Diabetes HTN And Right Foot Injury
A 65 Year old male with Diabetes, Hypertension and Right foot injury.
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I've been given this case to solve in an attempt 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 come up with a diagnosis and treatment plan.
CONSENT AND DEIDENTIFICATION:
The patient and the attenders have been adequately informed about this documentation and privacy of the patient is being entirely conserved. No identifiers shall be revealed through out the piece of work whatsoever.
This case is about a 65 year old Gentleman who was an RTC driver 15 years back , came with
Chief Complaints:
Decreased urine output (dysuria, hematuria, burning micturition ) since 20 days
SOB since 10 days
HOPI:
The patient was apparently asymptomatic 10 years ago then he felt weak and not well for a few days for which he visited local hospital and was diagnosed to be Hypertensive
He was kept to Antihypertensives and now is on
Atenolol Amlodipine 50mg/5mg
5 years ago:
The patient one day was helping someone who was cutting a tree by holding the branch which was being cut with the help of a rope
He got injured by a stone in the rope to his left palm
This was followed by pain, swelling and blackish discolouration
Then was when he was diagonosed incidentally as diabetic and was kept on medication
He is now on Tab. Metformin 500mg
4 years ago:
He drank and drove following which he had an accident and was taken to hospital from there.
He had
Fracture to his Left ribs (5,6,7) at mid clavicular line And Punctured his lung
30 days back:
While he was going out for work, he stepped over a sharp stone which penetrated through his right little toe
He used medications from the local medical store for about 10 days
He noticed:
1. Increase in pain gradual
2. Edema till his knee which was gradual
3. Bleb formation of about 3*3 cm on the dorsum of his foot which he ruptured by piercing a safety pin through it
There was bleeding from the site after piercing and it continued for a few days and formed into an ulcer.
4. Low grade on and off fever
5. There was also difficulty in urination
Burning micturition
Hematuria
Reduced urine output
He then went to a government hospital in Nalgonda and was diagnosed to be AKI on CKD and was transferred for private hospital for dialysis
There he developed SOB of grade 2-3, orthopnea and PND
He undergone through first session of Dialysis
He had itching at his abdomen, back and left and right Axilla
Then he was shifted to another hospital for Dialysis due to money restraints.
Timeline of events:
Past History:
Hypertensive since 10 years
Diabetic since 5 years
No History of Asthma, tuberculosis, epilepsy.
Family History:
The patients mother was a diabetic
None of the other family members have similar complaints
Drug History:
Atenolol+Amlodipine 50mg/5mg
Metformin500mg
No known allergies
Personal history:
Diet- mixed
Appetite-reduced since 3 days
Sleep - inadequate
Bladder - decreased
Bowel- regular
Alcoholic 90ml everyday since 40 years
Chronic smoker 1 pack since 40 years
General Examination:
The patient is conscious coherent cooperative, and well oriented to time place and person
He is moderately built and nourished
Pallor- absent
Icterus- absent
Cyanosis- absent
Clubbing-absent
Edema- present pitting Type
Lymphedenopathy - absent
VITALS:
Temperature- afebrile
Pulse rate- 68 beats per minute
Respiratory rate- 22 breaths per minute
B.P- 160/90 mm hg
SpO2- 99% at room air
SYSTEMIC EXAMINATION:
*CVS:
S1and S2 are heard
No murmurs are heard
*Respiratory system:
BAE- positive
Dyspnoea- present
Breath sounds- decreased breath sounds in right side
Vesicular breath sounds are normal
Rt side Fine Crepts present
*Central nervous system:
Patient was conscious coherent and cooperative.
Speech was normal.
No meningeal irritation signs
GAIT - Normal
*Abdomen:
Soft and non tender
INVESTIGATIONS:
Provisional Diagnosis:
Treatment:
Questions Discussed:
1)Adipocytes and Hypertension effect on Blood Vessels?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371623/
In a healthy person adipose tissue maintains a specifically balanced adipokine profile, which modulates vascular homeostasis via endocrine and paracrine pathways .
*Excessive accumulation of adipose tissue may alter the expression of the adipokine profile and consequently the physiological effects of adipokines on the vessels. Excessive weight gain contributes to increased blood pressure in most patients with essential hypertension. Blood pressure is a function of cardiac output and peripheral resistance.
* Weight gain leads to increased cardiac output and blood volume, which might be related to activation of SNS and RAS, and to physical compression of the kidneys by fat accumulation within and around the kidneys and excessive visceral fat. SNS activation and physical compression of the kidneys both cause activation of the RAS, and pharmacological blockade of either the RAS or the SNS attenuates obesity induced hypertension by at least 50-60%.
*Several mediators in the obesity-associated hypertension have been suggested, including hyperinsulinemia, angiotensin II, FFAs and leptin. Hyperinsulinemia could lead to a rise in blood pressure by enhancing sodium retention. Adipocytes secrete angiotensinogen, which can be converted to angiotensin I and then angiotensin II, a potent vasoconstrictor and promoter of sodium and water absorption.
*FFAs could promote hypertension by means of adrenergic stimulation, increase in oxidative stress, endothelial dysfunction, or stimulation of vascular cell growth. Leptin activates SNS by stimulating opiomelanocortin neurons, with subsequent activation of central nervous system melanocortin 4 receptors. The physiological importance of leptin in blood pressure regulation has been demonstrated in animal models. Obese Ob/ob mice deficient in leptin have significantly decreased blood pressure. Increased peripheral resistance due primarily to changes in vascular structure and function appear to be the fundamental abnormality in hypertension.
*Adipokines induce the functional and structural changes in the vessels by endothelial dysfunction, VSMC proliferation and migration and vascular inflammation, thereby regulating vascular responses to constrictor and dilator stimuli and contribute to the increased arterial pressure.
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