Block 16 Flashcards
(41 cards)
RNA polymerase types and location
DNA polymerase function and location
DNA endonuclease function and location
RNA polymerase I = found exclusively in the nucleolus , form essential ribosomal component (18S, 5.8 S, 28 S)
RNA polymerase II= found around the nucleus and nucleolus, responsible for making mRNA, snRNA, and micro RNA
RNA polymerase III= transcribes DNA to form snRNA such as tRNA and 5S rRNA.
DNA polymerase= responsible for replication and repair found throughout the nucleus.
DNA endonuclease= found in nucleoplasm and breaks phosphodiaster bonds within nucleotide chain, responsible for repair and RNA splicing
Mullerian aplasia
(Also called mayer rokitansky kuster hause syndrome)
Normally mullerian duct give rise to fallopian tubes, uterus cervix, and upper vagina by 20 weeks of gestation.
- defective development or congenital absence of organ or tissue —> variable uterine development, short vagina.
- amenorrhea with normal secondary sexual characterestics
- patients have normal ovaries which secretes estrogen —> secondary sexual characteristics.
Patients with mullerian aplasia (MRKH) , may have extra genital complication —> ?
Urological malformations such as Unilateral renal agenesis , ultrasound should be done
Efficacy vs potency
Efficacy = intrinsic ability of a drug to elicit and effect such as receptor activation or dilation of a vessel. Its a measure of the maximum ceiling of activity (E-max) of a drug with respect to particular pharmacodynamic end point.
Potency = refers to the dose of the drug that is required to produce a given effect. Its primarily affected by the affinity of the drug for its receptor and the amount of drug that is able to reach the target tissues, therefore a drug that binds to their receptors with a higher affinity have a greater potency.
The lower the ED50 , the more potent the drug is.
Fenoldopam
Dopamine- 1 receptor agonist,. Stimulates and activates cAMP —> vasodilation in most arterial beds —> decrease in Systemic BP.
- Renal vasodilation is particularly prominent and leads to increased renal perfusion, naturesis and diuresis.
Hypertensive emergency vs urgency
Urgency= severe hypertension with no evidence of end organ damage. Emergency= severe hypertension with end organ damage Such as (ACS, encephalopathy, pulmonary edema, AKI, aortic dissection, papilledema, aortic dissection) Treated with dopamine agonist (e.g fenledopam)
Changes after MI by time frame
0-4 hrs : minimal changes
4-12 hrs: early coagulation necrosis, edema , hemorrhage and wavy fibers.
12-24 hrs: coagulation necrosis and marginal contraction band necrosis
1-5 days: neutrophilic infiltrates
5-10 days : macrophage phagocytosis of dead cells
10-14 days: granulation tissues and neovascularization
2 weeks to 2 months: scar formationm
IL- 4 and IL-5 stimulate which Ig
IL-4 —> IgE (also IL-13)
IL-5 —> IgA
If a patient with angina cant tolerate aspirin he should receive
Clopidogrel
PAD drugs
Peripheral artery disease
Pentoxyfilline
Cilostazol
Phenylketonuria deficiency in which enzymes
- Most cases are due to phenylanine hydroxyalse deficiency —> deficient phenylanine.
- Less commonly deficiency in BH4 (tetrahydrobiopetric) due to deficiency in dihydropteridine reductase deficiency. This will lead to decrease serotonin (tryptophan cant be converted to 5-hydroxytryptophan which then converted to serotonin )
Peptidoglycan cell wall in Gram positive bacteria
Provides the shape of the bacterium as well as resistance to osmotic pressure.
-if treated with antibiotic that acts on it (e.g cephalosporins pencillins, and vancomycin) —> can disentegrate bacteria because it wont be resistant to osmotic pressure
Supplementation for breastfeed infants
- Vitamin D (especially with lack of sun exposure or african american)
- Iron (preterm/ low birthweight.
- Vitamin K (at delivery)
Bupropion side effect
- its an antidepressant that similar in structure of amphetamines —> inhibits reuptake of dopamine and NE. Commonly used to treat major depression.
- seziures are potential side effect of bupropion therapy, especially in high doses.
- contraindicated in sezuires history or bulemia/ anorexia history.
Vanlefexine AE
Hypertension
Fastest to slowest cardiac tissue conduction
- Prukinje —> atrial muscle —> ventricular muscle —> AV node
B12 deficiency in spinal cord lesion
- Subacute combined degeneration of dorsal coulmns( position and vibration sense, positive romberg ataxia)
- Lateral corticospinal (spastic paresis)
- Spinocerbellar tracts (ataxia)
- Pts may develop atrophic glossitis (smooth,shiny erythmatous tongue)
TPR equation
1/Rt= 1/TPR 1/Rt= 1/R1 + 1/R2 + 1/R3 +1/R4.... if for example all 1/R1 + 1/R2 + 1/R3 +1/R4 were equal to 2 So 1/TPR TPR= 1/2 +1/2 +1/2 + 1/2 = 2 mm 1/TPR = 0.5
Superior messenteric artery syndrome
- intermittent intestinal obstrucion symptoms (postprandial pain and billous vomiting)
- when transverse (third portion) part of dudenum gets compressed between SMA and aorta.
- occurs with low body weight and malnutrition usually.
Lamotrigine can cause (AE)
- SJS or toxic epidermal necrolysis
Acute adrenal crisis
Etiology
Clinical
Treatment
Etiology: adrenal hemorrhage or infarction, acute illness/ injury/surgery in patients with chronic adrenal insuffeciency or long term corticoids use
Clinical feature:
1. Hypotension and shock
2. Nausea/vomiting/abdominal pain and hypoglycemia
3. Weakness
4. Fever
5. Hypopegmentation
Treatment:
Hydrocortisone or dexamethasone with high IV fluids
Hepatodudenal ligament includes
Common bile duct Hepatic artery Hepatic portal vein (Portal triad) Occlusion of it can be done surgically to identify vascular source. If liver bleeding doesnt cease, its likely it hasnt been the cause of bleeding rather the IVC or hepatic veins.(pringle maneuver)
West nile virus - features, clinical and diagnosis.
- positive sense, ssRNA flavivirus transmitted by culex mosquitos most commonly in summer.
- Rash , neurological manifestaion (encephalitis associated with flaccid paralysis syndrome), meningitis
- diagnosis can be done with positive CSF anti-WNV antibodies.
- management -> supportive
Acid base disorders appropriate compensation
- metabolic acidosis = PaCO2= 1.5 (serum HCO3-) +8 +- 2
- metabolic alkalosis = increase in paCO2 by 0.7 mm Hg for every 1 mEq/L rise in HCO3-
- Acute respiratory acidosis= increase serum HCO3- by 1 mEq/L for every 10 mm Hg rise in PaCO2
- Acute respiratory alkalosis= decreased serum HCO3- by 2 mEq/L for each 10 mm Hg decrease in PaCO2.
