2/10 UWORLD test # 11 Flashcards
Q 1. Describe B cell development : somatic hypermutation, class switching, affinity maturation, VJ/VDJ recombination: what are they? where do they exactly occur?
VJ/VDJ recombination: happens during B cell maturation in bone marrow, generation of variable antigen binding sites
somatic hypermutation: after antigen presentation in secondary lymphoid structure (germinal center), production of slightly different antibodies, best fit antibody will be selected (affinity maturation)
class switching: after antigen presentation in secondary lymphoid structure (germinal center), class switching happens depending on cytokine signals
IL-4: IgM -> IgG/ IgE
IL-5: IgM -> IgA
Q 1. Difference between primary lymphoid organ and secondary lymphoid organ?
primary lymphoid organ: no antigen presentation, maturation of B/T cells, but not activated yet ( bone marrow- B cell, Thymus- T cell)
secondary lymphoid organ: antigen presentation -> activated B/T cell: spleen or lymph node
Q 2. What are three congenital heart abnormalities that are not cyanotic (That is L->R shunt)? What happens if these diseases are not corrected? What is it called? (hint: some syndrome)
- PDA
- VSD
- ASD
With uncorrected L->R shunt, right ventricular hypertrophy-> R->L shunt and cyanosis.
This is called Eisenmenger syndrome
Q 2. What is total anomalous pulmonary venous return? Is it cyanotic?
pulmonary vein returning back to SVC.
“TOTAL” : all oxygenated blood from pulmonary vein go back to SVC. Thus, cyanosis
Q 5. Loss of what gene on X chromosome gives short stature in Turner’s?
SHOX gene
SHOX is required for long bone growth
Q 6. Why do you worry when patient eats Rat poison (rodenticides)? How to reverse it?
Rat poison contains warfarin.
Reversed by FFP (fresh frozen plasma)
Q 9. What structures are derived from neural crest? (remember mnemonic?)
M- melanocyte O- odontoblasts T- trachea cartilage E- enterochromaffin cell (histamine release for gastric acid secretion) L- laryngeal cartilage P- parafollicular cells of thyroid A- adrenal medulla S- schwann cells S- spiral membrane
Q 10. orotic aciduria and hyperammonemia: what enzyme deficiency? Explain how these two build up with this enzyme deficiency
ornithrin transcarbamylase deficiency
- > build up of carbamoyl phosphate (which normally reacts with ornithin by ornithin transcarbamylase for urea cycle)
- > excess prymidine synthesis (megaloblastic anemia not seen as orotic aciduria due to defect in UMP synthase)
- > excess orotic acid synthesis
Q 10. What are signs of hyperammonemia? (6)
- asterixis (tremor)
- cerebral edema
- slurred speech
- blurred vision
- vomiting
- drowsiness
Q 11. How to distinguish between schizophrenia vs. major depressive episodes with psychotic features?
- Schizophrenia:
: Psychotic features: positive symptoms/ negative symtpoms, without prevalence of depressive features
- Major depressive episodes with psychotic features
: positive psychotic features (delusion, hallucination. disorganized speech) may also be noticed. But depression features (SIGECAPS) will be predominant and exclusively present. That is when mood symptoms kick in, psychotic features will not present
Q 12. What is the most common pathogen of community acquired pneumonia for immunocompetent host?
what about atypical pnuemonia? atypical pneumonia in infants? secondary pneumonia?
- community acquired pneumonia
Strep. pneumoniae - atypical pneumonia
Mycoplasma pneumoniae - atypical pneumonia in infants
RSV - secondary pneumonia (pre-existing URI)
Staph. Aureus
Q 13. Difference between aneroxia nervosa vs. avoidant/restrictive food intake disorder?
aneroxia nervosa
: severely thin, distorted view to body shaped
avoidant/restrictive food intake disorder
: no disturbance in body image
Q 13. What is BMI in aneroxia nervosa?
less than 18.5
Q 16. FAD is derived from what vitamin?
Riboflavin, B2
Q 16. What is the only one enzyme in TCA cycle that uses FAD as a cofactor? which reaction is this?
Succinate -> Fumarate
Succinate dehydrogenase
Fumarate, FAD: starts with F
dehydrogenase: FAD -> FADH2
