Firecracker AIN/ATN/STEMI Flashcards
categories of ATN
ischemic
nephrotoxic
etiology of ATN
disturbances in renal blood flow
tubular injury
renal ischemia causes
intrarenal vasoconstriction (afferent arteriolar)
decreased GFR
oliguria
parts of tubules most suseptible to hypoxic injury
straight portion of PT
thick ascendling limb
mechanisms of renal ischemia
loss of tubule cell polarity
endothelial damage
Ischemic ATN most commonly caused by
pre-renal failure
- effective circulating blood volume/preload
decreased cardiac output
NSAIDs, ACEIs
decreased effective circulating blood volume
hypovolemia
systemic vasodilation (shock)
cirrhosis
decreased cardiac output
CHF
cardiogenic shock
NSAIDs and ATN
decreased PGI2 (NSAIDS) decreased vasodilation of afferent arteriole
ACEIs and ATN
decreased ATII
decrease vasoconstriction of efferent arteriole
nephrotoxic ATN
1) aminoglycosides
2) amph b
3) cisplatinum
other causes of nephrotoxic ATN
heavy metals - lead, mercury
contrast
gram negative sepsis
myoglobinuria
Mechanism of nephrotoxic ATN
1) tubular toxicity
2) direct injury to PCT
3) mygolbin precepitation and tubular obstruction
ethylene glycol ATN
massive intratubular oxalate crystal deposits
ATN phases
initiation phase
maintenace (oliguric phase)
recovery (polyuric) phase
ATN initiation phase
first 36 hrs
slight decrease in urine output w increase in BUN
ATN maintenace phase
- sustained oliguria
- increased ECF
- hyperkalemia
- increased anion gap metabolic acidosis (retention of H and anions)
ATN recovery phase
2-3 wks after event
- brisk diuresis w/ loss of K, Ca, Mg, Ph
- hypokalemia
- BUN and Cr return to baseline
increased EcF
weight gain, edema, pulmonary vascular congestion
diagnosis of ATN
exclusion
muddy brown granular casts
FeNa > 3
ATN treatment
supportive
most common cause of AKI
ATN
hypokalemia EKG changes
flattening or inversion of T waves, U waves, depressed ST segments
PVCs
arrythmias
STEMI
thrombus occludes atherosclerotic coronary artery
slowly developing coronary stenosis
doesn’t cause STEMI
development of rich collateral circulation
more likely to cause unstable angina, NSTEMI
risk factors for STEMI
atherosclerotic RF (hld, smoking) unstable angina
other risk factors for STEMI
hypercoaguability, cocacine, collagen vascular dz, intracardiac thrombi which can embolize
pharmacologic treatment of STEMI
BEMOAN
beta-blocker, enoxaparin, morphine, oxygen, aspirin, nitrates
nitrates
preload reduction mainly
but also reduces afterload
beta blocker and STEMI
don’t give if acute heart failure is present
aspirin
prevents further platelet aggregation at site
contradicted in NSTEMI
glucocorticoids
NSAIDs
impair healing, risk for ventricular wall rupture
definitive treatment for STEMI
reperfusion therapy
chemical or percutaneous coronary intervntion
fibrinolysis/chemical reperfusion
tpa
streptokinase, tenecteplase, reteplase
absolute contraindications to chemical fibrinolysis
cerebrovascular hemorrhage, active internal bleeding, suspicion of aortic dissection, marked htn or stroke/cva in past year
CABG
primary reperfusion stratgey in patients with occlusion of left main coronary artery severe three vessel involvement
MI mot common complication
arrhythmia
post MI arrythmias
V fib – death
new onset AV or bundle branch blocks due to infarction of condution tissues
mechanical complications of MI
3-5 d post MI
ventricular free wall rupture
ventricular septal rupture
papillary muscle rupture
ventricular free wall rupture
pericardial tamponade
ventricular septal rupture
new ventricular septal defect murmur
papillary muscle rupture
severe MR, hemodynamic compromise
Dressler’s syndrome
2-3 weeks post MI
low grade fever, chest pain, pericarditis, and/or pericardial effusion
friction rub!
Dressler’s syndrome treatment
self limited
colchicine
post MI lifestyle modifications
smoking cessation
exercise
dietary modifications
post MI medications
B blocker, low dose Aspirin, ACE/ARB, nitroglycerin, statin
post MI pts w/ stents meds
clopidogrel or GpIIB/IIIa inhibitor
DKA
hyperglycemia
metabolic acidosis
ketone bodies
what can lead to increased glucose
physiological stress: infection, intoxication, lack of medication –> increase insulin demand
ketones
free fatty acids –> b hydroxybutyric acid, acetoacetic acid
DKA symptoms
abdominal pain, vomitting, fruity breath odor, profound dehydration
fruity breath odor
acetoacetic acid –> acetone
DKA mechanism of dehydration
glucosuria –> osmotic diuresis
MS changes
DKA - metabolic acidosis
increased carbonic acid in blood which is converted to Co2
increased co2 – deep, rapid breathing (kussmaul respirations)
DKA diagnosis
elevated gluc >300 anion gap metabolic acidosis urine + glucose and ketones normal or high potassium low sodium
K in DKA
potassium moves from ICF to ECF to compensate for electrolyte loss
low total body potassium
normal/high potassium on labs
treatment of DKA
normal saline
potassium
insulin and glucose
check potassium before insulin because
insulin can worse preexisting hypokalemia
DKA - fluid repletion
slowly over 1-2 days
prevent cerebral and pulmonary edema
DKA deaths in children
cerebral edema
optimal rate of glucose decline is
100mg/dl per hour
if glucose falls too fast
rebound ketosis
cerebral edema
insulin is given until
ketosis is corrected
DKA complications
hypoglycemia, hypokalemia
cerebral, pulmonary edema
