1. Case presentation on
Atherosclerosis

2. DEFINITION
A process of progressivethickening and hardeningof the walls of medium-
sized and large arteries as a result of fat deposits on their inner lining
leading leucocytes and smooth muscles into the intima, a process by which
plague are formed in the walls of arteries and blood vessels.
Risk factors for atherosclerosis include high levels of "bad" cholesterol,
high blood pressure (hypertension), smoking,diabetes and a genetic
family history of atheroscleroticdisease.
Atherosclerosis is responsible for much coronary artery disease
(angina and heart attacks) and many strokes.

4. Symptoms
Atherosclerosis develops gradually.
Mild atherosclerosisusually doesn'thave any symptomsuntil an artery is
so narrowed or clogged that it can't supply adequate blood to your organs
and tissues.
Sometimes a blood clot completely blocks blood flow, or even breaks apart
and can trigger a heart attack or stroke.

5. Causes
The damage may be caused by:
High blood pressure
High cholesterol
High triglycerides,a type of fat (lipid) in your blood
Smoking and other sources of tobacco
Insulin resistance, obesity or diabetes
Inflammationfrom diseases, such as arthritis, lupus or
infections, or inflammationof unknown cause

7. The healthy arterial wall consists of 3 layers: a thin tunica intima
consistingof endothelial cells, a thick tunica media composed of internal
and external elastic lamina and smooth muscle cells, and the tunica
adventitia composed of dense, irregular connective tissue and vasa
vasorum(small blood vesselssupplyingmuscles of the arterial wall).
Pathogenesis

8. The developmentof atherosclerotic lesions is thought to be a response to
endothelialdamage and dysfunction.Lesions begin as fatty streaks that
result from the accumulation of cells (macrophages, lymphocytes,and
smooth muscle cells) in the tunica intima, and the accumulation of lipid and
cellular debris as these cells undergo necrosis.

10. Most fatty streaks remain benign, but those that progress go on to become
atheroma.As smooth muscle cells continue to proliferate and more foamy
macrophages (full of lipid) accumulate, the atheroma develops a core
consistingof fatty tissue and necrotic cellular debris. Fibroblasts lay down
collagen and other extracellular matrix constituents to form a fibrous
tissue envelope around the atheroma. Cholesterol clefts form in the now
enlargedintima as necrotic cells liberate more and more lipid. Dystrophic
calcification occurs as an attempt to contain the lesion.

11. The sequelae of these patchy, multifocal lesions in the major arteries are
numerousand diverse in consequence.These lesionscan remain silent,
never causing the patient harm. They can also gradually diminishthe flow
of blood through the artery as the lesion grows and slowly beginsto
occlude the lumen. If the fibrous roof of the lesion gives way, the lesion can
thrombus,potentially leadingto an atheroembolism.

12. The presence of vaso vasorum in the adventitia of major arteries
increases the risk of hemorrhage into the lesion, which can lead to an
acute occlusion of the artery lumen as the hemorrhage swells and
raises the roof of the lesion into the lumen.
Atherosclerosis can also cause weakening of the arterial wall,
increasingthe risk of aneurysm (an excessive localized swelling of
artery walls) and arterial rupture.

13. NAME: xy
AGE: 55
SEX: M
D.O.A: 28/09/18
D.O.D: 33/09/18
Patient details

14. Patient history
H/O: Cramp on right calf 4 days back.
C/O: Fever, SOB (shortness of breath),
constipation, dry cough
Past medical history: Hypertension (HTN),
Diabetics Mellitus (DM)
Past medication history: Metformin 500mg
twice daily, Hydrochlorothiazide 25mg once daily.
Family history: NIL
Social history: Non-alcoholic, smoking 10 per
day

15. Physical examination
Weight: 80 kg
Pulse: 69 b/m
BP: 130/80 mmhg
Temperature: 99 degrees F
RR: 20 b/m
Heart: normal heart beat, no bruit
Abdomen: Bruit umbilical region

16. Systemic examination
CVS: S1 S2+
RS: BAE+
P/A: Soft and non-tender

17. LAB INVESTIGATION
Parameter Observed Value Normal value
BLOOD TEST
*RBC
*WBC
*Hb
4.06cub.mm( )
12,000cub.mm( )
9.7 g/dl( )
4-25.6 cub.mm
4,000- 10,000cub.mm
14-18 g/dl
PCo2 32.6 mmHg( ) 35-45 mmHg
PO2 159 mmHg( ) 80-100 mmHg
Ph. 7.5( ) 7.4
ABI 0.41-0.70( ) 0.90-1.30
sodium 128 mmol( ) 136-145 mmol

18. Globulin 4.1 g/dl ( ) 2-3.5 g/dl
haematocrit 30.8 % ( ) 39-59%
Albumin 2.8 g/dl ( ) 3.5-5.55 g/dl
Blood urea
nitrogen (BUN) 15 mg/dl 10-20 mg/dl
Creatinine 1.20mg/dl 0.84-1.21 mg/dl
Lipid profile test 258 mm/dl ( ) 150-200 mm/dl
Blood glucose test 115 mm/dl 100-125 mm/dl
LAB INVESTIGATION

19. Other lab tests;
Electrocardiogram (ECG OR EKG),ChestX-ray, Stress test, Magnetic
ResonanceAngiogram (MRA), Arteriogram, Computed
tomography(CT),Transcutaneous oximetry, Cardiac catherization,
Treadmill test.
Colour Doppler study of lower limb arterioles and veins;
Impression: Deep facial oedema, severe atheroscleroticarterial
wall in anterior tibial and posteriortibial arteries.
Ultrasonography of abdomen;
Impression: Bilateral pleural effusion with basal consolidation.

20. Assessment
The patient has diagnosed with severe atheroscleroticartery wall
disease.

21. Surgical procedures
Angioplasty and stent placement: In this procedure, your
doctor inserts a long, thin tube (catheter) into the blocked or narrowed
part of your artery.A second catheter with a deflated balloon on its tip is
then passed through the catheter to the narrowed area. The balloon is
then inflated, compressingthe deposits against your artery walls. A
mesh tube (stent) is usually left in the artery to help keep the artery open.
Fibrinolytic therapy. If you have an artery that's blocked by a
blood clot, your doctor may use a clot-dissolvingdrug to break it apart.

22. Drug chart
Drug Generic name Dose ROA Timing Category ADR’s
Inj.piptaz Piperacillin 4.5g IV TID Anti-biotic Vomiting
Duolin neb salbutamol Bronchus
dilator
Nasal
Congestion
Inj.pantop Pantoprazole 40mg IV OD Protein pump
Inhibitor
Nausea ,
Electrolyte
Imb.
Tab.
tolvapton
Tolvapton
nitrase
15mg O BD Vasopressin,
antagonist
Anorexia,
Urination
Inj.
fragmin
Daltepari -
sodium
5000
IU
S/C BD Anti-
coagulant
haematuria
Tab.
aspirin
acetylsalicylic
acid
25mg O OD Anti-
Platelets
Inhibit
TAX2

23. Drug Generic name Dose ROA Timing Category ADR’s
Tab.
clopilet
Clopidogrel 75mg O OD Anti-
platelets
Dizziness ,
hypotension
Tab.
gemer
Glimepiride &
Metformin HCl
1mg
500mg
O BD Sulphonyl
urease
Hypoglycemia
Tab.
actocor
Atorvastatin 40mg O OD Statins Diarrhea,
nausea
Tab.
ultracet
Tramadol HCl &
acetaminophen
10mg O BD Analgesic Anxiety,
sweating
Inj.clabid clarithromycin 500
MG
IV BD Macrolide Nausea
Drug chart

24. Drug interactions
Dalteparin – Clopidogrel,
Increase the risk of bleeding. If complications are seen
then discontinue the antiplatelet drug.
Clopidogrel – pantoprazole,
Decrease the activity of Clopidogrel. H2 receptor
antagonist is substituted if an interaction is suspected.
Clarithromycin – tramadol,
Electrolyte imbalance
Atorvastatin – Clopidogrel,
May have blood clots, chest pain, and swelling.

25. Patient counselling
About drugs
Tramadol and tolvapton should be taken with
glass full of water.
Clopidogrel and atorvastatin can be taken with
or without food.
Glimipride taken with breakfast.
Antiplatelet drugs taken with plenty of water as
prescribed by physician.
Pantoprazole should be taken after meal.

26. Lifestyle
Stop smoking. Smoking damages your arteries.
Exercise most days of the week. Physical activity can
also improve circulation and promote development of new blood vessels
that form a natural bypass around obstructions.
Eat healthy foods. A heart-healthy diet based on fruits,
vegetablesand whole grains and low in refined carbohydrates,sugars,
saturated fat and sodium can help you control your weight, blood pressure,
cholesterol and blood sugar.
Lose extra pounds and maintain a healthy
weight. If you're overweight, losing as few as 2.3 to 4.5 kilograms an
help reduce your risk of high blood pressureand high cholesterol.
Manage stress. Reduce stress as much as possible.

27. SOAP
Notes
Subjective-Objective-Assessment-planning
S A 55yrs old male was admitted in the hospital with H/O cramp on
right calf 4 days back.
O On examination lipid profile , ABI, complete blood count (CBC) are
not in normal range.
A From the above details we can assess him to have atherosclerosis
P Standard treatment.
Medication include antiplatelet, beta blockers, ACE inhibitors.
Surgical procedures like angioplasty and slent placement &
Fibrinolytic therapy.
soap notes