Firecracker AIN/ATN/STEMI Flashcards Preview

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Flashcards in Firecracker AIN/ATN/STEMI Deck (64):
1

categories of ATN

ischemic
nephrotoxic

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etiology of ATN

disturbances in renal blood flow
tubular injury

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renal ischemia causes

intrarenal vasoconstriction (afferent arteriolar)
decreased GFR
oliguria

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parts of tubules most suseptible to hypoxic injury

straight portion of PT
thick ascendling limb

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mechanisms of renal ischemia

loss of tubule cell polarity
endothelial damage

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Ischemic ATN most commonly caused by

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

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decreased effective circulating blood volume

hypovolemia
systemic vasodilation (shock)
cirrhosis

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decreased cardiac output

CHF
cardiogenic shock

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NSAIDs and ATN

decreased PGI2 (NSAIDS)
decreased vasodilation of afferent arteriole

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ACEIs and ATN

decreased ATII
decrease vasoconstriction of efferent arteriole

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nephrotoxic ATN

1) aminoglycosides
2) amph b
3) cisplatinum

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other causes of nephrotoxic ATN

heavy metals - lead, mercury
contrast
gram negative sepsis
myoglobinuria

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Mechanism of nephrotoxic ATN

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

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ethylene glycol ATN

massive intratubular oxalate crystal deposits

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ATN phases

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

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ATN initiation phase

first 36 hrs
slight decrease in urine output w increase in BUN

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ATN maintenace phase

- sustained oliguria
- increased ECF
- hyperkalemia
- increased anion gap metabolic acidosis (retention of H and anions)

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ATN recovery phase

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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increased EcF

weight gain, edema, pulmonary vascular congestion

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diagnosis of ATN

exclusion
muddy brown granular casts
FeNa > 3

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ATN treatment

supportive

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most common cause of AKI

ATN

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hypokalemia EKG changes

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

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STEMI

thrombus occludes atherosclerotic coronary artery

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slowly developing coronary stenosis

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

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risk factors for STEMI

atherosclerotic RF (hld, smoking)
unstable angina

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other risk factors for STEMI

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

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pharmacologic treatment of STEMI

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

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nitrates

preload reduction mainly
but also reduces afterload

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beta blocker and STEMI

don't give if acute heart failure is present

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aspirin

prevents further platelet aggregation at site

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contradicted in NSTEMI

glucocorticoids
NSAIDs
impair healing, risk for ventricular wall rupture

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definitive treatment for STEMI

reperfusion therapy
chemical or percutaneous coronary intervntion

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fibrinolysis/chemical reperfusion

tpa
streptokinase, tenecteplase, reteplase

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absolute contraindications to chemical fibrinolysis

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

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CABG

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

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MI mot common complication

arrhythmia

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post MI arrythmias

V fib -- death
new onset AV or bundle branch blocks due to infarction of condution tissues

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mechanical complications of MI

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

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ventricular free wall rupture

pericardial tamponade

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ventricular septal rupture

new ventricular septal defect murmur

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papillary muscle rupture

severe MR, hemodynamic compromise

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Dressler's syndrome

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

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Dressler's syndrome treatment

self limited
colchicine

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post MI lifestyle modifications

smoking cessation
exercise
dietary modifications

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post MI medications

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

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post MI pts w/ stents meds

clopidogrel or GpIIB/IIIa inhibitor

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DKA

hyperglycemia
metabolic acidosis
ketone bodies

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what can lead to increased glucose

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

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ketones

free fatty acids --> b hydroxybutyric acid, acetoacetic acid

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DKA symptoms

abdominal pain, vomitting, fruity breath odor, profound dehydration

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fruity breath odor

acetoacetic acid --> acetone

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DKA mechanism of dehydration

glucosuria --> osmotic diuresis
MS changes

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DKA - metabolic acidosis

increased carbonic acid in blood which is converted to Co2
increased co2 -- deep, rapid breathing (kussmaul respirations)

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DKA diagnosis

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

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K in DKA

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

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treatment of DKA

normal saline
potassium
insulin and glucose

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check potassium before insulin because

insulin can worse preexisting hypokalemia

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DKA - fluid repletion

slowly over 1-2 days
prevent cerebral and pulmonary edema

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DKA deaths in children

cerebral edema

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optimal rate of glucose decline is

100mg/dl per hour

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if glucose falls too fast

rebound ketosis
cerebral edema

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insulin is given until

ketosis is corrected

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DKA complications

hypoglycemia, hypokalemia
cerebral, pulmonary edema