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Description: APPG Crash Course 2016 Medicine Notes
@351. Construction worker sustained an injury to the vertebral column from a fall. Radiological examination revealed damage to right half of spinal cord at T7 level. Which one of the clinical findings is NOT TRUE in this patient ? (APPG 2014 First time)
(A) Ipsilateral loss of pain and thermal sensation below the level of lesion
(B) Ipsilateral loss of touch and pressure below the level of lesion
(C) Ipsilateral hyperesthesia at the level of lesion
(D) Ipsilateral motor and vasomotor paralysis
Ans. A
That eccentric experimentalist, Charles Edouard Brown-Sequard, flitted restlessly between the major cities of the old and new worlds in the nineteenth century, replacing outdated concepts with new ideas of his own concerning the operation of the nervous system in health and disease. He used the experimental approach to generate hypotheses but had no interest in showing by meticulous study that his views were correct, leaving this to others.
Patients with Brown-Séquard syndrome suffer from ipsilateral upper motor neuron paralysis and loss of proprioception, as well as contralateral loss of pain and temperature sensation. A zone of partial preservation or segmental ipsilateral lower motor neuron weakness and analgesia may be noted. Loss of ipsilateral autonomic function can result in Horner syndrom
@352. In Huntington Chorea the causative mutation in the protein huntingtin is a(APPG 2014 First time)
(A) Point mutation
(B) Gene deletion
(C) Frameshift mutation
(D) Trinucleotiderepeat expansion
Ans. D
HD is one of several trinucleotide repeat disorders which are caused by the length of a repeated section of a gene exceeding a normal range.. The HTT gene is located on the short arm of chromosome 4[14] at 4p16.3. HTT contains a sequence of three DNA bases—cytosine-adenine-guanine (CAG)—repeated multiple times (i.e. … CAGCAGCAG …), known as a trinucleotide repeat.
@353. Feeling as if grains of sand are lying under the skin or small insects are creeping on the skin giving rise to itching sensation (Magnan’s Symptoms) is the characteristic of(APPG 2014 First time)
(A) Atropa belladonna poisoning
(B) Dhaturafastuosa poisoning
(C) Chronic Cannabis sativa poisoning
(D) Chronic Cocaine poisoning
Ans D
Magnan’s sign is a clinical sign in which people with cocaine addiction experience paraesthesia which feels like a constantly moving foreign body, such as fine sand or powder, under the skin.
@354. A third cranial nerve palsy associated with pupillary dilatation, loss of ipsilateral light reflex, focal pain behind the eye may occur with(APPG 2014 First time)
(A) Aneurysm in the cavernous sinus
(B) Expanding supraclinoid carotid
(C) Expanding aneurysm at the junction of posterior communicating and internal carotid artery
(D) Expanding anterior cerebral artery aneurysm
Ans C
Third cranial nerve palsy, particularly when associated with pupillary dilation, loss of ipsilateral light reflex and focal pain above or behind the eye may occur in an aneurysm at the junction of posterior communicating artery and the internal carotid artery.
▪ Sixth nerve palsy may indicate an aneurysm in the cavernous sinus and visual field defects can occur with an expanding supraclinoid carotid or anterior cerebral artery aneuyrsm.
Occipital or posterior cervical pain may signal a posterior inferior cerebellar artery or anterior inferior cerebellar artery aneurysm.
@355. In Wemicke’s encephalopathy memory loss is correlated most closely with inflammation and necrosis of(APPG 2014 First time)
(A) Mamillary bodies
(B) Midline cerebellum
(C) Periacqueductal gray matter
(D) Dorsomedial thalamus
Ans A
Brain atrophy associated with WKS occurs in the following regions of the brain; the mamillary bodies, the thalamus, the periaqueductal grey, the walls of the 3rd ventricle, the floor of the 4th ventrical, the cerebellum, and the frontal lobe. The amnesia that is associated with this syndrome is a result of the atrophy in the structures of the diencephalon (the thalamus, hypothalamus and mamillary bodies),
and is similar to amnesia that is presented as a result of other cases of damage to the medial temporal lobe.[ It has been argued that the memory impairments can occur as a results of damage along any part of the mamillo-thalamic tract, which explains how WKS can develop in patients with damage exclusively to either the thalamus or the mamillary bodies
@356. One of the common variants of sickle cell anaemia frequently marked by lesser degree of haemolyticanaemia and greater propensity for the development of retinopathy and aseptic necrosis of bones is(APPG 2014 First time)
(A) Sickle all trait
(B) Haemoglobin SC disease
(C) Sickle thalassaemia
(D) Sickle – Hb E disease
Ans B
Patients with sickle thalassemia and sickle-HbE tend to have similar, slightly milder, symptoms, perhaps because of the ameliorating effects of production of other hemoglobins within the RBC. Hemoglobin SC disease, one of the more common variants of sickle cell anemia, is frequently marked by lesser degrees of hemolytic anemia and a greater propensity for the development of retinopathy and aseptic necrosis of bones.
@357. Polyarticular rheumatoid arthritis is diagnosed when more than joints are involved. (APPG 2014 First time)
(A) Two
(B) Three
(C) Four
(D) Five
Ans D
@358. All are recognized causes of Adult Respiratory Distress Syndrome (ARDS) EXCEPT(APPG 2014 First time)
(A) Smoke inhalation
(B) Malignant hypertension
(C) Hypothermia
(D) Viral pneumonias
Ans B
@359. A 60 years old man is being treated for pulmonary emphysema. He is admitted with laboured breathing at rest with marked use of accessory muscles. Arterial blood gas analysis revealed
pH 7.33
PaCO2 64 mmHg
PaO2 50 mmHg
HCO3 43 mEq/L
Possible diagnosis is(APPG 2014 First time)
(A) compensated metabolic alkalosis
(B) chronic compensated respiratory acidosis
(C) acute respiratory acidosis
(D) hyperventilation is the main factor
Ans B
Increase in Bicarbonate = (43-28 ) = 15
PCO2 = (64-45) = 20
With renal compensation, renal excretion of carbonic acid is increased, and bicarbonate reabsorption is increased
Normal
Bicarbonate 22-28 mEq/L
PCO 2 33-45 mm Hg 4.4-5.9 kPa
PO 2 75-105 mm Hg 10.0-14.0 kPa
• Acute respiratory acidosis – Bicarbonate increases by 1 mEq/L for each 10-mm Hg rise in PaCO 2.The acute change in bicarbonate is, therefore, relatively modest and is generated by the blood, extracellular fluid, and cellular buffering system.
• Chronic respiratory acidosis – Bicarbonate increases by 3.5 mEq/L for each 10-mm Hg rise in PaCO 2. The greater change in bicarbonate in chronic respiratory acidosis is accomplished by the kidneys. The response begins soon after the onset of respiratory acidosis but requires 3-5 days to become complete.
• Acute respiratory acidosis – Change in pH = 0.008 × (40 – PaCO 2)
• Chronic respiratory acidosis – Change in pH = 0.003 × (40 – PaCO 2)
@360. Locomotor ataxia, a late manifestation of syphilis due to parenchymatous involvement of the spinal cord is called(APPG 2014 First time)
(A) general paralysis of insane
(B) tabes dorsalis
(C) meningovascular syphilis
(D) syphiliticamyotrophy
(E) APPG 2014
Ans.B
Tabesdorsalis, also known as syphilitic myelopathy, is a slow degeneration (specifically, demyelination) of the nerves primarily in the dorsal columns (posterior columns) of the spinal cord (the portion closest to the back of the body). They help maintain a person’s sense of position (proprioception), vibration, and discriminative touch.
Symptoms may not appear for some decades after the initial infection and include: weakness, diminished reflexes, paresthesias (shooting and burning pains, pricking sensations, and formication), hypoesthesias (abnormally diminished cutaneous, especially tactile, sensory modalities), tabetic gait (locomotor ataxia), progressive degeneration of the joints, loss of coordination, episodes of intense pain and disturbed sensation (including glossodynia), personality changes, urinary incontinence, dementia, deafness, visual impairment,
positive Romberg’s test, and impaired response to light (Argyll Robertson pupil). The skeletal musculature is hypotonic due to destruction of the sensory limb of the spindle reflex. The deep tendon reflexes are also diminished or absent; for example, the “knee jerk” or patellar reflex may be lacking (Westphal’s sign). A complication of tabesdorsalis can be transient neuralgic paroxysmal pain affecting the eyes and the ophthalmic areas
Tabesdorsalis or general paresis indicating a parenchymal involvement by the organism
@361. All of the following are indicated in the management of acute hyperkalemia EXCEPT(APPG 2014 First time)
(A) Calcium gluconate
(B) Glucose with insulin
(C) Salbutamol nebulisation
(D) Cation exchange resin
Ans: D
Salbutamol can be used in the immediate management of hyperkalaemia
@362. Stored plasma is deficient in(APPG 2014 First time)
(A) factors 7 and 8
(B) factors 5 and 7
(C) factors 5 and 8
(D) factors 5, 7 and 8
Ans: C
@363. All the following statements are correct about treatment in chronic Immune Thrombocytopenic Purpura (ITP) EXCEPT(APPG 2014 First time)
(A) Most of the patients respond to immunosuppressive doses of glucocorticoids
(B) Relapse is rare
(C) Splenectomy is the treatment of choice for relapse
(D) Minority have refractory forms of ITP and difficult to treat
Ans: B
In 10% of adults, ITP runs a chronic course with relapse and remissions
364.Regarding Iron deficiency which of the following statements is TRUE (APPG 2014 Second time)
A. Commonest cause chronic blood loss
B. Reduced MCV precedes depletion of iron stores
C. Hepcidin levels are high in isolated iron deficiency
d. Out of an oral tablet of 325 nig. TID, 100 mg is absorbed
ANS A
Hepcidin levels are reduced in iron deficiency, and measurement of blood or urine hepcidin levels may enable evaluation of iron requirements and provide a powerful indicator of physiological iron deficiency
The most common cause of iron deficiency anemia is gradual, prolonged blood loss. For this reason, menstruating women are particularly prone to anemia. In men, the most common cause of iron deficiency is blood loss in the digestive tract, resulting from disorders such as peptic ulcer, inflammatory bowel disease, and stomach or colon cancer. Sometimes hemorrhoids bleed enough to result in anemia.
Hepcidin is a peptide hormone produced by the liver. It was discovered in 2000, and appears to be the principal regulator of iron homeostasis in humans and other mammals.[2] Hepcidin functions to regulate (inhibit) iron transport across the gut mucosa, thereby preventing excess iron absorption and maintaining normal iron levels within the body. Hepcidin also inhibits transport of iron out of macrophages (site of iron storage and transport). Thus, in states of high hepcidin levels (including inflammatory states), serum iron levels can drop because
iron is trapped inside macrophages. This may lead to anemia. I
There are many diseases where failure to adequately absorb iron contributes to iron deficiency and iron deficiency anaemia. The treatment will depend on the hepcidin levels that are present, as oral treatment will be unlikely to be effective if hepcidin is blocking enteral absorption, in which cases parenteral iron treatment would be appropriate. Studies have found that measuring hepcidin would be of benefit to establish optimal treatment,[13] although as this is not widely
available, C-reactive protein (CRP) is used as a surrogate marker.
.4
The loss of iron stores is reflected in the blood by a reduction in ferritin and reduced levels of iron bound to transferrin. As the iron stores become more severely depleted,
availability of transferrin-bound iron to the erythroid precursor causes reduced heme and hemoglobin production. This is reflected in a drop in the red blood cell count and mean corpuscular volume. The red cell count usually becomes abnormal before the mean corpuscular volume, which remains within the normal range until the hemoglobin reaches about 10 g/dl. Additionally, the red cell distribution width increases because the smaller, iron deficient cells are being mixed with normocytic cells. In the absence of therapy, erythrocyte production remains
inadequate and anemia develops. Importantly, many patients with iron deficiency anemia have normal red cell indices because the red cell count becomes abnormal before there is much change in red cell morphology.7 in those cases, more specialized testing of iron status may be required to confirm the diagnosis of iron deficiency anemia.
365. A tall male patient with arachnodactyly and subluxated lens came with sudden, sharp, severe chest pain and sweating. Left arm pulses are weak. ECG appears normal. Further steps include the following EXCEPT TRUE (APPG 2014 Second time)
A. IV hydralazine or sublingual nifedipine immediately to ‘reduce blood pressure and pain
B. Echo and CT angiogram
C. IV labetalol
D. Plan for surgery with an interposition graft
ANS A
Medical management remains the treatment of choice for descending aortic dissections unless they are leaking or ruptured. With the progress in stenting technology, descending dissections can be approached with this modality in selected cases.[6, 13, 26, 27, 28, 29] Medical therapy is also administered to surgical patients preoperatively, intraoperatively, and postoperatively to prevent progression or recurrence of aortic dissection.
Medical management consists of decreasing the blood pressure and the shearing forces of myocardial contractility in order to decrease the
intimal tear and propagation of the dissection. Medical management with antihypertensive therapy, including beta-blockers, is the treatment of choice for all stable chronic aortic dissections.[30]
Initiate therapy to reduce systemic arterial pressure and shear stress if the patient’s blood pressure allows for this type of intervention. The following agents are commonly used:
o Intravenous nitroprusside drip
o Intravenous labetalol: it has a dual effect of decreasing blood pressure and cardiac contractility
o Calcium channel blockers (eg, diltiazem): they lower blood pressure and cardiac contractility
Pain management is an important but difficult aspect of medical therapy. Narcotics and opiates are the preferred agents.
A number of advances have resulted in a decreased frequency of complications associated with surgery on the aorta. Dacron grafts with impregnated collagen or gelatin have been developed that are impervious to blood. The development of more impermeable grafts has greatly enhanced the surgical repair of thoracic aortic dissections. Such grafts include the following:
o Woven Dacron
o Collagen-impregnated Hemashield (Meadox Medicals) aortic grafts
o Gel-coated Carbo-Seal Ascending Aortic Prosthesis (Sulzer CarboMedics)
o Chest radiography is the initial imaging technique and may or may not reveal any abnormality. Computed tomography (CT) is useful in hemodynamically stable patients; emergency CT angiography with 3-dimensional reconstruction is rapidly becoming the diagnostic test of choice. Magnetic resonance imaging (MRI) is as accurate as CT and may
benefit patients who have adverse reactions to the use of intravenous contrast agents. For hemodynamically unstable patients, echocardiography is ideal.
o Aortography is still considered by some as the diagnostic criterion standard test for aortic dissection. However, it is being replaced by newer imaging modalities.
The following conditions contraindicate beta-blocker therapy:
o Hypersensitivity to drug/class
o Severe asthma
o Heart block
o Uncompensated heart failure
o Bradycardia (heart rate < 60 beats/min)
o Severe chronic obstructive pulmonary disease
o Hypotension
The following conditions contraindicate calcium channel blocker therapy:
• Hypersensitivity to drug/class
• Second- or third-degree atrioventricular block
• Sick sinus syndrome
• Hypotension
• Left ventricular dysfunction
• Pulmonary congestion
366. Which of the following is NOT a feature of Weil’s disease? (APPG 2014 Second time)
A. fever and jaundice
B. hepatic encephalopathy
C. renal failure
(4) conjunctival hyperemia and skin purpura
ANS B
The physical examination findings differ depending on the severity of disease and the time from onset of symptoms. Patients may appear mildly ill or toxic. Early in the disease, temperatures as high as 40°C and tachycardia are common. Hypotension, oliguria, and abnormal chest auscultation at presentation may portend severe illness. When fever is severe and prolonged, hypotension and shock due to volume depletion may also occur. The fever typically subsides within 7 days.
Early in the disease, the skin is warm and
flushed. Additional skin findings include a transient petechial eruption that can involve the palate. Later in severe disease, jaundice and purpura can develop. The classic ocular finding of conjunctival suffusion occurs early irrespective of disease severity. Conjunctival suffusion is characterized by redness of the conjunctiva that resembles conjunctivitis but that does not involve inflammatory exudates.
Uveitis is a common feature following acute leptospirosis; however, patients who receive antibiotics during the acute phase of illness may develop only mild uveitis.[7]
367. Chinese Restaurant syndrome after eating fried rice and vanilla sauce is due to(APPG 2014 Second time)
A. Clostridium perfringens
B. Bacillus cereus
C. Staphylococcus aureus
D. Clostridium botulinum
ANS B
368. The following causes Normal Anion Gap acidosis(APPG 2014 Second time)
A. Diarrhea
B. Starvation ketoacidosis
C. Methanol poisoning
D. All the above
ANS A
369. The following help to treat hiccups EXCEPT(APPG 2014 Second time)
A. Carbonated beverages
B. Valsalva maneuver
C. Carotid massage
D. Eating a spoon of dry granulated sugar
ANS A
Another popular remedy for minor cases of the hiccups, people using this treatment simply need to measure out a teaspoon-sized portion of regular granulated sugar and eat it in one bite. if the hiccups persist, try eating one more spoonful of sugar before moving onto another remedy.
CAROTID SINUS MASSAGE
Gently massaging the carotid sinus, which is located in the neck, can sometimes cure persistent hiccups. However, make sure that you have a professional health care provider
do this type of massage for you rather than attempting to do it yourself or having a friend or family member do it for you.
HOLDING YOUR BREATH
Like breathing into a paper bag holding your breath can be another way to try to control your diaphragm and make the hiccups stop. Hold your breath and concentrate on not allowing the hiccups to occur, if possible. Don’t hold your breath so long that you begin to get dizzy or lightheaded.
COLD WATER
This is one of the most commonly shared home remedies for hiccups. To use this remedy, drink a glass of cold water very quickly. Some people find that drinking as much of the cold water as they can without taking a breath is the most useful tactic with this remedy. Rest for a few moments after gulping the water to see if the hiccups have subsided.
370. A patient came with chronic postprandial diarrhea. His stool has increased osmotic gap and normal fecal fat content. The probable diagnosis is(APPG 2014 Second time)
A. Lactose intolerance
B. Pancreatic insufficiency
C. Irritable bowel syndrome
D. Zollinger Ellison syndrome
ANS A
Measurement of stool Na & K calculate osmotic gap
– Osmotic gap = 290 mOsm/Kg – 2 (Na + K)
– Small gap ( 100) = osmotic diarrhea
Definition
Stool weight of more than 300
Stool weight of more than 300 gm / 24 h more than 4 weeks gm / 24 h more than 4 week
– Measured osmolality < 290 addition of water or hypotonic urine.
– pH of stool water ↓ ( 100
Stool volume decrease with fasting
Gas, bloating ( fermentation–>fatty acids, CO2)
o Examples:
lactase deficiency laxative abuse
poorly absorbed CHO
Stool analysis
o Stool pH
o Laxative screen eg Mg,
Chronic secretory diarrhea:
o Diagnostic clues: Diagnostic clues:
o Large volume ( > 1 litre) – Large volume ( > 1 litre)
o Little change with fasting (except bile salt diarrhea)
o Normal osmotic gap
o Normal osmotic gap
Pancreatic exocrine insufficiency
o smaller stool volume and higher fat concentration / 100 gm stool. Fat concentration> 9.5 gm / 100 gm in patients with suspected maldigestion suggest pancreatic or biliary dysfunction.
o Oil is seen in stool.
o Fewer problems with vitamin deficiencies.
o Lower frequency of hypocalcemia (more common in small bowel mucosal diseases.
371. An alcoholic had a vomiting and continuous retching. This was followed by a bout of hematemesis. The most probable diagnosis of the following is(APPG 2014 Second time)
A. Bleeding peptic ulcer
B. Boerhaave’s syndrome
C. Mallory Weiss tear
D Acute gastric dilatation
ANS C
Mallory-Weiss syndrome (MWS) is characterised by upper gastrointestinal bleeding (UGIB) from mucosal lacerations in the upper gastrointestinal tract (GIT) (usually at the gastro-oesophageal junction or gastric cardia). Mallory and Weiss described the syndrome in 1929 in patients retching and vomiting after an alcoholic binge.
372. A Serum-Ascitic Albumin Gradient greater than 1.1 is seen in ascites due to the following EXCEPT(APPG 2014 Second time)
A. Alcoholic Cirrhosis
B. Nephrotic syndrome due to Minimal change disease
C. Congestive cardiac failure after one dose of diuretic
D Budd Chiari Syndrome
ANS B
o High gradient
o A high gradient (> 1.1 g/dL) indicates the ascites is due to portal This is due to increased hydrostatic pressure within the blood vessels of the hepatic portal system, which in turn forces water into the peritoneal cavity but leaves proteins such as albumin within the vasculature.
Important causes of high SAAG ascites (> 1.1 g/dL) include:
o high protein in ascitic fluid (> 2.5): heart
failure, Budd Chiari syndrome
o low protein in ascitic fluid (< 2.5): cirrhosis of the liver
Low gradient
o A low gradient (< 1.1 g/dL ) indicates causes of ascites not associated with increased portal pressure. Examples include tuberculosis, pancreatitis, nephrotic syndrome and various types of peritoneal cancer.
373. Choose the correct statement regarding Pseudomembranous colitis(APPG 2014 Second time)
A. causes yellowish adherent plaques and hyperemic colonic mucosa
B. is often due to vancomycin
C. is best treated by ampicillin
D. all the above are true
ANS A
Oral administration of vancomycin is the method of choice for treating antibiotic-associated pseudomembranous colitis
Antibiotics most commonly associated with pseudomembranous colitis include:
o Quinolones, such as ciprofloxacin (Cipro) and levofloxacin (Levaquin)
o Penicillins, such as amoxicillin and ampicillin
o Clindamycin (Cleocin)
o Cephalosporins, such as cefixime
374. Natalizumab is a(APPG 2014 Second time)
A. monoclonal Ab against TNF
B. monoclonal Ab against alpha-4 integrin used in multiple sclerosis
C. monoclonal Ab against IL-23 used in progressive multifocal leukoencephalopathy
D VEGF inhibitor used in hepatocellular carcinoma
ANS B
Natalizumab is a humanized monoclonal antibody against the cell adhesion molecule α4-integrin. Natalizumab is used in the treatment of multiple sclerosis and Crohn’s disease.
375. In which of the following situations would you use the P-SPIKES approach? (APPG 2014 Second time)
A. Soon after your patient has died in the lCCU
B. When you interview an alchoholic
C. When you assess level of consciousness in the Emergency room
D. When you assess for suspected depression
ANS A
STEP 1: S—SETTING UP the Interview
STEP 2: P—Assessing the Patient’s PERCEPTION
STEP 3: I—Obtaining the Patient’s INVITATION
STEP 4: K—Giving KNOWLEDGE and Information to the Patient
STEP 5: E—Addressing the Patient’s EMOTIONS with Empathic Responses
STEP 6: S—STRATEGY and SUMMARY
the protocol (SPIKES) consists of six steps. The goal is to enable the clinician to fulfill the four
most important objectives of the interview disclosing bad news: gathering information from the patient, transmitting the medical information, providing support to the patient, and eliciting the patient’s collaboration in developing a strategy or treatment plan for the future.
The task of breaking bad news can be improved by understanding the process involved and approaching it as a stepwise procedure, applying well-established principles of communication and counseling. Below we describe a six-step protocol, which incorporates these principle
376. Select the TRUE statement among the following : (APPG 2014 Second time)
A. Anti-D is used in Immune Thrombocytopenic purpura
B. DDAVP is used in von Willebrand disease type 3
C. DDAVP is used in severe form of Hemophilia A
D. EACA is used in Factor XI deficiency for minor bleeds
ANS D
. Patients with type 3 vWD are usually unresponsive to desmopressin
DDAVP is contraindicated in vWD type 2b because of the risk of aggravated thrombocytopenia and thrombotic complications.
Desmopressin (DDAVP) is a man-made hormone used to treat people who have mild hemophilia A. DDAVP isn’t used to treat hemophilia B or severe hemophilia A.
DDAVP stimulates the release of stored factor VIII and von Willebrand factor; it also
increases the level of these proteins in your blood. Von Willebrand factor carries and binds factor VIII, which can then stay in the bloodstream longer.
377. Following are useful in treatment of aplastic anemia EXCEPT(APPG 2014 Second time)
A. Epoetin and Filgrasatim
B. Equine ATG + Cyclosporine
C. Fluoxymesterone
D Autologous bone marrow transplantation
ANS A
Treating immune-mediated aplastic anemia involves suppression of the immune system, an effect achieved by daily medicine intake, or, in more severe cases, a bone marrow transplant, a potential cure.[5] The transplanted bone marrow replaces the failing bone marrow cells with new ones from a matching donor. The multipotent stem cells in the bone marrow reconstitute all three blood cell lines, giving the patient a new immune system, red blood cells, and platelets. However, besides the risk of graft failure, there is also a risk that the newly
created white blood cells may attack the rest of the body (“graft-versus-host disease”).
o Medical therapy of aplastic anemia often includes a course of antithymocyte globulin (ATG) and several months of treatment with a cyclosporin to modulate the immune system. chemotherapy with agents such as cyclophosphamide may also be effective but has more toxicity than ATG. Antibody therapy, such as ATG, targets T-cells, which are believed to attack the bone marrow. Corticosteroids are generally
ineffective,[citation needed] though they are used to ameliorate serum sickness caused by ATG.
One prospective study involving cyclophosphamide was terminated early due to a high incidence of mortality, due to severe infections as a result of prolonged neutropenia.[6]
378. Least likely cause of renal papillary necrosis(APPG 2014 Second time)
A. Sickle cell disease
B. Analgesic nephropathy
C. Posterior urethral valves
D Diabetes with UTI
ANS C
A useful mnemonic device for the conditions associated with renal papillary necrosis is POSTCARDS, which stands for the following:
o Pyelonephritis
o Obstruction of the urinary tract
o Sickle cell hemoglobinopathies, including sickle cell trait
o Tuberculosis
o Cirrhosis of the liver, chronic alcoholism
o Analgesic abuse
o Renal transplant rejection, radiation
o Diabetes mellitus
o Systemic vasculitis
379. Captopril enhanced renography is useful to exclude(APPG 2014 Second time)
A. Diabetic nephropathy
B. Renal vein thrombosis in a patient with Renal cell carcinoma
C. Renal artery stenosis in a young hypertensive
D A kidney donor who may be a mismatch
ANS C
Radioisotope renography is a form of kidney imaging involving radioisotopes. The two most common radiolabelled pharmaceutical agents used are Tc99m-MAG3 (Mercaptoacetyltriglycine) and Tc99m-DTPA (Diethylene Triamine Pentacaetic Acid)
A MAG3 scan is a diagnostic imaging procedure that allows a nuclear medicine physician, also known as a radiologist, to visualize the kidneys and learn more about how they are functioning. MAG3 is an acronym for mercapto acetyl tri glycine, a
compound that is chelated with a radioactive element – technetium-99m.
The technique is very useful in evaluating the functioning of kidneys. It is widely used before renal transplantation to assess the vascularity of the kidney to be transplanted and with a test dose of captopril to highlight possible renal artery stenosis in the donor’s other kidney,[4] and later the performance of the transplant.[5][6]
The use of the test to identify reduced renal
function after test doses of captopril (an angiotensin converting enzyme inhibitor drug) has also been used to identify the cause of hypertension in patients with renal failure.[7][8] Initially there was uncertainty as to the usefulness,[9] or best test parameter to identify renal artery stenosis, the eventual consensus was that the distinctive finding is of alteration in the differential function
380. A patient of Congestive Heart Failure was treated with IV Frusemide for 3 days. On the 3rd day, there was still pedal edema and he complained of anorexia and vomiting; he became apathetic and lethargic. BP 120/80. Pulse 90. Ser. Creat =1.6 mg%. K=3.5 Na=128. The next treatment in him would be(APPG 2014 Second time)
A. 1.5 li. of Normal saline over 2 hours
B. Judicious continuation of diuretic with restriction of free water
C. 9 IV Potassium chloride 2 amp. at a rate of 20 meq /hour
D Begin chlorthiazide and carbamazepine
ANS A
There are 2 indications for saline infusion in hyponatremia. Overt manifestations of hyponatremia are treated with hypertonic saline, whereas symptomatic hypovolemia associated with hyponatremia without overt symptoms is usually treated with isotonic saline.23–24 In both situations, the infusion of saline results in rising [Na]. This rise can be slower or faster than desired, with potentially dire clinical consequences
For the asymptomatic patient, the following treatments may be of use:
Hypovolemic hyponatremia: Administer isotonic saline to patients who are hypovolemic to replace the contracted intravascular volume (thereby treating the cause of vasopressin release). Patients with
hypovolemia secondary to diuretics may also need potassium repletion, which, like sodium, is osmotically active. Correction of volume repletion turns off the stimulus to ADH secretion, so a large water diuresis may ensue, leading to a more rapid correction of hyponatremia than desired. If so, hypotonic fluid such as D5/½ normal saline may need to be administered (see below under normovolemic hyponatremia for guidelines).
Hypervolemic hyponatremia: Treat patients who are hypervolemic with salt and fluid restriction, plus loop diuretics, and correction of the underlying condition. The use of a V2 receptor antagonist may be considered (see below).
381. Which of the following is NOT part of the Mini Mental State examination?
A. What is the year, month, date, day of Today
B. What is your name and age
C. Spell ‘World’ backward
(4) Follow a 3 stage command
ANS B
382. Which of the following is known as a ‘GREAT MASQUERADER’?
A. Leprosy
B. Syphilitic Aortic aneurysm
C. Pulmonary embolism
D Chronic HIV infection
ANS C
Pulmonary embolism as “one of the great masqueraders of medicine
383. A patient appears awake and is not talking. No voluntary movements. He can signal with vertical eye movements. The CT scan shows infarction of ventral pons. The diagnosis is
A. Coma
B. Abulia
C. Locked in state
(4) Catatonia
ANS C
384. A patient with Acute Kidney injury and RBCs and red cell casts in urine probably has
A. Thrombotic micro angiopathy
B. Pyelonephritis
C. Rhabdomyolysis
(4) Allergic interstitial nephritis
ANS D
acute interstitial nephritis (AIN) is associated with many intratubular red blood cells and red blood cell casts, consequent acute tubular injury and red blood cell phagocytosis by tubular cells
385. Calciphylaxis refers to
A. anaphylactic reaction to IV calcium in a patient on digoxin
B. tolerance to increasing calcium doses in patients with hyperkalemia
C. calcific arteriopathy in chronic kidney disease
D one variant of tachyphylaxis
ANS C
Calciphylaxis is a condition characterised by necrosis (cellular death) of the skin and fatty tissue. It is seen mainly in patients with end stage kidney disease. It is also sometimes called calcific uraemic arteriolopathy.
386. Following conditions must be fulfilled in a person before taking him as a kidney donor EXCEPT
A. ABO compatibility with recipient
B. Presence of two normally functioning kidneys
C. No HIV infection
D Zero HLA mismatch with recipient
ANS D
The association between HLA mismatches and rejection was not linear, with the greatest benefit of HLA matching appeared to be confined to those with
387. The following inheritance patterns are correct EXCEPT
A. Huntington’s Autosomal chorea Recessive
B. Marfan’s Autosmal Syndrome dominant
C. Duchenne’s Xlinkied myotonic Recessive dystrophy
(4) Romano Ward Autosmal Syndrome Dominant
ANS A
388. A 60 year patient with past history of Myodardial infarction , on irregular treatment came with a one year history of exertional dyspnea, occasional PND, easy fatigability and pedal edema. On examination, BP is 130/80. Mitral regurgitation+. X-ray shows cardiomegaly. Echo shows an EF . of 35%. Ser. creatinine = 1,5 mg%. In him, the following are true EXCEPT?
A. Enalapril is contraindicated
B. Frusemide will relieve symptoms though it has no mortality benefit
C. Digoxin is useful if he has atrial fibrillation
(4) Eplerenone is beneficial
ANS D
Eplerenone is specifically indicated for the reduction of risk of cardiovascular death in people with heart failure and left ventricular dysfunction within 3–14 days of an acute myocardial infarction, in combination with standard therapies and as treatment against hypertension. It appears equivalent to spironolactone but is much more expensive
Eplerenone is contraindicated in patients with hyperkalaemia, severe renal impairment (creatinine Cl less than 30 ml/min), or severe hepatic impairment (Child-Pugh score C). The manufacturer of eplerenone also contraindicates ( relative C.I. ) concomitant treatment with ketoconazole, itraconazole or other potassium-sparing diuretics (though the manufacturer still considers taking these
drugs to be absolute C.I.) Potential benefits should be weighted against possible risks.
loop diuretics reduce symptoms but have not been shown to reduce mortality
389. While auscultating the heart, a doctor heard an additional sound just after the second heart sound. The patient could be suffering from any of the following EXCEPT
A. Bicuspid aortic valve with moderate aortic stenosis
B. Mitral regurgitation with heart failure
C. Moderate Mitral stenosis in sinus rhythm
(4) Chronic constrictive pericarditis
ANS A
mitral opening snap of mitral stenosis occurs after A2
Mitral regurgitation with heart failure causes S3
Chronic constrictive pericarditis cause pericardial knock
390. A young male came with history of episodes of palpitation, cardiovascular examination – No Abnormality Detected. He says his doctor treated his palpitation by pressing the side of his neck. The ECG shows a PR interval of two small boxes (2mm) and a slurring of the initial part of the QRS complex. The diagnosis is
A. Brugada syndrome
B. Wolff Parkinson White syndrome
C. Lown Ganong Levine syndrome
D. Jervell Lange Nielsen syndrome
ANS B
o PR interval (beginning of P wave to the beginning of the next QRS).
o Normally, .2 seconds, it is a first degree block
o QRS interval (beginning of Q to the end of the S wave)
o Should be < .12 seconds ( .12, check for bundle branch block.
o A QRS > .12 and RR (2 peaks or R waves in QRS) occurring in the right chest leads (V1-V2) indicates a right bundle branch block
o QT interval (beginning of QRS to end of T
wave) should be less than half of the preceding RR interval – this varies with the rate. For normal rates, QT < .4 seconds (2 large boxes).
o “QT prolongation” (too long) can lead to a refractory form of ventricular tachycardia called torsades de pointes.
The Lown-Ganong-Levine syndrome (LGL) is a clinical syndrome consisting of paroxysms of tachycardia and electrocardiogram (ECG) findings of a short PR interval and normal QRS duration. LGL is usually categorized in a class of preexcitation syndromes that includes the Wolff-Parkinson-White syndrome (WPW), LGL,
and Mahaim-type preexcitation.[
Jervell and Lange-Nielsen syndrome (JLNS) is a type of long QT syndrome, associated with severe, bilateral hearing loss.
391. Microscopic polyangiitis is characterized by the following features EXCEPT
A. Involves small and medium sized arteries and veins
B. 75% cases are associated with ANCA positivity
C. .Palpable purpura, ulcers and vesiculobullous lesions seen
(4) Unlikely to cause pulmonary — renal syndrome .
ANS D
Microscopic polyangiitis (MPA) can manifest as a mild systemic vasculitis with mild renal insufficiency, or it can manifest as a full blown acute disease with rapid deterioration of renal function and respiratory failure due to pulmonary capillaritis. Treatment depends on the extent of disease, the rate of progression, and the degree of inflammation
Microscopic polyangiitis (MPA) is vasculitis of small vessels.
Antineutrophil cytoplasmic antibodies
o ANCA positive (80%)
o Perinuclear ANCA related to myeloperoxidase ANCA (60%)
o Cytoplasmic ANCA related to proteinase-3 ANCA (40%)
Symptoms of microscopic polyangiitis (MPA) include the following:
o Constitutional symptoms
o Fever (55%)
o Malaise, fatigue, flulike syndrome
o Myalgia (48%)
o Weight loss (72%)
o Skin manifestations – Skin rash (50%)
o Pulmonary manifestations
o Hemoptysis (11%)
o Dyspnea
o Cough
o Cardiovascular manifestations – Chest pain, symptoms of heart failure
o Gastrointestinal involvement
o Gastrointestinal bleeding
o Abdominal pain
o Nervous system manifestations
o More commonly, peripheral nervous system involvement manifesting as mononeuritis multiplex (57%)
o CNS involvement manifesting as seizures (11%)
o Arthralgias (10-50%)
o Myalgias (40%)
o Testicular pain (2%)
o Ocular manifestations (1%)
o Red eye
o Ocular pain
o Decreased visual acuity
o Symptoms of sinusitis (1%)
392. The following statements are True regarding Nephrogenic Systemic Fibrosis: EXCEPT
A. Commonly seen in patients of Chronic Kidney Disease with a GFR of above 30ml/min/1.73 sq.m.
B. % Increase in dermal spindle cells positive for CD34 and procollagen I
C. It is a multi-organ fibrosis involving muscle, lungs and heart
(4) Skin lesions include erythematous papules and woody painful skin
ANS A
Definitive diagnosis of NFD/NSF is made by full-thickness skin biopsy at the involved site. Characteristic histological findings include thickened reticular dermal collagen bundles with dermal spindle cells that stain positive for both CD34 and procollagen.7 These spindle cells are thought to have the immunophenotype of ‘circulating fibrocytes’, which are characterized as circulating cells of bone marrow origin that express markers of both connective tissue cells and circulating leukocytes.8 Extensive mucin deposition is often seen between collagen bundles, but in
contrast to other fibrosing disease states, inflammatory cells are usually absent.9 Although the etiology has yet to be elucidated, it seems that some antigenic stimulus associated with renal dysfunction upregulates these circulating fibrocytes and induces an aberrant form of wound healing.
The manifestations of NFD were initially thought to be confined to the skin; however, recent reports reveal systemic fibrosis on autopsy including skeletal muscles, diaphragm,
pleura, pericardium, myocardium, dura mater and vessels of the heart. This newly described systemic involvement prompted the name of the disease to be changed to nephrogenic fibrosing dermopathy/nephrogenic systemic fibrosis (NFD/NSF).
skin thickening, tightness and contractures are hallmarks of the clinical findings in nephrogenic fibrosing dermopathy.
393. ‘The following statements regarding autologous stem cell transplantation are true EXCEPT
A. It is used in some relapsed lymphomas that are responsive to chemotherapy
B. It is used in treatment of Acute Myeloid Leukemia
C. Hematopoeitic stem cells are “mobilised from the marrow into the blood using filgrastim
(4) Unlike allogenic stem cell, trplantation, there is no period of pancytopenia after myelosupression and before recovery of infused cells
ANS D
High-dose chemotherapy and autologous stem cell transplantation has been demonstrated to improve a patient’s chance of cure when incorporated into the initial treatment or delivered to patients in complete remission after standard chemotherapy
HDCT induces profound pancytopenia, lasting approximately 2 to 4 weeks until the stem cells restore hematopoiesis. During the period of granulocytopenia, life-threatening infectious complications may occur. GM-CSF and G-CSF have been shown to accelerate hematopoietic recovery after autologous transplantation [30,31] and to improve hematopoiesis in patients with graft failure –
Autologous stem cell transplantation
o The person’s own stem cells are collected and returned after treatment.
o Autologous transplants are sometimes used for people with AML who are in remission after initial treatment and who don’t have a matched donor for an allogeneic transplant.
o One problem with autologous transplants is
that it is hard to separate normal stem cells from leukemia cells in the bone marrow or blood samples. Even after purging (treating the stem cells in the lab to try to kill or remove any remaining leukemia cells), there is the risk of returning some leukemia cells with the stem cell transplant.
Allogeneic stem cell transplant
o Using donor cells for SCT for acute myeloid leukemia (AML) is preferred because leukemia is a disease of the blood and bone marrow, so giving the patient his or her own
cells back may mean giving leukemia cells. Donor cells are also helpful because of the “graft versus leukemia” effect. When the donor immune cells are infused into the body, they may recognize any remaining leukemia cells as being foreign to them and will attack them. This effect doesn’t happen with autologous stem cell transplants filgrastim and lenograstim used as single-agent mobilisers have been well established, with both agents having reliably demonstrated increased concentrations of circulating HSCs .41,42 G-CSF is thought to
stimulate HSC mobilisation by decreasing SDF-1α gene expression and protein levels while increasing proteases that can cleave interactions between HSCs and the bone marrow environment .
394. A patient with pleural effusion has the following test results.
Serum protein = 7G/dL.
Pleural fluid protein = 5 G/dL
Serum glucose = 90 mg/dL
Pleural fluid glucose = 20 mg/dL
Pleural fluid LDH = 300 units
Probable diagnosis is
A. CHF patient not on diuretics
B. CHF patient with diabetes and on insulin
C. Renal failure
D. Rheumatoid arthritis
Ans D
According to Light’s criteria , a pleural effusion is likely exudative if at least one of the following exists:[11]
• The ratio of pleural fluid protein to serum protein is greater than 0.5
• The ratio of pleural fluid LDH and serum LDH is greater than 0.6
• Pleural fluid LDH is greater than 0.6 or 2⁄3 times the normal upper limit for serum.
Different laboratories have different values for the upper limit of serum LDH, but examples include 200 and 300
Conditions associated with transudative pleural effusions:[17]
• Congestive Heart Failure (CHF)
• Hepatic cirrhosis
• Hypoproteinemia
• Nephrotic syndrome
• Acute atelectasis
• Myxedema
• Peritoneal dialysis
• Meig’s syndrome
• Obstructive uropathy
• End-stage renal disease
Once identified as exudative, additional evaluation is needed to determine the cause of the excess fluid,
and pleural fluid amylase, glucose, pH and cell counts are obtained.
• Pleural fluid amylase is elevated in cases of esophageal rupture, pancreatic pleural effusion, or cancer.
• Glucose is decreased with cancer, bacterial infections, or rheumatoid pleuritis.
• Pleural fluid pH is low in empyema ( 45 IU/L, interferon gamma > 140 pg/mL, or positive polymerase chain reaction (PCR) for tuberculous DNA).
395. A 30 year previously healthy male came with 2 days fever and cough with purulent sputum. Examination reveals an impaired note with bronchial breathing and crackles and increased vocal resonance. He is alert. BP = 100/70. Respiratory rate = 24/min. Blood urea =.20 mg%. Which of the following is the best treatment for him?
A. OP treatment with Clarithromycin 500 mg BID for one week
B. Admit ‘ in ward and give Levofloxacin orally 750 mg OD + Inj. Ceftriaxone 1G IV BID for one week
C. Admit in ICCU and give Inj. Ceftriaxone 2G IV OD + IV levofloxacin 750 mg OD for one week
D. Piperacillin + tazobactam 4.5 G qid for one week
Ans A
For mild to moderate community-acquired pneumonia shorter courses of antibiotics (3–7 days) seem to be sufficient according to a recent meta-analysis
Factors that increase the need for hospitalization include:
• Age greater than 65
• Underlying chronic illnesses
• Respiratory rate greater than thirty breaths per minute
• Systolic blood pressure less than 90 mmHg
• Heart rate greater than 125 beats per minute
• Temperature less than 35 or greater than 40°C
• Confusion
• Evidence of infection outside the lung
Healthy outpatients without risk factors
• This group, the largest, is composed of otherwise healthy patients without risk factors for DRSP, enteric Gram negative bacteria, Pseudomonas, or other less common causes of CAP. The primary microoganisms in this group are viruses, atypical bacteria, penicillin sensitive
Streptococcus pneumoniae, and Hemophilus influenzae. Recommended management is with a macrolide antibiotic such as azithromycin or clarithromycin for seven[15] to ten days.
Outpatients with underlying illness and/or risk factors
• This group does not require hospitalization; its members either have underlying health problems (such as emphysema or congestive heart failure) or is at risk for DRSP and/or enteric Gram negative
bacteria. Treatment is with a fluoroquinolone active against Streptococcus pneumoniae such as levofloxacin or a beta-lactam antibiotic such as cefpodoxime, cefuroxime, amoxicillin, or amoxicillin/clavulanate plus a macrolide antibiotic such as azithromycin or clarithromycin for seven to ten days.
396. A 70 year old diabetic and hypertensive patient was being investigated for angina and a coronary angiogram was performed. Two days later, he developed fever and abdominal discomfort and dyspnea and a mottled skin rash. His great toe appeared black. His BP increased to 180/100. His creatinine was found to have risen from a preangio level of 1.2 to 3.6mg/dl. He has eosinophilia. Which one of the following statements is TRUE regarding this condition.
1) N-acetylcysteine would have prevented this condition
2) Heparin is the treatment of choice
3) This is contrast induced nephropathy
4) Kidney biopsy will show microvessel occlusion with a cleft in the vessel
Ans D
Atherosclerotic renovascular disease (ARVD) is increasingly recognised as an important cause of both chronic and end stage renal failure. These patients tend to do badly on dialysis, which reflects their systemic atherosclerotic burden. In an effort to delay and perhaps prevent their need for renal replacement therapy, some patients are subjected to a variety of medical, radiological and surgical interventions, although evidence for each is sparse.
PLAQUE INSTABILITY
Recent data reports increased cardiovascular morbidity and mortality in patients with irregular as opposed to smooth carotid plaques.50 The increased risk, which must reflect a systemic predisposition to unstable atherosclerotic plaques, did not correlate with conventional risk factors and this suggests additional as yet unrecognised factor(s) for plaque progression.
Similarly, the very high incidence of recurrent disease after coronary angioplasty in haemodialysis patients suggests that plaques behave differently in uraemia.51 Unstable atherosclerotic plaques may embolise cholesterol crystals and other debris that lodge in the dependent circulation, even down to the capillary level.
In the kidney, cholesterol embolisation can lead to progressive microvascular obliteration, chronic inflammation and worsening renal failure, with the diagnosis clinched by the characteristic appearance of intravascular cholesterol clefts on renal biopsy
(A) Characteristic histological appearance on light microscopy of a cholesterol cleft in a small artery with evidence of intimal thickening, concentric hypertrophy, and interstitial inflammation. Embolised cholesterol crystals dissolve during the fixation process. (B) Electron micrograph demonstrating a cholesterol cleft in an afferent glomerular arteriole. The destination vessel depends on crystal size and this variability may determine the clinical presentation.
397. A 6 month infant presented with recurrent episodes of polyuria and dehydration. Lab. tests revealed serum Na of 130 meq/li., K of 3 meq/li Cl of 92 meq/li., bicarbonate of 30 meq/li. pH was 7.48. Ser creat was 0.4 mg/dl. The patient had hypercalciuria and ultrasound showed medullary nephrocalcinosis. Which one of the following is the most likely diagnosis?
1) Bartter syndrome
2) Distal renal tubular acidosis
3) Liddle syndrome
4) Gitelman syndrome
Ans A (APPG- 2015)
In 90% of cases, neonatal Bartter syndrome is seen between 24 and 30 weeks of gestation with excess amniotic fluid (polyhydramnios). After birth, the infant is seen to urinate and drink excessively (polyuria, and polydipsia, respectively). Life-threatening dehydration may result if the infant does not receive adequate fluids. About 85% of infants dispose of excess amounts of calcium in the urine (hypercalciuria) and kidneys (nephrocalcinosis), which may lead to kidney stones. In rare occasions, the infant may progress to renal failure.
People suffering from Bartter syndrome present symptoms that are identical to those of patients who are on loop diuretics like furosemide.
• The clinical findings characteristic of Bartter syndrome are hypokalemia, metabolic alkalosis, and normal to low blood pressure. These findings may also be caused by:
• Chronic vomiting: These patients will have low urine chloride levels (Bartter’s will have relatively higher urine chloride levels).
• Abuse of diuretic medications (water pills): The physician must screen urine for multiple diuretics before diagnosis is made.
• Magnesium deficiency and Calcium deficiency: These patients will also have low serum and urine magnesium and calcium
• Patients with Bartter syndrome may also have elevated renin and aldosterone levels.
Prenatal Bartter syndrome can be associated with polyhydramnios
398. The following are main diagnostic criteria for Allergic Bronchopulmonary Aspergillosis EXCEPT –
1) Bronchial asthma
2) Pulmonary infiltrates
3) Distal bronchiectasis
4) Peripheral eosinophilia
Ans C (APPG- 2015)
Allergic bronchopulmonary aspergillosis
ABPA is defined by abnormalities including the following:
• Asthma
• Eosinophilia
• A positive skin test result for Aspergillus fumigatus
• Serum IgE level > 1000 IU/dL
• Positive test results for Aspergillus precipitins (primarily IgG but also IgA and IgM)
Minor criteria for diagnosis include positive Aspergillus radioallergosorbent assay test results and sputum culture
Chest radiography results in ABPA may vary from fleeting pulmonary infiltrates to mucoid impaction to central bronchiectasis. Computed tomography (CT) is helpful for better defining bronchiectasis, and images may demonstrate that apparent lobulated masses are mucus-filled dilated bronchi. Areas of atelectasis related to bronchial obstruction from mucoid impaction may be present
399. Henoch Schonlein purpura is characterized by the following EXCEPT
1) Glomerulonephritis
2) Palpable purpura
3) Hematocchezia
4) Thrombocytopenia
Ans D
(APPG- 2015)
400. Characteristic antibodies of autoimmune hepatitis include all of the following EXCEPT
1) Anti -CCP antibodies
2) ANAs
3) Smooth muscle antibodies
4) Anti LKM antibodies
Ans A
Clinicians must consider the diagnosis of autoimmune hepatitis in any patient who has acute hepatitis or acute liver failure (defined by the new onset of coagulopathy). In addition to aminotransferase levels and other liver function studies, the workup of such patients should include the following assays:
• Serum antinuclear antibody (ANA)
• Anti–smooth muscle antibody (ASMA)
• Liver-kidney microsomal type 1 (LKM-1) antibody
• Serum protein electrophoresis (SPEP)
• Quantitative immunoglobulins
Urgent liver biopsy, transjugular if appropriate, may help to confirm the clinical suspicion of acute autoimmune hepatitis
Laboratory findings in autoimmune hepatitis include the following:
• Elevated serum aminotransferase levels (1.5-50 times reference values)
• Elevated serum immunoglobulin levels, primarily immunoglobulin G (IgG)
• Seropositive results for ANAs, SMAs, or LKM-1 or anti–liver cytosol 1 (anti-LC1) antibodies
Anti–citrullinated protein antibodies (ACPAs)
Anti–citrullinated protein antibodies (ACPAs) are autoantibodies (antibodies directed against an individual’s own proteins) that are directed against peptides and proteins that are citrullinated. They are present in the majority of patients with rheumatoid arthritis.
ACPAs have proved to be powerful biomarkers that allow the diagnosis of rheumatoid arthritis (RA) to be made at a very early stage.
(APPG- 2015)
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