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Internal Med > Firecracker AIN/ATN/STEMI > Flashcards

Firecracker AIN/ATN/STEMI Flashcards

1
Q

categories of ATN

A

ischemic

nephrotoxic

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2
Q

etiology of ATN

A

disturbances in renal blood flow

tubular injury

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3
Q

renal ischemia causes

A

intrarenal vasoconstriction (afferent arteriolar)
decreased GFR
oliguria

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4
Q

parts of tubules most suseptible to hypoxic injury

A

straight portion of PT

thick ascendling limb

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5
Q

mechanisms of renal ischemia

A

loss of tubule cell polarity

endothelial damage

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6
Q

Ischemic ATN most commonly caused by

A

pre-renal failure
- effective circulating blood volume/preload
decreased cardiac output
NSAIDs, ACEIs

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7
Q

decreased effective circulating blood volume

A

hypovolemia
systemic vasodilation (shock)
cirrhosis

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8
Q

decreased cardiac output

A

CHF

cardiogenic shock

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9
Q

NSAIDs and ATN

A 
decreased PGI2 (NSAIDS)
decreased vasodilation of afferent arteriole
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10
Q

ACEIs and ATN

A

decreased ATII

decrease vasoconstriction of efferent arteriole

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11
Q

nephrotoxic ATN

A

1) aminoglycosides
2) amph b
3) cisplatinum

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12
Q

other causes of nephrotoxic ATN

A

heavy metals - lead, mercury
contrast
gram negative sepsis
myoglobinuria

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13
Q

Mechanism of nephrotoxic ATN

A

1) tubular toxicity
2) direct injury to PCT
3) mygolbin precepitation and tubular obstruction

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14
Q

ethylene glycol ATN

A

massive intratubular oxalate crystal deposits

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15
Q

ATN phases

A

initiation phase
maintenace (oliguric phase)
recovery (polyuric) phase

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16
Q

ATN initiation phase

A

first 36 hrs

slight decrease in urine output w increase in BUN

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17
Q

ATN maintenace phase

A
  • sustained oliguria
  • increased ECF
  • hyperkalemia
  • increased anion gap metabolic acidosis (retention of H and anions)
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18
Q

ATN recovery phase

A

2-3 wks after event

  • brisk diuresis w/ loss of K, Ca, Mg, Ph
  • hypokalemia
  • BUN and Cr return to baseline
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19
Q

increased EcF

A

weight gain, edema, pulmonary vascular congestion

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20
Q

diagnosis of ATN

A

exclusion
muddy brown granular casts
FeNa > 3

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21
Q

ATN treatment

A

supportive

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22
Q

most common cause of AKI

A

ATN

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23
Q

hypokalemia EKG changes

A

flattening or inversion of T waves, U waves, depressed ST segments
PVCs
arrythmias

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24
Q

STEMI

A

thrombus occludes atherosclerotic coronary artery

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25
Q

slowly developing coronary stenosis

A

doesn’t cause STEMI
development of rich collateral circulation
more likely to cause unstable angina, NSTEMI

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26
Q

risk factors for STEMI

A 
atherosclerotic RF (hld, smoking)
unstable angina
27
Q

other risk factors for STEMI

A

hypercoaguability, cocacine, collagen vascular dz, intracardiac thrombi which can embolize

28
Q

pharmacologic treatment of STEMI

A

BEMOAN

beta-blocker, enoxaparin, morphine, oxygen, aspirin, nitrates

29
Q

nitrates

A

preload reduction mainly

but also reduces afterload

30
Q

beta blocker and STEMI

A

don’t give if acute heart failure is present

31
Q

aspirin

A

prevents further platelet aggregation at site

32
Q

contradicted in NSTEMI

A

glucocorticoids
NSAIDs
impair healing, risk for ventricular wall rupture

33
Q

definitive treatment for STEMI

A

reperfusion therapy

chemical or percutaneous coronary intervntion

34
Q

fibrinolysis/chemical reperfusion

A

tpa

streptokinase, tenecteplase, reteplase

35
Q

absolute contraindications to chemical fibrinolysis

A

cerebrovascular hemorrhage, active internal bleeding, suspicion of aortic dissection, marked htn or stroke/cva in past year

36
Q

CABG

A

primary reperfusion stratgey in patients with occlusion of left main coronary artery severe three vessel involvement

37
Q

MI mot common complication

A

arrhythmia

38
Q

post MI arrythmias

A

V fib – death

new onset AV or bundle branch blocks due to infarction of condution tissues

39
Q

mechanical complications of MI

A

3-5 d post MI
ventricular free wall rupture
ventricular septal rupture
papillary muscle rupture

40
Q

ventricular free wall rupture

A

pericardial tamponade

41
Q

ventricular septal rupture

A

new ventricular septal defect murmur

42
Q

papillary muscle rupture

A

severe MR, hemodynamic compromise

43
Q

Dressler’s syndrome

A

2-3 weeks post MI
low grade fever, chest pain, pericarditis, and/or pericardial effusion
friction rub!

44
Q

Dressler’s syndrome treatment

A

self limited

colchicine

45
Q

post MI lifestyle modifications

A

smoking cessation
exercise
dietary modifications

46
Q

post MI medications

A

B blocker, low dose Aspirin, ACE/ARB, nitroglycerin, statin

47
Q

post MI pts w/ stents meds

A

clopidogrel or GpIIB/IIIa inhibitor

48
Q

DKA

A

hyperglycemia
metabolic acidosis
ketone bodies

49
Q

what can lead to increased glucose

A

physiological stress: infection, intoxication, lack of medication –> increase insulin demand

50
Q

ketones

A

free fatty acids –> b hydroxybutyric acid, acetoacetic acid

51
Q

DKA symptoms

A

abdominal pain, vomitting, fruity breath odor, profound dehydration

52
Q

fruity breath odor

A

acetoacetic acid –> acetone

53
Q

DKA mechanism of dehydration

A

glucosuria –> osmotic diuresis

MS changes

54
Q

DKA - metabolic acidosis

A

increased carbonic acid in blood which is converted to Co2

increased co2 – deep, rapid breathing (kussmaul respirations)

55
Q

DKA diagnosis

A 
elevated gluc >300
anion gap metabolic acidosis
urine + glucose and ketones
normal or high potassium
low sodium
56
Q

K in DKA

A

potassium moves from ICF to ECF to compensate for electrolyte loss
low total body potassium
normal/high potassium on labs

57
Q

treatment of DKA

A

normal saline
potassium
insulin and glucose

58
Q

check potassium before insulin because

A

insulin can worse preexisting hypokalemia

59
Q

DKA - fluid repletion

A

slowly over 1-2 days

prevent cerebral and pulmonary edema

60
Q

DKA deaths in children

A

cerebral edema

61
Q

optimal rate of glucose decline is

A

100mg/dl per hour

62
Q

if glucose falls too fast

A

rebound ketosis

cerebral edema

63
Q

insulin is given until

A

ketosis is corrected

64
Q

DKA complications

A

hypoglycemia, hypokalemia

cerebral, pulmonary edema

Internal Med (23 decks)

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