Tuesday, 24 November 2020

Bimonthly assignment for November

I have been given the following cases to solve in an attmept to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.

This is the link of the questions asked regarding the cases:

https://medicinedepartment.blogspot.com/2020/11/blended-learning-bimonthly-assignment.html?m=1

Below are my answers to the Medicine Assignment based on my comprehension of the cases. 

Question 1) Pain in the epigastric region differentials

Inferior wall MI(normal ecg and echo)

Acute pancreatitis(radiation to the back)-usg finding and elevated serum amylase level

Perforated peptic ulcer 

Causes of acute pancreatitis-harrison pg no 2348



Gall stones :https://gi.org/topics/gallstone-pancreatitis/

This occurs at the level of the sphincter of Oddi, a round muscle located at the opening of the bile duct into the small intestine. If a stone from the gallbladder should travel down the common bile duct and get stuck at the sphincter, it blocks outflow of all material from the liver and pancreas. This results in inflammation of the pancreas that can be quite severe.



2)sob- acidosis due to renal failure

         ? Ards secondary to sepsis/pancreatitis

          Pleural effusion due to acute pancreatitis

          



3)decreased urine output-pre renal Aki secondary to volume loss(oliguric)

3rd space loss due to pancreatitis

Sepsis induced aki

4) abdominal distention with constipation and nausea

Secondary to paralytic ileus

2) pharmacological interventions

https://link.springer.com/article/10.1007/s00534-005-1050-8

1)fluid replacement

Increased vascular permeability in acute pancreatitis causes the loss of intravenous fluid and reduces plasma volume. In severe cases, in patients with massive ascites, pleural effusion, and retroperitoneal and mesenteric edema, circulating plasma volume decreases markedly. Hypovolemia may lead to shock and acute renal failure, and, because hypovolemic shock may impair the pancreatic microcirculation and promote pancreatic ischemia and necrosis, restoration and maintenance of plasma volume is crucial in severe acute pancreatitis.

2) antibiotics

On the other hand, a placebo-controlled, double-blind trial of ciprofloxacin  +  metronidazole in patients with predicted severe acute pancreatitis showed that prophylactic administration of these antibiotics did not prevent pancreatic infection (Level 1b).

3)analgesics


4) nebulization in view of b/l wheeze secondary to ?copd

5)diuretics for decreased urine output due to renal failure


Non pharmacological interventions

1)nill by mouth

https://pubmed.ncbi.nlm.nih.gov/27107634/

2)ryles tube catheterisation

3)oxygenation



Question 2:(55M)

https://aakansharaj.blogspot.com/2020/11/55-year-old-male-with-anemia.html?m=1

1)bone marrow and bones

2)kidneys

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3205153/

The pathophysiology of renal failure in multiple myeloma is often multifactorial but is mostly due to the high excretion of immunoglobulin free light chains. When the light chains combine with Tamm-Horsfall proteins, they form obstructing casts (5). Chemotherapy should therefore be initiated rapidly to decrease light chain production. Intravenous fluids can be given to treat volume depletion, hypercalcemia, or hyperuricemia.

3)lungs(infection-incrsead susceptibility)

https://www.cancer.org/cancer/multiple-myeloma/causes-risks-prevention/what-causes.html

Researchers have found that patients with plasma cell tumors have important abnormalities in other bone marrow cells and that these abnormalities may also cause excess plasma cell growth. Certain cells in the bone marrow called dendritic cells release a hormone called interleukin-6 (IL-6), which stimulates normal plasma cells to grow. Excessive production of IL-6 by these cells appears to be an important factor in development of plasma cell tumors.


A) pharmacological interventions


1. Antibiotics (?aytpical pneumonia-azithromycin)


https://www.intechopen.com/books/update-on-multiple-myeloma/infections-in-patients-with-multiple-myeloma-in-the-era-of-novel-agents-and-stem-cell-therapies


However, the infections encountered in patients with MM include: (1) bacterial infections, predominantly involving respiratory and urinary tract, caused by Streptococcus pneumonia, Staphylococcus aureus, Haemophilus influenzae, Klebsiella pneumonia, Escherichia coli (2) viral infections caused by herpes simplex virus (HSV), VZV, and cytomegalovirus (CMV); (3) fungal infections caused by Candida species and Aspergillus species; and (4) Pneumocystis jiroveci pneumonia


2. Blood transfusion




B)non pharmacological


1. Pleural fluid analysis


2. Imaging -xray skull, hrct chest


3. Serum electrophoresis,sputum culture



Question 3)


http://nithishaavula.blogspot.com/2020/11/51-yr-old-male-with-hfref.html?m=1


1)pedal edema with abdominal distention with sob suggestive of right heart failure or renal failure


B)etilogy of rt heart failure


https://www.ncbi.nlm.nih.gov/books/NBK459381/


chronic conditions of pressure overload may lead to RVF. These include:

Primary pulmonary arterial hypertension (PAH) and secondary pulmonary hypertension (PH) as seen in chronic-obstructive pulmonary disease (COPD) or pulmonary fibrosis)

Congenital heart disease (pulmonic stenosis, right ventricular outflow tract obstruction, or a systemic RV).

The following conditions result in volume overload causing RVF:

Valvular insufficiency (tricuspid or pulmonic) 

Congenital heart disease with a shunt (atrial septal defect (ASD) or anomalous pulmonary venous return (APVR)).

Another important mechanism that leads to RVF is intrinsic RV myocardial disease. This includes:

RV ischemia or infarct

Infiltrative diseases such as amyloidosis or sarcoidosis

Arrhythmogenic right ventricular dysplasia (ARVD)

Cardiomyopathy

Microvascular disease.

Lastly, RVF may be caused by impaired filling which is seen in the following conditions:

Constrictive pericarditis

Tricuspid stenosis

Systemic vasodilatory shock

Cardiac tamponade

Superior vena cava syndrome

Hypovolemia. 

2 )Pharmacological interventions

https://heart.bmj.com/content/104/5/407(meta analysis with each class of drugs)

Preload reducers

Diuretics

Afterload reducers-ace inhibitors

Rate controlling agents-beta blockers



Antiepileptics for known case of epilepsy

Insulin for glycemic control in diabetes.



Non pharmacological interventions

Salt and fluid restriction

https://pubmed.ncbi.nlm.nih.gov/23787719/

Individualized salt and fluid restriction can improve signs and symptoms of CHF with no negative effects on thirst, appetite, or QoL in patients with moderate to severe CHF and previous signs of fluid retention.



Question 4

1)heart(rt and left)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5851725/

Wet beriberi is one of the clinical syndromes associated with thiamine deficiency. Thiamine, in its phosphorylated form thiamine pyrophosphate (TPP), is the precursor for the cofactor of both pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, which are both key enzymes of the Krebs cycle. The Krebs cycle is an essential part of aerobic glucose metabolism. A decrease in the activity of these 2 enzymes due to thiamine deficiency may lead to the tissue accumulation of pyruvate and lactate.[1] Moreover, the accumulation of pyruvate and lactate decreases peripheral resistance and increases venous blood flow, increasing the cardiac preload. Increased preload and myocardial dysfunction ultimately leads to congestive heart failure.

https://www.medindia.net/patients/patientinfo/beriberi-disease.htm

Other conditions cause beriberi include:

Excessive alcohol usage, which results in inadequate intake in the diet as well as prevents the body from absorbing and storing vitamin B1.
Genetic beriberi, which is an inherited condition where people lose the ability to absorb thiamine from foods. Symptoms usually present during adulthood.
Pregnancy; pregnant women often present with vitamin B1 deficiency. Breastfeeding infants can suffer from vitamin B1 deficiency if the mother is deficient.
People with endocrine disorders like hyperthyroidism who require extra vitamin B1.
Chronic liver disease, which prevents the body from absorbing sufficient vitamin B1.
Kidney dialysis, which leads to a loss of vitamin B1.
A prolonged bout of diarrhea, which also leads to a loss of vitamin B1.

1) pharmacological interventions

Diuretics

Thiamine

2)non pharmacological interventions

Salt and fluid restriction




Saturday, 21 November 2020

A 65 yr old male with Delirium under evaluation , Pre-renal AKI, Non healing ulcer over right foot, Anemia: microcytic hypochromic under evaluation

This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent.


Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs. 


This E log book also reflects my patient-centered online learning portfolio and your valuable inputs on the comment box is welcome. 


CASE PRESENTATION


A 65year old male patient shepherd by occupation came with c/o ulcer over dorsum of lt foot since 6 months and disoriented speech since 1 day.

Pt was apparently asymptomatic 6months ago then he sustained trauma to his right lower limb and developed ulcer and right lower limb edema. Pt has been on regular dressings for the ulcer with RMP.

3months ago pt developed left lower limb edema also

1week ago h/o giddiness and fall(pt did not eat food that day),pt did not remember the event of fall but according to attendors there was no loss of consciousness,no trauma,no seizures

Since 5days c/o involuntary micturation,involuntary passing stools and spitting everywhere,altered behaviour, irrelevant talk,visual hallucinations,no orientation to person place

Pt not sleeping since 4days

Decreased appetite since 1week

Occasional alcoholic 

smoker since 40 years

Past history:

Not a k/c/o DM,HTN,CAD,CVA, Epilepsy

Personal history:

Mixed diet

Decreased  appetite 

Sleep not adequate 

Bowel and bladder involuntary 

Occasional alcoholic

Smoker since 40 yrs

O/E

Pt is conscious, not orientated to time,place and person, thin built

Vitals

Pt is Afebrile

BP - 110/70 mmhg

PR - 82bpm

RR - 16 CPM

CVS - S1S2 heard

RS - BAE present 

P/A - soft , non tender 

CNS - No neck rigidity, signs of meningitis

           Motor and sensory not elicitable


Psychiatry notes:

Day 1:

C/O : sleep disturbance, irrelevant talk , irritability, self talking, decreased appetite since 3 days

Pt was apparently asymptomatic 1week back,he was sitting in the field during day time, pt fell down and was brought to home by village people, pt was taken to a nearby hospital, after 3 days pt started behaving abnormally ,sleep decreased, appetite decreased,self talking,visual hallucinations, irrelevant talk, spitting frequently, involuntarily passing urine

H/O consumption of whiskey 90ml , toddy 500ml occasionally, h/o tobacco smoking since 20 yrs , 2 cigarettes per day , stopped 3 months back (OD denies withdrawal symptoms)

No H/O suspiciouness ,self smiling, low mood , crying spells, fear , palpitations , repititive thoughts, suicidal ideation

MSE - GAB- pt is sitting on bed , frequently trying to go outside of ward 

ETEC negative

PMA Normal, rapport CNBE

further MSE CNBE 

No Orientation to time ,place , person

DAY 2:

Pt reports  to have slept well, decreased  irritability 

MSE - GAB : pt sitting on the wheel chair, responding to oral commands.  PMA normal ETEC present not sustained, rapport established with difficulty

RT increased,  relevant,  coherent 

Affect - dysphoric

Thought and perception - CNBE

Not oriented to time , orientated  to place, person.


INVESTIGATIONS:



LFT

TB 0.66

DB 0.2

SGOT 17

SGPT 17

ALP 279

TP 4.7

Alb 2

RBS 70



DIAGNOSIS:

Delirium under evaluation

Pre-renal AKI

Non healing ulcer over right foot

Anemia:microcytic hypochromic under evaluation


TREATMENT:

1. RF FEEDS 200 ML MILK WITH PROTEIN POWDER 2ND HRLY, 100ML PLAIN WATER4TH HRLY

2. IVF 1 UNIT NS , 1 UNIT DNS @ 75ML/HR

3. INJ OPTINEURON 1AMP IN 100ML NS/IV/OD 

4. INJ PANTOP 40MG IV/OD

5. TAB OROFER XT PO/BD

6. TAB OLANZAPINE 2.5 MG PO/BD

7. INJ HALOPERIDOL 2.5 MG IM

8. INJ LORAZEPAM 2 MG IM/ SOS IF SLEEPLESS

9. ZYTEE GEL FOR L/A

10. GRBS CHARTING 6TH HRLY 

11. I/O CHARTING 

12. SYP LACTULOSE 15 ML PO/BD 



Friday, 13 November 2020

27 yr old female with GERD , Surgical premature menopause , Pyrexia Of Unknown Origin , ? K/C/O Pulmonary Koch's

This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent. 


Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs. 


This E log book also reflects my patient-centered online learning portfolio and your valuable inputs on the comment box is welcome. 


CASE PRESENTATION


27 yr old female married at age of 11 years , consanguinous marriage, mother of 2, 1st pregnancy at age of 14 years, 2nd pregnancy at 16 yrs c-section
6 months after c-section pt noticed pain abdomen which is continuous, daily. H/o Irregular menstrual cycles, white discharge
Used medication for regularisation of cycles. This continued for 1 yr and later she underwent hysterectomy (done 1 yr back )

After 20 days pt noticed low grade fever ,nausea,loss of appetite for 2-3 months. Later she was hospitalized for 1-2 days and treated for typhoid (widal test +), fever subsided only with medication and recurred when stopped.

H/o using ATT for 6 months I/V/O low grade fever, after ATT pt felt some improvement

HOPI
C/O low grade fever nocturnal, easy fatiguabality, nasuea since 3 yrs, vomitinngs intermittently,bowel regular, retro sternal heart burn +, regurgitation sym+ , abdominal fullness +, pt avoids food because of nasuea and abd fullness, belching +, generalised weakness, multiple joint pains, early morning stiffness+

No H/O palpitations,SOB,pain abdomen, rash , pet exposure, palpable, no H/O allergies,  swelling over body

PERSONAL HISTORY:

Normal appetite 
Mixed diet
Sleep adequate
Bowel and bladder regular  
No addictions 

O/E:

Pt is C/C/C 
Moderately built and nourished
Pt is febrile
BP: 100/60 mm/hg
PR: 106 bpm
RR: 20 cpm
SPO2: 99% at room air
CVS: S1,S2 +
RS: NVBS +, BLAE +
CNS: NAD

INVESTIGATIONS:






DIAGNOSIS:

GERD
Surgical premature menopause
Pyrexia Of Unknown Origin 
? K/C/O Pulmonary Koch's

TREATMENT:

1. Inj. Optineuron 1 amp in 500ml NS/IV/OD
2. TAB. PANTOP 40 mg PO/OD
3. TAB. ULTRACET /PO/QID
4. TEMP. CHARTING  4th hrly

Sunday, 8 November 2020

Decompensated Alcoholic Liver Disease with Rt pleural effusion , pityriasis versicolor

This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent. 


Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs. 


This E log book also reflects my patient-centered online learning portfolio and your valuable inputs on the comment box is welcome. 


CASE PRESENTATION

33yr old male pt came with c/o abdominal distension since 7 days insidious in onset , gradually progressive and associated with pedal edema upto knee , pitting type from 7days and sob on exertion since 5 days, yellowish discolouration of eyes from 5days
C/o fever since 10days on and off,relieved with medication,low grade, not associated with chills and rigor

No H/O cold, cough, burning micturation, decreased output, chest pain , palpitation, giddiness, Malena, hemetemesis, vomiting, 

Alcoholic from 15yrs daily 90ml stopped one month ago
Smoker beedi 10 per day 

Past history:
Not a k/c/o DM , HTN, 
H/o jaundice 4yrs back used medication (unknown)

Personal history:
Appetite normal
Sleep adequate
Bowel movements regular

O/E

Pt is conscious, coherent, cooperative moderately built and moderately nourished

Pallor Present
No cyanosis, clubbing, lymphadenopathy,
Pedal edema present , pitting type

Hypo pigmented patches present over neck and upper region of chest diagnosed as pytriasis versicolor
Wood lamp examination:

Vitals:

Pt is afebrile
Bp: 140/90 mmHg
Pulse: 78bpm
RR: 18cpm
CVS: S1 S2 heard
RS: Absent breath sounds in rt IAA area
CNs: NAD
Per abdomen distended


Investigations:
Diagnosis: 

1. Chronic alcoholic liver disease with portal hypertension 
2. Right pleural effusion
3. Normocytic normochromic anemia
4. Pityriasis versicolor
5. Hypokalemia resolving

Treatment:

1.INJ. CEFOTAXIM 2gm IV/BD
2. FLUID RESTRICTION < 1.5 Lt/day
3. 2-3 egg whites/ day
4. INJ. THIAMINE 1AMP IN 100ML NS/IV/BD
5. TAB. ALDACTONE 25 mg/PO/OD
6. TAB. PROPRANALOL 10mg/PO/OD
7. SYP. POTCHLOR 10ml in 1 glass water
8. T. PANTOP 40mg PO BD
9. Wt, AG measurement daily
10. INJ. OPTINEURON 1amp in 100 NS/IV/OD
11. TAB. RIFAGUT 550 mg PO BD
12. SYP. HEPAMERZ 10ml PO TID
13. CANDID TV LOTION/ WEEKLY TWICE for 2 weeks

Friday, 6 November 2020

51 yr old male with Heart failure with reduced ejection fraction Metabolic syndrome K/c/o DM ,HTN ,CVA ,Seizures

This is an online E log book to discuss our patient's de-identified health data shared after taking his/her/guardian's signed informed consent. 


Here we discuss our individual patient's problems through series of inputs from available global online community of experts with an aim to solve those patient's clinical problems with collective current best evidence based inputs. 


This E log book also reflects my patient-centered online learning portfolio and your valuable inputs on the comment box is welcome. 


CASE PRESENTATION

A 51 year old male patient who is a k/c/o DM since 7 yrs and HTN since 5 yrs have  H/O 1 episode of seizures(GCTS) in feb 2017 and got admitted  in our hospital  and was on tab. Phenytoin 100mg TID medication ecg taken at that time showed atrial  fibrillation  and EF was 54% 

Similar H/o 1 episodes of seizure after 1 year of 1st episode was given. Then in Aug 2019 he presented with c/o B/L pedal edema and generalised edema since 10 days which subsided with medication 2d echo showed EF of 30% 

Then now he presented to the opd with complaints of B/L pitting pedal edema from 5 to 6months,abdominal distension from 2 to 3 days,SOB from 3days.

Pedal edema is aggrevated from 2 to 3 days and decreased urine output from 2 days for which pt used T. Amiloride, Furosemide  40mg since 2 days

Sob since 3 days grade 2 , orthopnoea and PND are present.

Abdominal  distention  since 3 days

No H/O chestpain,palpitations,giddiness,sweating,yellowish discolouration of eyes, fever.

K/c/o DM from 7yrs on tab glimi M2 bd

K/c/o HTN from 5yrs on tab telma 40mg od 

K/c/o epilepsy from 5yrs on tab phenytoin 100mg bd

Occasional alcoholic from 10yrs

Tobacco chewing from 40yrs

Personal history - 

Appetite  normal

Mixed diet

Sleep adequate

Bowel regular

O/E 

Patient is C/C/C moderately built and nourished

Pallor present 

No icterus clubbing cyanosis lymphadenopathy

Pedal edema present upto knees , pitting type 


Vitals:

Patient is afebrile

BP 150/90mm hg

PR 96 bpm

RR 24cpm

Spo2 95 on RA

CVS :

Inspection-

   precordium no bulging

   No visible  pulsations,  no engorged  veins, no scars, no sinuses

Palpation- 

   no tenderness 

Apical impulse -

Auscultation - S1 S2 heard

RS : BLAE Present NVBS 

P/A : distended 

Abdominal girth - 106 cms


CNS : NAD


Investigations-


2d echo global hypokinesia 

EF 28%

Severe TR Severe PAH

Diastolic dysfunction 

ivc 2.4 non collapsing 

CXR - PA view



DIAGNOSIS :

Heart failure with reduced ejection fraction 

Metabolic syndrome

K/c/o DM ,HTN ,CVA ,Seizures


TREATMENT :

1. Fluid restriction < 1.5 lt/day and salt restriction <2.5gm/ day

2. Inj lasix 40 mg /IV/BD IF SBP>110 mg

3. TAB. MET XL 12.5 mg/PO/OD

5. TAB. PHENYTOIN  100 mg/PO/TID

6. ECOSPRIN IV (75/10mg) PO/OD

7. TAB. PAN 40 MG/PO/OD

8. INJ. HAI S.C according to sliding scale

9. DAILY WT MEASURING 

10. STRICT I/O CHARTING 

11. GRBS CHARTING  6TH HRLY 

12. TAB. PREGABLIN 75mg PO HS

13. INJ. OPTINEURON 1amp in 100ml NS/IV/OD

14. TAB. ENALAPRIL 2.5 mg OD