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  #1  
Old 12-03-2014
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RBC My NBME 15 DISCUSSION!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Just took my nbme 15, and want to solve every quetion, and understand where occur my mistake in solving, one thing is that i do it very rapidly, remaining about 10 to 15 minutes free after every block...
Who want and know corect answers please be actively here...
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  #2  
Old 12-03-2014
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Post Kidney

what is with this child kidney? if coraliform stones is incorect, that Hydronephrosis?
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Post Hi

Quote:
Originally Posted by sashabeliimd View Post
what is with this child kidney? if coraliform stones is incorect, that Hydronephrosis?
Of course Hydronephrosis, because on image is seen atrophy of the cortex, classic presentation...
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Quote:
Originally Posted by sashabeliimd View Post
Of course Hydronephrosis, because on image is seen atrophy of the cortex, classic presentation...
The classic presentation and what is shown in the picture is actually distention/DILATION of the renal pelvis and calyces im not sure you can figure out where the compression atrophy is taking place in this picture. The dilation is pretty self-evident tho.
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Quote:
Originally Posted by 10blade View Post
The classic presentation and what is shown in the picture is actually distention/DILATION of the renal pelvis and calyces im not sure you can figure out where the compression atrophy is taking place in this picture. The dilation is pretty self-evident tho.
It depends on what stage of disease, patient is investigates, you know stones formation is not a 1 day process...

Dilation of calyces is related to progreession of disease..
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Quote:
Originally Posted by sashabeliimd View Post
It depends on what stage of disease, patient is investigates, you know stones formation is not a 1 day process...

Dilation of calyces is related to progreession of disease..
stone formation is what will lead to the distention of the caayces due to fluid accumulation within those areas. Which is where HYDRO comes from. the Distension LEADS to compression atophy, so it comes LATER, from the subsequent pressure exerted on the renal parnechyma.

Watch pathoma.
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Thumbs Up Hi

Quote:
Originally Posted by 10blade View Post
stone formation is what will lead to the distention of the caayces due to fluid accumulation within those areas. Which is where HYDRO comes from. the Distension LEADS to compression atophy, so it comes LATER, from the subsequent pressure exerted on the renal parnechyma.

Watch pathoma.
I know man, obstruction of urine pathway, and decreased glomerular filtration rate, renal plasma flow remain same, function of glomeruli will decrease, and also ATROPHy will occur...
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Default Anatomy

A little anatomy..,
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Post Metal worker

A 35 year old metal worker collapses after exposure to an unknown chemical at a factory. He is dyspneic but is noncyanotic and smells of burnt almonds. The most appropiate nextt step is to administer which of the following???

Amyl nitrite
Errythopoietin
Ethanol
Hyperbaric oxygen wrong
Physiostigmine
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  #10  
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Star Vaccines

The vaccine against diphtheria confers protective immunity by inducing the formation of antibodies against a preparation composed of which of the follwing?????

Killed bacterial cell
Live attenuated wrogn
Purified bacterial peptidoglycan
Purified capsular polysaccharide
Purified inactivated toxin
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  #11  
Old 12-04-2014
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Post Hi

Hey please someone , explane posted nbme tests...
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Post Hi

Pain related to developed peritonitis...

Common examples of referred pain are scapular pain due to biliary colic

groin pain due to renal colic

shoulder pain due to blood or infection irritating the diaphragm.
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Correct Answer Hi

Quote:
Originally Posted by sashabeliimd View Post
The vaccine against diphtheria confers protective immunity by inducing the formation of antibodies against a preparation composed of which of the follwing?????

Killed bacterial cell
Live attenuated wrogn
Purified bacterial peptidoglycan
Purified capsular polysaccharide
Purified inactivated toxin
PUrified inactivated toxin

Diphtheria vaccine is based on purified diphtheria toxin that is chemically inactivated. The inactivated toxin is referred to as a toxoid. As it is the toxin rather than the bacterium that causes the majority of diphtheria symptoms, producing antibodies to the toxin protects against symptomatic disease even though it does not prevent infection with the bacteria.
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Default Hi

Quote:
Originally Posted by sashabeliimd View Post
A little anatomy..,

Internal sphincter muscle of urethra

Anatomical terms of muscle
The internal sphincter muscle of urethra is a urethral sphincter muscle which constricts the internal urethral orifice. It is the junction of the urethra with the urinary bladder. The muscle is made of smooth muscle, so therefore it is under involuntary control. It is kept tonically contracted by Lumbar plexus of the sympathetic nervous system.

Function[edit]
During micturition it is relaxed via branches from the pelvic plexus (S2-S4) parasympathetic nervous system. This is the primary muscle for maintenance of continence of urine. Its two major roles are:

Prevent urine leakage as the muscle is contracted via sympathetic stimulation (via the Inferior hypogastric plexus).
During ejaculation, the contraction of the muscle prevents reflux of semen in the urinary bladder
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A previously healthy 48-year-old man is brought to the emergency department
because of a 1-hour history of nausea and crushing chest pain that radiates to his
left arm. An ECG and evaluation of serum cardiac enzyme activity confirm a
diagnosis of a myocardial infarction of the anterior wall. Fourteen hours after
arrival, he has a cardiac arrest. Resuscitation efforts are successful after
approximately 30 minutes. He then immediately develops severe oliguria. Serum
studies show increased urea nitrogen and creatinine concentrations. Microscopic
examination of this patient's urine is most likely to show which of the following?
A) Degenerating epithelial cells and dirty brown granular casts
B) Degenerating WBCs and colorless hyaline casts
C) Dysmorphic RBCs and yellow granular casts
D) Lymphocytes and RBC casts
E) Numerous eosinophils and red hyaline casts
F) WBCs and RBC casts

Problems with heart, means some ischemia to kidneys., >>>> acute tubular necrosis Key findings, muddy brown, granular casts...
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Correct Answer Hi

24) A 75-year-old woman is brought to the physician because of a 1-day history of fever and back pain. Her temperature is 39.5°C (103.1°F), pulse is 111/min, respirations are 32/min, and blood pressure is 115/79 mm Hg. Physical examination shows left-sided costovertebral angle tenderness. Laboratory studies show a leukocyte count of 17,000/mm3 (with 9% bands) and pyuria. Urine cultures grow Escherichia coli. It is determined that the patient's fever is partially due to interleukin-6 (IL-6), which was induced by the IL-1 produced during the immune response. Which of the following best describes the role of I
κ
B in the nuclear factor-kappa B (NF-κB) signal transduction pathway from IL-1 binding to IL-6 induction in this patient?


Attaches to cytokine receptor Facilitates proteolytic cleavage of NF-
κ
B dimers Phosphorylates NF-
κ
B Releases NF-
κ
B after undergoing phosphorylation Translocates to the nucleus after undergoing phosphorylation


Releases NF-κB after undergoingphosphorylation



Phosphorylation of NF-kappaB and IkappaB proteins: implications in cancer and inflammation.
Viatour P1, Merville MP, Bours V, Chariot A.
Author information
Abstract
Nuclear factor-kappaB (NF-kappaB) is a transcription factor that has crucial roles in inflammation, immunity, cell proliferation and apoptosis. Activation of NF-kappaB mainly occurs via IkappaB kinase (IKK)-mediated phosphorylation of inhibitory molecules, including IkappaBalpha. Optimal induction of NF-kappaB target genes also requires phosphorylation of NF-kappaB proteins, such as p65, within their transactivation domain by a variety of kinases in response to distinct stimuli. Whether, and how, phosphorylation modulates the function of other NF-kappaB and IkappaB proteins, such as B-cell lymphoma 3, remains unclear. The identification and characterization of all the kinases known to phosphorylate NF-kappaB and IkappaB proteins are described here. Because deregulation of NF-kappaB and IkappaB phosphorylations is a hallmark of chronic inflammatory diseases and cancer, newly designed drugs targeting these constitutively activated signalling pathways represent promising therapeutic tools.
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Correct Answer Hi

3) An investigator is studying Helicobacter pylori stains isolated from the same patient over several years. The immune response to proteins produced by these strains is observed. It is found that the original H. pylori isolate from the patient expresses one protein recognized by the patient's antibodies, but subsequent isolates do not express this protein. Sequencing of the gene encoding the protein from the original and subsequent isolates is done. It is found that subsequent isolated have nine consecutive cytidine residues, whereas the original isolate has eight. The results are show.

Original isolate:
... ACC CCC CCC ACT CAA ATT GAA CCT AGC ....
... Thr Pro Pro Thr Gln lle Glu Pro Ser .....

Subsequent isolates:
... ACC CCC CCC CAC TCA AAT TGA ACC TAG ...
... Thr Pro Pro His Ser Asn STOP

Which of the following mechanisms best explains this genetic change?
A) Crossing over
B) DNA excision repair
C) Slipped-strand mispairing
D) Thymidine dimer formation
E) Transposon insertion

Slipped-strand mispairing may cause deletions resulting in frameshift mutation
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27) An investigator wishes to test the hypothesis that a number of CD44 splice variants correlate with aggressive disease progression and risk of relapse in patients with Hodgkin disease, especially if the variant protein CD44v10 is expressed. The investigator plans to retrospectively screen archives of fresh frozen tissue and paraffin-embedded biopsy specimens from documented Hodgkin disease patients. Assuming the necessary reagents are available, which of the following methods would be the most effective in screening the archives for the variant protein?

Affinity column chromatography Density gradient centrifugation Immunohistochemistry
Northern blot
Polymerase chain reaction (PCR)
Reverse transcriptase
PCR
Southern blot



Immunohistochemistry or IHC refers to the process of detecting antigens (e.g., proteins) in cells of a tissue section by exploiting the principle of antibodies binding specifically to antigens in biological tissues.[1] IHC takes its name from the roots "immuno," in reference to antibodies used in the procedure, and "histo," meaning tissue (compare to immunocytochemistry). The procedure was conceptualized and first implemented by Dr. Albert Coons in 1941.[2]

Immunohistochemical staining is widely used in the diagnosis of abnormal cells such as those found in cancerous tumors. Specific molecular markers are characteristic of particular cellular events such as proliferation or cell death (apoptosis). IHC is also widely used in basic research to understand the distribution and localization of biomarkers and differentially expressed proteins in different parts of a biological tissue.
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Fire Thread

34) A healthy 25-year-old man participates in a study of muscle function. The electrophysiologic observations made on a muscle biopsy specimen are shown. Via iontophoresis, 1
μ
M acetylcholine (ACh) was applied to the muscle surface. Extracellular Ca2+ concentration was decreased to prevent end-plate potentials from acting as a suprathreshold for muscle action potentials. epp Amplitude mepp Amplitude Response (in mV) to ACh (in mV) (in mV) (1
μ
M) Normal muscle 10 1 1 epp=end-plate potential; mepp= miniature epp Based on these findings, which of the following electrophysiologic characteristics is expected in a muscle biopsy specimen from a patient with acute botulism? epp Amplitude mepp Amplitude Response (in mV) to ACh (in mV) (in mV) (1
μ
M)

A)1 0.5 0.5

B)1 1 1 >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

C)2 0.2 0.2

D)5 0.2 0.1

E)15 1 1

can anybody explane why???? B
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Correct Answer

13. A 59-year-old man comes to the physician because of a 10-day history of shortness of breath, fatigue, and cough. His respirations are 12/min. The lungs are clear to auscultation and percussion. Laboratory studies show: Hemoglobin 11.8 g/dL Hematocrit 36% Leukocyte count 146,400/mm3 Segmented neutrophils 47% Bands 12% Eosinophils 1% Basophils 5% Lymphocytes 2% Monocytes 2% Metamyelocytes 7% Myelocytes 18% Prornyelocytes 2% Other cells 4% Platelet count 804,000/mm3 Which of the following is the most appropriate pharmacotherapy for this patient?


A) Anti-interleukin-S (IL-5)
B) Cytarabine
C) Hydroxyurea

D) lmatinib >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

E) Interferon alfa


Patient have chronic myelocytic leukemia


Imatinib (INN), marketed by Novartis as Gleevec (Canada, South Africa and the USA) or Glivec (Australia, Europe and Latin America), and sometimes referred to by its investigational name STI-571, is a tyrosine-kinase inhibitor used in the treatment of multiple cancers, most notably Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML).[1]

In order to survive, cells need signaling through proteins (signal cascade) to keep them alive. Some of the proteins in this cascade use a phosphate group as an "on" switch. This phosphate group is added by a tyrosine kinase enzyme. In healthy cells, these tyrosine kinase enzymes are turned on and off as needed. In Ph-positive CML cells, one tyrosine kinase enzyme, BCR-Abl, is stuck on the "on" position, and keeps adding phosphate groups. Imatinib blocks this BCR-Abl enzyme, and stops it from adding phosphate groups. As a result, these cells stop growing, and even die by a process of cell death (apoptosis).[2] Because the BCR-Abl tyrosine kinase enzyme exists only in cancer cells and not in healthy cells, imatinib works as a form of targeted therapy—only cancer cells are killed through the drug's action.[3] In this regard, imatinib was one of the first cancer therapies to show the potential for such targeted action, and is often cited as a paradigm for research in cancer therapeutics.[4]


Imatinib, Mechanism of action: philadelphia chromosome bcr-abl tyrosine kinase inhibitor...
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  #21  
Old 12-04-2014
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Star Hi

Quote:
Originally Posted by sashabeliimd View Post
34) A healthy 25-year-old man participates in a study of muscle function. The electrophysiologic observations made on a muscle biopsy specimen are shown. Via iontophoresis, 1
μ
M acetylcholine (ACh) was applied to the muscle surface. Extracellular Ca2+ concentration was decreased to prevent end-plate potentials from acting as a suprathreshold for muscle action potentials. epp Amplitude mepp Amplitude Response (in mV) to ACh (in mV) (in mV) (1
μ
M) Normal muscle 10 1 1 epp=end-plate potential; mepp= miniature epp Based on these findings, which of the following electrophysiologic characteristics is expected in a muscle biopsy specimen from a patient with acute botulism? epp Amplitude mepp Amplitude Response (in mV) to ACh (in mV) (in mV) (1
μ
M)

A)1 0.5 0.5

B)1 1 1 >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

C)2 0.2 0.2

D)5 0.2 0.1

E)15 1 1

can anybody explane why???? B
It;s simple in reality, because all remain same, out of amplitude on graph of action potential, because receptors are busy with antibodies binded to them and do not respond as well as without those antibodies...
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  #22  
Old 12-04-2014
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Post Hi

A signal for insulin


In islet beta cells, glucokinase activity serves as a principal control for the secretion of insulin in response to rising levels of blood glucose. As G6P is consumed, increasing amounts of ATP initiate a series of processes that result in release of insulin. One of the immediate consequences of increased cellular respiration is a rise in the NADH and NADPH concentrations (collectively referred to as NAD(P)H). This shift in the redox status of the beta cells results in rising intracellular calcium levels, closing of the KATP channels, depolarization of the cell membrane, merging of the insulin secretory granules with the membrane, and release of insulin into the blood.

It is as a signal for insulin release that glucokinase exerts the largest effect on blood sugar levels and overall direction of carbohydrate metabolism. Glucose, in turn, influences both the immediate activity and the amount of glucokinase produced in the beta cells.

Regulation in beta cells[edit]
Glucose immediately amplifies glucokinase activity by the cooperativity effect.

A second important rapid regulator of glucokinase activity in beta cells occurs by direct protein-protein interaction between glucokinase and the "bifunctional enzyme" (phosphofructokinase-2/fructose-2,6-bisphosphatase), which also plays a role in the regulation of glycolysis. This physical association stabilizes glucokinase in a catalytically favorable conformation (somewhat opposite the effect of GKRP binding) that enhances its activity.

In as little as 15 minutes, glucose can stimulate GCK transcription and glucokinase synthesis by way of insulin. Insulin is produced by the beta cells, but some of it acts on beta cell B-type insulin receptors, providing an autocrine positive-feedback amplification of glucokinase activity. Further amplification occurs by insulin action (via A-type receptors) to stimulate its own transcription.

Transcription of the GCK gene is initiated through the "upstream," or neuroendocrine, promoter. This promoter, in contrast to the liver promoter, has elements homologous to other insulin-induced gene promoters. Among the probable transacting factors are Pdx-1 and PPARγ. Pdx-1 is a homeodomain transcription factor involved in the differentiation of the pancreas. PPARγ is a nuclear receptor that responds to glitazone drugs by enhancing insulin sensitivity.

Association with insulin secretory granules[edit]
Much, but not all, of the glucokinase found in the cytoplasm of beta cells is associated with insulin secretory granules and with mitochondria. The proportion thus "bound" falls rapidly in response to rising glucose and insulin secretion. It has been suggested that binding serves a purpose similar to the hepatic glucokinase regulatory protein—protecting glucokinase from degradation so that it is rapidly available as the glucose rises. The effect is to amplify the glucokinase response to glucose more rapidly than transcription could do so.[20]
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Old 12-04-2014
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gen l/a,ct=enlage paraaortic ln, bx=prolif histiocyte neutrophil,AFB[MAI] IG A,IG G, IG M, B,T LYMPHOCYTE,CD4,CD8 [ALL NORMAL] DEFECTIVE PROTEIN? A.MHC 1
B. IFN GAMMA
C.NADPH OXIDASE
D. LEUCOCYTE FUN ASSO ANTIGEN 1 FEVER, BACK PAIN,103 F.PR 111, RES32,BP 115/79, L CVA TENDER, WBC 17000, PYURIA, E COLI, F

Persistent Mycobacterium avium infection following nonmyeloablative allogeneic peripheral blood stem cell transplantation for interferon-gamma receptor-1 deficiency.
Horwitz ME1, Uzel G, Linton GF, Miller JA, Brown MR, Malech HL, Holland SM.
Author information
Abstract
Interferon-gamma receptor-1 (IFNgammaR1) deficiency is a rare inherited immunodeficiency. We performed a nonmyeloablative allogeneic stem cell transplantation on a boy with complete IFNgammaR1 deficiency and refractory disseminated Myco- bacterium avium infection. Despite the patient's profound immune defect, early donor stem cell engraftment was low. Full donor engraftment was accomplished only following multiple donor lymphocyte infusions. Detection of IFNgammaR1 expression on peripheral blood monocytes and neutrophils corresponded with establishment of stable, complete donor hematopoietic chimerism. However, expression of, and signaling through IFNgammaR1 disappeared shortly thereafter. Disseminated Mycobacterium avium infection persisted and the patient died. Coculture of Myco- bacterium avium with normal myeloid cells resulted in an IFNgamma signaling defect similar to that observed in vivo. Active disseminated Mycobacterium avium infection may significantly compromise normal immune reconstitution following allogeneic stem cell transplantation. Patients with IFNgammaR1 deficiency should receive transplants before developing refractory mycobacterial infections.
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Old 12-05-2014
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Listening Carbon dioxide affinity

Which of the following best explains why deoxygenated blood can carry more carbon dioxide for a given Poo, than oxygenated blood?
A) Deoxyhemoglobin does not bind to 2.3-bisphosphoglycerate as efficiently as oxyhemoglobin
B) Deoxyhemoglobin has a lower capacity to form carbamino compounds than oxyhemoglobin
C) Deoxyhemoglobin has a lower pKa than oxyhemoglobin 0) Deoxyhemoglobin is a better buffer of hydrogen ions than oxyhemoglobin
E) Oxygen and carbon dioxide compete for the same binding site in hemoglobin (wrong)
F) Oxyhemoglobin binds nitric oxide with a higher affinity than deoxyhemoglobin
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Old 12-05-2014
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Romania Hi

Quote:
Originally Posted by forza-interna View Post
Which of the following best explains why deoxygenated blood can carry more carbon dioxide for a given Poo, than oxygenated blood?
A) Deoxyhemoglobin does not bind to 2.3-bisphosphoglycerate as efficiently as oxyhemoglobin
B) Deoxyhemoglobin has a lower capacity to form carbamino compounds than oxyhemoglobin
C) Deoxyhemoglobin has a lower pKa than oxyhemoglobin 0) Deoxyhemoglobin is a better buffer of hydrogen ions than oxyhemoglobin
E) Oxygen and carbon dioxide compete for the same binding site in hemoglobin (wrong)
F) Oxyhemoglobin binds nitric oxide with a higher affinity than deoxyhemoglobin



Hemoglobin
The oxygen-carrying molecule of the red blood cells of vertebrates. This protein represents more than 95% of the solid constituents of the red cell. It is responsible for the transport of oxygen from the lungs to the other tissues of the body and participates in the transport of carbon dioxide in the reverse direction.

Each molecule of hemoglobin comprises four smaller subunits, called polypeptide chains. These are the protein or globin parts of hemoglobin. A heme group, which is an iron-protoporphyrin complex, is associated with each polypeptide subunit and is responsible for the reversible binding of one molecule of oxygen. The polypeptide chains and the heme are synthesized and combine together in nucleated red cells of the bone marrow. As these cells mature, the nuclei fragment and the cells, now called reticulocytes, begin to circulate in the blood. After sufficient hemoglobin has been formed in the reticulocyte, all nuclear material disappears and the cell is then called an erythrocyte, or red blood cell. Each hemoglobin molecule lasts as long as the red cell, which has an average life of 120 days. See Porphyrin

Normal adult males and females have about 16 and 14 g, respectively, of hemoglobin per 100 ml of blood; each red cell contains about 29 × 10-12 g of hemoglobin. Red cells normally comprise 40–45% of the volume of whole blood.

The reversible combination of hemoglobin and oxygen can be represented by the reaction shown below. The equilibrium constants for each step are not the same because an oxygen molecule on one heme group changes the affinity of the other hemes for additional oxygen molecules. This alteration in binding affinity during oxygenation is called heme-heme interaction and is due to small changes in the three-dimensional structure of the molecule.

Hemoglobin combines reversibly with carbon monoxide about 210 times more strongly than with oxygen. This strong affinity for carbon monoxide accounts for the poisoning effects of this gas.

Hemoglobin binds carbon dioxide by means of free amino groups of the protein but not by the heme group. The reversible combination with carbon dioxide provides part of the normal blood transport of this gas. Hemoglobin serves also as a buffer by reversible reactions with hydrogen ions. The acidic property of oxyhemoglobin is greater than deoxygenated hemoglobin. The extra binding of hydrogen ion by deoxyhemoglobin promotes the conversion of tissue carbon dioxide into bicarbonate ion and thus increases the amount of total carbon dioxide which can be transported by blood
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  #26  
Old 12-06-2014
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Quote:
Originally Posted by sashabeliimd View Post
A 35 year old metal worker collapses after exposure to an unknown chemical at a factory. He is dyspneic but is noncyanotic and smells of burnt almonds. The most appropiate nextt step is to administer which of the following???

Amyl nitrite
Errythopoietin
Ethanol
Hyperbaric oxygen wrong
Physiostigmine
Amyl Nitrite is the answer, burnt almond is related to cyanide intoxication..
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  #27  
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Quote:
Originally Posted by sashabeliimd View Post
A little anatomy..,
ans is ureteric orifice i got it right
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Quote:
Originally Posted by sashabeliimd View Post
A 35 year old metal worker collapses after exposure to an unknown chemical at a factory. He is dyspneic but is noncyanotic and smells of burnt almonds. The most appropiate nextt step is to administer which of the following???

Amyl nitrite
Errythopoietin
Ethanol
Hyperbaric oxygen wrong
Physiostigmine
amyl nitrite. smell of burnt almond is cyanide poisoning plus he is non cyanotic
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