2004 gen med48.Ans: A: epinephrine 1: 1000Ref: harrison 17/ e pg 117, KDT,6/E- Pg 130Exp: adrenaline is a life saving drug in anaphylaxis and given 0. 2 0.5 mg SC/ IM . It not only increases BP but also counteracts bronchospasm or laryngeal edema and hence the choice of drug in anaphylaxis( Type I hypersensitivity reaction).Additional info: a detailed description is given in 2005 gen med paper- Q-41.49.Ans:C: excessive sweatingRef: harrison 17/ e- pg 5Exp:Although all options are correct but minmal losses is likely to occur in sweating compared to the other options given.hence the chopice of answer.Additional info:Hyponatremia:Hyponatremia This is defined as a serum [Na+] 18 mM within the first 48 h.

Third, the response to interventions, such as hypertonic saline or vasopressin antagonists, can be highly unpredictable, such that frequent monitoring of serum Na+ (every 24 h) is imperative.

Treatment of acute symptomatic hyponatremia should include hypertonicsaline to acutely increase serum Na+ by 12 mM/h to a total increase of 46mM; this increase is typically sufficient to alleviate acute symptoms, after serum [Na+] should be monitored every 24 h during and after treatment with hypertonic saline.

The administration of supplemental O2 and ventilatory support can also be critical in acute hyponatremia. Vasopressin antagonists are highly effective in SIADH and in hypervolemic hyponatremia due to heart failure or cirrhosis.close monitoring of the response of serum [Na+] is essential to adjust therapy.

Also note:Bailey and love surgery- 25/ e- pg 226

The following are the approximate daily requirements of some electrolytes in adults: sodium: 5090mMday1; potassium: 50mMday1; calcium: 5mMday1; magnesium: 1mMday

50.Ans: B: acidic urine excretionRef: Harrison 17 / e- pg 20Exp:persistent vomiting causes hypocholeremia , hypokalemia, hypoventilation metabolic alkalosis with paradoxical acidic urine excretion. Thus both B and C are alternatives. Hypocholeremia is found in both initial as well as compensatory phase but paradoxiacal aciduria exists only when there is severe hypokalemia. Since the question specifically asks about the likely event B is the choice of answer.

Additional info:

Metabolic alkalosis:

Metabolic alkalosis is due to a primary increase in serum [HCO3 ], distinguished from chronic respiratory acidosiswith a compensatory increase in renal HCO3 reabsorptionby the associated increase in arterial pH (normal or decreased in chronic respiratory acidosis).

Causes and patho phsiology:

Administered, exogenous alkali (HCO3, acetate, citrate, or lactate) may cause alkalosis if the normal capacity to excrete HCO3 is reduced or if renal HCO3 reabsorption is enhanced.

Metabolic alkalosis is primarily caused by renal retention of HCO3 and isdue to a variety of underlying mechanisms. Pts are typically separated into twomajor subtypes: Cl-responsive and Cl-resistant. Measurement of urine Cl affordsthis separation in the clinical setting .

persistent vomiting produces loss of fluid with high chloride and hydrogen ion concentration, hypochlorermia in blood and excess bicarbonate accumulation ( metabolic alkalosis.

This contraction of ECF volume stimulates maximal reabsorption of sodium to maintain volume. Since there is less of chloride in glomerular filtrate for reabsorptiuon of sodium in the PCT ,more sodium must be absorbed in the distal tubule, where sodium reabsorption occurs in exchange of potassium and hydrogen ( if potassium is depleted).

Hypokalemia from continued vomiting and above exchange mechanism encourages exchange of hydrogen for sodium .since less potassium is available. If this continues, alkaline urine becomes acidic with excretion of hydrogen ions in it.

causes and the diagnostic approach is given in table 2-6 ( Harrison 17/ e pg 19)most of these pts are hypokalemic, volume-expanded, and/or hypertensive.

Diagnosis:

Common forms of metabolic alkalosis are generally diagnosed from the history,physical examination, and/or basic laboratory tests.

ABGs will help determine whether an elevated [HCO3 ] is reflective of metabolic alkalosis or chronic respiratory acidosis; ABGs are required for the diagnosis of mixed acid-base disorders.

Measurement of urinary electrolytes will aid in separating Cl-responsiveand Cl-resistant forms. Urinary [Na+] may thus be >20 meq/L in Cl-responsivealkalosis despite the presence of hypovolemia; however, urinary [Cl] will bevery low.

Notably, urinary [Cl] may be variable in pts with diuretic-associated alkalosis, depending on the temporal relationship to diuretic administration.

Other diagnostic testse.g., plasma renin, aldosterone, cortisolmay be appropriatein Cl-resistant forms with high urinary [Cl].

treatment:

The acid-base disorder in Cl-responsive alkalosis will typically respond to saline infusion; however, the associated hypokalemia should also be corrected.

Pts with true or apparent mineralocorticoid excess require specific treatment to blockade of the mineralocorticoid receptor with spironolactone or eplerenone.

Finally, severe alkalosis in the critical care setting may require treatment with acidifying agents such as acetazolamide or HCl.

51.

Ans: C: idiopathic ipsilateral paralysis of the facial nerve.Ref: Harrison 17/ e- pg 1021Exp: bell s paralysis is an idiopathic lower motor neuron type of lesion of facial nerve of acute onset. pathogenesis is not known . Associated with herpes simplex lesion.

Additional info:

Bells palsy:

Most common form of idiopathic facial paralysis; affects 1 in 60 persons over a lifetime.

The facial nerve can be damaged at the cerebellopontine angle, within the internal auditory meatus, within the middle ear, at the skull base and within the parotid gland.

Association with herpes simplex virus type seen.

Clinical features and Symptoms:.

Onset is acute. Mild pain at stylomastoid foramen for a few days may precede the palsy.

Weakness evolves over 1248 h, sometimes preceded by retroaural pain.

Hyperacusis may be present.

Paralysis of all the facial muscles of expression on the side of palsy.

Drooping of the corner of the mouth, creases and skin fold on the affected side.

Weakness of frowning and eye closure since the upper facial muscles are weak.

Deviation of the angle of mouth away from the side and drooping of saliva from the angle of the mouth.

On attempted closure of the eyelid , the eye on the paralysed side rolled upwards( bell phenomenon)

Diagnosis:Diagnosis can be made clinically in pts with (1) a typical presentation, (2) no risk factors or preexisting symptoms for other causes of facial paralysis, (3) no lesions of herpes zoster in the external ear canal, and (4) a normal neurologic examination with the exception of the facial nerve.

In uncertain cases, an ESR, testing for diabetes mellitus, a Lyme titer, angiotensin-converting enzyme level, and chest x-ray for possible sarcoidosis, a lumbar puncture for possible Guillain- Barre syndrome, or MRI scanning may be indicated.

Treatment:

Protect the eye with paper tape to depress the upper eyelid during sleep.

Prednisone (6080 mg/d over 5 days, tapered off over the next 5 days) when startedearly appears to shorten the recovery period and modestly improve functional outcome. A recently published trial found no added benefit of acyclovir compared to prednisolone alone; the value of valacyclovir (usual dose 1000 mg/d for 57 days) is not known

prognosis:

Full recovery within several weeks or months in 80%; incomplete paralysis in first week is the most favorable prognostic sign. Older patients may show poor prognosis.

Also note:( harrisson 17/ e- pg 1021)

Ramsay Hunt syndrome is caused by herpes zoster infection of geniculate ganglion; distinguished from Bells palsy by a vesicular eruption in pharynx and external auditory canal, and by frequent involvement of eighth cranial nerveBilateral facial weakness may occur in Guillain-Barre syndrome, sarcoidosis, Lyme disease, and leprosy. Hemifacial spasm may occur with Bells palsy, irritative lesions (e.g., acoustic neuroma, basilar artery aneurysm, an aberrant vessel compressing the nerve), or as an idiopathic disorder.Melkerrson Rosenthal syndrome has a triad of recurrent facial paralysis, facial edema and scrotal tongue.

52.Ans: A : loss of diurnal variationRef: cyclic cushings syndrome- a clinical challenge by-J R Meinardi,B H Wolffenbuttel and R P F DullaartExp: patients with cushings syndrome classically lack the normal circadian rhythm . In normal individuals the serum levels of cortisol reach their lowest levels at midnight. In patients with cushings disease , this diurnal variation is lost and serum levels of cortisol remain same throughout 24 hrs. levels of cortisol changes in urine and hence loss of diurnal variation is the earliest manifestation of cushings syndrome. This is used as a diagnostic protocol in cushings syndrome.

Additional info:

Cushings syndrome: This disorder is caused by any condition that produces an elevation in glucocorticoid levels Causes:

The most common cause of Cushings syndrome is iatrogenic, due to administration of glucocorticoids for therapeutic reasons.

Endogenous Cushings syndrome results from production of excess cortisol (and other steroid hormones) by the adrenal cortex.

The major cause is bilateral adrenal hyperplasia secondary to hypersecretion of adrenocorticotropic hormone (ACTH) by the pituitary (Cushings disease) or from ectopic sources such as small cell carcinoma of the lung; medullary carcinoma of the thyroid; or tumors of the thymus, pancreas, or ovary.

Adenomas or carcinoma of the adrenal gland account for about 25% of Cushings syndrome cases.

Clinical Features

Some common manifestations (central obesity, hypertension, osteoporosis psychological disturbances, acne, amenorrhea, and diabetes mellitus)are relatively nonspecific.

More specific findings include easy bruising, purple striae, proximal myopathy, fat deposition in the face and interscapular areas (moon facies and buffalo hump), and virilization.

Glucocorticoids induce gluconeogenesis and inhibit the uptake of glucose by cells, with resultant hyperglycemia, glucosuria, and polydipsia, mimicking diabetes mellitus.The catabolic effects on proteins cause loss of collagen and resorption of bone. Thus, the skin is thin, fragile, and easily bruised; cutaneous striae are particularly common in the abdominal area. Bone resorption results in the development of osteoporosis, with consequent increased susceptibility to fractures.

Because glucocorticoids suppress the immune response, patients with Cushing syndrome are also at increased risk for a variety of infections.

Additional manifestations include hirsutism and menstrual abnormalities, as well as a number of mental disturbances, including mood swings, depression, and frank psychosis.

Extra-adrenal Cushing syndrome caused by pituitary or ectopic ACTH secretion is usually associated with increased skin pigmentation, because of melanocyte-stimulating activity in the ACTH precursor molecule.Hypokalemia and metabolic alkalosis are prominent, particularly with ectopic production of ACTH.

Microscopical feature: The morphologic features in the adrenal include bilateral cortical atrophy (in exogenous steroid-induced disease), bilateral diffuse or nodular hyperplasia (most common finding in endogenous Cushing syndrome), or an adrenocortical neoplasm.

Diagnosis

The diagnosis of Cushings syndrome requires demonstration of increasedcortisol production and abnormal cortisol suppression in response to dexamethasone.

For initial screening, measurement of 24-h urinary free cortisol, the 1-mg overnight dexamethasone test [8 A.M. plasma cortisol < 1.8 g/dL (50 nmol/L)] or late night salivary cortisol measurement is appropriate.

Repeat testing or performance of more than one screening test may be required.

Definitive diagnosis is established in equivocal cases by inadequate suppression ofurinary [