2015.04.11 (2)

Question 1

Common causes of bacterial meningitis

Answer 1

Streptococcus pneumoniae (Gram + cocci - lancet shaped diplococci)

Listeria monocytogenes (Gram + rods)

Neisseria meningitidis (Gram - cocci - bean shaped diplococci)

Escheria coli (Gram - rods)

Haemophilus influenzae (Gram - coccobacilli)

Question 2

Histone H1

Answer 2

located outside of the nucleosome core and helps to package nucleosomes into more compact structures by binding and linking DNA between adjacent nucleosomes.

Question 3

Androgenetic alopecia

Answer 3

Most common cause of hair loss in both males and females.

Polygenic inheritance (influenced by multiple genes) with variable penetrance.

Question 4

Otitis media causing organisms

Answer 4

most common:

Streptococcus pneumoniae

Haemophilus influenzae

Moraxella

Recurrent infections with these organisms indicate humoral immunodeficiency.

Question 5

Severe Combined Immune Deficiency (SCID)

Answer 5

Recurrent infections caused by bacteria, viruses, fungi, and opportunistic pathogens as well as failure to thrive and chronic diarrhea within the first year of life.

Profound hypoplasia of both B-lymphocyte and T-lymphocyte tissue.

Lymphopenia and hypogammaglobulinemia.

Question 6

Pneumocystis and chronic mucocutaneous candidiasis

Answer 6

associated with underlying T-cell deficiency

Question 7

Charcot-Bouchard aneurysms

Answer 7

Associated witih hypertension

Located: Basal ganglia, cerebellum, thalamus, pons

Size < 1mm

Result of rupture: intracerebral hemorrhage

Symptoms: progressive neurologic deficits, headache

Question 8

Saccular (berry) aneurysms

Answer 8

Associated with ADPKD, Ehlers-Danlos syndrome, hypertension.

Located: Circle of Willis

Size: variable, 2-23mm

Result: subarachnoid hemorrage

Symptoms: sudden severe headache, focal neurologic deficits uncommon

Question 9

Vitamin A Toxicity

Answer 9

Subdivided into:

Acute - NV, vertigo, blurred vision.

Chronic - alopecia, dry skin, hyperlipidemia, hepatotoxicity, hepatosplenomegaly, and visual difficulties

Teratogenic - microcephaly, cardiac anomalies, fetal death

Intracranial hypertension, skin changes, hepatosplenomegaly

Question 10

Niacin Deficiency

Answer 10

3 D’s of pellagra: dementia, dermatitis, diarrhea

Question 11

Where is body’s satiety center located?

Answer 11

Ventromedial nucleus of the hypothalamus.

Neurons here detect glucose elevations and signal satiety.

Lesions cause hyperphagia and obesity.

Rage/savage behavior sometimes noted.

Most commonly caused by tumor invasion.

Question 12

Lateral Nuclei of the hypothalamus

Answer 12

signals hunger.

lesions would cause one to lose desire to eat

Question 13

Suprachiasmatic nuclei

Answer 13

above the optic chiasm

receive visual input from the retina via the optic tract.

regulate circadian rhythms by relaying light information to other hypothalamic nuclei and to the pineal gland

Question 14

Anterior hypothalamic nuclei

Answer 14

when body temperature rises, it signals cooling by stimulating the parasympathetic nervous system to produce vasodilation and sweating.

Lesions cause uncontrolled hyperthermia and death.

Question 15

Posterior hypothalamic nuclei

Answer 15

regulate heat conversation and heat production when the body is cold.

Question 16

Standard error

Answer 16

SD/sqrt(n)

Account for variability due to sampling and helps estimate the true mean of the underlying population

Question 17

Red blood cell fragments, burr cells, and helmet cells

Answer 17

Associated with either microangiopathic hemolytic anemia or mechanical red cell destruction.

In patients with prosthetic valves, RBCs are exposed to excessive shear and turbulence in the circulation, causing damage from mechanical trauma.

Question 18

Obstructive Sleep Apnea Syndrome

Answer 18

recurrent nocturnal upper airway obstruction and apnea (daytime sleepiness, poor energy).

Each nocturnal episode of reduced ventilation causes transiet hypercapnea and hypoxemia resulting in reflexive systemic and pulmonary vasoconstriction as well as sympathetic cardiac stimuolation.

Can result in pulmonary hypertension and right heart failure.

Question 19

Left ventricular systolic failure

Answer 19

Usually due to to myocardial ischemia and causes heart failure, which decreases ejection fraction and increases end-systolic ventricular volume.

S3 sound (ventricular gallop) is audible from blood rushing into a partially filled ventricle or stiff ventricle.

S3 best heard with bell (low frequency sounds) in left lateral decubitus position with the patient exhaling to bring the heart closer to the chest wall.

Question 20

Straining phase of Valsalva manuever (bearing down against closed glottis)

Answer 20

Differentiates between causes of systolic murmur in the left heart.

Decrease venous return to the heart, reducing left ventricular volume and blood pressure.

Murmurs associated with MVP and hypertrophic cardiomyopathy become more audible.

Murmurs associated with aortic stenosis are less audible.

Question 21

Supine hypotension syndrome (Aortocaval compression syndrome)

Answer 21

Hypotension, pallor, sweating, nausea, and dizziness that occurs when a pregnant woman lies supine. Symptoms resolve when standing or left lateral decubitus position.

Due to gravid uterus compressing and obstructing IVC (reduces venous return, which lowers CO and leads to hypotension).

Question 22

Alcoholics and pulmonary infections

Answer 22

Alcoholics are at increased risk for aspiration pneumonia because alcohol intoxication impairs the gag and cough reflexes. Poor oral hygiene, impaired phagocytic and/or bactericidal action of alveolar macrophages.

Pulmonary infections usually polymicrobial: anaerboic (Bacteriodes, Prevotella, Fusobacterium, Peptostreptococcus) admixed with aerobic (Streptococcus, Klebsiella).

Clindamycin covers most of these organisms - antibiotic of choice for treating lung abscesses.

Question 23

Anemia associated with neurologic abnormalities

Answer 23

Vitamin B12 deficiency .

Hematological manifestions are megaloblastic anemia and pancytopenia.

Cofactor for methylmalonyl CoA mutase (methylmalonyl CoA into succinyl CoA). Leads to elevated methylmalonic acid which result in myelin synthesis abnormalities (subacute, combined degeneration of posterior and lateral spinal columns).

Loss of position and vibration sensation, ataxia, and spastic paresis.

Question 24

Decrease progression of diabetic nephropathy

Answer 24

ACE-I class of drug with Angiotensin receptor blockers

Question 25

tRNA regions

Answer 25

Acceptor stem - helps to mediate correct tRNA recognition by the proper aminoacyl tRNA synthetase (load correct amino acid)

3’ CCA tail - recognition sequence by proteins. recognize tRNA molecules, necessary for protein translation. hydroxyl group at the ened is binding site for the amino acid

D arm - contains dihydrouracil residues

Anticodon arm - complementary to mRNA codon (read in 3’ to 5’)

T arm - TWC sequence necessary for binding of tRNA to ribosomes. Presence of thymidine, pseudouridine, and cytidine

5’ terminal phosphate

Question 26

HbS

Answer 26

Valine (nonpolar) is in place of glutamic acid in 6th aa position of beta subunit.

Promotes hydrophobic interaction among hemoglobin molecules when no oxygen is bound and results in polymerization of HbS molecules and RBC distortion.

Question 27

HbM

Answer 27

mutation in heme binding pocket of either alpha or beta chain.

results in an iron phenolate complex that resists the reduction of iron to the ferrous state

Question 28

β-hCG

Answer 28

produced by human conceptus (blastocyst) 6 days after ovulation.

Successful implantation is required in order for there to be hCG in the maternal serum (begins day 6 and may require up to 11 days to appear)

Question 29

Primary osteoporosis

Answer 29

Osteoporosis not caused by a medical disorder

in postmenopausal osteoporosis, cancellous bone is involved (predominant in vertebral column, distal radius, hip and neck of femur)

Serum calcium phosporus, and PTH levels are typically normal.

Question 30

Pentazocine

Answer 30

Opioid narcotic with partial agonist activity and weak antagonist activity at mu receptors.

Can cause withdrawal symptoms to patients dependent on morphine due to its antagonist effects.

Question 31

Treatment of overdose on β-blcokers

Answer 31

Glucagon - increases hr and contractility independent of adrenergic receptors.

Glucagon activates GPCRs on cardiac myocytes, causing activation of adenylate cyclase and raising intracellular cAMP. This results in calcium release from intracellular stores and increased SA node firing.

Question 32

Where are β1 receptors found?

Answer 32

Cardiac tissue and renal juxtaglomerular cells.

β-blockers will decrease intracellular cAMP levels.

Question 33

Gs, Gq, Gi

Answer 33

Gs - activates adenylyl cyclase which converts ATP to cAMP. Increases in cAMP activate protein kinase A.

Gi - inhibits adenylyl cyclase and decreases cAMP.

Gq - activates phospholipase C which degrades membrane lipids into DAG and IP3. Protein kinase C is activated by DAG and Calcium is released from SR under the influence of IP3

Question 34

Proto-oncogenes (Tumor promotors)

Answer 34

Ras: bladder, lung, colon, pancreas, kidney cancers

N-myc: neuroblastoma, small cell carcinoma of the lung

ERB-B1: squamous cell carcinoma of the lung

ERB-B2: breast and ovarian cancer

TFG-a: astrocytoma, hepatocellular carcinoma

sis: astrocytoma, osteosarcoma

abl: CML, ALL

Question 35

Anti-oncogenes (Tumor suppressors)

Answer 35

BRCA-1,2 (DNA repair genes): breast and ovarian cancer

NF-1: neuroblastoma, neurofibromatous type 1, sarcomas

APC/β-catenin: gastric, colonic, and pancreatic cancer; familial adenomatous polyposis coli

DCC: colon cancer

p53: majority of cancers, Li-Fraumeni syndrome

RB: retinoblastoma, osteosarcoma, others

WT-1: Wilms tumor

Question 36

How does diptheria toxin work?

Answer 36

AB exotoxin. A subunit transfers a ribose residue from NAD to elongation factor-2 and inactivates it. This inhibits protein synthesis and causes cell death.

Question 37

How does C. perfringins exotoxin work?

Answer 37

Lecithinase is the exotoxin.

Degrades membrane phospholipids (including lecithin), leading to cell membrane destruction and cell death.

Causes gas gangrene.

Question 38

How does Bordetella pertussin toxin work?

Answer 38

AB exotoxin that stimulates G-proteins to icrease cAMP production, leading to increased insulin production, lymphocyte and neutrophil dysfunction, and increased sensitivity to histamine.

Question 39

Which bacterial toxins inactivate 60s ribosomal subunit?

Answer 39

Shigella’s shiga toxin

EHEC’s shiga-like toxin

Question 40

Transamination

Answer 40

occurs between amino acid and a-keto acid (turning the a-keto acid into an amino acid)

Pyrodixal phosphate (Vitamin B6) is a cofactor for transamination and decarboxylation.

Question 41

Cofactors for biochemical reacions

Answer 41

Thiamine (B1): transketolase, a-ketoglutarate dehydrogenase, pyruvate dehydrogenase

Riboflavin (B2): dehydrogenase rxns involving FMN and FAD

Niacin: forms NAD and NADP required for dehydrogenases

Biotin: pyruvate carboxylase, acetyl CoA carboxylase, propionyl CoA carboxylase, 3-methylcrotonyl-CoA carboxylase

Folic acid: nucleic acid synthesis

Question 42

Difference between membranous and membranoproliferative glomerulonephritis

Answer 42

Membranoproliferative glomerulonephritis: LM shows large hypercellular glomerui

Membranous: Diffudse thickening of capillary wall without an increase in cellularity, “spike and dome” and IgG and C3 deposits ane

Question 43

How does Rb protein work?

Answer 43

Regulates G1-S phase transition.

It is active when hypophosphorylated.

Inactive when hyperphosphorylated (due to proliferation signals like CDK4 - cyclin-dependent kinase-4)