CARDIO PATH
CARDIO PHARM
RENAL PATH
RENAL PHARM
100
What would we expect to see on an EKG for both STEMIs and NSTEMIs?
STEMI - Pathologic Q waves
NSTEMI - T wave inversions
100
Nitroglycerin causes an increase in _____ which causes vasodilation
cGMP
100
Most common cause of acute cystitis
E coli
100
Name a medication that would be recommended for someone who is experiencing a persistent cough after taking captopril.
Losartan, candesartan, valstartan.. any "ARTAN"
200
"Rib notching" on CXR with enlarged intercostal arteries. Hypertension in the upper extremities. Lower extremities are cold with weak pulses (brachiofemoral delay).
Coarctation of the Aorta
200
Statins are primarily responsible for inhibiting this enzyme
HMG-CoA reductase
200
You look under a microscope and see muddy brown granular casts
Acute Tubular Necrosis (ATN)
200
What is the MOA for Aliskiren?
Direct renin inhibitor, blocks conversion of angiotensinogen to AI.. Alkiskiren kills renin
300
Age-related degeneration of SA node. ECG can show bradycardia, sinus pauses, sinus arrest, junctional escape beats.
Sick Sinus Syndrome (SSS)
300
Pt comes in with adverse effects from medication: Nausea, Vomiting, Diarrhea... blurry yellow vision.. arrhythmias
Digoxin toxicity
300
Type IV collagen mutation... glomerular basement membrane alterations... X linked DOM... Basket weave appearance due to longitudinal splitting of GBM
Alport Syndrome
300
Pt has severe systemic histoplasmosis infection.. he then received appropriate treatment and then developed RTA type 1. What was he treated with?
Amphotericin B
400
Early cyanosis - "blue babies". Often diagnosed prenatally or becomes evident immediately after birth. Name at least 4 out of the 5 pathologies associated with this phenomena. (Hint: Think 5 T's)
1. Truncus arteriosus (1 vessel)
2. Transposition of the great vessels (2 switched vessels)
3. Tricuspid atresia
4. Tetralogy of Fallot
5. Total anomalous pulmonary venous return (TAPVR)
400
Name 2 agents that can be used to treat metoprolol overdose
Atropine or glucagon
400
Wilms Tumor (nephroblastoma) is highly associated with this loss of function mutation on chromosome 11 in this age demographic. Name both the gene(s) and demo.
Genes: WT1 or WT2
Age: Toddlers to young children (2-4)
400
Pt comes in with bilateral flank pain. Has a hx of ethylene glycol ingestion. Urinalysis shows enveloped shaped crystals. What diuretic would be most appropriate for treatment?
Pt has calcium oxalate kidney stones. Thiazides would be most appropriate to use because they reduce presence of Ca in the kidney
500
How does atherosclerosis progress? Starts with damaged endothelium --> ends with calcification. There are 7 steps in between
Damaged Endothelium --> Macrophage and LDL accumulation --> foam cell formation --> fatty streaks --> smooth muscle cell migration (involving PDGF and FGF) --> proliferation and ECM deposition --> fibrous plaque --> complex atheroma --> calcification
500
Draw what would happen to an action potential in the presence of Procainamide, Flecainide, and Lidocaine
Procainamide (Class 1A), Flecainide (Class 1C), Lidocaine (Class 1B)
500
Pt has a history of Hep C. IgG autoantibodies are present. This patient is at risk for developing what kind of deficiency?
MPGN, nephritic factor stabilizes C3 convertase.. leads to persistent complement activation which will lead to low C3 levels.
500
What parts of the nephron do these diuretics target? What is their MOA? Acetazolamide, Hydrochlorothiazide, Spironolactone, Torsemide
Acetazolamide - CA inhibitor, decrease total body HCO3 stores, affects PCT
Torsemide - loop diuretic, inhibits cotransport Na/K/Cl in the thick ascending limb. Prevents concentration of urine. Increases Ca excretion
Hydrochlorothiazide - inhibits NaCl reabsorption in early DCT, decrease diluting capacity of the nephron decreases Ca excretion
Spironolactone - K+ sparing diuretic. competitive aldosterone receptor antagonist at cortical collecting tubule