Kidney diseases Flashcards

1
Q

Is kidney injury a slow process?

A

NO - rapid progression

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2
Q

Fxn of kidneys

A

F&E homeostasis, rid body of water-soluble waste (many drugs) via urine, endocrine functions like making erythropoietin, activating vit D, making renin (regulate BP)

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3
Q

Is kidney injury reversible?

A

It can be

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4
Q

What is GFR a measure of?

A

how well the kidneys are working; insufficiency is 25% of normal GFR

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5
Q

Are kidneys greedy?

A

Yes - require 1L/minute of blood (20% CO)

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6
Q

AKI

A

body causes inflammation when it sense injury causing inc kidney cell death

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7
Q

Causes of AKI

A

ischemic injury r/t loss of blood volume and dec perfusion from toxins (OD) or sepsis (3rd space), acute blood loss

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8
Q

Pre-renal AKI

A

volume loss (surgery) or dehydration
- most common

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9
Q

intrarenal AKI

A

acute tubular necrosis (drug OD, kidney cell death), vascular disease, glomerulonephritis

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10
Q

post-renal AKI

A

not as common, obs causes cell death, tumor; in ureter or bladder

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11
Q

CM of AKI

A

1st day after hypotensive event and lasts 1-3 weeks; oliguria, FVE (edema), metabolic acidosis, hyponatremia, hyperkalemia, waste product accumulation, neuro dx

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12
Q

Oliguria of AKI

A

under 400 mL/24h or under 30 mL/1h

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13
Q

Tx for AKI

A

address cause, fluids, drug antidote, electrolytes, address fluid shift

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14
Q

What determines the stage of injury with CKD?

A

GFR

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15
Q

Stage 5 CKD

A

urinemic - urea in blood; excess AA in metabolic end products
- urine in blood bc body can’t excrete

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16
Q

Best tx for CKD

A

Prevent by controlling causes (often chronic conditions like DM - 1, HTN - 2, glom or AKI, other probs)

17
Q

Risks for CKD

A

family history, CAD, HLD, atherosclerosis, older than 60Y, men, Black, HTN, DM, SMOKING, overwt and obese

18
Q

Patho of CKD

A

lack BF to kidney cells and proteinuria from leaky GBM accumulates in the interstitial space in nephrons, causing injury; inflammatory system activated and angiotensin 2 activates, causing arterial vasoconstriction which normally would inc glom HTN but due to the leaks it causes more proteinuria

19
Q

CM of CKD

A

Most body sys are affected by waste products from the kidneys are everywhere
- inc systemic inflammation

20
Q

Integumentary sx of CKD

A

itchy, red, dry, scaly

21
Q

Psych sx of CKD

A

anx and dep

22
Q

Neuro sx of CKD

A

fatigue, HA, sleep prob, encephalopathy

23
Q

CV sx of CKD

A

heart failure, HTN, CAD, pericarditis, PAD

24
Q

GI sx of CVD

A

anorexia, N/V, gastritis, bleeding

25
Q

What sign of CVD indicates dialysis is needed?

A

Pulmonary edema - biggest concern

26
Q

CKD fx of poor F&E homeostasis

A

edema, INC K, inc P, and inc Mag, metabolic acidosis

27
Q

CKD CM of no waste ridding

A

anorexia, malnutrition, itching, CNS change from things crossing BBB (AMS), uremic frost

28
Q

CKD fx of dec erythropoitein

A

anemia; gradual adjustment to hgb of 5 or 6

29
Q

CKD fx of dec activation of vit D

A

renal osteodystrophy, weak bones

30
Q

Drugs used to slow progression of CKD

A

ACE inhibitors OR ARBs - keep BP under 140/90
Tx HLD (under 200) with statins, diet

31
Q

How to tx CKD

A

Tx the symptoms and complications with usual tx - overload (diuretics and low salt), inc K (hemodialysis, Kayexalate), acidosis (NaHCO3), hyperphos (phosphate binder like Calcium carbonate) anemia (erythropoitein), renal osteodystrophy (calcitriol–activated vit D)

32
Q

Drug monitoring with CKS

A
  • dec drug elimination with CKD
  • monitor levels closely - may need to adjust to kidney fxn - RENALLY DOSED
33
Q

Which drugs do you need to watch closely with CKD?

A

Digoxin, diabetic agents like glyburide, Metformin, abx like VANC, opioids (can cause severe resp dep bc kidneys won’t clear it)

34
Q

Normal GFR

A

Over 90

35
Q

Stage 1 and 2 CKD CM

A

Often asymptomatic

36
Q

Stage 3 CM

A

HTN - tx it

37
Q

Why don’t we want to lower BP too much?

A

Kidneys won’t get perfused at the rate that they are used to - slow titration
- goal is SBP 110-130