DIT notes Flashcards
What hormone is increased or decreased in:
1) Cushing’s syndrome?
2) Conn’s syndrome?
3) Addison’s disease (aka primary adrenal insufficiency)?
4) Graves’ disease?
1) increased cortisol
2) increased aldosterone
3) decreased cortisol and decreased aldosterone
4) increased thyroid hormone
Function of MacConkey’s agar?
1) Select out gram (+), only gram (-) grow (crystal violet and bile salts inhibit gram (+) growth)
2) Distinguish lactose and non-lactose fermenters. Lactose is only carb that grows in agar; lactose fermenters form PINK colonies; non-lactose fermenters form other color or white colonies.
List 5 classes of drugs used to treat Glaucoma:
1) alpha-agonists
2) Beta-blockers
3) Diuretics (carbanic anhydrase inhibitors like acetazolamide, and mannitol)
4) Cholinergic agonists (cholinomimetics)
5) Prostaglandins (PGF-2alpha)
Symptoms:
- facial angiofibroma
- ash-leaf spots of skin depigmentation
- history of seizures
- mental retardation
Tuberous scelorosis
–> patients are at increased risk of developing these neoplasms: cardiac rhabdomyoma, astrocytoma, angiomyolipoma
What’s the cause of achalasia?
How is it diagnosed?
Achalasia = failure of relaxation of lower esophageal sphincter (LES) d/t loss of myenteric (Auerbach’s) plexus.
–> uncoordinated peristalsis –> progressive dysphagia to solids AND liquids.
DX by barium swallow: shows dilated esophagus with an area of distal stenosis. “Birds beak” on barium swallow.
Associated with increased risk of esophageal carcinoma.
Leading causes of death in 15-24 year olds:
- injury
- homicide
- suicide
- cancer
- heart disease
Leading causes of death in 25-64 year olds:
- cancer
- heart disease
- injuries
- suicide
- stroke
anti-GBM antibodies (Immunofluorescence)
Goodpasture’s syndrome
Kimmelstein-Wilson lesions (LM)
Diabetic nephropathy
“spike-and-dome” appearance (EM)
Membranous GN
“tram track” of subendothelial humps (EM):
membranoproliferative GN
subepithelial humps (EM)
Post-streptococcal GN
clinical uses for Metronidazole:
GET GAP: Giardia Entamoeba Trichomonas Gardnerella vaginalis Anaerobes (Bacteriodes, C. dificile) H. Pylori (triple therapy = metronidazole + bismuth + amoxicillin or tetracycline)
- note: pts must avoid alcohol while on this drug – has disulfiram-like reaction with alcohol
- side effects = headache, metallic taste
2 most common post-MI complications?
1) Cardiac arrhythmias –> ventricular fib = most lethal/severe complication
2) LV failure –> leads to pulmonary edema and Right-sided heart failutre
What is Dressler’s syndrome?
autoimmune disease, occurs post-MI’s, results in fibrinous pericarditis
What is the WAGR complex?
a mnemonic for Wilm's tumor (nephroblastoma) = a renal tumor; most common tumor of early childhood (spec 2-4 yo) Wilms' tumor Aniridia (lack of an iris) Genitourinary malformation Retardation - mental-motor
What’s the cause of chronic granulomatous disease?
What are the consequences of chronic granulomatous disease?
Cause: Lack of NADPH oxidase activity
Results in: “impotent neutrophils or phagocytes”; lysosomes don’t work
Consequences = susceptible to opportunistic infections (because no neutrophils)
4 main pharmacokinetics equations:
1) Vd = amount of drug given (by IV) / [drug in plasma]
2) Clearance:
CL = (0.7 X Vd) / t1/2
= k X Vd
( where k=elimination constant = 0.7/t1/2)
3) Loading Dose:
LD = Css X Vd
(where Css = concentration of steady state = desired concentration)
4) Maintenance Dose:
MD = Css X CL
What’s the pKa?
pKa = acid dissociation constant = ph at which the amount of the non-protonated form = the amount of protonated form
if pH < pKa:
this is an acidic environment; have more of hte protonated form; basic drugs gets trapped
if pH > pKa:
this is a basic environment; there will be more of hte non-protonated form; acidic drugs get trapped
How to treat an acidic drug OD (ie salicylates = aspirin)?
Give NaHCO3 –> traps the acidic drug in basic urine
How to treat basic drug OD (ie amphetamines)?
Give NH4Cl (ammonium chloride) –> traps basic drug in the acidic urine
What are the symptoms of excess parasympathetic activity?
DUMBBELSS: Diarrhea Urination Miosis Bradycardia Bronchospasm Excitation of skeletal muscle and CNS Lacrimation Salivation Sweating
*Parasympathetic drugs make you “leaky”!
Ptosis or Diplopia that worsens throughout the day?
Myasthenia gravis
Tensilon test = Endrophonium test:
Dx for myasthenia gravis; give endrophonium, if symptoms improve then dx as MG
4 treatment options for myasthenia gravis:
1) acethylocholinesterase inhibitors (indirect cholinergic agonists) (b/c in MG have abs to ach receptor; so ach-ase inhibitors increase ach in synapse)
2) corticosteroids
3) thymectomy
4) plasmapheresis
What drug regenerates acetylcholinesterases after organophosphate poisoning?
(organophosphates = anti-cholinesterases = parathion = insecticide)
Pralidoxime (regenerates active AchE); also can give atropine to treat symptoms
What are symptoms of inhibiting parasympathetic activity? (ie from giving atropine)
Hot as a hare (increased body temp)
Dry as a bone (decreased sweating)
Red as a beet (flushed skin)
Blind as a bat (cycloplegia= ciliary body paralysis–> loss of accommodation = blurry, near vision)
Mad as a hatter (disorientaion, delirium)
Bloated as a toad (constipation, urinary retention)
What anti-cholinergics are used to treat urge-type urinary incontinence?
- oxybutinin
- tolterodine
- darifenacin and solifenacin
- trospium
What drugs inhibit parasympathetic activity?
- atropine, homatropine, tropicamide (all muscarinic antagonists)
- benztropine
- scopolamine
- ipratropium
- oxybutynin
- glycopyrrolate
- methscopolamine
- propatheline
In what disease/s does one have increase Ach?
In what disease/s does one have decrease Ach?
- increased Ach in: Parkinson’s disease (treat with muscarinic antagonists)
- decreased Ach in Huntington’s disease and in Alzheimer’s disease (treat with cholinergic drugs)
In what pt populations is atropine contraindicated?
- Glaucoma
- Prostatic hypertension or any urinary retention
- GI obstruction (ie ileus)
- Dementia, Delirium, Elderly
- Infant with fever (because can cause hypoterhmia in infants)
G-protein second messengers:
- receptors and G-protein class
- second messengers; what each class does
qiss and qiq until you're siq of sqs α1 --> Gq α2 --> Gi B1 --> Gs B2 --> Gs M1 --> Gq M2 --> Gi M3 --> Gq D1 --> Gs D2 --> Gi H1 --> Gq H2 --> Gs V1 --> Gq V2 --> Gs
Gq —> Phospholipase C —> converts lipids to PIP2 –> PIP2 forms DAG and IP3
-DAG (diacylglycerol) –> Protein kinase C
-IP3 (inositol triphosphase) –> increased incracellular Ca2+
(q-c = “cutesy”)
Gs–> stimulates adenylyl cyclases –> converts ATP to cAMP —> CAMP activates protein kinase A —> get increased intracellular Calcium (in heart) and inhibition of myosin light-chain kinase in smooth muscle.
Gi –> inhibits adenylyl cyclase
Drugs that inhibit cytochrome P-450:
PICK EGS: Protease inhibitors Isoniazid Cimetidine Ketoconazole Erythromycin Grapefruit juice Sulfonamides
Cholinomimetic Drugs:
- Direct cholinergic agonists
- Indirect cholinergic agonists
Direct agonists:
- Bethanechol
- Carbachol
- Pilocarpine
- Methacholine
Indirect Agonists = Anticholinesterases:
- Neostigmine
- Pyridostigmine
- Edrophonium
- Physostigmine
- Echothiophate
- Donepezil
