3/15/16 Flashcards
Converted to pyridoxal phosphate and participates as a cofactor in transamination reactions (ALAS cofactor)
- Pyridoxine (Vitamin B6)
- Given with isoniazid
- Succinyl CoA to aminolevulinic acid done by ALAS and its B6 cofactor
Treats: leukemias, Hodgkin and non-Hodgkin’s lymphoma, Wilm’s Tumor, and choriocarcinoma. Can cause NEUROTOXICITY including areflexia (absent reflexes) and peripheral neuritis (tingling in extremities)
- Vincristine (binds tubulin to inhibit microtubule formation)
- Vinca alkaloid
Alkylating agent also known as mustard gas. Used to treat testicular cancer, breast cancer, and lymphomas
Ifosfamide
-Note all alkylating agents can cause myelosuppression
Paclitaxel ADR:
Myelosuppression
HYPERSENSITIVITY (remember skin are also site of stem cells)
During exercise, there is increased sympathetic outflow→vasoconstriction (alpha 1) of splanchnic regions, kidney, skin, and inactive muscles…so why during exercise is there a cumulative DECREASE in TPR?
Selective vasodilation of active musculature is achieved because metabolic factors such as lactate, potassium, and adenosine overcome sympathetic effects in these areas (overall leads to a cumulative decrease in TPR).
Exercise leads to vasodilation in skeletal muscle beds→ decreased TPR. What happens to the following in exercise? CO? Pulmonary resistance? Venous oxygen pressure?
Increased CO (due to increased HR) via sympathetic activity Decreased pulmonary resistance→increased pulmonary flow→better gas exchange Venous oxygen pressure is decreased due to maximum oxygen being unloaded to the tissues
Right sided heart valve pathology…first two things you suspect?
IV drug use or carcinoid tumor
AFP tumor marker
- Gonadal germ cell tumors (yolk sac carcinoma)
- Hepatocellular carcinoma
CA-125 tumor marker
- Monitor the response to treatment and detect recurrence of …
- OVARIAN CANCER
Carbohydrate antigen 19-9 (CA-19-9) tumor marker:
Monitor progress of pancreatic adenocarcinoma
Hunter Syndrome Inheritance
X-linked recessive deficiency in iduronate sulfatase
What is seen in HURLER syndrome (AR) but is absent in Hunter syndrome (XR)? Both are lysosomal storage disorders with accumulation of heparan sulfate and dermatan sulfate (Mucopolysaccharidoses)
-Corneal clouding is absent in Hunter syndrome
Mucopolysaccharidoses Lysosomal Storage Disorder: Hunter Syndrome (X-linked recessive)
Deficiency in iduronate sulfatase→builds up of heparin sulfate and dermatan sulfate
Mild Hurler + aggressive behavior (NO corneal clouding)
Minimal change disease first line treatment
Corticosteroid → Prednisone
Immunosuppressive agent that binds FK-binding protein to inhibit SECRETION of IL-2
Tacrolimus
Immunosuppressive agent that acts as an antagonist to PURINE metabolism (fucks up cell proliferation)
Azathioprine
- MTOR-receptor (mammalian target of rapamycin)
- Binds FK-binding protein→ acts to block SIGNAL transduction of IL-2 receptor
Sirolimus
Warfarin metabolism
CYP450 system (CYP2C9 member) Inducers of CYP450 cause increased metabolism of warfarin
CYP-450 Inducers: Chronic alcoholics Steal phen-phen and Never Refuse Greasy Carbs
- Chronic alcohol use
- St. John’s wort
- Phenytoin
- Phenobarbital
- Nevirapine
- Griseofulvin
- Carbamazepine
Inhibitors of P-450: AAA RACKS IN GQ Magazine
Try this one instead: Crack Amingos GQ
- Acute Alcohol Abuse
- Ritonavir
- Amiodarone
- Cimetidine/ciprofloxacin
- Ketoconazole
- INH (isoniazid)
- Grapefruit juice
- Quinidine
- Macrolides (except azithromycin)
Patients with chronic renal insufficiency are at risk for developing renal osteodystrophy due to decreased conversion of vitamin D from its inactive (25-hydroxyvitamin D) to its active (1,25 dihydrocholecalciferol) forms. How do you treat renal osteodystrophy?
-Calcium, phosphate binders, and calcitriol (synthetic vitamin D3) supplementation
Toxoid vaccine (example diphtheria-tetanus-pertussis vaccination)
- Toxoid = toxin like
- No longer toxic like toxin but maintains some antigenic similarity (share enough epitopes)
- CROSS REACTIVITY of TOXOID via van der Waals forces
Shigella flexneri vaccine is created how?
By linking shigella to an exoprotein A of Pseudomonas aeruginosa as a carrier
MMR and varicella are what types of vaccines?
Live attenuated (weakened form of infectious agent or killed version of virus is given to patient)
Hemolytic anemia lab values (secondary to drug…Ribavirin)
- Decreased serum haptoglobin (binding to Hb from lysed cells)
- Increased lactate dehydrogenase (released from lysed cells)
- Indirect hyperbilirubinemia
Saquinavir
- Protease inhibitor used to treat HIV
- ADR: nausea, diarrhea, and hyperglycemia
PrPSC (misfolded protein) accumulates in CNS as amyloid plaques
Creutzfeldt-Jakob
Achondroplasia and Marfan’s Inheritance
Autosomal DOMINANT mutation in FGFR3
Autosomal DOMINANT mutation in Fibrillin 1
ATRA (All-trans retinoic acid) is also known as…
Tretinoin
-Induce remission in APL
Oprelvekin (interleukin-11)
- Thrombopoietic growth factor
- Used to combat thrombocytopenia
Myxopapillary ependymomas
Adults = spinal cord (especially filum terminale) Children= fourth ventricle
Pilocytic astrocytomas
- Low-grade astrocytomas typically found in posterior fossa of children.
- Uncommon in adults
What is the active form of prednisone?
Prednisolone (catalyzed by 11-beta-hydroxysteroid dehydrogenase)
Selective alpha-1 antagonist that is used to treat HTN and urinary retention in the setting of benign prostatic hyperplasia
Doxazosin
Activated form of methionine is a very common methyl group donor:
S-adenosyl-L-methionine
Homogentisic acid builds up in the body and polymerize to form alkapton bodies, deposit to cause dark urine and dark cartilage. Patients suffer from decreased joint mobility and arthralgia; but are otherwise healthy.
Congenital deficiency of homogentisic acid oxidase = Alkaptonuria (AR)
Disruption in tyrosine degradation pathway
-Ablating part of the Globus Pallidus Internal (GPi) segment would reduce tonic inhibition of the thalamus in REFRACTORY Parkinson’s cases.
Pallidotomy
Fungal meningitis and encephalitis CSF findings:
High opening pressure
Increased WBC w/lymphocytic and monocytic predominance
High protein
Low glucose
India Ink showing encapsulated yeast is suggestive of Cryptococcus…if Cryptococcus meningitis…how do you treat?
Amphotericin B and flucytosine → when clinical improvement is seen you can drop these to and start FLUCONAZOLE for the next 8 weeks
When a temperate bacteriophage carry genes that transform the phenotype of the host once incorporated this is called LYSOGENIC CONVERSION. Examples of this that increase pathogenicity include:
GAS- scarlet fever
Corynebacterium diphtheriae- diphtheria
Clostridium Botulinum- botulism
Lesch-Nyhan syndrome inheritance
-X-linked recessive
PCOS (polycystic ovarian disease) drugs used to treat:
Spironolactone- anti-androgen (will reduce hirsutism)
Oral contraceptives, gonadotropin analogs, clomiphene
Minoxidil
Rogaine (hair growth)
GAA trinucleotide repeat
Friedreich’s Ataxia
CTG trinucleotide repeat
Myotonic dystrophy
Fragile X trinucleotide repeat
CGG
ANP is released by cardiac myocytes in response to increased atrial stretch during times of volume expansion
Volume contraction (ex: furosemide) would cause ANP levels to drop
Prevents an ethical physician from giving in to a patient’s request for unnecessary testing
The principle of nonmaleficence
Methemoglobinemia may occur as an adverse effect of oxidizing agents such as:
Sulfonamides
Dapsone
Nitro drugs (?)
Local anesthetics (ex: benzocaine)
Methemoglobinemia first line treatment is methylene blue (increases conversion of Fe3+ back to Fe2+)…what is an alternative treatment?
Ascorbic acid (Vitamin C)
NAC (N-Acetylcysteine). Name 3 mechanisms
- Increases glutathione (because is a precursor)
- Binds N-acetyl-p-benoquinone imine directly
- It enhances conjugation with sulfates into a water-soluble product
Cyanide Toxicity treatment
- Sodium thiosulfate
- Sodium nitrates
- Amyl nitrates
Esophageal varies and ascites suggest portal hypertension
Think chronic alcoholism
Follicular thyroid carcinoma mutation
RAS
Alcohol fucks shit up in weeks 3-8 of gestation…how?
Inhibition of cell migration
Impairment of cell differentiation
Impaired or excessive apoptosis
Alteration in cell metabolism
Papillary thyroid carcinoma mutation (most common thyroid malignancy)
Braf
Exposure to radiation
MERRF (myoclonic epilepsy with ragged red fibers)
Mitochondrial inheritance
GM-CSF acts to stimulate the growth of the common progenitor stem cell of neutrophils, basophils, eosinophils, macrophages, and platelets:
The myeloid stem cell
