March 26 - NBME Flashcards
Blood gas in chronic bronchitis
Lung is poorly ventilated due to mucus plugging and shunting resulting in low pO2 and high pCO2. Bicarb goes up to compensate for respiratory acidosis.
Methylphenidate
Ritalin. CNS stimulant for ADHD and narcolepsy
Sertraline
SSRI
T4/5 dermatome
nipple
T10 dermatome
umbilicus
L1 dermatome
inguinal area
L4 dermatome
anterior knee
S1/2 dermatome
back of thigh (via sciatic nerve)
Alcoholic hepatitis: pathophysiology and pathology
Pathophysiology: Oxidative damage due to increased CYP450 resulting in increased ROS and increased toxic metabolites. Inflammation due to endotoxins from the gut going to the liver via the portal tract.
Pathology: centered around the portal vein. Mallory bodies are classic due to increased acetaldehyde which causes lipid peroxidation and cytoskeletal damage. Body is intracellular accumualtion of intermediate filaments
Gout vs pseudogout crystals
Gout: negatively birefringent monosodium urate crystals
Pseudogout: positively birefringent calcium pyrophosphate crystals
Calcium kidney stones
Can be calcium oxalate or calcium phosphate. Radioopaque stones. Most commonly formed due to increased urine Ca++ with normal serum Ca++.
Can also be seen due to increased oxalate. In Crohns or gastric bypass, fat that doesn’t get absorbed binds Ca++ leaving oxalate free to be absorbed. Vitamin C abuse also increases oxalate.
Struvite kidney stones
Ammonium, magnesium, and phosphate stones. Seen in the setting of a UTI with urease positive bacteria (proteus, staph, kelbsiella). These bacteria create alkaline urine that allows them to form.
Can form staghorn calculi: stone material precipitates out and forms cast of renal pelvis and calcies. These require surgery; failure to treat forms a nidus for recurrent infection.
Uric acid kidney stones
Causes: increased uric acid such as in gout, leukemia, myeloproliferative disease. Acidic urine
Radiolucent stones that are not visible on x-ray. Form in distal tubule and collecting duct which have the lowest pH. Treated medically, not surgerically
Cystine stones
Seen in kids with cystinuria who cannot absorb cystine in their tubules. Can form staghorn calculi
Ascites treatment
Spironolactone is first line: gets at the pathophysiology of inappropriate RAAS activation due to perceived volume depletion.
Add loop diuretic if ineffective
Pseudohyponatremia
Caused by hyperglycemia: increased glucose in the blood pulls water into the vasculature, diluting out sodium
Hypocalcemia presentation
muscle spasms/tremor/tetany increased blood pressure arrhythmias confusion seizures
Hypercalcemia presentation
N/V, anorexia, increased thirst confusion to acute psychosis kidney and biliary stones bone pain and muscle weakness polyuria leading to dehydration
Fibromuscular dysplasia
Narrowing and weakness of blood vessels. Risk of dissection and aneurysm. Classically a string of beads appearance of renal vein in middle aged woman. Causes HTN and renal bruit
NSAID nephropathy
Prostaglandins dilate the afferent arteriole. Angiotensin II is still constricting the efferent, so RPF goes down.
Normal saline
0.9% saline
Omeprazole interactions
CYP450 inhibitor: increases levels of many drugs, decreases activation of clopidogrel
Decreases stomach acidity which decreases azole absorption
Glucocorticoids: mechanisms
- inhibits NFkappaB decreasing production of inflammatory cytokines
- inhibits formation of inflammatory mediators by inhibiting phospholipase A2 and COX
- Decreases adhesion molecules, decreasing leukocyte emigration
- Decreases T cell activation via inhibition of cytokine production
Classification of burns
First degree: only epidermis; skin red and dry
Second degree: epidermis and dermis; skin red, moist, blistering, very painful
Third degree: extends to hypodermis; painless; patchy appearance
Glue sniffing symptoms
Dizziness, loss of coordination, slurred speech, hallucinations
Vascular supply to female pelvis
Uterine a, vaginal a, and internal pudendal all branch off of internal iliac a. Internal pudendal gives rise to inf rectal and supplies the clitoris/penis and labia/scrotum
Phases of clinical trials
I: small number of healthy people; assess safety
II: small number with the disease; assess efficacy
III: large number randomly assigned; assess if better than what’s already on the market
IV: post-market surveillance; look for long term outcomes/side effects
