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Chronic pancreatitis:
Abdominal pain radiated to back
If s. amylase is low it can be excluded
Guarding is characteristic
NSAIDs are not contra-indicted.…
Guarding and abdominal pain that directly radiates to the back are characteristic of acute pancreatitis.
In chronic pancreatitis pain is either epigastric / left upper abdomen and can be band like.
Reduced with bending forward or sitting.
And both serum lipase and amylase can be normal with the chronic pancreatitis.
NSAIDS ARE CONTRAINDICATED DUE TO THE POSSIBILITY OF GASTRIC ULCERATION.
Xerostomia:Antidepressant treatment Sjogren’s syndromeElderlySialdenitisBeta blockers treatment
What are the immediate effects of transection of spinal cord ar vertibal level T 12Exaggerated reflexesHypotoniaHypertonic bladderPlantar upgoingSensory loss- umbilical level
All
malignancies:
Malignant melanoma – lung metastasis
Endometrial CA – early menapuse is a risk factor
Cervical CA- menorrhagia is a early characteristic feature🚀
Oesophageal CA- appetite is good
Everted edge- basal cell CA
Ok
Acute left ventricular failure management:
IV Frusemide
Aminophyllin
Beta blocker
Invasive ventilation
40% oxygen via CPAP mask
HypercalcaemiaOf primary hyperparathyroidism readily responds to steroidsCan be due to familial hypocalciuria when presents with recurrent renal stonesBone pain is typical of primary hyperparathyroidismThey can present with peptic ulcersForced dieresis and hydration are key RX51.WOF type of arthritis is not seen in psoriatic arthritisSymmetrical small joint arthropathyJaccoud’s arthropathySacroilitisMonoarthritisDIP joint arthropathy52. WOF is not aarecognized factor for osteoporosisEarly menarcheSmokingLow dietary calcium intakeSedentary lifestyleSlender body habbitus53. Following are recognized extra articular manifestations of rheumatoid arthritis exceptCaplans syndromePyoderma gangrenosumPhotosensitive rashScleromalacia perforansPeripheral neuropathy54.Following are poor prognostic factors in RA exceptPersistent synovitisEarly erosive changesExtra articular findingsNegative anti-CCP antibodiesPositive rheumatoid factor55. Features of temporal arteritis includeHeadacheNormal ESRScalp tendernessFeverJaw claudication56.Recognized side effects of steroid use includeAtypical features of infectionsProximal myopathyChronic pancreatitisAvascula necrosis of boneBone marrow suppression57. recogniozed side effects of MTX includeCirrhosisBM suppressionMouth ulcersAcute interstitial pneumonitisMaculopathy58. An 80 yr old male presented with painful swelling of his left knee joint of 2 weeks duration. A knee joint effusion was detected on examination.waht is the most likely causePseudogout of the kneeTrauma to the kneeSeptic arthritis of the kneeRheumatoid arthritis of the kneeOsteoarthritis of the knee59. Following are red flag signs of backache in a 60 yr old femalePain when getting up from the seated positionPresence of fever and weight lossShooting pain down the right legAssociation with bladder symptomsWorse early morning60. WOF are beneficial in Rx in acute goutColchicineAllopurinolCorticosteroidsNSAIDs Febuxostat61. A coronary angiogram with a view to revascularization is indicated inAll post infarct ptsA positive exercise ECG at a high workload not on anti anginal medicationAll unstable angina ptsAcute anterior STEMI with CI to thrombolyticsCardiogenic shock due to post MI VSD62. Recognized causes of sinus bradycardia includeHypoglycaemiaCholestatic jaundiceMyocarditisDigitalis toxicityRaised ICP63. Drugs safe to use in AF with WPW syndrome include the followingDigoxinVerapamilAmiodaroneSotalolFlecainide64. Acuired prolonged QT interval is known to be caused byHypercalcaemiaHypomagnesaemiaHyperkalaemiaAstemazole Erythromycin65. T/F regarding thrombolytic therapy in acute MIThrombolysis within 12 hours reduces ventricular damage and mortality rateActs in synergy with aspirin 150-300mg chewedTissue type plasminogen activator achieves higher reperfusion rates than skIV heparin therapy is mandatory after sk therapyPrimary PCI achieves higher reperfusion rates than thrombolytics66. Drugs known to prolong survival in unstable angina includeNitratesBeta blockersACEILMWHClopidogrel67. Following are known to prolong survival in acute MIPrimaty angioplastyACEIAspirinBeta blockersStatin68.T/F regarding coronary artery disease preventionGoal LDL cholesterol level for secondary prevention is <130mg/dlGoal LDL level for primary CAD prevention in diabetics is <160mg/dlGoal BP for diabetics is 140/90Goal LDL for primary CAD prevention in a hypertensive and a smoker is<130mg/dlStatin therapy is beneficial immediate post MI irrespective of the cholesterol level69. Drugs used in the primary prevention of CAD includeAspirinStatinBeta blockersClopidogrelNitrates70. Drugs known to prolong survival in heart failure includeNitrates with hydralazineDigoxinACEIARBSIvabradine71. Treatments known to prolong survival in heart failure includeMetoprololEplerononeAICDCardiac resynchronization therapyCardiac transplant72. Recognized indications for warfarin therapy includeIntermittent AFMS with sinus rhythmAF with a TIAAF with HT and DMPrimary pulmonary hypertension73. T/F regarding LMWHFondaparinaux is superior in efficacy to enoxaparinA standard dose of fondaparinaux is given to all pts irrespective of their bosy weightDose adjustment is required in renal dysfunctionAnticoagulant effect can be reversed with protamineLevel of anticoagulation can be monitored with activated factor x levels[Xa]74.Regarding severe hypercalcaemiaSymptoms occur when serum calcium is >3mmol/lRarely can present as comaST segment depression responsive to Rx of hypercalcaemia may be seenCalcitonin is the first line RX in MxGlucocorticoids should be considered in pts with vitamin D dependent hypercalcaemia75. Ischaemic strokeCan be reliably diagnosed at the bedside by a neurologist Surgery may be indicated in some pts with ischaemic strokeEarly administration of aspirin minimizes the cerebral damage due to the incident strokeHeparin should be considered in pts with progressive symptomsDexamethasone is standard care for large infarcts with progressive symptoms76. TIATo diagnose according to the new criteria a brain scan is requiredTIA with transient weakness is more likely to lead a disabling stroke than a TIA causing amaurosis fugaxEarly investigation is the key to preventing a strokeCHAD score helps prognosticate TIAsIf a pt with TIA has 99% occlusioj of the corresponding ICA he should be heparinised77. CI for thrombolysis includeCurrent aspirin useBeing on warfarinA minor stroke 1 month beforeAge over 80yrsDemonstrable clot occluding the ICA78.Parkinson’s diseaseBradykinesia is a typical featureHas a better prognosis than MSAHearing impairment may preceed motor symptomsSense of smell is often affected in PDEarly memory impairment suggests alternative diagnosis79. MSAThose with early autonomic dysfunction have a worse prognosisDiagnosis is made clinicallyMRI is helpful in the evaluation Humming bird sign is seen in MRIAnal sphincter EMG may show denervation changes80.TremorParkinsonian tremor is the most disabling type of tremorAction tremor is typically seen in essential tremorIntention tremor is seen in cerebellar diseaseBetablockers are very effective in controlling intention tremorOrthostatic tremor responds to clonazepam81. SleepHypersomnolence is the most common sleep disorderMost of adult sleep is in REMNormal person has about 10 sleep cycles every night Dreaming occurs in REMSleep walking occurs in NREM82. Subacute combined degeneration of the spinal cord80% of pts with pernicious anaemia suffer from this neurological conditionMost pts have associated megaloblastic anaemiaIs excluded if the pt has a normal Hb levelClinical features are caued by demyelination of posterior columns and spinothalamic tractsSphincters may get involved in later stagesCopper deficiency could present with similar clinical findings
HypercalcaemiaOf primary hyperparathyroidism readily responds to steroidsCan be due to familial hypocalciuria when presents with recurrent renal stonesBone pain is typical of primary hyperparathyroidismThey can present with peptic ulcersForced dieresis and hydration are key RX51.WOF type of arthritis is not seen in psoriatic arthritisSymmetrical small joint arthropathyJaccoud’s arthropathySacroilitisMonoarthritisDIP joint arthropathy52. WOF is not aarecognized factor for osteoporosisEarly menarcheSmokingLow dietary calcium intakeSedentary lifestyleSlender body habbitus53. Following are recognized extra articular manifestations of rheumatoid arthritis exceptCaplans syndromePyoderma gangrenosumPhotosensitive rashScleromalacia perforansPeripheral neuropathy54.Following are poor prognostic factors in RA exceptPersistent synovitisEarly erosive changesExtra articular findingsNegative anti-CCP antibodiesPositive rheumatoid factor55. Features of temporal arteritis includeHeadacheNormal ESRScalp tendernessFeverJaw claudication56.Recognized side effects of steroid use includeAtypical features of infectionsProximal myopathyChronic pancreatitisAvascula necrosis of boneBone marrow suppression
Polymyalgia rheumatic:
Proximal muscle weakness
High CPK
Associated with malignancy 🚀
Common in fourth decadem
High ALP
Can be associated with malignancy
Angiotensin:🚀
Secrete vasopressin
Secrete noradrenalin
Constrict efferent arterioles
Sodium and water resorption
Diuresis
Angiotensin II (Ang II), a potent vasoconstrictor, stimulates the formation and secretion of aldosterone from the adrenal gland, and has pleiotropic effects on cellular growth.
The majority of Ang II is derived from the precursor angiotensin I (Ang I), which originates from angiotensinogen, produced by the liver. The formation of angiotensin I from angiotensinogen is rate-limited by the protease renin which is produced from the juxtaglomerular cells of the kidney.
Primary stimulation for renin secretion includes:
impaired renal perfusion,
salt depletion, and adrenergic stimulation.
Ang II inhibits renin secretion, via negative feedback loop. Although the majority of Ang I is converted to Ang II primarily through the activity of ACE, non-ACE pathways also exist and modulate the production of Ang II.
The highest concentration of ACE exists within the pulmonary circulation; however, many studies have documented the existence of local tissue RAAS.Ang II is involved with vascular tone and endothelial function, cardiac contractility, and impulse propagation, and stimulates the formation and secretion of aldosterone; it has pleiotropic effects on cellular growth and apoptosis.
Regarding wernicke’s encepahalopathy
May be precipitated by a high protein diet
Vegetarianism is a common cause
B/L lateral rectus palsies may occur
Papilloedema is common
MRI may help in the diagnosis
Signs and symptomsIn addition to the classical triad of symptoms—encephalopathy, ataxic gait, and oculomotor dysfunction—clinical signs of WE may include the following:Acute confusion/DeliriumAtaxiaOphthalmoplegiaMemory disturbanceHypothermia with hypotensionDelirium tremens
DiagnosisThe clinical diagnosis of WE in alcoholics requires two of the following four signs:
(i) dietary deficiencies
(ii) eye signs,
(iii) cerebellar dysfunction, and (iv) either an altered mental state or mild memory impairment. Although WE remains a clinical diagnosis with no characteristic abnormalities in diagnostic studies, the use of laboratory and radiographic tests remains important to exclude alternate or coexisting medical conditions.ManagementRapid correction of brain thiamine deficiency is the goal of therapy.
Administration of thiamine improves the patient’s condition to some degree in almost all cases; however, persistent neurologic dysfunction is common. Oral absorption is unreliable in patients at risk of Wernicke encephalopathy, which emphasizes the importance of parenteral treatment.
Although as little as 2 mg of thiamine may be enough to reverse symptoms, the dose of thiamine required to prevent or treat WE in most alcoholic patients may be as high as greater than 500 mg given once or, preferably, 2 or 3 times daily parenterally, intravenous is preferred to intramuscular administration.
EtiologyCausesThiamine deficiency is characteristically associated with chronic alcoholism, because it affects thiamine uptake and utilization. In long-term alcoholics, malnutrition can reduce intestinal thiamine absorption by 70%, decreasing serum levels of thiamine to between 30% and 98% below the lower level established for normal subjects. Thiamine acts as a coenzyme in the metabolism of glucose and lipids, and, as stores of water-soluble vitamins are limited in the body, deficiency can present within 2 to 3 weeks of cessation of intake.
Chronic alcohol consumption does not necessarily result in WE if dietary thiamine intake is adequate. It may induce thiamine deficiency through several potential mechanisms: genetic predisposition, replacement of vitamin-containing foods by the high calorific value of alcohol, impaired absorption of thiamine from the gut, impairment of storage by the liver, thiamine transport problems, other nutritional deficiencies, decreased phosphorylation to thiamine pyrophosphate and excessive requirements for the metabolism of alcohol.
WE may develop in nonalcoholic conditions, such as prolonged starvation, hyperemesis gravidarum, and bariatric surgery.
The numerous reports of severe thiamine deficiency after obesity surgery have led to the expression "bariatric beriberi.” Other causes of thiamine deficiency include total parenteral nutrition deficient in thiamine, formula deficient in thiamine, and hemodialysis-induced thiamine deficiency in patients with end-stage renal disease.Other uncommon etiologies of WE are:
forced or self-imposed starvation, protein-energy malnutrition resulting from inadequate diet or malabsorption (from celiac sprue), conditions associated with protracted vomiting (eg, hyperemesis gravidarum), carbohydrate loading in the presence of marginal thiamine stores (feeding after starvation), other gastric bypass surgeries, . A correlation between hemodialysis and WE has been demonstrated possibly secondary to inadvertent dialysis of the water-soluble thiamine combined with malnutrition in the end-stage renal disease population.
The most common inciting factor precipitating WE in the setting of thiamine deficiency is infection. Concomitant illnesses, such as pneumonia or even meningitis, do not exclude a co-diagnosis of WE.
Iatrogenic exacerbation of WE can occur with prolonged glucose or carbohydrate loading in the setting of thiamine deficiency.
However, a single, acute administration of glucose does not appear to cause this effect. Nutritionally deficient patients receiving glucose should also receive thiamine, but urgent administration of glucose should not be delayed pending thiamine administration.
Subacute combined degeneration of the spinal cord
80% of pts with pernicious anaemia suffer from this neurological condition
Most pts have associated megaloblastic anaemia
excluded if the pt has a normal Hb level
Clinical features are caued by demyelination of posterior columns and spinothalamic tracts
Sphincters may get involved in later stages
Copper deficiency could present with similar clinical findings
The neurologic features are attributable to pathology in the peripheral and optic nerves, posterior and lateral columns of the spinal cord (subacute combined degeneration), and in the brain.
Interestingly, hematologic and neurologic manifestations are occasionally dissociated.
An inverse correlation in the severity of both manifestations has been suggested. In patients with neuropsychiatric abnormalities, 28% lack anemia or macrocytosis.
Clinical manifestations due to vitamin B-12 deficiency are unrelated to etiology. In a prospective comparative study between antiparietal cell antibody positive and negative patients, no significant difference was shown in clinical, electrodiagnostic, and radiological features.
Although the clinical features of vitamin B-12 deficiency may consist of a classic triad of weakness, sore tongue, and paresthesias, these are not usually the chief symptoms.
Onset is subacute or gradual, although more acute courses have been described, in particular after N 2 O exposure.
Onset is often with a sensation of cold, numbness, or tightness in the tips of the toes and then in the fingertips, rarely with lancinating pains. Simultaneous involvement of arms and legs is uncommon, and onset in the arms is even rarer.
Paresthesias are ascending and occasionally involve the trunk, leading to a sensation of constriction in the abdomen and chest.
Untreated patients may develop limb weakness and ataxia.In 1991, Healton et al performed detailed neurologic evaluations of 143 patients with vitamin B-12 deficiency; 74% presented with neurologic symptoms. [19]Isolated numbness or paresthesias were present in 33%.Gait abnormalities occurred in 12%.Psychiatric or cognitive symptoms were noted in 3%.Visual symptoms were reported in 0.5%.
Symptoms include subacute progressive decrease in visual acuity, usually caused by bilateral optic neuropathy and rarely pseudotumor cerebri or optic neuritis.
Rare autonomic features include orthostasis, sexual dysfunction, and bowel and bladder incontinence.
Other symptoms include lightheadedness and impaired taste and smell.
Nonneurologic symptoms, some of which may also reflect autonomic nervous system involvement, were present in 26%.
Constitutional symptoms, including anorexia and weight loss occurred in 50%. Low-grade fever that resolves with treatment occurred in 33% of cases. Other symptoms include fatigue and malaise.
Cardiovascular symptoms include syncope, dyspnea, orthopnea, palpitations, and angina.
Gastrointestinal symptoms include heartburn, flatulence, constipation, diarrhea, sore tongue, and early satiety.PhysicalMost patients exhibit signs of peripheral nervous system (PNS) or spinal cord involvement, but the extent of PNS involvement remains unclear, in part because both neuropathy and myelopathy can cause impaired vibration sense, ataxia, and paresthesias. Either can be affected first in the early stages. Objective sensory abnormalities usually result from posterior column involvement and less often from PNS disease.Isolated neuropathy was reported in 25% of patients.Myelopathy occurred in 12% of cases.A combination of neuropathy and myelopathy was noted in 41%.
Neuropsychiatric manifestations, such as recent memory loss with reduced attention span and otherwise normal cognition, depression, hypomania, paranoid psychosis with auditory or visual hallucinations (megaloblastic madness), violent behavior, personality changes, blunted affect, and emotional liability, were reported in 8% of patients.
Ocular findings included a cecocentral scotoma and occurred in 0.5% of cases. Others have described optic atrophy, nystagmus, small reactive pupils, and chiasmatic lesion causing bitemporal hemianopia.
Early in the course, poor joint position and vibration sense predominate. Typically, the legs are affected before the arms. Rarely are all limbs affected simultaneously. A Romberg sign is commonly found. The gait may be wide based.
On presentation, 50% of patients have absent ankle reflexes with relative hyperreflexia at the knees. Plantars are initially flexor and later extensor. A Hoffman sign may be found.
As the disease progresses, ascending loss of pinprick, light touch, and temperature sensation occurs. Later, depending on the predominance of posterior column versus cortical spinal tract involvement, ataxia or spastic paraplegia predominates. Then, PNS involvement causes distal limb atrophy.
Cognitive testing may reveal mild impairment or frank dementia.
Nonneurologic manifestations include the following:General - Lemon-yellow waxy pallor, premature whitening of hair, flabby bulky frame, mild icterus, and blotchy skin pigmentation in dark-skinned patientsCardiovascular - Tachycardia, congestive heart failureGastrointestinal - Beefy, red, smooth, and sore tongue with loss of papillae that is more pronounced along edgesCausesInadequate vitamin B-12 absorption is the major pathomechanism and may result from several factors.Intrinsic factor deficiencyPA accounts for 75% of cases of vitamin B-12 deficiency.
It is an autoimmune attack on gastric IF. Antibodies are present in 70% of patients. They may block the formation of the cobalamin-IF complex or block its binding with cublin. Other antibodies are directed at parietal cell hydrogen-potassium adenosine triphosphatase (ATPase).Destruction of gastric mucosa can occur from gastrectomy or Helicobacter pylori infection. Deficient vitamin B-12 intake: Intake may be inadequate because of strict vegetarianism (rare), breastfeeding of infants by vegan mothers, alcoholism, or following dietary fads.Disorders of terminal ileum: Tropical sprue, celiac disease, enteritis, exudative enteropathy, intestinal resection, Whipple disease, ileal tuberculosis,Competition for cobalamin: Competition for cobalamin may occur in blind loop syndrome or with fish tapeworm (Diphyllobothrium latum).Abnormalities related to protein digestion related to achlorhydria: Abnormalities include atrophic gastritis, pancreatic deficiency, proton pump inhibitor use, and Zollinger-Ellison syndrome, in which the acidic pH of the distal small intestine does not allow the cobalamin-IF complex to bind with cublin.Medications: Medications include colchicine, neomycin, and p -aminosalicylic acid.
In AIDS, vitamin B-12 deficiency is not infrequent. Although the exact etiology remains obscure, it is likely a multimodal process involving poor nutrition, chronic diarrhea, ileal dysfunction, and exudative enteropathy. Low vitamin B-12 levels may be more common in late than in early HIV disease.
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