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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
slowly developing coronary stenosis
doesn't cause STEMI development of rich collateral circulation more likely to cause unstable angina, NSTEMI
26
risk factors for STEMI
``` atherosclerotic RF (hld, smoking) unstable angina ```
27
other risk factors for STEMI
hypercoaguability, cocacine, collagen vascular dz, intracardiac thrombi which can embolize
28
pharmacologic treatment of STEMI
BEMOAN | beta-blocker, enoxaparin, morphine, oxygen, aspirin, nitrates
29
nitrates
preload reduction mainly | but also reduces afterload
30
beta blocker and STEMI
don't give if acute heart failure is present
31
aspirin
prevents further platelet aggregation at site
32
contradicted in NSTEMI
glucocorticoids NSAIDs impair healing, risk for ventricular wall rupture
33
definitive treatment for STEMI
reperfusion therapy | chemical or percutaneous coronary intervntion
34
fibrinolysis/chemical reperfusion
tpa | streptokinase, tenecteplase, reteplase
35
absolute contraindications to chemical fibrinolysis
cerebrovascular hemorrhage, active internal bleeding, suspicion of aortic dissection, marked htn or stroke/cva in past year
36
CABG
primary reperfusion stratgey in patients with occlusion of left main coronary artery severe three vessel involvement
37
MI mot common complication
arrhythmia
38
post MI arrythmias
V fib -- death | new onset AV or bundle branch blocks due to infarction of condution tissues
39
mechanical complications of MI
3-5 d post MI ventricular free wall rupture ventricular septal rupture papillary muscle rupture
40
ventricular free wall rupture
pericardial tamponade
41
ventricular septal rupture
new ventricular septal defect murmur
42
papillary muscle rupture
severe MR, hemodynamic compromise
43
Dressler's syndrome
2-3 weeks post MI low grade fever, chest pain, pericarditis, and/or pericardial effusion friction rub!
44
Dressler's syndrome treatment
self limited | colchicine
45
post MI lifestyle modifications
smoking cessation exercise dietary modifications
46
post MI medications
B blocker, low dose Aspirin, ACE/ARB, nitroglycerin, statin
47
post MI pts w/ stents meds
clopidogrel or GpIIB/IIIa inhibitor
48
DKA
hyperglycemia metabolic acidosis ketone bodies
49
what can lead to increased glucose
physiological stress: infection, intoxication, lack of medication --> increase insulin demand
50
ketones
free fatty acids --> b hydroxybutyric acid, acetoacetic acid
51
DKA symptoms
abdominal pain, vomitting, fruity breath odor, profound dehydration
52
fruity breath odor
acetoacetic acid --> acetone
53
DKA mechanism of dehydration
glucosuria --> osmotic diuresis | MS changes
54
DKA - metabolic acidosis
increased carbonic acid in blood which is converted to Co2 | increased co2 -- deep, rapid breathing (kussmaul respirations)
55
DKA diagnosis
``` elevated gluc >300 anion gap metabolic acidosis urine + glucose and ketones normal or high potassium low sodium ```
56
K in DKA
potassium moves from ICF to ECF to compensate for electrolyte loss low total body potassium normal/high potassium on labs
57
treatment of DKA
normal saline potassium insulin and glucose
58
check potassium before insulin because
insulin can worse preexisting hypokalemia
59
DKA - fluid repletion
slowly over 1-2 days | prevent cerebral and pulmonary edema
60
DKA deaths in children
cerebral edema
61
optimal rate of glucose decline is
100mg/dl per hour
62
if glucose falls too fast
rebound ketosis | cerebral edema
63
insulin is given until
ketosis is corrected
64
DKA complications
hypoglycemia, hypokalemia | cerebral, pulmonary edema

Internal Med (23 decks)

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