outpatient > Renal Portion > Flashcards

Flashcards in Renal Portion Deck (36):
1

renal failure

azotemia

what is this?

due to?

symptomatic?

excess of urea and nitrogenous compounds in the blood

due to breakdown of proteins

metabolism of carbohydrates and fats yields water and CO2

if symptoms are present use the term uremia

2

renal failure

 

3 test you should consider ordering for renal failure

4

2

1

 

 

1. US

you can see obstructions and size very well!! so this is good!

non invasive

no risky dye contrast dye

readily avaliable

2. plain Xray

pyelogram

retrograd pyelogram

3. CT

probally better but risk of dye and raising creatinine

3

what are 6 complications of acute renal faillure?

1. volume overload

decreased sodium and water excretion

resultant weight gain, heart failure, and edema

2. hyponatremia

3. hypocalcemia

paresthesias, cramps, seizures, confusion

4. hyperkalemia (increases), phosphatemia (increases), magnesemia

5. metabolic acidosis

6. HTN

 

4

what are the 5 tx of acute renal failure?

1. prevention!!!

(avoid nephrotoxins, diabetes control etc)

 

2. reverse poisons

(ETOH, bicarbonate in acidosis)

 

3. restore fluid volume and electrolyte balance

(saline/crystalloids, colloids, blood)

 

4. dialysis when needed

(acute if responsive or dialyzable toxin or CRF)

 

5. relieve obstruction

(easiest way to fix ARF)

5

how long does it take acute renal failure to come on?

 

are there symptoms?

hours to days

 

typically little symptoms found randomly on lab tests

6

what are the 3 classifications of acute renal failure?

what one is most common?

1. prerenal renal failure (renal hypoprofusion) 55%

2. renal/parenchyma/intrinsic 45%

3. post renal (obstructive) 5%

 

pre renal azotemia (failure) most common

7

acute renal failure

prerenal azotemia

 

what are the two things that cause this the most often?

permanent/reversible?

damage to kidney?

 

3 things that cause the first?

4 things that cause the second

due to renal hypoprofusion and Hypovolemia

usually reversible if restoring renal blood flow (RBF)

parenchyma usually not damaged

in severe cases, ischemia/injury

 

1. hypovolemia

a. fluid loss

b. decreased cardiac output

c. decreased systemic vasculature

causing:

-epi relase and vasoconstriction

-RAA activation

-arginine vasopressin rlease

 

2. renal hypoprofusion

a. vasoconstriction from epi

b. cycloxygenase inhibitors

c. hyperviscosity syndrome

d. hepatorenal syndome

 

8

acute kidney failure

prerenal azoturia:

hepatorenal syndrome causing hypoprofusion of kidneys

 

what is this?

what does it do?

cirrhosis leads to intrarenal vasoconstriction

sodium retention

 

 

precipitated by:

bleeding

paracentesis

diuretics

vasodilation

cycloocygenase inhibitors

9

acute renal failure

prerenal azouremia

 

2 signs

4 symptoms

2 tests and 1 result

 

 

symptoms

thirst

dizzy

 

signs

low BP

tachycardia

orthostasis

low urine output

 

    lab evaluation

urine volume

urine microscopy

hyaline/bland casts due to concentrated urine

10

acute renal failure:

intrinsic renal failure

 

what are the two main categories of this?

2 in fist

6 im second

WHAT ONE IS THE MOST COMMON CAUSE OF intrinsic renal disease?

1. renovascular cause

a. obstructed renal artery (atherosclerosis/thrombus)

b. renal vein obstruction

 

 

2. glomerular/microvascular disease

a. glomerulonephritis

b. vasculitis

c. acute tubular necrosis *MOST COMMON CAUSE OF INTRINSIC RENAL FAILURE*

d. ischemia/neprotoxin

e. intersitial nephritis

11

what are 6 nephrotoxins that can cause acute intrinsic renal failure?

1. radioconstrast dye

2. aminoglycosides

3. cyclosporine

4. chemo

5. solvents (ETOH)

6. endogenous nephrotoxin (things in the body taht can be toxic if too much is present, rhabdomylosis, hemolysis, UA etc.

12

Acute intrinsic renal failure

nephrotoxins:

radiocontrast dye

 

what does this cause?

how long after exposure?

what are the 4 features?

how can you prevent this?

tx?

intrarenal vasoconstriction resulting in acute tubular necrosis (ATN)

 

24-48 hours after contrast exposure

 

 

FEATURES:

1. decrease eGFR

2. sediment

3. reversible

4. elevation of BUN

 

HOW TO AVOID:

use  NON IONIC contrast, more expensive

 

resolves 1-2 weeks

13

what are 7 RF for having a negative rxn to contrast dye and having it cause acute intrinsic renal failure?

age over 80

CKD

diabetes

CHF

hypovolemia

multiple myeloma

chemotherapy, antibiotics

14

 acutre intrinsic renal failure

 

1. are there symptoms?

2. signs?

3. what might you see on labs (5)

4. tx?

often no sxs

 

signs:

azotemia on lab tests

 

labs:

1. muddy brown casts (ischemia/nephroxic)

2. red cell cats (nephritis/acute glomerular)

3. eosinophilic cats (allergic nephritis)

4. white cell casts (interstitial nephritis)

5. proteinuria

15

what are the 4 signs of nephritic syndrome?

1. olioguria

2. edema

3. HTN

4. urine sediment

16

acute postrenal kidney failure

what is this?

what are 6 things that can cause it?

urinary outflow obstruction

single kidney or urethral obstruction leading to anuria

 

 

causes:

1. prostate disease

2. neurogenic bladder (spinal cord injuries)

2. anticholinergics

3. blood clots

4. stones

5. tumor or other extrarenal obstruction

17

acute postrenal failure

 

what are 4 signs of this?

what are the 2 tx options?

 

SIGNS:

1. bladder distension

2. abdominal pain-colic

3. renal distension (check with US)

4. hx of RF (prostate disease, stones etc)

 

 

TREATMENT:

fix the plumbing!

1. urologist

2. nephrostomy tube or suprapubic catherer

18

what might dopamine promote?

water and sodium excretion

19

what are 5 conditions that might warrent dialysis?

1. uremia

2. hypervolemia

3. hyperkalemia

4. acidosis

5. toxins (multiple, digoxin)

20

end stage chronic renal failure

characterized by what 3 things?

1. proteinuria

2. hematuria

3. 3 month of disease and eGFR less than 60/ml

21

what are the stages and values for eGFR of CKD?

A image thumb
23

currently what are the two most common causes of end stage CKD/uremia?

1. diabetes

2. HTN

24

uremia

what is this?

azotemia

+

syndrome of anemia, malnuitrition, and metabolic problem

25

what are 5 sxs of end stage CKD?

anorexia (weight loss/loss of appetite)

nausea/vomiting

malaise

headache

itching

26

what are 3 metabolic effects you see with chronic kidney disease?

1. hypothermia: decreased Na transport; source of energy/head

 

2. impaired carbohydrate metabolism: “pseudodiabetes”, slower handling of glucose load to insulin resistance

 

3. increased triglycerides

27

when does decreased K excretion occur? what does this leave the chronic kidney disease patient at risk for?

typically occurs if GFR less than 10 cc/min

 

at risk for hyperkalemia

28

why does CKD cause calcium disorders?

what is the nickname for this? what two things contribute to fracture risk? explain the process?

"renal osteodystrophies"

 

osteomalacia and osteitis fibrosa cystica due to hyperthyroidism increase fracture risk

 

Reasoning:

1. decreased conversion of vitamin D to 1,25 dihydroxy (activated) vitamin D

2. decreased calcium in serum since less active vitamin D to absorb it

3. increase in PTH in response to low Ca

4. results in weakness of bones because it sucks the  the Ca out

 

 

29

phosphorus disorders

seen in CKD

 

why is this increased?

what is the domino effect of increase phosphorus?

what are 3 tx options?

decreased phosphorus excretion in CKD so it accumulates in the blood

 

Domino effect of bad things:

1. causes low calcium

2. increase in PTH

3. bone reabsorption

4. weak bones/fractures

 

 

TX:

1. decrease serum phosphate

-diet restriction of proteins, dairy, colas

-calcium carbonate

-selevemer

30

what is the most common complication of end stage renal disease?

hypertension

31

what are 7 random other things you can see with CKDs?

1. pericarditis (toxin induced)

2. anemia

3. metabolic acidosis

4. thrombocytopenia

5. bruising/bleeding

6. platelet dysfunction

7. infection

 

32

anemia in CKD

 

what are 5 causes of this?

what helped to sove this problem?

decreased need for?

Causes:

1. bone marrow toxins

2. decreased eryhtropoetin

3. hemolysis

4. hemodilution

5. decreased RBC

 

**this used to be aa HUGE problem in CKD patients, but now with ERYTHROPOETIN we can fight it!! REVOLUTION!** and helps to limit the need for transfusion

33

explain what sxs you would see in CKD for:

neuromuscular

gastro

*don't memorize just read it*

neuromuscular

decreased concentration

drowsiness

insomnia

hiccups

cramps/twitches

periphreal neuropathy/restless leg syndrome

more severe

stupor

seizure

coma

 

 

gastrointestinal

anorexia

N/V

hiccups

uremic fetor/ bad breath

mucosal irritation

34

when is transplant or dialysis appropriate?

where can you get it from?

creatinine greater than 8

creatinine clearance less than 10

 

donor

cadaver

35

hemodialysis

what are the three ways you can accomplish this?

what alows you to accomplish this?

what are the 2 requirements?

what are 2 things you must monitor?

1. requires a shunt that connects artery and vein, "must ripen", allow for diffusion across semipermeable membrane

2. artificial options

3. IV cathertic into IJ

 

REQUIREMENTS:

300-450 ml/min blood flow

9-12 hour commitment a week

 

 

MONITOR:

KT/V

urea pre and post dialysis

36

peritoneal dialysis

 

what is this process?

what are 3 advantges?

catheter- can use immediately, goes in the stomach, put catheter in the belly dump fluid in there with certain osmolarity and you keep doing it over and over again and it comes out, makes you less likely to be able to receive a kidney

 

push fluid for 4-6 hours

intermittent tx

can do at night, cyclic

 

Advantages:

1. no heparin

2. independence

3. no vascular acess

37

what are 3 disadvantes of periotoneal dialysis?

1. DONT USE IN LUNG DISEASE

2. PERITONITIS major risk( may be so risky that they can be disqualified from recieving a kidney transplant)

3. need to be trained