Exam 2 Clinical Flashcards
When do you use cardiac monitor with kidney problems?
pts with low K+
Stage 1 HTN tx
thiazides
Stage 2 HTN tx
thiazides + ACEI/ARB/CCB/BB
1st line for all HTN
lifestyle modification
HTN with hypothyroidism
diastolic HTN
Renal artery stenosis dx test
renal angiography
Labs seen with primary aldosteronism
increased aldosterone
low renin
Labs seen with renal artery stenosis
increased aldosterone and renin
Drug tx for high renin activity
ACEI
Beta blockers
Drug tx for low renin activity
alpha blockers
CCB
diuretics
Cause of renal artery stenosis in young adults
medial fibroplasia
Sign of endocrine HTN
imbalance of electrolytes
low renin, high aldosterone
Tx for endocrine HTN
surgery (if unilateral)
spironolactone/triamterene in bilateral
Pheochromocytoma impact
catecholamine release
abnormal lipid levels
hyperglycemia
HTN
Tx for pheochromocytoma
surgery
alpha blockers
volume expansion
Cushing syndrome
increased ACTH production (microadenoma of pituitary)
part of MEA syndrome
increased cortisol in morning and evening
Metabolic acidosis with anion gap causes
Methanol Uremia DKA Paraldehyde Iron/INH Lactic acid Ethylene glycol Salicyclates
Renal tubule acidosis type II
loss of max resorption bicarb in prox tubule decreased bicarb (15-20mEq/L) hypokalemia assc with myeloma/Fanconi syndrome can be caused by CAI's (acetazolamide)
Some causes of hypernatremia
water loss
diabetes insipidus
mannitol/hyperglycemia
Correction of hypernatremia
infuse water
if over 48hrs, no more than 10mEq/L a day correction
Drug causes of diabetes insipidus
lithium
demeclocycline
Causes of inappropriate hyponatremia
SIADH
hypothyroid
adrenal insufficiency
Causes of appropriate hyponatremia
CHF
cirrhosis
volume loss
all are euvolemic hyponatremia
Hyponatremia correction risk
can cause central pontine myelinolysis
from rapid correction of hyponatremia
cracks myelin sheath
Tx for hypovolemic hyponatremia
0.9% saline
Tx for euvolemic hyponatremia
3% saline (acutely)
saline must be more conc than urine osmolarity
demeclocycline/salt for chronic tx
Tx for hypervolemic hyponatremia
underlying disorder tx
diuretics/aquaretics
Tx for hypernatremia
D5W/hydration
Risks of hypokalemia
cardiac arrhythmia (excitability) rhabdomyolysis (releases K+ into serum) alkalosis
Insulin/K+ relationship
causes transport of K+ into cells
decreases serum K+
can tx hyperkalemia acutely
Causes of K+ loss
diarrhea villous adenoma DKA/RTA increased aldosterone Bartter's & Gitelman's
Hypokalemia and RMP
increased excitability
causes increased firing
hyperpolarizes cells
delays repolarization
Hyperkalemia and RMP
depolarization of membrane
increased inactivation time
decreased firing
Catecholamines/K+ relationship
increase Na+/K+ ATPase
drives K+ into cell
Normal K+ range
3.6-5.1
Causes of hyperkalemia
metabolic acidosis
hyperglycemia (insulin)
digoxin
beta blockers (less Na+/K+ ATPase)
Signs of hyperkalemia
muscle weakness
peaked T waves/wide QRS
bradycardia
Alkalosis impact on O2 dissociation curve
shift to the L
less H+ to compete with oxygen binding on Hb
Acidosis impact on O2 dissociation curve
shift to the R
more H+ competes with oxygen and displaces it on Hb
Causes of metabolic alkalosis
antacid
vomiting
diuretics
Methanol absorption
all routes, even skin contact
4mL blindness/15mL death ingestion
Methanol metabolism
alcohol DH converts to formic acid
regulated by folic acid system
Formic acid toxicity
metabolic acidosis/anion gap ocular toxicity seizures/coma/increased ICP CSF with WBCs/xanthochromia (putamen damage) increased amylase
Tx for methanol poisoning
bicarb therapy
folic acid
dialysis
EtOH
Ethylene gylcol characteristics
sweet taste/aromatic odor
ingestion toxicity
metabolized by liver into acids
Ethylene glycol poisoning
CNS stage-acidosis/intox/coma
Cardiopulmonary stage-HTN/cyanosis
Renal stage-crystalluria/ATN/renal failure
Acids produced from ethylene glycol metabolism
glycoaldehyde
glycolic acid/glyoxylic acid
oxalic acid (precipitates in organs/kidneys)
formic acid
Dx of ethylene glycol poisoning
wood lamp exam
increased osmolar gap (early)
decreased serum Ca2+
large anion gap
Digoxin characteristics
excreted via kidneys
alters Na+ transport in cardiac m./increased IC Ca2+
Sx of digoxin toxicity
N/V seizures amnesia/confusion yellow/green vision dysrhythmia
Causes of digoxin toxicity
erythromycin/tetracycline (decreased bacterial metabolism of digoxin)
electrolyte imbalances
hepatic/renal disease
Tx for Dig toxicity
Digibind
FAB fragment
Salicylate metabolism
mostly liver (kidney if excess) rapid absorption
Aspirin overdose
alkalosis (hyperventilation) decreased factor VIII (increased PT time) acute renal failure metabolic acidosis from organic acids ox-phos uncoupling (hyperthermia)
Sx of aspirin OD
hyperpnea
coma/seizures/vomiting
tinnitus
hyperpyrexia
Tx for salicylate OD
salicylate nomogram (within 6hrs) supportive care
Acetaminophen toxicity
Phase 1: 30min-4hrs, N/V
Phase 2: 24-72hrs, liver abn, increased transaminase
Phase 3: 3-5 days, jaundice/encephalopathy/hepatic necrosis
Phase 4: 7-8 days, return to normal/continue decline
Prognosis factor for acetaminophen OD
serum concentration
Tx for acetaminophen OD
nomogram within 4 hrs
N-acetylcysteine within 24 hrs
donates sulfhydryl group for nontox elimination
Acetylcholinesterase inhibitors
carbamates and organophosphates
organophosphates absorbed all routes
Carbamates
acetylcholinesterase inhibitor
lower toxicity/shorter duration
does not cross BBB
Organophosphates
acetylcholinesterase inhibitor
stimulates ANS/skeletal m./CNS
garlic odor of insecticides
Muscarinic effects of organophosphates
SLUG BAM salivation lacrimation urination GI upset/motility Bradycardia Abd pain Miosis
Nicotinic effects of organophosphates
MTWtHF (days of week) midriasis tachycardia weakness HtN fasciculations
Cause of death with acetylcholinesterase inhibitors
respiratory failure (prolonged contraction)
Intermediate syndrome
24-96hrs post poisoning of acetylcholinesterase inhibitors
paralytic sx for days
no atropine response
Tx for acetylcholinesterase inhibitors
atropine for muscarinic effects
pralidoxime for nicotinic/CNS effects
Cyanide characteristics
decreases ATP production
cell membranes are permeable to CN
bind iron on Hb tightly
Cyanide metabolism
B12 incorporation
thiocyanate conversion
rhodanase
Dx of cyanide toxicity
LOC/metabolic acidosis
almond odor
bright red venous blood
Lee-Jones test
Tx for cyanide
amyl nitrate/sodium nitrate (converts to oxyhemoglobin)
Na+ thiosulfate (convertes to thiocyanate)
Phases of iron intoxication
1: 30-120min, acidosis/N&V
2: 2-24hrs, apparent recovery
3: 12-48hrs, acidosis/coma/shock
4: 2-4 days, hepatic necrosis/bleeding diathesis
5: 2-4wks, GI scarring/cirrhosis/CNS sx
Dx of iron intox
pills on x-ray
bloody stool/diarrhea
damage after iron saturates ferritin (300-450ug/dL)
Tx for iron intox
deferoxamine (chelator)-complexes and kidney secretion
use if iron over 350ug/dL in serum
Anticholinergic drug action
blocks muscarinic sites (parasympathetics)
Anticholingergic syndrome
dilated pupils/blurred vision
flushing/dry skin
HTN/hyperthermia
Tx for anticholinergic toxicity
lidocaine for VT
valium for psychotic sx
anticholinesterases (physostigmine)
cold packs for hyperthermia
Physostigmine characteristics
for anticholinergic OD
can cross BBB
do not use with GI/GU obstructions
caution with DM/glaucoma/asthma/heartblock
