block 4

1Aaortic regurgitation

FA 255 , 2010

AR ---

high pitched blowing diastolic and decrescendo, which is best heard at aortic area;

Austin Flint murmur, a soft mid-diastolic rumble heard at the apical area

AS-- A diamond-shaped (crescendo-decrescendo) systolic ejection murmur following ejection click

MS --opening snap , followed by mid diastolic murmur

MR -- holosystolic murmur high pitched , loudest at apex, radiates to axialla

TR --- holosystolic murmur high pitched , loudest at Tricuspid area, radiates to R sternal border

TS ----A mid diastolic murmur over the left sternal border, tricuspid opening snap with wide splitting
S2. May increase in intensity with inspiration (Carvallo's sign)

PR ----Early decresendo diastolic murmur at the left lower sternal border.

- Graham Steell murmur of pulmonary hypertension -- a high-pitched, early diastolic decrescendo

murmur over the left upper-to-left midsternal area

PS : a crescendo-decrescendo harsh murmur at pulmonic area , radiating into the neck or back

2CAtrial flutter ---saw tooth appearance

FA 259, 2010

b) AV reentrant tachycardia ---delta wave -WPW $

c) sinus tachycardia ---P wave precedes each QRS complex , rate > 100/min

d) ventricular fibrillation --- totally erratic shape no identifiable waves

e) ventricular tachycardia --- repeated large wide QRS complexes originates in ectopic focus

atrial fibrillation -- chaotic and erratic baseline ( irreg irreg) with no discrete p waves between
irregularly spaced QRS complexes

3E

bronchop'nia

chronic malabsorption -------- CF

Pseudomonas aeruginosa

a) coccidioides immitis --- in desert sand SW US

b) legionella ---airconditioning , common showers, esp over 50 yrs , heavy smokers, drinkers

c) mycoplasma -- atypical p'nia --walking p'nia-- X ray features more severe than clinical ones

d) PCP ---AIDS , premature, groundglass x ray with honeycomb exudate with silver staining cysts,

Pneumonia followed by flu Staph. Aureus (lung abscess), H.influenzae, Strep. Pneumonae

from forums

NeonatoStrep Gpo B (baby)

6wks to 18 YO.RSV,Chlamydia, Mycoplasma

18- 40 YO.Mycoplasma, Chlamydia, Strep. Pneumoniae

40-65YO..Strep Pneumoniae, H influenza, anaerobios

> 65 YOStrep Pneumoniae, Virus, Anaerobios

Alcoholics,.Strep Pneumoniae, Klebsiella

Immuno depress ptStaph, PCP ....

MCC of pneumonia in immunocompramised still remains streptococcus pneumonia ;;PCP will be

AIDS defining

Aspiration...anaerobios

Community aquire atypical pneumoniae.Legionella

Nosocomial.Staph, G- (e. colli)

Cystic fibrosis..Pseudomona.

Sickle cell..Strep Pneumoniae

IVDU: S.aureus

Atypical pneumonias: 3 zoonotic and 3 non-zoonotic

CAP in older adults: Str. pneumoniae; H. influenzae

1 to 3 Months: febrile- RSV; afebrile- Chlamydia trachomatis

3-12 Months: RSV

2-5 Years: Respiratory viruses (parainfluenza, influenza, adenoviruses), S. pneumoniae, H. influenzae

5 Years to 18 Years: Mycoplasma pneumonia4C

5DDiarrhea

symptom --- past 5 weeks

-Giardia lamblia -- 1-2 wks to yrs

a) Bacillus cereus ---> 6hrs, heat labile toxin., meat and vegetables

b) Campylobacter --- 3-5 days,poultry, MC bact Diarrhea in US

c)Cryptosploridium -- 2-4 weeks , children, AIDS, daycare center, acid fast oocytes in stool

d) Shigella sonnei -- 1-7 Days -- daycare , bloody D

6F--early cyanotic --5 days old

systolic murmur

TOF ( MC cyanotic cong HD)

g) TGA ----increased risk in infants of DM mothers

a) ASD -- acyanotic -- systolic ejection murmur , fixed splitting of S2

b) bicuspid aortic valve -- AS Systolic Ejection M following ejection click

c) COA--mid systolic murmur over ant part of chest and back , rib notching

e) PDA ---continuous machinery murmur

h) VSD --acyanotic , holosystolic murmur

7Dbeta 2 agonist --- albuterol, salmeterol --- relaxes smooth m/s of bronchioles

a) constriction of pul bronchioles -------will worsen asthma

pul vas resistance --- ass with pul hypertension -- not asthmatic attack

pul surfactant -- for the surface tension lowering thereby preventing collapse

8B24 hrs after missing insulin dose

DKA

decreased in pH

decreased in HCO3--- anion gap meta acidosis

acidotic breathing --- decreased in PCO2

9CC is the right answer

T3 bind to the receptor and activate DNA binding activity on intracellular receptor. T3 like other steroid
hormones PET CAT are lipophilic and relatively insoluble in plasma,there fore must circulate in blood
bound to specific binding globulins,which increase sollubilty and increase delivery to target organ.The
need for gene trascritiopn and protein synthesis delays the onset of action of these hormones

10B
11Ehttp://www.idph.state.il.us/HealthWellness/fs/congenitalhypo.htm

Thyroid agenesis (or thyroid dysgenesis) is a cause of congenital hypothyroidism[1] where the thyroid
is missing, ectopic, or severely underdeveloped.

It should not be confused with iodine deficiency, or with other forms of congenital hypothyroidism
where the thyroid is present but not functioning correctly.

It can be associated with PAX8.[2]This gene is a member of the paired box (PAX) family of
transcription factors. Members of this gene family typically encode proteins which contain a paired box
domain, an octapeptide, and a paired-type homeodomain. This nuclear protein is involved in thyroid
follicular cell development and expression of thyroid-specific genes.

12E ...here is the order how ovulation occurs.

1-estrogen level rise above certain level,they no longer inhibit the release of LH and FSH .Instead they
stimulate the release of LH and FSH (negative feedback loop to positive feedback loop )
2-This causes surge in the release of LH and FSH .Only the LH isurge is essential for the induction of
ovulation and the formation of corpus luteum.Therfore if estrogens are still rising ovulation hasnot
occured.
3-Graffian follicular rupture occurs 24-36 hours after the onset of the LH surge .
4-Luteal phase starts .And the metabolic pathways are then altered in the granulosa and thecal cells in
favor of progesterone production.

5-luteal cells (transformed granulosa and thecal cells ) start to produce considerable progesterone and
some estrogen.....

so in my thinking it is Progesterone level in the serum that shows ovulation has occurred ....

13F
14c- hPL stimulates DNA synthesis in mammary tissue. hPL may have actions either on the
development (mammogenesis) or the function (lactogenesis) of the mammary gland.

http://books.google.com/books?
id=iuhCuejgZD8C&pg=PA485&dq=human+placental+lac...gen&f=false

STAGES OF Lactation

1-Mammogenesis (UPTO MIDPREGNACY )....due to proliferation of ducts and glandular system

under estrogen and progesterone

2-LACTOGENESIS ,STAGE 1--MID PREGNANCY TO DA2 2 POSTPARTUM-differentiation of

alveolar cells from secretory cells...under estrogen,prolactin,and human placental lactogen

3-Lactogenesis ,Stage 2--day 3-day 8...triggered by rapid drop in mother's progesterone level(the
inhibitor)...onset of copious secretion of milk...

4-Galactopoiesis-day 3 upto involution...maintenance of established secretion...under prolcatin and

oxytocin

5-Involution ...average 40 days after last breast feeding---due to high sodium levels

15C C http://genomebiology.com/content/figures/gb-2001-2-5-research0016-1.jpg A zinc finger is a

large superfamily of protein domains that can bind to DNA.
16B

DCM: walls get dilated due to various etiology commonly autoimmune/post viral...hypertrophy is not
uniform..someplaces thin others thick..resulting in bizzare contraction behaviour..whats the effect walls
loose ability to pump ..low ef..forward heart failure

HCM: walls get hypertrophied due to overactivity of LV against increased after load resulting in
uniform hypertrophy...iniatlly ef normal or more...ultimately loose ef

RCM: LV size decreases and overall chamber size smaller..ef low from begining

atrial myxoma common with DCM why?

nonuniform hypertrophy leads to bizzare contraction causing blood stagnation in few places which
leads the nidus for atrial myxoma

Atrophic & Hypertrophic" myocytes combination is characteristic of DCM.

also pt is showing symptoms of CHF with decreased Ef and blood backing up.
17DD.is the right answer

DVT from bed rest leading to Pulmonary Infarction

A in bronchopneumonia the lung has patchy are of consolidation

B in lobar pneumonia lower lobe is consolidated

C in lung abscess the lung will be filled in necrotic tissue

E in pulmonary metastasis there is multiple nodule in the lungy

18A
19B

Although several substances have been investigated as potential mediators of anginal pain, at
present only two molecules have been convincingly demonstrated to be involved in the genesis of
cardiac ischemic pain in man: adenosine and bradykinin....As bradykinin is released in large
amounts by the heart during ischemia, it can be a natural stimulus for causing, via arachidonic
acid metabolites, excitation of the sensory receptors signaling pain during myocardial ischemia."

atherosclerosis = blockage of blood supply to heart

therefore heart does not get nutrients and 02.

whenever heart contracts it uses ATP.

where does ATP come from? glycolysis and 02.

since we blocked off nutrients and 02, myocytes try to make ATP by anaerobic metabolism.
Anaerobic metabolism increases lactic acid production.

increased lactic acid potentiates bradykinin.

bradykinin = pain.

http://www.uptodate.com/patients/content/topic.do?topicKey=~GSM9MBDcFS

mechanism of angina

ischemia reduces the formation of adenosine triphosphate (ATP), resulting in the development of
acidosis, the loss of the normal ATP sodium-potassium pump, the loss of myocardial membrane
integrity, and the release of chemical substances that stimulate chemosensitive and mechanoreceptive
receptors innervated by unmyelinated nerve cells found within cardiac muscle fibers and around the
coronary vessel The substances that are released include lactate, serotonin, bradykinin, histamine,
reactive oxygen species, and adenosine In addition there are substances released from platelets, which
often spontaneously aggregate in the area of a coronary artery stenosis, which may also be responsible
for myocardial ischemia and angina. These include serotonin, thromboxane A2, and 5-
hydroxytyrptamine [

Mechanisms of pain in angina pectorisA critical review of the adenosine hypothesis

There is substantial evidence that the primary mediator of angina is adenosine, via stimulation of the
A1 adenosine receptor [11-14]. It is also possible that venodilation as a response to ischemia can
activate these receptors. The nerve fibers travels along the sympathetic afferent pathways from the
heart and enter the sympathetic ganglia in lower cervical and upper thoracic spinal cord (C7-T4).
Impulses are then transmitted via the ascending spinothoracic pathways to the medial and lateral
thalamus and ultimately activate several areas of the cerebral cortex

20DDDD

i read it somewhere that even though there is increased in ventilation and metabolic rate during exercise
but these parameters stay close to normal(PaO2,PaCO2 and pH).

increase CO
increase Respiratory rate (increased PAO2---> increased A-a gradient--->increased diffusion)
increase O2 extraction by muscles---> decreased PO2 of mixed venous blood
improved V/Q mismatch( opens up more capillaries and alveoli)

CO and Resp. rate are adjusted according to the metabolic rate.

21A
b) is essential for male reproductive devt -- 3 things have to have for male normal devt ( SRY Gene on
Y chr, MIF, androgen) while female fetus does not require any factors for reproductive devt

22D
23D
-on the Y axis...minute ventilation ( Minute Ventilation =TIDAL VOLUME x BREATHS/MIN)
on the X axis inspired oxygen concentration

Factors affecting minute ventlation are depth of breathing and Rate of breathing as we can see in the
formula.
And the ones which regulate these factors (depth and rate of breathing ) are Central Chemoreceptors
and Peripheral Chemoreceptors.

Central chemoreceptors (MEDULLA )directly monitor and and are stimulated by CSF H+ and CO2....
Whereas Peripheral Chemoreceptors (Carotid bodies and Aortic Bodies..the carotid one is the most
important ) respond to both PO2 and H+/CO2 ...but mainly respond to low level of oxygen in the
blood....PO2 < 60 MMHG

Hence in this graph we are looking for the response of Carotid Bodies in response to the level of
Oxygen...The way to read the graph is from right to left (which means from high inspired oxygen
concentration to low oxygen concentration ...as WE go from right to left on the normal graph we see an
increase(which was constant ) in minute ventilation because of a decrease in PO2 < 60 mmhg (this
response is mediated by carotid bodies)...

So in the experimental animal we removed the carotid bodies and there is no response (increase ) in
minute ventilation if there is a decrease in the PO2 ...which is DDDD

The key is to read the graph from right to left on the x axis (not the usual left to right )

Carotid bodies are peripheral chemoreceptors that sense Oxygen. When oxygen is on the between 100-
60 mmHg they are of little if any importance ( the flat limb of the priginal graph ) and they will start
firing when the oxygen saturation is dramatically low below 50 mmHg increasing ventilation the ( the
upward limb of the original graph)

When you remove the carotid bodies there will be no response to the decreased oxygen so the curve is
expected to be flat as in response D
24C lung underdevelopment lung due to oligohydramnios. An appropriate volume of amniotic fluid
(produced by the kidneys) is necessary for complete and proper branching of the bronchial tree and
alveoli
25ATHE ASCENDING AND DESCENDING COLON(BUT NOT SIGMOID AND transverse colon)

Duodenum-2nd n 3 rd parts(but not 1st n 4 th parts)

Pancreas-head,neck n body (but not tail ) are retro -peritoneal.

Primarily retroperitoneal:
o urinary
adrenal glands
kidneys
ureter
bladder
o circulatory
aorta
inferior vena cava
o digestive
esophagus (part)
rectum
o Reproductive
uterus
Secondarily retroperitoneal:
o the head and neck of the pancreas (but not the tail)[1]
o the duodenum, except for the proximal first segment[2]
o ascending and descending portions of the colon
26D
27C
28FIn menopause the decreased estrogen causes a decrease in Sex Hormone Binding Globulin
(SHBG), thus increasing FREE TESTOSTERONE (not total testosterone, which stays normal). This
increased FREE TESTOSTERONE and related decreased FREE ESTROGEN are causing her
hirsutism. Its a ratio thing.
29F
cclusion or lesion of pit stalk -- decreased secretion if all ant and post pit hr except prolactin which is
controlled by inhibitory effects of dopamine ( chr inhibitory source of inhibition of PIF is removed)

Panhypopituitarism--The anterior pituitary produces the hormones thyrotropin (thyroid-stimulating

hormone [TSH]), corticotropin (adrenocorticotropic hormone [ACTH]), luteinizing hormone (LH),
follicle-stimulating hormone (FSH), growth hormone (GH), and prolactin (PRL). The posterior
pituitary produces vasopressin (antidiuretic hormone [ADH]) and oxytocin.
Prolactin hormone counteracts the effect of
dopamine, which is responsible for sexual arousal. This is thought to cause the sexual refractory period.
[3] The
amount of prolactin can be an indicator for the amount of sexual satisfaction and relaxation. Unusually
high
amounts are suspected to be responsible for impotence and loss of libido (see hyperprolactinemia
Symptoms).
Prolactin also stimulates proliferation of oligodendrocyte precursor cells. These cells differentiate into
oligodendrocytes, the cells responsible for the formation of myelin coatings on axons in the central
nervous
system.[

30A
31C
32B
well capillary hydrostatic pressure increase will promote more fluid to move out of the capillary and
increased lymph volume.

the fluid in the interstitium flows to lymph vessel by direct diffussion..more fluid available in
interstitium more lymph flow...now here is the catch if the fluid is hyptonic to lymph then only fluid
will enter lymp vessel..lymph is isotonic with plasma

option b,c,d,e all will make interstitium hypotonic but if colloid osmotic pressure is low fluid will
return to the vessel...so colloid osmotic pressure is most important in guiding lymph flow.
.. D n E- it plasma along with some proteins wil come out.
which may increae the lymph flow along with increasing its protein content.

C- increase in resistance wil decrease flow right ?

this the reason isotonic fluid is not adviced in septic shock as it will add up the edema..usually albumin
infusion is given in septic shock..septic shock increases the cappillary permeability leading to edema

33C this is gonococcal urethritis and the co

mplications of gonococcal urethritis are mainly to reproductive organs ...like epidydimis,prostate ...If it
had been Ecoli urethritis more of urinary organs get the complication ...hence i think epidydimitis is the
better choice as the complication of gonococcal urethritis.
male--epididymis (epididymitis); prostate gland (prostatitis) and urethral structure (urethritis
pelvic inflammatory disease, - infertility.
Other perihepatitis,[7] a rare complication associated with Fitz-Hugh-Curtis syndrome; septic arthritis in
the fingers, wrists, toes, and ankles; septic abortion; chorioamnionitis during pregnancy,neonatal or
adult blindness from conjunctivitis; and infertility
34Chttp://medicineworld.org/images/renal-cell-cancer.jpg
multiple and/or bilateral, with median age 45 yrs at diagnosis/autosomal /associated with the Von
Hippel-Lindau syndrome, and the Lynch syndrome IIdominant

35G Parietal cells secrete HCl and intrinsic factor. Which stimulated by Ach, gastrin, and histamine
g.parietal cells
a- secrete alkaline mucus to neutralize acid
b- A nonsecretory cell of a pancreatic ductule occupying the lumen of an acinus. Also calledLangerhans
cell.secrete bicarbonate
c-Enteroendocrine cells
the contents of the gland lumen and release their hormones based on their sensing response.
d- secrete pepsinogen
e-mucus secretion
f.Paneth cells provide host defense against microbes in the small intestine. They are functionally similar
to neutrophils. When exposed to bacteria or bacterial antigens, Paneth cells secrete a number of
antimicrobial molecules into the lumen of the crypt, thereby contributing to maintenance of the
gastrointestinal barrier.
h. secrete mucus

36Bb glucose wld increase after eating carbohydrate.

A starch digestion
c. any one, or the mixture, of the water-soluble, intermediate polysaccharides formed during the
hydrolysis of starch to sugar.and a preparation of such formed by boiling starch and used in pharmacy
d-a polymer of sugar acids of fruit that forms gels with sugar at the proper pH; a purified form obtained
from the acid extract of the rind of citrus fruits or from apple pomace is used as an antidiarrheal and as
a pharmaceutic aid.
E-sucrose made from fructose and glucose.

37CFF = GFR/RPF
Increased glomerular hydrostatic pressure due to efferent constriction will increase GFR
Increased resistance would decrease flow (remember: flow = pressure gradient/resistance)
Hence, filtration fraction will increase due to the increased GFR and decreased RBF
38E
39C http://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/A83_Alveoli_TypeI...&II_40X.jpg
40A
41Ee ..meckel diverticulum.
a.small bowel obstruction related ?
b. Absent intestinal muscularis - Neonatal gastrointestinal perforation Neonatal intestinal obstruction
c.failure of normal recanalization-Intestinal obstruction - Intestinal atresia - Duplication Newborn
d-The term malrotation is used when the normal process of rotation and fixation of the midgut goes
awry. Malrotation may lead to 2 critical complications: mechanical obstruction of the proximal
intestine and ischemia of part or all of the mid

42D Gilbert-elevated level of unconjugated bilirubin because of reduced activity of the enzyme
glucuronyltransferase- no serious consequences-Mild jaundice may appear under conditions of
exertion, stress, fasting, and infections.
43D[6:56:29 PM] Jagraj: Bitemporal hemianopsia (or Bitemporal hemianopia) is the medical
description of a type of partial blindness
where vision is missing in the outer half of both the right and left visual field. It is usually associated
with
lesions of the optic chiasm, the area where the optic nerves from the right and left eyes cross near the
pituitary
gland.
44D is D
reference BRS patho pg 128
medium and large size arteries @ aortic arch and branches imflamation and stenosis: aortic branch
syndrome
clinical: absent pulses
related to this low BP in upper limbs, claudication(no suficient blood reaching these limbs)
non specific fever, night sweats, malaise,myalgia,arthritis,arthralgia, eye problems and paiful skin
nodules
young asian females
angiogram corkscrew,widened aorta
the other giant cell arteritides is Temporal arteritis

akayasu's arteritis is an inflammatory disease of unknown etiology that affects the aorta and its
branches.
Although it has been reported worldwide, it shows a predilection for young Asian women. Females
with this
disease outnumber males by 8-9:1
Patients may have lower blood pressure and pulses in the upper extremities as compared to the lower
extremities, and cold or numb fingers.
Weak upper extremity pulses may be found

This large-vessel vasculitis predominantly involves the aorta and its proximal branches.

Histologically, the lesions in Takayasu arteritis are similar to giant cell arteritis.

45C
46DD) 2
During expiration, the lungs have a positive pressure causing the alveoli to collapse, while the chest
wall puts an opposing negative preuusre on the lungs.. Expiration ends when these two pressures are
equal (and opposite).. In the figure, this occurs at a volume of 2L. because at the end of expiration
mean F R C and this volume is in the middle of lung curve and chest wall curve and when you see the
both curves you notice that they have the same NO at the middle of both of them ,- similar graph in
Kaplan book
q46-the question asks the value of Functional Residual Capacity...(volume of gas in the lungs at the end
of passive expiartion ,the neutral point for the respiratory system....At FRC the forces on the chest wall
and lung are in equilibrum(that means the pressure on both systems cancels out at FRC) ...
so let us try the pressures on the chest wall and lung at the given volumes in the choice
A-Volume 0.5 ....Pressure on the chest wall -20 ,pressure in the lung + 5...not canceled out
B-Volume 1 .......Pressure on the chest wall -17 ,pressure in the lung +7...not canceled out
C-volume 1.5....pressure on the chest wall - 14,pressure in the lung + 8...not canceled out
D-Volume 2......pressure on the cheast wall -10 ,pressure in the lung + 10..canceled out
E-Volume 2.5..pressure on the chest wall -5 ,pressure in the lung +13,not canceled out
Hence the answer in my thinking is DDDD as it the volume of the gas in the liungs where the forces are
at equilibrum (FRC )...

47A--If bronchioli are obstructed, the space beyond them would have very little oxygen, and whatever
oxygen is there it would be carried out by the pulmonary veins. Also they would bring the CO2 there.
Respiratory acidosis: hypercapnia hypoxia.. in Alvioli beyond the obstruction , there is no gas exchange
, therefor pO2 and pCO2 will reach there values in mixed venous blood which are 40 - 46 respectufully
48D
49ECRF-->Decreased Vit-D--->Decreased Calcium--->Secondary Hyper-Parathyroidism---
>However,The increased po4 excretion action of PTH does not occur due to inability of the kidney to
excrete po4.

So,Lab will look like increased po4 and decreased Calcium.

Phosphate Retention Occurs very early in the Disease which doesnt lead to High Serum due to Inc.
Serum PTH which leads to Phosphate excretion. But later on as the GFR decs the Renal Excretion of
Phospate decs.

Hyperphosphatemia suppresses the renal hydroxylation of inactive 25-hydroxyvitamin D to calcitriol,

so serum calcitriol levels are low when the GFR is less than 30 mL/min. Hypocalcemia develops
primarily from dec. intestinal calcium absorption because of low plasma calcitriol levels and possibly
from calcium binding to elevated serum levels of phosphate.If serum levels of PTH remain elevated,
osteitis fibrosa develops.

Other Findings Include: Hyperkalemia, low serum bicarbonate, hypocalcemia, hyperphosphatemia,

hyponatremia (in ESRD with free-water excess)
50C

[10:46:27 PM] Meryum: cozzsplicing provides a mechanism for producing a wide variety of proteins
from a small number of genes. While we humans may turn out to have only some 23 thousand genes,
we probably make at least 10 times that number of different proteins. It is now estimated that 92-94%
of our genes produce pre-mRNAs that are alternatively-spliced. There is evidence that the pattern of
alternative splicing differs consistently in different tissues and so must be regulated. But whether all the
products are functional or that many are simply the outcome of an error-prone process remains to be
seen.

[10:36:29 PM] Meryum: Antibody induced with polysaccharide vaccines has less functional activity
than that induced by protein antigens. This is because the predominant antibody produced in response
to most polysaccharide vaccines is IgM, and little IgG is produced.
[10:37:13 PM] Meryum: http://www.immune.org.nz/?t=916
T-cell independent antigens, including polysaccharide vaccines, are not consistently immunogenic in
children <2 years of age. Young children do not respond consistently to polysaccharide antigens,
probably because of immaturity of the immune system.
[11:04:10 PM] Meryum: so if we consider A
[11:04:40 PM] Meryum: it wouldnt elicit igm
[11:04:42 PM] Meryum: in kids