Block 1

1 Bpainful vesicular lesions --herpes

famiclovir, acyclovir,

a) penicillin, cephalosporins, vancomycin, aztreonam, imipenem/meropenem

c) etoposide

d) azoles

e) protease inhibitors-- -navirs( saquinavir, ritonbavir, nelfinavir, amprenavir)

f) RTI -- AZT, ddC, ddI , nevirapine ---

g) clindamycin, tetracycline, chloramphenicol, macrolides ----

2 --C from the primodial gut and contains ganglia supplied by enteric neurons

pancreas

a) adrenal gl -- medulla - neural crest cells, cortex -- mesoderm

b) kidney ---nephros, uretic bud

d) spleen--dorsal mesentery of stomach ( dorsal mesogastrium)

e) ureters--metanephric blastema

Pancres: comes from the foregut (endoderm).... spleen is dorsal mesentery (mesoderm) although is
supplied by SMA from foregut. Kidney is mesoderm (metanephros) as it is ureter (ureteric bud from
mesonephros)... adrenal is neural crest (medulla) and can't recall where does the cortex of medulla
comes.

3Ccarbidopa -- inhibit dopa decarboxylase in periphery preventing L dopa fr being converted to DA in

periphery -------so that L dopa can cross BBB and converted to DA in brain

a) benztropine -- antimuscurinic --- parkinsonism

b) bromocryptine -- DA agonist -- hyperprolactinemia , pitutary adenoma ( causes shrinage)

d) DA-- low dose( D1 activation) --increase renal perfusion , mod dose ( beta1 activation) -- in shock,
high dose ( alpha 1 activation) -- VCn

e) alpha methydopa -- alpha 2 agonist ---for hypertension in preg

f) pergolide --- DA agonist ( PIH) -- hyperprolactinemia

g) selegiline---selective MAO -B inhibitor -- parkinson d/s

estrogen deficiency secondary to anovulation secondary to stress in training, change of body

composition as result of training ex. decrease in fat in the body
4B autoinhibitory effects of NE: how NE inhibit Epinephrine release from nerve terminal.
The qs is asking about the receptor: a2 is the answer???

drug mimics autoinhibitory effects of NE ---

a) reserpine -- prejunctional availability -- not inhibitory

c) reuptake carriers --- also make available for NE -- so not inhibitory

d,e,f) postsyn receptors --- can get NE effects -- not inhibitory effect

5B-HMO --- members pay a fixed payment/month , no additional ( or only minimal ) payment is made
when services are used

a) fee-for service --payment rendered after service is delivered --not lowest

c) personal tax exempt H care account ---The U.S. government, unlike some other countries, does not
treat employer funded health care benefits as a taxable benefit in kind to the employee, ---she is
recently employed , can't be the lowest

d) point of service POS---based on the basic managed care foundation: lower medical costs in exchange
for more limited choice

e) preferred provider organization PPO ---fee for service at a DISCOUNT which is substantial ( 30%
below std fees for primary care , 50% below std fees for specialists)

http://en.wikipedia.org/wiki/Health_care_in_the_United_States
http://en.wikipedia.org/wiki/Point_of_service_plan
6 D..GM-CSF? hemopoietic GF

dyspnea, m/s pain, sinus tachycardia, vomiting, hypotension ( MC with first dose)

Sargramostim-GM CSF

low dose --- primary response -- neutrophilic,

larger dose --- monocytosis, eosinophilia

GM-CSF leads to increased eosinophils which causes anaphylaxis.

"In the presence of ATRA and granulocyte colony-stimulating factor (G-CSF), the cells showed
polymorphonuclear neutrophil differentiation accompanied by expression of surface CD11b, CD15,
CD10, positive activity for neutrophil alkaline phosphatase (NAP), and NAP mRNA expression. In
cultures with ATRA and granulocyte-macrophage colony-stimulating factor (GM-CSF), IL
(interleukin)-3, or IL-5, HT93 showed remarkable eosinophil maturation at day 8 as determined by
luxol fast blue staining, in addition to expression of eosinophil peroxidase and major basic protein."

a) erythropoietin---exacerbate retinopathy ( b of angiogenic effects), CVS complication in kidney

disease pt ( if Hb> 13 g/dl)

b) filgastrim (G CSF) --granulocytes series --bone pain, tenderness over inj site,

c) PDGF---mild , edema, nausea, rash, m/s pain ,

e) thrombopoietin ---thrombocytosis, thrombosis, veno occlusive

7Chypoplastic mandible , malleus -- fr 1st arch

a) cricothyroid -- 4th arch

e) thyroid cartilage -- 4th arch

b) greater genu of hyoid bone -- 3rd arch

d) Stapes --2nd arch

8BINH

slow and fast acetylators

a) GI enzymes

c) tyrosine hydroxylase - DA

d) succinylcholine

e) most enz -affects bioavailability ..

9AA is the right answer

Alcohol withdrawal is life threatening peak 2-5 days form last drink

symptoms are autonomic symtoms hyperactivity(tachcardia,tremors,anexiety,seizures),

psycotic symptoms(halucinations,delusions) and confusion

C.Wernicke_korskoff syndrome caused by thiamin defecincy .Triad

1 confusion

2.opthalmopledia

3. ataxia(Wernick;es encephalopathy

May progress to irreversible memory loss Korsokoff phsycosis

10F-11Deoxycortisol (or cortodoxone) is a steroid, and an immediate precursor to the production of

cortisol. It functions as a mineralocorticoid, though is less potent than cortisol. It can be synthesized
from 17-hydroxyprogesterone. In 11-beta-hydroxylase deficiency, 11-deoxycortisol levels increase
dramatically, causing hypertension (as opposed to 21-alpha-hydroxylase deficiency, in which patients
have hypotension from a lack of mineralocorticoids).

11B ----vagus nerve stimulates both ECL and Parietal cells right ECL has M1 and parietal has M3
receptors both of them are Gq coupled so any shud be IP4

Sinus bradycardia can be defined as a sinus rhythm with a resting heart rate of 60 beats per minute or
less.

Drug treatment of sinus bradycardia is usually not indicated for asymptomatic patients. In symptomatic
patients, underlying electrolyte or acid-base disorders or hypoxia should be corrected. Intravenous
atropine may provide temporary improvement in symptomatic patients, although its use should be
balanced by an appreciation of the increase in myocardial oxygen demand this agent causes.2

12E P. ovale and most P. vivax: Primaquine is recommended for the radical cure of P. vivax malaria, the
prevention of relapse in P. vivax malaria or following the termination of chloroquine phosphate
suppressive therapy in an area where P. vivax malaria is endemic. [5:26:08 PM] physiology: Because
primaquine is not generally active against asexual erythrocytic forms of plasmodia, a blood
schizonticidal agent, preferably chloroquine, is always given in conjunction with primaquine

[5:26:22 PM] physiology: http://www.malaria-ipca.com/primaquine.html

chloroquine, 600-mg base (1,000 mg chloroquine phosphate) PO single dose, followed by 300-mg base
PO 6, 24, and 48 hours later.

plus primaquine phosphate, 15.3-mg base (26.5 mg salt) PO daily, for 14 days to prevent relapse.
Glucose 6-phosphate dehydrogenase deficiency must be ruled out before primaquine is initiated

13A amphotericin is the treatment of choice of Mucormycosis., bcoz it causes release of histamine so
pretreatment with NSAIDS, STEROIDS AND ANTIHISTAMINE.
Fever and shills(shake and bake)

Hypotension

Nephrotoxicity and hydration reduce nephrotoxicity

Arrhythmia due to QT prolongation which exacerbated by changes in potassium and magnesium

levels

Anemia

IV phlebitis(amphoteriible)

14Dhttp://www.medicineonline.com/drugs/N/3126/NALOXONE-HYDROCHLORIDE-Injection-
USP.html

the mechanism of action is to antagonizes opioid effects(not agonist) by competing for the mu,
kappa, and sigma opiate receptor sites in the CNS, with the greatest affinity for the mu receptor.
 Naloxone prevents or reverses the effects of opioids including respiratory depression, sedation and
hypotension. Also, Naloxone can reverse the psychotomimetic and dysphoric effects of agonist-
antagonists, such as pentazocine.

Naloxone is an essentially pure opioid antagonist, i.e., it does not possess the agonistic or
morphine-like properties characteristic of other opioid antagonists. When administered in usual doses
and in the absence of opioids or agonistic effects of other opioid antagonists, it exhibits essentially no
pharmacologic activity.

Naloxone has not been shown to produce tolerance or cause physical or psychological dependence.

15E

Rheunatic fever includes 1- Carditis (inflammation of the heart), 2-Polyarthritis , 3-Erythema

Marginatum , 4- Chorea , 5- Sub cutaneous nodules.It is desirable to give penicillin to prevent
recurrence of rheumatic fever to prevent damage of the heart by another attack.if the Strep bacteria is
killed by antibiotics (like Penicillin) before the body has a chance to make antibodies, then damage to
the heart will not occur.

16B Tobacco smoking is the main known cause of urinary bladder cancer: in most populations,
smoking causes over half of bladder cancer cases in men and a sizeable proportion in women. There is
a linear relationship between smoking and risk, and quitting smoking reduces the riskOther risk factors
dye rubber leather industries, cycolophosphamide ,arsenic ,bear consumption due to nitrosamine and
shistosomiasis

17A
18A
19B
20A angina pectoris.. thyroid hormones may aggravate heart conditions, especially in older patients;
therefore, doctors may start these patients on a lower dose & work up to avoid risk of heartattack

Effect of thyroxine
Increases cardiac output
increases basal metabolic rate
potentiates the effects of catecholamines (i.e. increases sympathetic activity)
Thickens endometrium in females

cardiac wall thickness, increase in heart rate, and cardiac contractility and may precipitate angina or
arrhythmias. Patient with coronary artery disease receiving levothyroxine treatment should be monitored
closely during surgical procedures, since the possibility of precipitating cardiac arrhythmias may be greater in
those treated with levothyroxine. Concomitant administration of levothyroxine and sympathomimetic agents to
patients with coronary artery disease may precipitate coronary insufficiency.

4 B -- brain maturation, Bone growth, Beta adrenergic effects, BMR increase

21E
22B
23E glucagon-binds with receptor-activate G protein-GDP to GTP-alpha unit separate and activate
adenylate cyclase-increase intracellular cAMP-protein kinaseA-action

Basically it is working as beta 1-same effect.

Glucagon binds to the glucagon receptor, a G protein-coupled receptor located in the plasma
membrane. The conformation change in the receptor activates G proteins, a heterotrimeric protein with
, , and subunits. The subunits breakup as a result of substitution of a GDP molecule with a GTP
mol, and the alpha subunit specifically activates the next enzyme in the cascade, adenylate cyclase.

Glucagon does this as its receptor is Gs Protein coupled. This means it increase cAMP (just like the
Beta-1 receptor). Basically it is a back door way to "activate" Beta-1 by causing the same
downstream effects in the same target organ, without using the Beta-1 receptor.

1. beta2 receptor activation --> increased glycogenolysis--> increased blood glucose. beta
blockers block this pathway and glucagon restore it;
2. beta1 and 2 receptors activate adenylate cyclase (AC) --> increased in tracellular cAMP,
beta blocker decrease cAMP, and glucagon, again, increase cAMP through activation of AC.

24A
25B
26E
27B Cimetidine is known to impair the hepatic microsomal oxidation of diazepam, reducing its
clearance and prolonging its half-life

coadministration of cimetidine to diazepam-treated patients causes a large increase in plasma diazepam

and desmethyldiazepam concentrations, the increase is of minimal clinical importance

28D bact strain X resis to ampi, sens to kanamycin.bact strain Y resis to kanamycin and resis to
ampi.bact strains X and Y r grwn in mixed c/r in medium without abx then c/r is plated on medium
containing both ampi and kana.bact colonies grw o plates .in second exp.. DNAse is added to mixe c/r
med, when this mixed c/r is plated on med containing both abx no colonies grw.assuming that bac cells
r impermeable to dnase which of flwng process best explns ? a) conjug b) utatuion,c) transduction d)
transformation e) transposition
plz i beg those who ans plz leave a key point hw to ans these bact genetics if any one knws,i hv always
being ans wriong these q,thnk u.plz explain

[6:15:57 PM] physiology: DNAase added to culture medium => that DNA was present in the
extracellular space....has to be transformation

Transformation means the "uptake" of DNA from the environment by the bacterium

transduction (introduction of DNA by virus) and conjugation( by cell to cell contact).

DNAse destroys all extracellular DNA, so D

Transposition is a "mutation" (chromosomal segment is transferred to a new position on the same or

another chromosome)

29B
30A Active smoking or substance abuse

Co-existing failure of organs other than the lungs. (Such a patient may, however, be a candidate for
multiple organ transplantation.)

Current diagnosis of malignancy, including lung cancer ; some types of skin cancer may not exclude a
patient for consideration

HIV disease or infection

Irreversible left heart failure

Lack of medical insurance

Inability to walk with a poor potential for improvement through rehabilitation

Severe connective tissue disease with extensive extrathoracic manifestations

Severe, untreated psychiatric disorders or a history of medical non-compliance

Uncorrectable coronary artery disease

Relative Contraindications for Lung Transplantation

The following factors tend to make lung transplantation a less viable option:
Age greater than 60 for heart-lung transplantation

Age greater than 70 for bilateral lung

Age greater than 75 for single lung transplantation

Bilateral pulmonary sepsis (single lung only)

31c
32c- PHYSICAL COMPLICATIONS:

Complications of anorexia include:

Death

Anemia

Heart problems, such as mitral valve prolapse, abnormal heart rhythms and heart failure

Bone loss, increasing risk of fractures later in life

In females, absence of a period

In males, decreased testosterone

Gastrointestinal problems, such as constipation, bloating or nausea

Electrolyte abnormalities, such as low blood potassium, sodium and chloride

Kidney problems

mental disorders :

Depression

Anxiety disorders

Personality disorders

Obsessive-compulsive disorders

Drug abuse
33-A AAA- cocaine has the direct effect on vascular endothelial cells releasing ENDOTHELIN-1(a
potent vasoconstrictor).

34A
35B
36C ligase - ligation, polymerase - syn , endonuclease , exonuclease - break ----all for DNA

37D
38E PTH up-regulates 25-hydroxyvitamin D3 1-alpha-hydroxylase, the enzyme responsible for -alpha
hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This
activated form of vitamin D increases the absorption of calcium (as Ca 2+ ions) by the intestine via calbindin

39E
40DTreatment for a thyroglossal cyst is surgical resection, often requiring concomitant removal of the
midsection of the hyoid bone (sistrunk procedure), to prevent recurrence

thyroglossal cyst presents as a midline neck lump (in the region of the hyoid bone) that is usually
painless, smooth and cystic, if infected pain can occur. There may be difficulty breathing,dysphagia
(difficulty swallowing), and/or dyspepsia (discomfort in the upper abdomen), especially if the lump
becomes large.

The most common locations for a thyroglossal cyst is midline or slightly off midline, between the
isthmus of the thyroid and the hyoid bone or just above the hyoid bone. A thyroglossal cyst can develop
anywhere along a thyroglossal duct, though cysts within the tongue or in the floor of the mouth are
rare.

A thyroglossal cyst will move upwards with protrusion of the tongue.

Thyroglossal cysts are associated with an increased incidence of ectopic thyroid tissue. Occasionally, a
lingual thyroid can be seen as a flattened strawberry-like lump at the base of the tongue.

The thyroglossal tract arises from the foramen caecum at the junction of the anterior two-thirds and
posterior one-third of the tongue

2nd -4 cleft

41Awater loss- increase in osmolarity will increase in ADH well there are two things cz the release of ADH
1-increase osmolarity (as is the case with right after giving 400 mM mannitol)
2 decrease in volume ( which remove the "chronic vessles stretch" negative-inhibiton on ADH and let it
release and since the person is HEALTHY (not hypervolumic) we end up decreasing volume and that as well
increases ADH)
so in either case ADH and plasma osmolarity will increase.

it is not like ADH continuosly being released. it get to released in above cases in "HEALTHY Individual". so it
can not be such thing as decrease in ADH if above two mechanisms are intact.
42E
43E corticospinal tract (coming from cerebral hemisph.
it is the medulla given u can see from the olives to identify it is the rostral medualla if the crebral hemisheres
are not developed then the pyramids shud be absent the ans shud be E here
44A

a- nucleus solitaries

b =hypoglossal nucleus

c- =inf cerebellar peduncle

d=inf olive

e=corticospinal tract

45A
46A
47E
48C
49A
50B