Myocardial Infarction

                           Myocardial Infarction 

• M.I. is define as Damage or Death of myocardial muscle due to Abrupt blood flow to the Heart.
• the blockage may be cause by formation of thrombus in coronary artery ,sudden progression of atherosclerosis,prolong narrowing of arteries.

Etiology:

• atherosclerosis
• arteries
• prolong narrowing
• thrombus
• agnoist

Risk factor:

• genetic cardial disorder
• smoking 
• alcohol consumption
• diet - like high cholesterol, high fat
• activity - low physical exercise

Pathophysiology:

• due to etiological factor
• myocardial ischemia 
• decrease myocardial oxygen supply
• increase cellular hypoxia
• decrease myocardial contractility
• decrease arterial pressure
• stimulation of baro-receptor and chemo-receptor 
• sympathetic response
• increase myocardial contractility
• increase heart rate
• increase myocardial oxygen demand 
• further myocardial ischemia
• necrosis of myocardial cells
• myocardial infarction or Heart Attack

Clinical manifestation:

• sever chest pain(more then angina pectoris )
• pain may radiant to the chest, shoulder, neck , jaw , back
• nausea
• unexplained anxiety
• dizziness
• dysponea
• sweating

Diagnostic Evaluation:

• ECG (elevated S & T segment)
• laboratory test : serum createnin kinase, myoglobin, cardiac troponin, ESR, (all level is increased)

Management:

Early management :

• morphine sulfate
• Anti-hematic : Domperidon, Alizapride
• Acute deperfusion therapy
• Primary percutaneous coronary intervention
• Maintaining vessel potassium
• Adjuncentive therapy

late management :

• life style modification : Diet control, stop smoking, regular exercise
• Secondary prevention : Anti-platelets , beta-blocker

Nursing management :

       The probable nursing diagnosis will be :

• pain related to an imbalance in oxygen supply and demand.
• Anxiety related to chest pain, fear of death, threatening environment.
• Decrease cardiac output related to impaired contractility.
• Activity intolerance related to insufficient oxygenation to perform ADL and deconditioning effect of bed-rest.
• Risk for injury related to dissolution of protective clot.

Angina Pectoris

                                 Angina Pectoris

• Angina pectoris occurs when myocardial demands exceeds, myocardial oxygen supply decreased usually caused by obstruction of coronary artery.
• chest pain due to an inadequate supply of oxygen to the heart muscle is characterized by feeling of suffocation.

Etiology :

• atherosclerosis
• prolong narrowing

Risk factor :

• thromboanxietis abliterance (inflammation of small and medium vein and thrombosis of extrimities.
• Polycythemia vera (thickness of blood)
• Polyarthritis nodosa (inflammation of aretery due to infiltraion of eosonophils.)

{Note : Angina can be triggered by exercise ,cold, or anything that incfreases the work load of heart}

Clinical manifestation :

• Pain : -  location: 90% of the clients experience pain slightly left to the sternum 

                        duration : Angina usually last fir 10 min. however attacks precipitate by emotional                                                 disturbance last for 15-20 min.

                        Severity : the pain is described as mild or moderate or often called as Discomfort.

• Dyspnea, weakness, light headache, nausea, vomiting, emptyness, restlessness.

Pattern of Angina :

1.  Stable Angina :- it is a acute chest pain triggered by exercise or emotion.
2. Unstable Angina :- it is also acute pain but unpredictable degree or cause.
3. Varient Angina:- it is also called as perinzmetals angian and it is for longer                                        duration.
4. Noctural Angina :- it is possibly associated with rapid eye movement during                                       sleeping or dreaming.
5. Angina Decubitis :- it is proximal chest pain that occur when client stand up.
6. Post Infarction Angina :- pain occur after heart attack.

Diagnostic Evaluation :-

• ECG
• Coronary Angiography
• Blood test
• Echo cardio gram
• Electron beam computed domography [EBCD]

Management :-

• the objective of the medical management in angina are to decrease oxygen demand of the myocardial and to increase the oxygen supply.
• medically these objectives are meet through pharmacological therapy and control of risk factor. Medical management focus on these three points :-

1. Relieve the acute pain.
2. Risk of coronary blood flow.
3. Prevent further attack to reduce the risk of myocardial infarction.

      A : Aspirine and anti-anginal therapy
      B : beta-blocker and blood pressure control
      C : cigarette smoking and cholesterol control
      D : Dietary modification
      E : Education and exercise.  

• Restore blood supply
• PTCA
• Intracoronary straind
• Laser ablation
• CABG (coronary artery bypass grafting)

Nursing management :-

          Diagnosis :

• Acute chest pain related to decrease blood supply to the heart resulting from coronary artery obstruction,
• Ineffective tissue perfusion related to decreased cardiac output as evidence by cyanosis ,decrease arterial oxygen and dyspnea.
• Risk of heart failure related to disease process.
• Anxiety and fear related to hospital admission, fear of death, fear of treatment procedure and disease process.
•  Risk of impaired skin integrity related to bed rest, edema, and decrease tissue perfusion.

Varicose vein

                                Varicose Vein (varicoty)

• Varicose vein or varicoty are abnormally dilated, tortuas superficial vein cause by incompetent venous valve.
• varicose vein are permanently distended veins that develop from the loss of valvular competence faulty valves elevated venous pressure causing distention and torluosity of superficial veins.
• varicose vein is divided in two types according to cause :-

1. Primary
2. Secondary

1. Primary varicose vein :-  vein after resting from congenital, genetic, or familial predisposition that                                               leads to loss of elasticity of the veins valve.

2.Secondary varicose vein :- it occurs when trauma , obstruction deep vein thrombosis or                                                                   inflammation cause damage of valves.

Etiology and Risk factor :-

• Prolong standing 
• Genetic predisposing factor
• Weakness of vein valves
• Congenital deformities
• Pregnancy

Clinical manifestation :-

• Dull-ache
• weakness
• moderate swelling
• malaise
• fever
• noctural cramps
• edema
• Pigmentation
• Ulceration
• susceptibility to injection
• Unslightly appearance of legs

Diagnostic evaluation :-

• Duplex scan :- to asses or find out anatomy of veins
• Venous blood pressure
• Venography

Management :-

1. General management :-

• the patient is instructed to avoid activity that cause venous stasis such as wearing light shocks or constructive griddles crossing. the legs at the thigh or sitting or standing at the long period. Instruct the client for changing the position frequently, elevating the legs which feels tired & getting up to walk for several minutes of every hour to promote circulation.
• the patient should be encouraged to walk 1-2 mile per day.
• Elastic wrap need to be wrapped twice daily so that greatest pressure is at the ankle with lessor pressure gradually applied at the level of knee.

     2.  Surgical management :-

• Sclerotherapy :- (using a fine therapy) :-  Sclerotherapy is the injection of a sclerosis agent      into varicose vein. The agent damage the vein and endothelial causing to swell the blood to clot. the vein turn into sear tissue that many eventually fade from view.It is used for spider veins of varicose veins up to 15 millimeter in diameter have been treated successfully.  
• Vein ligation and Stripping :- surgical management of varicose vein consist of ligation of        greator sphenous vein with its tributaries at the sphenofemoral junction. Combind with removal of the sphenous vein (stripping) & ligation of incompetent performance vein.Removal of vein is performed through multiple short incision. An increase made at the ankle over the sophenous vein and a nylon wire is threaded up vein to groin.
• Saphenofemoral ligation :- some client requires only typing of the junction of the saphenous  & femoral vein at the groin. this involves one short incision often local anesthesia & no hospital stay.

Nursing management:-

• Maintain firm elastic pressure over whole limb.
• Promote regular movement &exercise of legs.
• Elevate the foot to bed 6-9 inches so the legs are above the heart level which the client is in bed rest.
• Instruct client to walk rather than stand or sit.
• Asses for any signs of complications such as infection , hemorrhage , nerve damage etc. 

Rheumatic Heart Disease

                                 Rheumatic Heart Disease

•    Rheumatic Heart Disease is usually affect the children and it is still the most common cause of acquired heart disease in childhood and adolescence.

Incidence :-

• R.H.D. is usually affects 5-15 years child.
• 1-2 case / lakh in developed countries.
• 100 case/ lakh in developing countries.
• 3% people affect after the beta-hemolytic strptococci infection.

Pathophysiology :-

• due to etiological factor
• persistent infection of through streptococci.   
• Antigen of beta-hemolytic streptococci react.
• cross react with myosin and sarcolema membrane.
• bind the receptor on the heart.
• Inflammatory response in the cardiac muscle.
• severe & permanent heart damage.

Clinical Manifestation  :-

• carditis 
• cardiomegaly
• murmur
• pericarditis
• chest pain
• AV deffect
• Arterial fibrillation
• fever
• dysrhythmia
• Pnemonia signs
• Involuntry movement or speach after 3 month of disease.

Diagnostic Evaluation :-

• blood test
• throat swab
• chest x-ray
• ECG
• 2D echo

Management :-

Medical management :-

• Anti-biotics
• Aspirine
• Corticosteroid
• Bed rest & Supporting therapy

Nursing Management :-

• Chronic pain related to inflammatory response.
• Activity intolerance related to reduce cardiac pressure and inforced bed-rest.
• Imbalanced nutrition less the body requirement related to sever inflammation & fatigue.
• Risk for ineffective therapeutic resimen management related to need for life long threapy.    

Coronary Heart Disease

                                 Coronary Heart Disease

In coronary heart disease atherosclerosis develop in coronary arteries causing them to becoming narrow and block this leads to decrease or stop blood supply to the heart muscles.

Etiology :-

1. Non modifiable :-

• Genetic Heredity :- Children whose parents had heart disease are at a higher risk of C.H.D.
• Race :- The African & American have 45% greater chances of developing CHD.
• Age:- with increasing age risk & severity of CHD are increases.
• Gender :- males of younger age and females after menopause are at high risk of CHD.

     2. Modifiable factor :-

• Elevated serum lipid level
• Habitual diet high in fat and cholesterol
• Obesity 
• Cigarette smoking 
• Heavy alcohol consumption  
• Personality types
• Sedatory live
• Psychological strem
• Improper life style

Pathophysiology :-

• Due to etiological factor
• Localized accumulation of lipid, fibrous tissue, or thrombus
• Arterial narrowing or occulusion
• vascular changes occur that affect the functional ability or coronary arterial
• Deficit in myocardial oxygen supply
• Angina pectoris M.I. / cardiac arrest 
• Death

Types :-

• Type 1 st :- fatty, streaks lipid deposit in the int em of arteriol wall.
• Type 2 nd :- Inflammatory response takes macrophage to ingest lipid.
• Type 3rd :- Smooth muscle cell proliferate and form a fibrous capat are the deal fatty cell.
• Type 4th :- Fibrotic layer and plaque formation.
• Type 5th :- Distributed internal structure along with moderate disease that cause decrease in                         the size of lumen.
• Type 6th :- Rupture of plaque producing cavity thrombus with partial occlusion of lumen.

Clinical Manifestation :-

• Disrhythmia 
• Restlessness
• Fatigue
• Malase

Complication :-

• \Heart Failure
• Heart block
• Angina pectoris

Diagnostic Evaluation :-

• ECG
• 2D Echo
• Angiography
• Blood Investigation
• LFT

Management :-

1. Reduce Risk Factor :-

• Primary and secondary prevention cause are use for all major risk factor.
• Health professionals provide guidance & counselling related to disease condition.
• Health profession team motivate the client to stop smoking and alcohol consumption.
• maintain ideal body weight through the physical exercise
• Dietary modification according to disease condition & according to dietitian prescription.
• Encourage the client to perform physical activity and participate in exercise.
• Behavioral therapy or diversional therapy to reduce stress.

     2. Restore blood supply :-

• PTCA
• PCA
• Intra coronary stent
• laser ablation

    3. Pharmacological management :-

• Analgesics to relieve pain
• Vasoldilatiors
• ACE inhibitors

Raynaud's Disease

                                    Raynaud's Disease

Ranaud diseaseis a condition in which the small arteries and arterioles causing temporarily pallor or cynosis of digits & change in skin temperature.

Etiology :-

the exact cause of Raynaud disease is unknown but believe that some risk factor are responsible this condtion :-

• Hypersensitivity of digital arteries to clot.
• Reduce of serotonin [ Normally release in trauma for vasoconstriction ]
• Congenital predisposition
•  Eating disorder [ Anorexia nervosa ]
• Obstructive disorder

Types :-

1. Primary Raynaud Disease  :- The cause of primary raynaud disease is unknown. It is vasoseptive disorder & rarely lead to impaired tissue perfusion.
2. Secondary Raynaud Disease :- It is associated with connective tissue and collagen vascular disorder such as :-

• Scleroderma  [ hardening of skin]
• Systemic lupus Erythromatus  
• Rheumatoid Arthritis
•  Dermatomycitis [ inflammation of skin]
• Poliomyelitis

Clinical Feature :-

• Palor skin become bluish
• Numbness
• Tingling, sensation
• Burning pain
• Cynosis
• Gangrene formation

{ Note :- Raynaud's phenomena is used to localized intermittent episode of vasoconstriction of small arteries of feet and hand }

Management :-

• Avoid the particular stimuli such as cold , tobacco, drugs, etc.
• keep hand and feet warm and dry.
• Protecting all parts of body from cold, and exposure to prevent reflex, symptomatic vasoconstriction of the digits.
• Exposure to cold must be minimize and the patient remain indoor as much as possible.
• Provide protection with less of cloth , when comes out.
• Hat and gloves should be wore at all the times when outside.

  

 

Acute Venous Disorder

                                 Acute Venous Disorder

Acute venous disorder are due to thrombus formation that obstruct venous flow and develop blockage when occur in both superficial and deep veins.

Types :-

1. Superficial Venous Disorder :-It is resulting from careless insertion of intravenous line, intravenous catheter or performing diagnostic procedure.
2. Deep Venous Disorder :- Deep vein thrombosis refer to the thromboflabitis of deep vein with obstruction of veins , edema, and swelling of the extremity because of the outflow of the venous blood in inhibited.

Etiology :-

1. Venous stasis
2. Hyper coagulator
3. Trauma injury of venous wall
4. Obstruction Disease
5. Inflammatory Conditions 

{ Note :- these three phenomena(1,2,3) are together called VirChow's syndrome.}

Venous Stasis :- Immobilization or absence of the calf muscles pump or tight bending or tight clotting causes the venous stasis.

other condition that may cause stasis are surgery , paralysis , immobility , obesity , pregnancy.

Hypercoagulity :- It is often accomplished by malegnent , dehydration , and blood dyscariasis may rise the platelet count.                                                                                       Decrease fibrinolysis increase clotting factor and increase the viscosity of blood.oral contraceptives and hematogenic disorders may also cause the coagulity of the blood.

 Vein Wall Trauma :- condition that may cause the vein wall trauma are IV injection , thromboangitis obliterance fracture , chemical injury, from sclerotic agent, radiographics and certain antibiotics.

Risk Factor :-

• Surgery , specially orthopedic surgery, abdominal surgery, and renal transplantation.
• Congesting heart disease
• Cardiomyopathy
• Immobilization
• Stronger prolong travel
• Malignancy
• Previous deep vein thrombosis
• Pregnancy , particularly in purperium period and after cesarean section.
• Trauma
• Estrogen Therapy and contraceptives 
• Obesity

Pathophysiology :-

• Injury ,trauma, inflammation 
• Thrombus formation by platelets
• Adherence to endothelium
• Platelet adhere to collagen
• Adinosindiphosphate release from damage tissue
• Venous Obstruction
• Acute Venous Disorder   

    

  

Aneurysm

                                          Aneurysm

Aneurysm is defined as a permanent localized dilation , stretching and ballooning of an artery or blood vessels to around 50% increases in the size.

Etiology :-

The exact cause is unknown.

Risk factor :-

• Atherosclerosis 
• congenital defect is arterial wall
• Genetically weakness of wall
• Hypertension
• Trauma or injury
• Micro-tic infection
• Elevated cholesterol level
• Impaired nutrition

Classification :-

1. According to location :- they are described according to specific vessels in which they develop. Example: Aortic aneurysm , iliac aneurysm , thoracic aneurysm , lastly more preciously according to the area of vessels they affect.
2. According to Etiological factor :- Aneurysm is classified according to cause such as atherosclerotic aneurysm,microtic, aneurysm, hypertension aneurysm, traumatic aneurysm.
3. According to Appearance :- Classification of aneurysm is sometime based on shape and anatomic feature or size.
4. Sacular Aneurysm :- Sacular aneurysm involves all three layers of artery. A out pouching of an artery at point where the media is thin.
5. Fusiform Aneurysm :- Fusiform aneurysm involves the entire circumference of the vessels. It is localized uniform dilation of an artery.
6. Dissecting Aneurysm :- In disecting aneurysm hematoma is present in the arterial wall that separates the layers of arterial wall.
7. False Aneurysm :- False aneurysm results from the development of a sac around a hematoma that maintain a communication with the leumen of an artery where wall has been ruptured or penetrated.

Pathophysiology :-

Abdominal aortic aneurysm four types more often then the thorasic aneurysm. the Natural cause of untreated aneurysm is to expand or rupture.The aorta is under greater stress then the rest of the arterial system because of its large diameter and its exposure to high pressure during each systolic ejection of blood.

Clinical Manifestation :-

• Awareness of pulsation mask in the abdomen.
• Abdominal pain and back pain
• Pain in lower abdomen , groin, and genitalia
• Decrease hemoglobin
• Sign of hemorrhage
• Shock
• Abdominal Distension

Diagnostic Evaluation :-

• Physical Examination
• USG
• CT Scan
• Abdominal Aortography

Complication :-

• Coronary artery disease
• Pulmonary obstructive disease
• Pre-renal failure
• Spinal cord ischemia
• Change in sexual function
• Severe bleeding

Management :-

1. Surgical Management :-  Surgery is usually not perform on clients with a less symptomatic abdominal aortic aneurysm smaller then 4-5cm. In Every six month a USG is indicated to determine whether any change in the size occurred.

• Endovascular Procedure :- It is a newer method for lower emergency treatment to repair abdominal aneurysm. small incision are made in the groin and a vascular into the aorta. deflated balloon and tightly wrapped polyester cloth graft is placed , when properly position the graft is securely place by inflation the balloon and opening the graft of the diameter needed to prevent blood clot in the aneurysm then the balloon is deflated and remove along with the catheter at the each end of the graft hooks are present that help secure it to the inner walls of aorta.
• Aneurysm Repair :- Surgical repair is usually recommended for all aneurysm greater then 6cm. find 

Benign Prostate Hypertrophy / Hyperplasia (B.P.H.)

BPH is also called Benign Enlargement of Prostate or Benign Prostate Enlargement is a non-cancers increase in the size of the prostate .

It is Enlargement of prostate gland and obstruct the out flow of the urine.

Incidence :- 

• Approximately 50% clients after 50 years of age and after 80 years of age BPH develops in 90% of males. 

Etiology :- 

• the exact cause is unknown / idiopathic.

Risk Factor :- 

• Aging ( fibrosis and beginning of the muscular tissues in the prostate)
• Hormonal change / imbalance : specially DHT ( di-hydro testosterone). A metabolite of testosterone is the critical mediator of pro-static growth.
• Diet :( Animal protein)
• Hereditary / genetic
• malfunction of testis
• Sexual activity
• Local or abnormal growth

Pathophysiology :-

• Due to any risk factor
• Enlargement of prostate gland
• Obstruction and compression on urethra and bladder
• Bladder can not expel complete urine on each voiding
• Urinary obstruction
• Hydronephrosis
• Renal damage

1. The enzymes aromatase and 5-alpha reductase increase in activity. Aromatase and 5-alpha reductase of enzyme are responsible for converting androgen or testosterone hormones into estrogen and di-hydro testosterone.
2. This metabolism of androgen hormone leads to decrease in testosterone but raised level of DHT and estrogen. estrogen and DHT has a keep role in the growth of cells in the prostate.

Sign and Symptoms :-

• Anorexia 
• Nausea
• Vomiting
• Dysurea
• Increase frequency of urination
• Nocturis
• Acute urinary retention
• Decrease muscle tone of urinary
• Bladder leads to loss pf bladder control or inability to urinate
• Fatigue
• Hydronephrosis
• U.T.I.

Investigation :- 

• Physical examination
• History collection
• Urine Analysis
• U.S.G. of testis , prostate, kidney

1. Translateral ultrasound :- It is done to identify or visualization of prostate gland through the rectum,
2. P.S.A. test ( Prostate specific antigen) :- To identify the kidney damage or prostate cancer.
3. Cytosopy
4. R.F.T. or K.F.T.
5. C.B.C.

Acute Kidney Injury [ Acute Renal Failure]

Definition :- 

AKI Previously called Acute Renal Failure is an abrupt loss of kidney functions that develops within 7 days.

It is characterized or manifested by decrease glomerular filtration rate, level of serum creatinine and urea nitrogen rise and oligourea or anurea. 

 Etiology :-

It's cause are numerous. Generally it occurs because of damage to kidney tissue caused by decreased blood flow (ischemic kidney), low blood pressure or hypotension, exposure to substance harmful to kidney, inflammatory process or an obstruction of the urinary tract.

The causes of AKI can be categorized by into 3 major area's :-

1. Pre-Renal cause
2. Intra-Renal cause
3. Post Renal cause

     1. Pre-Renal Cause :-

• Pre-Renal causes are those that decrease effective blood flow to the kidney and cause to decrease in GFR.
• Low blood volume in the body (hypovolemia) [due to vomiting, diarrhea, hemorrhage, burns and excessive use of diuretics.]
• Hypotension
• Decreased cardiac output
• Heart failure
• Renal artery stenosis

      2. Intra-Renal / Intrinsic cause :-

Process which directly damage kidney itself :

• Glomerular Nephritis
• Tubular Necrosis
• Renal Surgery
• Injury, Trauma, Crush
• Electric Shock
• Diabetes Malitus
• Infectious Disease
• Rejection of transplant kidney
• Genetic Factors

      3. Post Renal cause :-

Caused by disease states / condition down stream of the kidney.

• Urinary tract obstruction.
• Uritral or urethral structures (stenosis)
• B.P.H.
• calculi
• cancer or tumor of bladders & uretor's
• Surgical Accidents
• Spinal cord injury leads to decrease bladder emptying of functional obstruction.

Mechanism / Pathogenesis :- 

The mechanism of AKI is not specific or not clear there are some mechanism which are :-

• Ischemic kidney
• Activation R.A.S.
• Tubular injury or infection
• Fibrosis and scare formation
• Renal Calculi
• Decreased osmotic pressure

Clinical Manifestation :-

• Headache 
• Fatigue
• Nausea , Vomiting
• Diarrhea
• Constipation 
• Loss of Apetite
• Flank pain
• Edema
• Shortness of breath
• Hematuria
• Oligurea or Anurea 
• Hypertension
• Hand tremors
• Decrease G.F.R.
• Increase Serum Keratinine
• Acidosis
• Ureanitrogen level Increase
• Fluid and Electrolyte Imbalance
• Hyperkelemia
• Hyponatriemia
• Hypocalcemia
• Hyperattrisemia

Investigation :-

• Serum Creatinine level (increases)
• Blood ureanitrogen
• Serum pottasium
• Urine analysis
• Radiological study (CT, MRI, X-ray)

Management :-

The management of AKI is divided into 4 stages or phases :-

1.  Initiating / onset phase :-  This phase covers the period from the precipitation event to the development of renal manifestation and continue until the sign and symptoms.It can last for few hours to week.
2. Oliguric phase :- The most common initiative manifestation of AKI is oligurea caused by a reduction in the G.F.R. oligurea usually occur within 24 hours. The longer oliguric phase clast the poor prognosis for recovery of complete renal function. (1 to 8 week).
3. Diuretic phase :- The diuretic of AKI begin with a gradual increase of urine output of 1 to 3 lit. per day but may reach to 3 to 5 liter per day or more although output increased in case nephrones are still  not fully functioning. At this stage the uremia may still be serve as infected by the low creatinine clearance , elevated serum creatinine, BUN level, and persistent sign and symptoms of dehydration because of large of loss of fluid and electrolyte . ( 25- 30 % of death dehydration)
4. Recovery phase :- The recovery phase begins when the GFR increases allowing the BUN and serum creatinine level decrease some individual do not recover or progress to chronic kidney failure. The older adults patient are less likely recovery to fully kidney function.The treatment of recovery phase last for some month or a year in severe cause dialysis or kidney transplantation may be prescribed.

Medical Management :-

• Avoidance of substance that are toxic to the kidneys called Nephrotoxics, it include NSAID.
• Iodinated contrast or contrast medium use in radio-graphic examination specially CT scan and MRI.
• Antibiotics 
• In lower BP :- Non epinephrine, Inotrops, steroid, Dobutamine
• In high BP :- calcium channel blocker, ACE inhibitor, Diuretics.
• In metabolic acidosis administer sodium bicarbonate 

Surgical management :-

• Nephrotomy
• Catheterization
• Dialysis
• Renal Transplantation

Nursing Management :-

• Fluid volume excess related to inability to kidney to promote or excrete urine.
• Fluid volume deficit.
• Altered  nutrition level .
• Risk for infection.
• Disturb thought process.
• Risk for impaired normal skin integrity related to edema.    

   

  

Chronic kidney disease ( chronic Renal failure )

Definition :-

CKD is a type of kidney disease in which there is gradual loss of kidney function over a period of months or years.

CKD is progressive irreversible destruction and dimension in renal function resulting in uremia and azotemia.

It occurs from several days or months to years.

Etiology :-

• Diabetes mallitus 
• Hypertension
• Recurrent episodes of AKI
• Chronic glomerulo nephritis
• Recurrent polynephritis
• Hypotension
• Polycystic kidney Disease
• Obstruction in urinary tract
• Renal artery obstruction or stenosis
• Autoimmune disease (SLE)
• Vasico uretral reflex
• Medication or Drugs
• Poor intake of fluids

Pathophysiology :-

• Due to etiological factor
• Deterioration or destruction of nephrone with progressive loss of renal function
• GFR falls and clearance of waste is reduced.
• Serum creatinine and urea nitrogen level rise 
• Hypertrophy in remaining nephrones as they required to filter large load of solutes.
• kidney losses their ability to concentrate urine adiquatening 
• In an attempt to continue excreting the solutes. large volume of dilute urine may be passed.
• fluid depletion (loss)
• Tubules gradually loss their ability to reabsorb electrolytes.
• Polyurea and results large amount of Na and water excretion 
• Disease progress toxic condition or toxicity
• Renal Failure

 Clinical Manifestation :-

Nervous System :-

• Confusion
• Disorientation 
• Weakness
• Fatigue ,malaise, restlessness

Cardio vascular system :-

• Hypertension
• cardia Disrrhythemia
• Pericarditis
• Pericardial Effusion
• Myocarditis
• Endocarditis

Intiguimatory System :-

• Palor appearence
• Orange,green, or grey in color of skin (because of retaining of Urochrome ligand)
• Thin and brittle nails and hair
• Ecchymosis (bruise) >1cm
• Petechie
• Purpura
• Puritis (severe form of itching)
• Edema of Enasarca

G.I. Tract :-

• Nausea ,Vomiting
• Constipation,Diarrhea
• Hiccups
• Anorexia
• Mouth ulcers
• Gastritis
• Stomatitis 
• Gingivitis
• Esophagitis
• Bitter or salty taste
• Ammonic or fishy odor from the breath 

Respiratory System:-

• Respiratory Distress
• dyspnea
• Shortness of breath

Blood or Hematology :-

• Anemia

Reproductive System :-

• amnorrhea
• Infertility (impotence & sterility)
• Oligospermia
• Testicular atrophy
• Decreased livido

Musculo skeletal System :-

• Fatigue
• Muscular cramps
• Decrease muscular strength
• Bone pain

Urinary system :-

• Polyurea
• Oligurea
• Hematurea
• Renal insufficiency with azotemia

Metabolic changes :-

• Metabolic acidosis
• Increased BUN
• Serum creatinine
• Serum uric acid
• Decreased GFR

Investigation :-

• History collection
• Physical examination
• Urine culture and urine routine
• Urine measurment
• BUN
• CT scan of K.U.B.
• I.V.P. (Intravenous pylography)
• Renal Angiography

Medical Management :-

• Calcium preparation and phosphorus binders .
• Aluminium based Antacids
• Antihypertensive 
• Diuretics
• Vitamine and minerals supplements
• Iron sulfate and follic acid (in severe anemia)
• Sodium bicarbonate (administered to correct metabolic acidosis)

Surgical management :-

• Catheterization
• Dialysis
• Renal transplantation

Nursing Management :-

• Fluid volume excess related to inability to kidney to promote or excrete urine.
• Fluid volume deficit.
• Altered  nutrition level .
• Risk for infection.
• Disturb thought process.
• Risk for impaired normal skin integrity related to edema.    

 

  

  

   

Osteoporosis

• Abnormal rarefaction of bone which may be idiopathic or secondary to other condition.
• This disorder leads to thinning of skeletal and decrease precipitation of lime salt.
• Osteoporosis is defined as systemic skeletal disease characterized by low bone mass and micro-architectural determination of bone tissue that leads to increase bone fragility and susceptibility to fracture or breakdown (hips,vertebrae,forearm)

Etiology :-

• increase aged
• Poor diet(low calcium and vitamin D)
• chronic alcoholism
• Tobacco,smoking
• Lack of exposure to sunlight
• lack of physical exercise
• Hyperthyroidism
• Estrogen deficiency after menopause
• surgical removal of ovaries
• Excessive secretion of parathyroid hormone 
• Certain medication (chemotherapy,Anti-seizure)
• Family history of genetic 
• Excessive consumption of soft drinks(increase amount of phosphoric acid)

Pathophysiology :-

1. Due to any etiological factor
2. calcium resorption
3. increase in osteoclast activity
4. Brittle or fragile bones
5. Reduction in resistance of bone towards physical stress
6. Fracture ,improper gait and reduction in height 

•   Bone is dynamic tissue that undergoes that continue remodeling (the process by which old bone is replaced by new bone)
• the remolding sequence start with activation of osteoclast which resorb a small portion of bone over a relatively short period of time (7-10 days)bone formation then take place as osteoblast form an organic matrix that is subsequently mineralized.

Clinical Manifestation :-

• Sudden onset of severe back pain .
• Kyphosis (posterior curvature of spine or humpback)
• Abdominal distention 
• Impaired respiration due to restricted lung expansion
• Loss of denture or teeth (due to loss in mandible) and finally fracture specially hip,vertebrae,forearm
• Improper gait, and reduction in height

Investigation :-

• Physical examination 
• Family history
• dual energy X-ray 
• Blood test 
• Urine calcium level
• CT,MRI

Management :-

Medial management :-

• Bisphosphonate
• Estrogen therapy (in early menopause)

Nursing management :-

• Pain related to fracture
• Altered nutrition less then body requirement related to calcium and vitamin D deficiency
• Risk of fracture due to disease condition softening of bone
• Impaired physical activity due to disease condition.

Nursing Responsibility :-

• Adequate intake of calcium and vitamin D
• Regular weight bearing exercise 
• Avoidance of alcohol and tobacco
• Assess clients at risk of fracture for activity level and dietary adiquency and programme appropriate teaching to prevent fracture
• Assessment include visual assessment medication that may cause dizziness or postural HTN.
• Difficulties with balance or co-ordination as well as the home environment for potential safety from hazards.
• Evaluation of the bone setting is performed via admission assessment discussion with the client consultation with specialist in social service and home safety evaluation by visiting nursing.
• Instruct the client who are prompt to dizziness to get up slowely from a lying position sitting on the site of the bed first.
• An aid to ambulation such as a cane or walker may also the indicated to prevent falling.
• Hand rails should be also available or provided specially in bathroom or toilets.     

Osteomalacia

• Osteomalacia is the disease in which the bone become abnormally soft because of a disturb calcium and phosphorus balance and secondary to vitamin D deficiency.
• It is characterized by wide spread decalcification and softening of bone specially in the a spine , pelvis and lower extremities.
• Osteomalacia is softening of the bone caused by impair bone metabolism primarily due to inadequate levels of the available calcium ,phosphorus and vitamin D or because excessive re-absorption of calcium.

Etiology :-

• Improper diet
• Strict vegeterianism
• vitamin D deficiency
• less expose to sunlight
• Renal failure
• Tumor induced or oncogenic osteomalacia 
• Hyperthyroid induced osteopenia
• Chronic or prolong used by Anti-convulsent drugs

Pathophysiology :-

• Due to vitamin D deficiency or other risk factor
• Improper or lack of calcium metabolism
• Reduced the absorption of calcium in the bones
• Bone become soft and bend
• Susceptible to or leads to fracture

Clinical manifestation :-

• Severe muscular and bone pain
• Fatigue ,malaise
• muscular weakness
• Pseudo fracture / Milkman syndeome,stripe form in bones and seems like fracture 

Investigation :-

• CT,MRI
• X-ray
• Dual energy X-ray
• Blood test 
• Biopsy (in case of oncogenic osteomalacia) 

Medical management :-

• Analgesic to reduce severe pain
• Expose to sunlight 
• Dietary intake of vitamin D rich food or sources
• 2000-10000 IV vitamin D ,4-6 weeks orally if malabsorption administered through injection 

Nursing management :-

• Pain related to fracture
• Altered nutrition less then body requirement related to calcium and vitamin D deficiency
• Risk of fracture due to disease condition softening of bone
• Impaired physical activity due to disease condition.

Hiatus Hernia

Definition :-

A type of hernia in which part of the stomach protrudes up through the esophageal opening of the Diaphragm.Hiatus hernia is an anatomical abnormality in which the part of the stomach protrudes up through the diaphragm into the chest.

Causes:-

   The exact cause is unknown.It may be due to ,

• Increased pressure within the abdominal cavity. It may be due to - Heavy lifting,Pregnancy,Ascites,Frequent or hard coughing,Boilent vomiting,Starving.
• Weak LES
• Obesity
• Aging

Types:-

1. type 1st :- Sliding Hiatus Hernia :-

• Herniation of both the stomach and gastro-esophageal function in thorax.
• most common type of hiatus hernia (90%).

      2.Type 2nd :- Paraesophageal Hiatus Hernia :-

• It is also known as rolling hiatus hernia.
• Herniation of all or part of stomach through the esophagus into the thorax,with an undisplaced G.E.junction.
• It is less common (10%).

Clinical Features :-

1. In most of cases hiatus hernia remains asymptomatic,the disease discovers accidentally.
2. the clinical feature are :-

• Heart burn.
• Dull chest pain. 
• Shortness of breath.
• Regurgitation.
• Disphasia.
• Palpitaion.
• Reteosternal chest pain.

Diagnosis :-

• Endoscopy.
• Barium swallow X-ray.
• Chest X-ray.
• C.T. scan.

Complications :-

• GERD (most common).
• Esophagitis.
• Esophageal ulcer.
• Aspiration pneumonia.
• Perforation (cutting of mucus membrane).

Gastritis

Definition :-

Inflammation of the gastritis mucus membrane is called Gastritis.It may occur as a short episode or may be of a long duration.

Types of Gastritis :-

Clinically Gastritis is classified into two types :-

1. Acute Gastritis 
2. Chronic Gastritis

On the basis of histology / endoscopic appearance.Gastritis is classified into three types :-

1. Erosive/Hemorrhagic Gastritis :- Acute
2. Non-Erosive Gastritis :-chronic
3. Specific Gastritis

  Etiology :-

      Most common causes includes :-

• Infection of helicobacter pylori
• NSAID's
• Heavy alcohol drinking

     less common cause includes :-

• Excessive stress
• May develop after major surgery of stomach
• Irritating food/contaminated food

Clinical Features :-

1. Anorexia 
2. Nausea and vomiting
3. Abdominal discomfort
4. Epigastric tenderness
5. Heart burn after eating
6. Belching
7. Frequent hiccough
8. Dehydration
9. Acidic test in mouth.

Diagnosis :-

      Diagnosis made on the basis of :-

• Clinical feature
• Feature of anemia
• upper G.I. endosopy
• Blood test to check H-pylori
• CBC for check the anemia

Medical Management :-

• Antacid :- are a common treatment for mild to moderate gastritis.when antacids do not provide enough relief ,medication such as H2 receptor blocker and proton pump inhibitors are given to client to reduce the amount of acid.
• Antibiotics

Diet management :-

• Blend diet,less spicy.
• prefer liquid food.
• Frequent small meals.

Nursing management :-

• Provide liquid diet to client,the diet should be less spicy and less irritate.
• Provide small and frequent diet.
• Encourage patient to avoid foods and drinks that triggers heart burn.
• Assess the patient for hematemesis.

 

Gastro Esophageal Reflex Disease (GERD)

• GERD is reflex (return) of gastric content (mainly acid) towards the mouth resulting in esophageal tissue damage.
• This is a chronic disease that occur when stomach acid (HCL) or bile flows into the food pipe and irritates the inner lining.
• GERD also known as Acid Reflex.

Causes or Etiology :-

• Hital Hernia
• Obesity
• Zollinger Ellison Syndrome :-Hyper-secretion of gastric acid 
•  delayed gastric emptying
• delayed esophageal clearance
• Increases intra abdominal pressure
• Inappropriate relaxation of LES (lower esophageal sphincter) :- It is most common cause
• Reduce tone of LES (seen in scleroderma or systemic sclerosis)
• Food (Alcohol,caffine,tobacco,spicy food,fried food etc)

Clinical Feature :-

most common feature are:-

• Acidic taste in mouth
• Regurgitation (back flow)
• Heart burn

less common feature include :-

• pain with swollowing
• Short throat
• Increase salivation (water brash)
• Chest pain 
• Coughing
• Frequent bleching

GERD sometimes causes injury to the esophagus/ Complication :-

• Reflex esophagitis :- Inflammation of esophageal epithelium which can cause ulcers near the juction of stomach and esophagus
• Esophageal stryctures (narrowing) :-the persistent narrowing of the esophagus causes by reflex induced inflammation.
• Barredd's Esophagus :- Abnormal changes in the cells of the lower esophagus.
• Esophageal Adinocarcinoma :- A form of cancer.

Diagnosis :-

1. EGD :- Esophago Gastro Duedenoscopy:- visualization of the esophagus stomach and first part of small intestine.
2. Barium Swallow X-ray :- to assess the presence of esophageal strecture
3. Esophageal PH monitoring.

Medical management :-

•   Proton pump inhibitor
• H2 receptors antagonist
• Antacids
• Avoiding drugs like :- Aspirin,ibuprofen
• Avoiding of alcohol,tea,coffee etc.

Surgical Management :-

• Nissen Fundoplication :- In this procedure the upper part of the stomach is wrapped along the lower esophageal sphincter to strengthen the sphincter and prevent acid reflex.

Nursing Management :-

• Nursing management of GERD involves teaching the client to avoid situation that decrease lower esophageal sphincter pressure or cause esophageal irritation.

Nursing Intervention :-

• Monitor vital sign of the client.
• Assess abdomen for distention and intra abdominal pressure.
• Encourage the client to small frequent meals of high calories and high protein foods.
• Instruct the client remain upright position , at least two hours after meals and avoiding eating three hours before bed time.
• Instruct client to eat slowly and masticate food well.
• Advice to client to avoid spicy food and acidic food.
• Encourage the client to quit smoking and to loose weight if over weight.