Brainscape's Knowledge GenomeTM

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


See full index

Patho > Chapter 46: acute kidney injury and chronic kidney disease > Flashcards

Chapter 46: acute kidney injury and chronic kidney disease Flashcards

1
Q

AKI
what?
accompanied by?

A

Rapid loss of kidney function with
-rise in creatine and/or fall in urine output
-High BUN and K+
-Azotemia = accumulation of nitrogenous wastes

High mortality rate! –> usually affects people with other issues

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

Prerenal causes of AKI

A

factors that reduce systemic circulation, causing less renal bloodflow, leading to oliguria –> dehydration, heart failure, low CO

Autoreg mechs try to preserve the flow
-retains water and sodium and decreases urine output

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

Intrarenal causes of AKI

A

conditions that cause direct damage to kidney tissue

-prolonged ischemia
-nephrotoxins
-hemoglobin released from hemolyzed RBCs
-myoglobin released from necrotic muscle cells
-kidney diseases – acute glomerulonephritis and SLE

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

Intrarenal causes of AKI: acute tubular necrosis: ATN

A

-Hypoperfusion
-Results from ischemia, nephrotoxins, or sepsis
-ischemia disrupts basement membrane and creates patches in tubular epithelium
-nephrotoxic agents kill tubular epithelial cells and clog the tubules
-possible reversible

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

Postrenal causes of AKI

A

mechanical obstruction of outflow –> leads to reflux in renal pelvis, fucking up renal function —> BPH, prostate cancer, calculi, trauma, and extrarenal tumors

Bilateral ureteral obstruction is even worse! –> hydronephrosis –> Might be able to recover if you clear the obstruction within 48 hours

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

Three phases of AKI and how to classify progression

A

phases: oliguric, diuretic, and recovery

RIFLE classification

Risk
Injury
Failure
Loss
End stage renal disease

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

Oliguric Phase: urinary changes

A

Oliguria
-less than 400 ml/day
-happens within 1-7 days after injury
-lasts 10-14 days (your probs gonna die if it lasts longer)
-urinalysis = casts, RBCs, WBCs, protein
-specific gravity is 1.010
-osmolality is 300 mOsm/kg

Half of people with AKI don’t even have oliguria though

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

Oliguric phase: fluid volume

A

Hypovolemia might worsen AKI

Less urine output leads to retension
-neck and veins distended
-bounding pulse
-edema
-hypertension

Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions

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

Oliguric phase: metabolic acidosis

A

messed up kidneys can’t get rid of H+ or acids

serum bicarbonate production goes down -> defective reabsorption and regeneration

severe acidosis –> Kussmaul respirations increase exhaled CO2

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

Oliguric phase: sodium and potassium

A

loss of sodium due to messed up tubules –> low Na can cause cerebral edema

Too much K bc kidneys can’t get rid of it
-increased risk with massive tissue trauma
-usually asymptomatic
-ECG stuff

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

Oilguric phase:
hematologic disorders
waste accumulation
neurologic disorders

A

Hematologic
-leukocytosis - infection may be fatal - side effects in urinary and respiratory system

waste
-more BUN and creatinine

Neurologic
-fatigue and difficulty concentrating
-seizures, stupor, coma

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

Diuretic phase
how long?
urine output?

A

1-3 weeks

1-3 L, but up to 5

Osmotic diuresis from high urea and inability of tubules to concentrate urine

Monitor for hypo- volemia, tesion natremia, kalema and dehydration

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

Recovery phase
how long?

A

up to 12 months

increased GFR, decreased BUN and creatinine

influenced by severity of injury and complications

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

Diagnostic studies for AKI

A

thorough history
serum creatinine, BUN, and electrolytes
UA
renal ultrasound
renal scan
CT scan
renal biopsy

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

AKI diagnostic study contraindictions for contrast

A

MRI or MRA with gadolinium contrast could KILL the person –> CIN

Diabetics need to stop taking melformin 48 hrs before and after contrast to avoid lactic acidosis

If absolutely necessary to use contrast in risky situation, use low dose and optimal hydration

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

Interprofessional care: fluid

A

make sure intravascular volume and CO are good
-use loop or osmotic diuretics

monitor intake during oliguric phase
-fluid restriction calculation : O for past 24 hrs + 600 mL

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

Interprofessional care: hyperkalemia therapies

A

move K into cells with insulin and sodium bicarbonate –> for acute issues

use calcium gluconate to stabilizy myocardium

use kayexalate or Veltessa or dialysis to excrete K –> slower, not for acute cases

dietary restriction

18
Q

Indications for renal replacement therapy RRT

A

volume overload
high K
metabolic acidosis
BUN > 120 mg/dL (43 mmol/L)
significan mental status changes
pericarditis, pericardial effusion, or cardiac tamponade
clinical status of patient

19
Q

Types of RRT

A

Peritoneal dialysis (PD)
- not common –> most closely resembles actual kidney func

Intermittnet hemodialysis (HD)
-emergent therapy

Continuous renal replacement therapy (CRRT)
-cannulation of artery and vein
-continuously 24 hrs

20
Q

Nutrition therapy

A

get enough calories –> mostly carbs and lots of fat (to prevent ketosis)–> also enough protein to prevent breakdown

limit Na, K and phosphate

Ca supplements of Phosphate-bidig agents

enteral or parenteral nutrition

21
Q

Why are old ppl more susceptible to AKI?

A

slower GFR already due to aging

Dehydration from polypharmacy, illness, and immobility

HT, diuretic therapy, aminoglycoside therapy, obstructive disorders, surgery, infection, and contrast medium

less able to recover –> can still do RRT though

22
Q

Chronic kidney disease
more or less common than AKI? Why?

A

more common

aging population, obesity, diabetes, HTN

23
Q

How does KDIGO define CKD?

A

Kidney damage and low GFR

Kidney damage
-pathologic abnormalities
-markers of damage = blood, urine, and imaging tests

Low GFR
-less than 60 mL/min/1.73m^2 for over 3 months

24
Q

Leading causes of CKD

A

Diabetes - 50%
HTN - 25%
Other - glomerulonephritis, cystic diseases, urologic diseases

ppl with CKD are often asymptomatic and go untreated

25
Q

Stages of GFR during CDK

A

1) >90
2) 60-89
3a) 45-59
3b) 30-44
4) 15-29
5) <15 or dialysis –> ESRD

26
Q

clinical action plan for stages of CDK

A

1) diagnose and treat –> reduce CVD risk
2) estimation of progression
3a) evaluate and treat complications
3b) get more aggressive with treatment
4) prepare for RRT (dialysis or transplant)
5) RRT if uremia present and patient wants treatment (alternative is death)

27
Q

Ethnicity CKD

A

blacks 4x more likely than whites (HTN)
native americans 2x more likely (diabetes)
Hispanics 1.5x more likely

28
Q

how much does medicare cover?

A

80%

29
Q

Early stages of CDK manifestations

A

no change in urine output
polyuria might be present due to diabetes

as CDK progresses, increase fluid retention –> need diuretic

After a while on dialysis, patients become anuric

30
Q

Clinical manifestations of CDK: hyperkalemia

A

most serious electrolyte disorder of kidney disease

Fatal dysrhythmias –> when K reaches 7-8

Decreased excretion, breakdown of cellular protein, bleeding, and metabolic acidosis lead to increased K
—-also foot, dietary supplements, drugs and IVs

31
Q

Clinical manifestations of CDK: sodium

A

could be high, low, or normal

Impaired excretion –> Na and water retention

Dilutional hyponatremia could happen –> edema, HTN, heart failure

32
Q

CDK clinical manifestation: metabolic acidosis

A

From kidney’s inability to excrete acid
Also defective reabsorption and regeneration of bicarbonate

Plasma bicarbonate level usually falls to 16-20 mEq/L

33
Q

clinical manifestations of CDK: Anemia

A

Bc less EPO produced –> usually stimulates bone marrow to make RBCs

Also, nutritional deficiencies, RBCs die quicker, more hemolysis, blood sampling, GI bleeding, HD, and increased PTH

Decreased iron stores

Folic acid lost in dialysis

34
Q

Which condition is closely linked with CKD? Why?

A

Cardiovascular disease
-myocardial infarction , ischemic heart disease, peripheral arterial disease, HF, cardiomyopathy, and stroke

Traditional CV risk factors that are common in CDK patients = HTN and high lipids

Nontraditional CV risk factors = vascular calcification and arterial stiffness

35
Q

HTN in CKD patients

A

Both a cause and a consequence
- aggravated by Na and H2O retention
-increased renein production might contribute

HTN, ECF volume overload, and anemia might dvlp into left ventricular hypertrophy which could lead to cardiomyopathy and HF
-HTN can cause retinopathy, encephalopathy, nephropathy

36
Q

What’s one of the most important goals in CKD treatment?

What causes dysrhythmias?

Uremic pericarditis progression and presentation

A

BP cotrol

Hyperkalemia and decreased coronary artery perfusion

progresses to effusion and tamponade –> friction rub, chest pain, and fever

37
Q

Clinical manifestation of CDK: Integumentary issues

A

Pruritus
- calcium-phosphate deposits and sensory neuropathy
-itching might be intense –>leads to bleeding or infection

Uremic frost
-urea crystalizes on skin
-happens when BUN > 200 mg/dL

38
Q

Clinical manifestations of CKD: Reproductive issues

A

Infertility and decreased libido
-dudes have low sperm count –> girls have amenorrhea

Sexual dysfunction
-physical, psychological, and medication side effects

Pregnancy during dialysis is super risky for mom and baby

39
Q

How to treat CKD: Hypertension

A

weight loss (if indicated)
Therapeutic lifestyle changes
Diet recommendations (DASH Diet)
Antihypertensive drugs –> usually need 2+
***if diabetic, give ACE inhibitors and ARBs

40
Q

How to treat CKD: anemia –> EPO

A

Get them EPO
-Epoetin alfa (epogen and procrit)
-Darbepoeitin alfa (Aranesp)
-Give IV or subcutaneously
-HGB and Hct might take 2-3 weeks to increase
-Side effects = thromboembolism and HTN

41
Q

How to treat CKD: anemia –> supplements

A

Iron supplements
-Give if plasma ferritin level is <100 ng/mL
-Side effects: gastric irritation and constipation
-Might make stool dark in color

Folic acid supplements
-needed for RBC formation
-removed by dialysis

42
Q

What to avoid when treating CKD –> esp when it comes to anemia

A

blood transfusions
-increase the development of antibodies –> makes finding kidney donor hard
-might lead to iron overload

Can do it if significant blood loss or symptomatic anemia

Patho (44 decks)

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