BIMONTHLY ASSESSMENT
BIMONTHLY EXAM NOVEMBER :
DR K VAISHNAVI - GEN MED PGY2
Online question paper link :
https://medicinedepartment.blogspot.com/2020/11/blended-learning-bimonthly-assignment.html?m=1
First patient question :
1)"55 year old male patient came with the complaints of
Chest pain since 3 days ;Abdominal distension since 3 days
Abdominal pain since 3 days and decreased urine output since 3days and not passed stools since 3days
https://sreejaboga.blogspot.com/2020/11/is-online-e-log-book-to-discuss-our.html?m=1
a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes ?
Ans ) This case is a 55 yr old male with sudden onset of abdominal pain and distension.
A) Anatomical location of problems and their etiologies:
1) Acute pancreatitis - secondary to gall stones obstructing common bile duct and pancreatic enzymes secretion not reaching dueodenum and are activated within acinar cells causing auto digestion of pancreas and inflammation .
Alcohol and smoking could be confounding factors.
Gallstones continue to be the leading cause of acute pancreatitis in most series (30–60%). The risk of acute pancreatitis in patients with at least one gallstone <5 mm in diameter is fourfold greater than that in patients with larger stones. Alcohol is the second most common cause, and risk increases if patient is also a smoker causing endothelial dysfunction.
Autodigestion is a currently accepted pathogenic theory; according to this theory, pancreatitis results when proteolytic enzymes (e.g., trypsinogen, chymotrypsinogen, proelastase, and lipolytic enzymes such as phospholipase A2) are activated in the pancreas acinar cell rather than in the intestinal lumen. A number of factors (e.g., endotoxins, exotoxins, viral infections, ischemia, oxidative stress, lysosomal calcium, and direct trauma) are believed to facilitate premature activation of trypsin. Activated proteolytic enzymes, espe-cially trypsin, not only digest pancreatic and peripancreatic tissues but also can activate other enzymes, such as elastase and phospholipase A2. Spontaneous activation of trypsin also can occur.
3 phases of acute pancreatitis are :
1) Initial phase - There is intra pancreatic activation of enzymes and acinar cell injury.
2) The second phase of pancreatitis involves the activation, chemoattraction, and sequestration of leu-kocytes and macrophages in the pancreas, resulting in an enhanced intrapancreatic inflammatory reaction.
3) The third phase of pancreatitis is due to the effects of activated proteolytic enzymes and cytokines, released by the inflamed pancreas, on distant organs. The active enzymes and cytokines then digest cellular membranes and cause proteolysis, edema, interstitial hemorrhage, vascular damage, coagulation necrosis, fat necrosis, and parenchymal cell necrosis.
Cellular injury and death result in the lib-eration of bradykinin peptides, vasoactive substances, and histamine that can produce vasodilation, increased vascular permeability, and edema with profound effects on many organs.
The systemic inflam-matory response syndrome (SIRS) and acute respiratory distress syn-drome (ARDS), as well as multiorgan failure, may occur as a result of this cascade of local and distant effects.
Reference : HARRISON 20 EDITION - pg 2439
2) Ascitis and pleural effusion and hypotension - They are all complications of acute pancreatitis due to third space loss.
Pt is having sob due to Acidosis of renal failure or ARDS seen in acute pancreatitis.
Due to inflammation there is liberation of bradykinin peptides, vasoactive substances, and histamine that can produce vasodilation, increased vascular permeability.
Also ascitic fluid amylase is high indicating one of the cause of ascitis as pancreatitis.
Elevation of ascitic fluid amylase occurs in acute pancreatitis as well as in (1) ascites due to disruption of the main pancreatic duct or a leak-ing pseudocyst and (2) other abdominal disorders that simulate pan-creatitis (e.g., intestinal obstruction, intestinal infarction, or perforated peptic ulcer). Elevation of pleural fluid amylase can occur in acute pan-creatitis, chronic pancreatitis, carcinoma of the lung, and esophageal carcinoma.
3) Pt dint pass stools due to paralytic ileus.
4) Pt developed acute renal failure again due to decreased intra vascular volume because of increased vascular permeability and vasodilation.(Distributive shock )
5) Thyroid status usually should not be evaluated ideally in acute stress conditions in icu .
Critical illness is often associated with alterations in t thyroid hormone concentrations in patients with no previous intrinsic thyroid disease.
Sick euthyroid syndrome is the commonest endocrine change seen in critically ill patients.
The most common thyroid hormonal change reported in critically ill patients is reduced serum T3 level. Under normal circumstances 100% of T4 and 10-20% of T3 are directly secreted by the thyroid gland. 5`deiodinase causes peripheral
monodeiodination of T4 contributing to 80-90% of T3 and also increases the clearance of the inactive isomer reverse T3 (rT3) .
Critical illness decreases 5`deiodinase activity, thereby, decreasing T4 to T3 conversion and rT3 clearance
.Thus, T3 decreases and rT3 increases .
Pt was in SIRS ..having more than 2 points
And is having severe acute pancreatitis
Severe acute pancreatitis is characterized by persistent organ failure (>48 h). Organ failure can be single or multiple. A CT scan or magnetic resonance imaging (MRI) should be obtained to assess for necrosis and/or complications.
Sequence of events :
Gall stones , alochol , smoking --Acute pancreatitis ---- SIRS ---Increased vascular permeability -
Third space loss --- AKI --Hypercoagulable state.
Intially fluid challenge was given..but due to refractory metabolic acidosis and decreased urine output and no improvement overall hemodialysis was initiated.
Pt tlc started raising later so was started on antibiotics. But there is no role of prophylactic antibiotics in Acute pancreatitis unless there is proven infected necrosis.
Timeline of events :
a1) Added 17/11/2020 Mention the optimal diagnostic interventions in the patient done and that you may further order in a low resource setting to fathom the etiologic possibilities.
Ans ) CECT Abdomen can be done to look for necrosis and other local complications of pancreatitis.
But if there is any gall stones obstructing, an ERCP with stenting would be the final treatment and prevention of recurrence.
Rectal NSAID and ERCP with stenting would prevent post ERCP pancreatitis.
b) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them?
B) Pharmacological interventions -
Iv Fluids to maintain intra vascular volume.
Iv antibiotics are usually not indicated ,unless there is infected necrosis.
Second patient question :
A 55 year old male, shepherd by occupation, presented to the OPD with the chief complaints of fever (on and off), loss of appetite, headache, body pains, generalized weakness since 2 months, cough since 2 weeks and vomitings and pain abdomen since 2 days.
https://aakansharaj.blogspot.com/2020/11/55-year-old-male-with-anemia.html?m=1
a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
Ans) Pt has Anemia ,acute renal failure, lytic bony leisons , cxr and sputum reports showing pneumonia.
On evaluation for Anemia , retic count showing hypoproliferative picture with absolute retic count 0.3 and reticulocyte index 0.13 .
With total proteins being so high (12.4 g/dl) and albumin (1.84 g/dl) - raises a suspicion of high gamma gap ( alpha ,beta ,gamma globulins )
There is excessive production of gamma globulins indicating multiple myeloma .
-MGUS - is a pre malignant condition where there is a)no end organ damage
b) Serum monoclonal protein less than 3 g/dl
c) Clonal bone marrow plasma cells less than 10%
-Smoldering myeloma -
a)No end-organ damage
b)Monoclonal protein equal to or over 3 g/dl
c) Clonal bone marrow plasma cells 10% to 59%
Multiple myeloma is a plasma cell dyscrasia ,where there are clone of plasma cells causing excessive production of immunoglobulins ,but these immunoglobulins are defective hence confer no immunity and these people are prone for more infections .
Multiple myeloma (MM) is a clonal plasma cell proliferative disorder characterized by the abnormal increase of monoclonal paraprotein leading to evidence of specific end-organ damage.
Anatomical locations of problems and their etiologies:
1) Bone marrow - Monoclonal proliferation of plasma cells
The exact etiology of MM is unknown. However, there is evidence that suggests genetic abnormalities in oncogenes such as CMYC, NRAS, and KRAS may play a role in the development of plasma cell proliferation. MM has also been associated with other factors such as drinking alcohol, obesity, environmental causes such as insecticides, organic solvents), and radiation exposure
2) Lytic bony leisons on skull ("pepper pot skull") - Myeloma bone disease results from overexpression of RANKL by bone marrow stroma. RANKL activates osteoclasts, which resorb bone. Several intracellular and intercellular signaling cascades, numerous chemokines and interleukins are implicated in this complex process.
3) Anemia -
Bone marrow occupation by the expanding plasma cell clone usually manifests as anemia, thrombocytopenia, and leukopenia
4) Renal failure and metabolic acidosis - Excess monoclonal immunoglobulin can cause hyperviscosity, platelet dysfunction and renal tubular damage, leading respectively to neurologic derangement, bleeding, and renal failure.
Renal insufficiency can be acute or chronic. A variety of etiologic mechanisms may be involved, including those related to the excess production of monoclonal light chains (light- chain cast nephropathy), deposition of intact light chains causing nephrotic syndrome, light chain amyloidosis, hypercalcemia, hyperuricemia, dehydration.
These patients can also have bleeding manifestations due to thrombocytopenia and anitbody coated platelets which are defective.
5) Head ache ,paresthesia and blurring of vision- are features of hyper viscosity.
6) Lungs : showing Moderate to gross right pleural effusion and Multilobar consolidations of the right lung, involving upper and middle lobes With Passive collapse of basal segments of right lower lobe .
Pneumonia is because of immunodeficiency state ,as the immunoglobulins produced are defective.
Pleural fluid analysis showing exudative picture suggesting parapneumonic effusion.
7) Multiple myeloma patients can have carpal tunnel syndrome and peripheral neuropathy secondary to amyloidosis.
Data collected from :
https://www.ncbi.nlm.nih.gov/books/NBK534764/
Timeline of events :
b) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them?
ANS ) The preferred treatment for those under the age of 65 is chemotherapy, commonly with bortezomib-based regimens, and lenalidomide-dexamethasone, followed by high-dose therapy with melphalan and autologous hematopoietic stem-cell transplantation (ASCT).
Median survival for newly diagnosed MM is about 44.8 months . MM cannot be cured , but new drugs are available to manage patients with MM.
https://www.hindawi.com/journals/bmri/2016/6848902/
3) Third patient question:
51 Year old man with complaints of B/L pitting pedal edema from 5 to 6months,abdominal distension from 2 to 3 days,SOB from 3days.
nithishaavula.blogspot.com/2020/11/51-yr-old-male-with-hfref.html?m=1
a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
Ans ) 51 year old male with diabetes and hypertension which are risk factors for atherosclerosis and heart failure.
1) Macrovascular and Microvascular dysfunction:
One known hypothesis is adipokine mediated endothelial dysfunction :
Adipokines are cytokines, chemokines and hormones secreted by adipose tissue that couple the regulation of lipid accumulation, inflammation, and atherogenesis, and therefore serve to link obesity with cardiovascular disorders. Obesity-related disorders including metabolic syndrome, diabetes, atherosclerosis, hypertension, and coronary artery disease are associated with dysregulated adipokine(s) expression .
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3006473/#!po=15.3061
2) Heart failure with reduced ejection fraction-.
Lv failure in this patient is secondary to chronic Pressure overload state - hypertension.
Lv failure ---leading to reduced ejection fraction and dilatation of la and increased pulmonary arterial hypertension and pulmonary edema .
Right heart failure is due to PAH.
Left heart failure being the most common cause of right heart failure.
Data collected from harrison 20 edition -1764 pg
3) Atrial fibrillation - In addition to underlying Heart failure, diabetic and hypertension are also risk factors for AF.
Cardiac remodeling, particularly of atria, results in structural and electrical changes that eventually become the cause of deranged rhythm in AF. Structural remodeling is caused by the changes in myocytes and the extracellular matrix, and fibrous tissue deposition also plays a major role in some etiologies. On the other hand, tachycardia and shortening of the refractory period lead to electrical remodeling.
Cardiac remodeling happens in long standing cardiac failure .
4) Due to AF - there is formation and dislodgement of thrombus , leading to stroke in this patient.
Atrial fibrillation is the leading cardiac cause of stroke.
5) Seizures in this patient is again due to stroke .
(Infarct in right frontal lobe ).
Timeline of events:
Q) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them?
ANS) For persistant AF - Patient has to be started on rate controlling drugs like beta blockers ( met-xl)
If the patient is hemodynamically unstable should go for cardioversion ,but here patient was stable.
Non-pharmacological therapy includes ablation therapy. Pacemaker placement is considered in severe cases resulting in heart failure in atrial fibrillation.
The patient should be risk-stratified using the CHADs-2-Vasc score, which is helpful in estimating the risk of stroke per year.
If the patient receives a 0 score, it is considered "low-risk" and anticoagulation is not recommended in such cases.
If the patient receives a score of 1, it falls in the "low-moderate" risk category; the providers should consider anticoagulant or antiplatelet therapy.
If the patient receives a score of greater than 2, they are in the "moderate-high" risk category, and anticoagulation therapy is indicated.
Rate or rhythm control should also be given to the patient; medications such as beta-blockers, calcium channel blockers, amiodarone, dronedarone, and digoxin are available options. HAS-BLED is also a scoring system that can be used to asses the risk of bleeding for the patient.
Non-vitamin K oral anticoagulants (apixaban, dabigatran, edoxaban, and rivaroxaban) are recommended over warfarin.
- CHRONIC HEART FAILURE TREATMENT :
Preload reducing agents - Diuretics ,
Afterload reducing agents - vaso dilators ,ace inhibitors and arb
Beta blockers for preventing cardiac remodeling and reduce mortality.
https://pmj.bmj.com/content/79/937/634
4) Fourth patient question:
35 yr old man with B/L pedal edema with scrotal and penile swelling since 2 months
https://nairaditya97.blogspot.com/2020/11/31-yr-old-male-with-bl-pedal-edema-with.html?m=1
a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
Ans )
1) Heart failure -
As patient is chronic alocholic and will be having thiamine deficiency (wet beri beri )
2) Peripheral neuropathy is again because of thiamine deficiency .
3) It is a high output cardiac failure leading to pedal edema ,raised jvp ,congested hepatomegaly,
Pulmonary edema and pleural effusion.
Timeline of events:
B) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them?
Ans ) Correcting thiamine deficiency is of prime importance.
Reduce the preload by adding diuretics.
Adequate salt and fluid restriction
Bed rest .
Administration of thiamine for wet beriberi varies among authors . Generally, alcohol-related beriberi patients were administered a higher dose of thiamine than non-alcohol-related beriberi patients, because alcohol can inhibit the uptake of vitamin B1 and the phosphorylation of its active form (TPP).
For non-alcohol-related wet beriberi patients, currently, the most common treatment is a daily intravenous treatment of 100 to 200 mg of thiamine.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5851725/
THANK YOU !
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