firecracker 11/28 Flashcards
RHF
right ventricle cannot pump blood into lungs
blood accumulates in systemic venous system
most common cause of RHF
left heart failure
also:
pulmonary HTN, L2R shunt, Tricuspid valve regurg
most common cause of RHF if no LSHF
COPD
cor pulmonale
rhf due to chornically elevated pulmonary artery pressures
RSHF symptoms
HSM
peripheral edema
jugular venous distension
hepatomegaly in RSHF
venous congestion of hepatic veins of liver
can cause portal htn
hepato-jugular reflux
pressing on RUQ elcitis distension of right jugular vein
peripheral edema cause
increase in venous hydrostatic pressure
jugular venous distension
increased venous pressure in superior venous cava
>4cm abnormal
severe pulmonary hypertension ECG
P pulmonale
peaked P waves >2.5 in inferior leads II, III, avf
right axis deviation
right ventricular hypertrophy
treatment for cor pulmonale
adequate oxygenation
correct respiratory acidosis
treat underlying infections
decrease work of breathing using positive pressure or bronchodilators
HIT
immune mediated reaction after exposure to heparin products
paradoxically pro-thrombotic state
pathophysiology of HIT
auto-antibodies to platelet factor 4:heparin complex Ab cross react with platelets peripheral activation (thrombosis) and destruction (thrombocytopenia)
HIT risk factors
unfractionated (vs LMWH)
higher doses
female
recent surgery
timing of hit
5-10 days after exposure
early onset within 24 hrs if exposed to heparin in past 3 months
thrombocytopenia in HIT
drop in platelet count >50%
thrombosis in HIT
venous>arterial
skin necrosis at injection sites
limb gangrene
organ ischemia or infarction
4 T score of HIT
thrombocytopenia
timing
thrombosis
oTher causes not present
HIT diagnosis
immunoassay test anti-PF4 antibodies
serotonin release assay
management of HIT
stop heparin
start direct thrombin inhibitor (argatroban or bivalirudin)
fondaparinux
HIT - pts with renal dysfunction
argratroban
HIT - pts with hepatic dysfunction
fondaparinux
gout
deposition of monosodium urate crystals in joints
primary gout
hyperuricemia due to nucleic acid metabolism disorders or underexcretion of uric acid
secoundary gout
diseases with high metabolic turnover (leukemia, psorasis)
gout age groupd
men, 40-60
overproduction of uric acid
obesity, cancer, hemoglobinopathies
underexcretion of uric acid
renal disease
diuretic use
podagra
first metatarsophalangeal joint
gout diagnosis
needle shaped negatively birefringent crystals
not uric acid
tophi
x ray imaging that shows bony erosions and soft tissue crystal deposition
gout treatment
nsaids, colchicine, corticosteroids
chronic gout treatment
allopurinol (decrease UA production)
probenecid (inhibit renal UA reabsorption)
pleural effusion
collection of fluid between parietal and visceral pleura
causes of exudative pleural effusions
lung infections, tb
cancer
pulmonary embolism
impaired pleural lymphatic drainage
transudative
increased hydrosatatic pressure or decreased serum oncotic pressure
exudate
increased vessel permeability
causes of transudative pleural effusion
CHF
nephrosis, cirrhosis
injuries to pleural lining
injuries to pleural lining
central venous catheter misplacement
pulmonary emobolism - type of pleural effusion
trans or exud
chylous effusions
iatrogenic (surgery)
traumatic
malignant
pleural effusion symptoms
dyspnea
pleuritic chest pain
worsens with time
associated symptoms (night sweats, wt loss, swelling)
pleural effusion physical exam
decreased breath sounds
dullness to percrussion
decreased fremitus
pleural effusion cxr
blunting of costophrenic angle
transudative - bilateral, exudative - unilateral
lateral decubitus cxr
most sensitive
light’s criteria
pleural prot/serum >.5
pleural ldh/serum ldh >.6
pleural ldh greater than 2/3 of normal serum ldh
treatment of parapneumonic effusions (around a pneumonia)
antibiotics if uncomplicated
chest tube drainage if complicated
ischemic atn most common cause
pre renal failure
- decreased effective circulating load/preload
- decreased cardiac output
- nsaids
DKA potassium levels
low total body levels
normal/high on labs
common cause of nephrotoxic ATN
aminoglycosides, amph b, cisplatinum
heavy metals, contrast, gram negative sepsis, myoglobinuria
meds for pts with coronary interventions
clopidogrel
gb11a/111b inhibitor
decreased effective circulating blood volume
hypovolemia
systemic vasodilation/septic shock
cirrhosis